Vision Realtors

Interpretation

The range is usually defined as the set of values 95 percent of the normal population falls within (that is, 95% prediction interval), or two standard deviations from the mean, although the definition may differ (see Definition of reference range). It is determined by collecting data from vast numbers of laboratory tests.

Plasma or whole blood

All values (except the exceptions below) denote blood plasma concentration, which is approximately 60-100% larger than the actual blood concentration if the amount inside red blood cells (RBCs) is negligible. The precise factor depends on hematocrit as well as amount inside RBCs. Exceptions are mainly those values that denote total blood concentration, and in this article they are:

All values in Hematology – red blood cells (except hemoglobin in plasma)

All values in Hematology – white blood cells

Platelet count (Plt)

A few values are for inside red blood cells only:

Vitamin B9 (Folic acid/Folate) in red blood cells

Mean corpuscular hemoglobin concentration (MCHC)

Units

Mass concentration (g/dL or g/L) is the most common measurement unit in the United States. Is usually given with dL (decilitres) as the denominator in the United States, and usually with L (litres) in, for example, Sweden.

Molar concentration (mol/L) is used to a higher degree in most of the rest of the world, including the United Kingdom and other parts of Europe and Australia and New Zealand.

International units (IU) are based on measured biological activity or effect, or for some substances, a specified equivalent mass.

Enzyme activity (kat) is commonly used for e.g. liver function tests like AST, ALT, LD and -GT in Sweden.

Arterial or venous

If not else specified, a reference range for a blood test is generally the venous range, as the standard process of obtaining a sample is by venipuncture. An exception is for acid-base and blood gases, which are generally given for arterial blood.

Still, the blood values are approximately equal between the arterial and venous sides for most substances, with the exception of acid-base, blood gases and drugs (used in therapeutic drug monitoring (TDM) assays). Arterial levels for drugs are generally higher than venous levels because of extraction while passing through tissues.

Inaccuracy

Main article: Reference range#Inaccuracy

References range will vary with age, sex, race, diet, use of prescribed or herbal drugs, stress and even the instruments used. The samples may deviate from normal distribution. Furthermore, reference ranges only denote what are usual values in the population, and do not directly correlate with the ranges for optimal health. In case of substantial difference, there may additionally be an optimal range specified for the substance. Finally, the test procedure itself may be erroneous or inaccurate.

Sorted by concentration

A separate printable combined image is available for mass and molarity

Smaller, narrower boxes indicate a more tight homeostatic regulation when measured as standard “usual” reference range.

By mass and molarity

Hormones predominate at the left part of the scale, shown with a red at ng/L or pmol/L, being in very low concentration. There appears to be the greatest cluster of substances in the yellow part (g/L or nmol/L), becoming sparser in the green part (mg/L or mol/L). However, there is another cluster containing many metabolic substances like cholesterol and glucose at the limit with the blue part (g/L or mmol/L).

To translate a substance from the molar to the mass concentration scale above:

Numerically: molar concentration x molar mass = mass concentration

Measured directly in distance on the scales:

, where distance is in number of decades or “octaves” to the right the mass concentration is found. To translate from mass to molar concentration, the dividend (molar mass and the divisor (1000) in the division change places, or, alternatively, distance to right is changed to distance to left. Substances with a molar mass around 1000g/mol (e.g. thyroxine) are almost vertically aligned in the mass and molar images. Adrenocorticotropic hormone, on the other hand, with a molar mass of 4540, is 0.7 decades to the right in the mass image. Substances with molar mass below 1000g/mol (e.g. electrolytes and metabolites) would have “negative” distance, that is, masses deviating to the left.

Many substances given in mass concentration are not given in molar amount because they haven’t been added to the article.

By units

Units don’t necessarily tell anything about molarity or mass.

A few substances are below this main interval, e.g. thyroid stimulating hormone, being measured in mU/L, or above, like rheumatoid factor and CA19-9, being measured in U/mL.

By enzyme activity

White blood cells

Clinical biochemistry

Clinical chemistry (also known as “clinical biochemistry”, “chemical pathology” or “pure blood chemistry”) is the area of pathology that is generally concerned with analysis of bodily fluids.

Electrolytes and Metabolites

Electrolytes and Metabolites: For iron and copper, some related proteins are also included.

Test
Patient type

Lower limit
Upper limit

Unit

Comments

Sodium (Na)

135, 137

145, 147

mmol/L or mEq/L

31 , 32

33 , 34

mg/dl

Potassium (K)

3.5 , 3.6

5.0 , 5.1

mmol/L or mEq/L

See hypokalemia or hyperkalemia

14

20

mg/dl

Chloride (Cl)

95, 98, 100

105, 106, 110

mmol/L or mEq/L

340

370

mg/dl

Osmolality

275, 280, 281

295, 296, 297

mOsm/kg

Plasma weight excludes solutes

Osmolarity

Slightly less than osmolality

mOsm/l

Plasma volume includes solutes

Urea

1.2, 3.0

3.0, 7.0

mmol/L

BUN – blood urea nitrogen

7

18, 21

mg/dL

* Uric acid

0.18

0.48

mmol/L

Female

2.0

7.0

mg/dL

Male

2.1
8.5

mg/dL

Creatinine

male

60 , 68

90 , 118

mol/L

May be complemented with creatinine clearance

0.7 , 0.8

1.0 , 1.3

mg/dL

female

50 , 68

90 , 98

mol/L

0.6 , 0.8

1.0 , 1.1

mg/dL

BUN/Creatinine Ratio

5

35

-

Plasma glucose (fasting)

3.8 , 4.0

6.0 , 6.1

mmol/L

See also glycosylated hemoglobin (in hematology)

65, 70, 72

100, 110

mg/dL

Full blood glucose (fasting)

3.3

5.6

mmol/L

60

100

mg/dL

Total serum iron (TSI)

male

65, 76

176, 198

g/dL

11.6 , 13.6

30, 32, 35

mol/L

female

26, 50

170

g/dL

4.6 , 8.9

30.4

mol/L

newborns

100

250

g/dL

18

45

mol/L

children

50

120

g/dL

9

21

mol/L

Total iron-binding capacity (TIBC)

240, 262

450, 474

g/dL

43 , 47

81 , 85

mol/L

Transferrin

190, 194, 204

326, 330, 360

mg/dL

25

45

mol/L

Transferrin saturation

20

50

 %

Ferritin

Male

12

300

ng/mL

27
670

pmol/L

Female

12

150

ng/mL

27
330

pmol/L

Ammonia

10, 20

35, 65

mol/L

17 , 34

60 , 110

g/dL

Copper

70

150

g/dL

11
24

mol/L

Ceruloplasmin

15

60

mg/dL

1
4

mol/L

Lactate (Venous)

4.5

19.8

mg/dL

0.5

2.2

mmol/L

Lactate (Arterial)

4.5

14.4

mg/dL

0.5

1.6

mmol/L

Pyruvate

300

900

g/dL

34
102

mol/L

Acid-base and blood gases

Further information: Acid-base homeostasis

Further information: Arterial blood gas

If arterial/venous is not specified for a acid-base or blood gas value, then it generally refers to arterial, and not venous which otherwise is standard.

Acid-base and blood gases are among the few blood constituents that exhibit substantial difference between arterial and venous values. Still, pH, bicarbonate and base excess show a high level of inter-method reliability between arterial and venous tests, so arterial and venous values are roughly equivalent for these.

Test

Arterial/Venous

Lower limit

Upper limit

Unit

Comments

pH

Arterial

7.34, 7.35

7.44, 7.45

Venous

7.31

7.41

[H+]

Arterial

36

44

nmol/L

3.6
4.4

ng/dL

Base excess

Arterial & venous

-3

+3

mEq/L

oxygen pressure (pO2)

Arterial

10 , 11

13 , 14

kPa

75, 83

100, 105

mmHg or torr

Venous

4.0

5.3

kPa

30

40

mmHg or torr

Oxygen saturation

Arterial

94, 95, 96

100

 %

Venous

Approximately 75

Carbon dioxide (CO2)

Arterial

4.4, 4.7

5.9 , 6.0

kPa

Designated pCO2

33, 35

44, 45

mmHg or torr

23

30

mmol/L

100

132

mg/dL

Venous

5.5

6.8

kPa

41

51

mmHg or torr

Bicarbonate (HCO3, )

Arterial & venous

18

23

mmol/L

110

140

mg/dL

Standard bicarbonate (SBCe)

Arterial & venous

21-22

27-28

mmol/L or mEq/L

134

170

mg/dL

Liver function

Further information: Liver function tests

Test

Patient type

Lower limit

Upper limit

Unit

Comments

Total Protein

60, 63

78, 82, 84

g/L

see hypoproteinemia

Albumin

35

48, 55

g/L

see hypoalbuminemia

3.5

4.8, 5.5

U/L

540

740

mol/L

Globulins

23

35

g/L

Total Bilirubin

1.7, 2, 3.4, 5

17, 22, 25

mol/L

0.1, 0.2, 0.29

1.0, 1.3, 1.4

mg/dL

Direct/Conjugated Bilirubin

0.0 or N/A

5 , 7

mol/L

0

0.3, 0.4

mg/dL

Alanine transaminase (ALT/ALAT)

1, 5, 7, 8

20, 21, 56

U/L

Also called serum glutamic pyruvic transaminase (SGPT)

Female

0.15

0.75

kat/L

Male

0.15

1.1

Aspartate transaminase (AST/ASAT)

Female

6

34

IU/L

Also called

serum glutamic oxaloacetic transaminase (SGOT)

0.25

0.60

kat/L

Male

8

40

IU/L

0.25

0.75

kat/L

Alkaline phosphatase (ALP)

Female

42

98

U/L

Male

53

128

(Enzyme activity)

0.6

1.8

kat/L

Gamma glutamyl transferase (GGT)

5 , 8

40, 78

U/L

Cardiac tests

Test

Lower limit

Upper limit

Unit

Comments

Creatine kinase (CK) – male

24, 38, 60

174 , 320

U/L

or ng/mL

Creatine kinase (CK) – female

24, 38, 96

140 , 200

CK-MB

0

3, 3.8, 5

ng/mL or g/L

Troponin Values 12 hrs after onset of pain:

Test

Lower limit

Upper limit

Unit

Comments

Troponin-T

0.02

ng/mL or g/L

Upper limit of normal

Troponin-I

0.2

ng/mL or g/L

Upper limit of normal

Troponin-T

0.02

0.10

ng/mL or g/L

Acute Coronary Syndrome

Troponin-I

0.2

1.00

ng/mL or g/L

Acute Coronary Syndrome

Troponin-T

0.10

n/a

ng/mL or g/L

Myocardial Infarction likely

Troponin-I

1.00

n/a

ng/mL or g/L

Myocardial Infarction likely

Other enzymes and proteins

Test

Lower limit

Upper limit

Unit

Comments

Lactate dehydrogenase (LDH)

50

150

U/L

0.4

1.7

mol/L

LDH (enzyme activity)

1.8

3.4

kat/L

< 70 years old

Amylase

25, 30, 53

110, 120, 123, 125, 190

U/L

0.15

1.1

kat/L

C-reactive protein (CRP)

n/a

5, 6

mg/L

200 , 240

nmol/L

D-dimer

n/a

500

ng/mL

Higher in pregnant women

0.5

mg/L

Lipase

7, 10, 23

60, 150, 208

U/L

Angiotensin-converting enzyme (ACE)

23

57

U/L

Acid phosphatase

3.0

ng/mL

Eosinophil cationic protein (ECP)

2.3

16

g/L

Other ions and trace metals

Further information: Trace metals

Test

Lower limit

Upper limit

Unit

Ionized calcium (Ca)

1.03 , 1.10

1.23 , 1.30

mmol/L

4.1 , 4.4

4.9 , 5.2

mg/dL

Total calcium (Ca)

2.1 , 2.2

2.5, 2.6, 2.8

mmol/L

8.4, 8.5

10.2, 10.5

mg/dL

Phosphate (HPO42)

0.8

1.5
mmol/L

Inorganic phosphorus (serum)

1.0

1.5

mmol/L

3.0

4.5

mg/dL

Copper (Cu)

11

24

mol/L

Zinc (Zn)

60 , 72

110 , 130

g/dL

9.2 , 11

17 , 20

mol/L

Magnesium

1.5 , 1.7

2.0 , 2.3

mEq/L or mg/dL

0.6 , 0.7

0.82 , 0.95

mmol/L

Selenium (optimal range)

120

g/L

Lipids

Further information: Blood lipids

Test

Patient type

Lower limit

Upper limit

Unit

Therapeutic target

Triglycerides

10 39 years

54

110

mg/dL

< 100 mg/dL

or 1.1 mmol/L

0.61

1.2
mmol/L

40 59 years

70

150

mg/dL

0.77

1.7

mmol/L

> 60 years

80

150

mg/dL

0.9

1.7

mmol/L

Total cholesterol

3.0 , 3.6

5.0, 6.5

mmol/L

< 3.9
120, 140

200, 250

mg/dL

< 150
HDL cholesterol

female

1.0, 1.2, 1.3

2.2

mmol/L

> 1.0 mmol/L
> 40 or 60 mg/dL

40 , 50

86

mg/dL

HDL cholesterol

male

0.9

2.0

mmol/L

35

80

mg/dL

LDL cholesterol

(Not valid when

triglycerides >5.0 mmol/L)

2.0, 2.4

3.0 , 3.4

mmol/L

< 2.5
80 , 94

120 , 130

mg/dL

< 100

LDL/HDL quotient

n/a

5

(unitless)

Tumour markers

Further information: Tumour markers

Test

Lower limit

Upper limit

Unit

Comments

Alpha fetoprotein (AFP)

0

44

ng/mL

Beta Human chorionic gonadotrophin (bHCG)

n/a

5

IU/l or mU/ml

in male and non-pregnant female

CA19-9

n/a

40

U/ml

CA-125

n/a

30 , 35

kU/L or U/mL

Carcinoembryonic antigen (CEA)

non-smokers at 50 years

n/a

3.4 , 3.6
g/l

Carcinoembryonic antigen (CEA)

non-smokers at 70 years

n/a

4.1

g/l

Carcinoembryonic antigen (CEA) – smokers

n/a

5

g/l

Prostate specific antigen (PSA)

n/a

2.5 , 4

g/L or ng/mL

below age 45 <2,5 g/L

PAP

0

3

units/dL (Bodansky units)

Thyroid hormones

Further information: Thyroid hormone

Test

Patient type

Lower limit

Upper limit

Unit

Thyroid stimulating hormone

(TSH or thyrotropin)

Adults -

standard range

0.3, 0.4, 0.5, 0.6

4.0, 4.5, 6.0

mIU/L or IU/mL

Adults -

optimal range

0.3 , 0.5

2.0 , 3.0

mIU/L or IU/mL

Infants

1.3

19

mIU/L or IU/mL

Free thyroxine (FT4)

Normal adult

0.7 ,0.8

1.4, 1.5

ng/dL

9, 10, 12
18 , 23

pmol/L

Infant 0-3 d

2.0

5.0

ng/dL

26

65

pmol/L

Infant 3-30 d

0.9

2.2

ng/dL

12

30

pmol/L

Child/Adolescent

31 d – 18 y

0.8

2.0

ng/dL

10

26

pmol/L

Pregnant

0.5

1.0

ng/dL

6.5

13

pmol/L

Total thyroxine

60

140, 160

nmol/L

4, 5.5

11, 12.3

g/dL

Free triiodothyronine (FT3)

Normal adult

0.2

0.5

ng/dL

3.1

7.7

pmol/L

Children 2-16 y

0.1

0.6

ng/dL

1.5

9.2

pmol/L

Total triiodothyronine

0.9 , 1.1

2.5 , 2.7

nmol/L

60, 75

175, 181

ng/dL

Thyroxine-binding globulin (TBG)

12

30

mg/L

Thyroglobulin (Tg)

1.5

30

pmol/L

1

20
g/L

Sex hormones

Further information: Sex steroid

Test

Patient type

Lower limit

Upper limit

Unit

Testosterone

Male, overall

8 , 10

27 , 35

nmol/L

230 , 300
780 – 1000

ng/dL

Male < 50 years

10

45

nmol/L

290

1300

ng/dL

Male > 50 years

6.2

26

nmol/L

180

740

ng/dL

Female

0.7

2.8 – 3.0

nmol/L

20

80 – 85

ng/dL

17 Hydroxyprogesterone

male

0.06

3.0

mg/L

Female (Follicular phase)

0.2

1.0

mg/L

Follicle-stimulating hormone (FSH)

Prepubertal

<1
3

IU/L

Adult male

1

8
Adult female (follicular

and luteal phase)

1

11

Adult female (Ovulation)

6

95% PI (standard)

26

95% PI)

5

90% PI (used in diagram)

15

(90% PI)

Post-menopausal female

30

118

Luteinizing hormone (LH)

Female, peak

20

90% PI (used in diagram)

75

(90% PI)

IU/L

Female, post-menopausal

15

60
Estradiol (an estrogen)

Adult male

50

200
pmol/L

1.4

5.5

ng/dL

Adult female (follicular phase, day 5)

70

95% PI (standard)

500
95% PI

pmol/L

110

90% PI (used in diagram)

220

90% PI

1.9 (95% PI)

14 (95% PI)

ng/dL

3.0 (90% PI)

6.0 (90% PI)

Adult female (preovulatory peak)

400

1500

pmol/L

11

41

ng/dL

Adult female (luteal phase)

70

600

pmol/L

1.9

16

ng/dL

Post-menopausal female

N/A
< 130

pmol/L

N/A

< 3.5

ng/dL

Progesterone

Female at day of ovulation

2.2 (90% PI)

9 (90% PI)

nmol/L

70 (90% PI)

280 (90% PI)

ng/dL

Androstenedione

Adult male and female

60

270

ng/dL

Post-menopausal female

< 180

Prepubertal

< 60

Other hormones

Further information: Hormones

Test

Patient type

Lower limit

Upper limit

Unit

Adrenocorticotropic hormone (ACTH)

4.4

18 ,22

pmol/L

20

80 , 100

pg/mL

Cortisol

09:00 am

140

700

nmol/L

5

25

g/dL

Midnight

80

350

nmol/L

2.9

13

g/dL

Growth hormone (fasting)

0

5

ng/mL

Growth hormone (arginine stimulation)

7

n/a

ng/mL

Prolactin

Female

n/a

20

ng/mL or g/L

Male

15

Parathyroid hormone (PTH)

10 , 17

65 , 70

pg/mL

1.1 , 1.8

6.9 , 7.5

pmol/L

25-hydroxycholecalciferol (a vitamin D)

-Standard reference range

8 , 9

40 , 80

ng/mL

20 , 23

95 , 150

nmol/L

25-hydroxycholecalciferol

-Therapeutic target range

30 , 40

65 , 100

ng/mL

85 , 100

120 , 160

nmol/L

Amino acids

Test

Sex

Age

Lower limit

Upper limit

Unit

Elevated

Therapeutic target

Homocysteine

Female

1219 years

3.3
7.2

mol/L

> 10.4 mol/L

or

> 140 g/dl

< 6.3 mol/L
or

< 85 g/dL

45

100

g/dL

>60 years

4.9
11.6
mol/L

66

160

g/dL

Male

1219 years

4.3
9.9
mol/L

> 11.4 mol/L

or

> 150 g/dL

60

130

g/dL

>60 years

5.9
15.3
mol/L

80

210

g/dL

Vitamins

Test

Patient type

Standard range

Unit

Optimal range

Lower limit

Upper limit

Lower limit

Upper limit

Vitamin A

30

65

g/dL

Vitamin B9

(Folic acid/Folate) – Serum

Age > 1year

3.0

16

ng/mL or g/L

5
6.8

36

nmol/l

11

Vitamin B9

(Folic acid/Folate) – Red blood cells

200

600

ng/mL or g/L

450

1400

nmol/L

Pregnant

ng/mL or g/L

400

nmol/L

900

Vitamin B12 (Cobalamin)

130 , 160

700 , 950

ng/L

100 , 120

520 , 700

pmol/L

Vitamin C (Ascorbic acid)

0.4

1.5

mg/dL

0.9

23

85

mol/L

50

25-hydroxycholecalciferol (a vitamin D)

8 , 9

40 , 80

ng/mL

30 , 40

65 , 100

20 , 23

95 , 150

nmol/L

85 , 100

120 , 160

Vitamin E

mol/L

28

mg/dL

1.2

Toxins

Test

Limit type

Limit

Unit

Lead

Optimal health range

< 20 or 40

g/dL

Ethanol

Limit for drunk driving

0, 0.2, 0.8

or g/L

17.4

mmol/L

Hematology

Hematology is the branch of biology (physiology), pathology, clinical laboratory, internal medicine, and pediatrics that is concerned with the study of blood, the blood-forming organs, and blood diseases.

Red blood cells

These values (except Hemoglobin in plasma) are for total blood and not only blood plasma.

Test

Patient

Lower limit

Upper limit

Unit

Comments

Haemoglobin (Hb)

male

2.0 , 2.1

2.5 , 2.7

mmol/L

Higher in neonates, lower in children.

130, 132, 135

162, 170, 175

g/L

female

1.8 , 1.9

2.3 , 2.5

mmol/L

Sex difference negligible until adulthood.

120
150, 152, 160

g/L

Hemoglobin in plasma

0.16

0.62

mol/L

Normally diminutive compared with inside red blood cells

1

4

mg/dL

Glycosylated hemoglobin (HbA1c)

< 50 years

3.6

5.0

 % of Hb

> 50 years

3.9

5.3

Haptoglobin

< 50 years

0.35

1.9

g/L

> 50 years

0.47

2.1

Haematocrit (Hct)

male

0.39, 0.4, 0.41, 0.45

0.50, 0.52,0.53 , 0.62

female

0.35, 0.36,0.37

0.46, 0.48

Child

0.31

0.43

Mean cell volume (MCV)

Male

76, 82

100, 102

fL

Cells are larger in neonates, though smaller in other children.

Female

78

101

fL

Red blood cell distribution width (RDW)

11.5

14.5

 %

Mean cell haemoglobin (MCH)

0.39

0.54

fmol/cell

25, 27

32, 33, 35

pg/cell

Mean corpuscular hemoglobin concentration (MCHC)

31, 32

35, 36

g/dL

4.8 , 5.0

5.4 , 5.6

mmol/L

Erythrocytes/Red blood cells (RBC)

male

4.2, 4.3

5.7, 5.9, 6.2, 6.9

x1012/L

Female

3.5, 3.8, 3.9

5.1, 5.5

x1012/L

Infant/Child

3.8

5.5

x1012/L

Reticulocytes

26

130

x109/L

Adult

0.5

1.5

 % of RBC

Newborn

1.1

4.5

 % of RBC

Infant

0.5

3.1

 % of RBC

White blood cells

These values are for total blood and not only blood plasma.

Test

Patient type

Lower limit

Upper limit

Unit

White Blood Cell Count (WBC.)

Adult

3.5, 3.9, 4.1, 4.5

9.0, 10.0, 10.9, 11

x109/L

x103/mm3 or

x103/L

Newborn

9

30

1 year old

6

18

Neutrophil granulocytes

(A.K.A. grans, polys, PMNs, or segs)

Adult

1.3, 1.8, 2

5.4, 7, 8

x109/L

45-54

62, 74

 % of WBC

Newborn

6

26

x109/L

Neutrophilic band forms

Adult

0.7

x109/L

3

5

 % of WBC

Lymphocytes

Adult

0.7 , 1.0

3.5, 3.9, 4.8

x109/L

16-25

33, 45

 % of WBC

Newborn

2

11

x109/L

Monocytes

Adult

0.1, 0.2

0.8

x109/L

3, 4.0

7, 10

 % of WBC

Newborn

0.4

3.1

x109/L

Mononuclear leukocytes

(Lymphocytes + monocytes)

Adult

1.5

5

x109/L

20

35

 % of WBC

CD4+ cells

Adult

0.4 , 0.5

1.5 , 1.8

x109/L

Eosinophil granulocytes

Adult

0.0, 0.04

0.44, 0.45, 0.5

x109/L

1

3, 7

 % of WBC

Newborn

0.02

0.85

x109/L

Basophil granulocytes

Adult

40

100, 200, 900

x106/L

0.0

0.75, 2

 % of WBC

Newborn

0.64
x109/L

Coagulation

Test

Lower limit

Upper limit

Unit

Comments

Platelet/Erythrocyte count (Plt)

140, 150

350, 400, 450

x109/L

Prothrombin time (PT)

10, 11, 12

13, 13.5, 14, 15

s

PT reference varies between laboratory kits – INR is standardised

INR

0.9

1.2

The INR is a corrected ratio of a patients PT to normal

Activated partial thromboplastin time (APTT)

18 , 30

28, 42, 45

s

Thrombin clotting time (TCT)

11

18

s

Fibrinogen

1.7, 2.0

3.6 , 4.2

g/L

Antithrombin

0.80

1.2

kIU/L

Bleeding time

2

9

minutes

Viscosity

1.5

1.72

cP

Immunology

Category

Test

Patient

Lower limit

Upper limit

Unit

Comments

Acute phase protein

markers of Inflammation

Erythrocyte sedimentation rate

(ESR)

Male

0

Age2

mm/hr

ESR increases with age and tends to be higher in females.

Female

(Age+10)2
C-reactive protein (CRP)

n/a

5, 6

mg/L

200 , 240

nmol/L

Alpha 1-antitrypsin (AAT)

20 , 22

38 , 53

mol/L

89 , 97

170 , 230

mg/dL

Immunoglobulins

IgA

Adult

70 , 110

360 , 560

mg/dL

IgD

0.5

3.0

IgE

0.01

0.04

IgG

800

1800

IgM

54

220

Autoantibodies

Antinuclear antibodies (ANA)

Extractable nuclear antigen (ENA)

Rheumatoid factor (RF)

0

20-30

IU/mL

High levels not specific for Rheumatoid Arthritis alone.

Serology

Antistreptolysin O titre

(ASOT)

Preschoolers

n/a

100

units/mL

School age

250

Adult

125

See also

Blood test

Cardiology diagnostic tests and procedures

Comprehensive metabolic panel

Medical technologist

Reference range

References

^ Page 34: Units of measurement in Medical toxicology By Richard C. Dart Edition: 3, illustrated Published by Lippincott Williams & Wilkins, 2004 ISBN 0781728452, 9780781728454 1914 pages

^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg ch ci cj ck cl cm cn co cp cq cr cs ct cu cv cw cx cy cz da db dc dd de df dg dh di dj dk dl dm dn do dp dq dr ds dt du dv dw dx dy Reference range list from Uppsala University Hospital (“Laborationslista”). Artnr 40284 Sj74a. Issued on April 22, 2008

^ a b c Arterial versus venous reference ranges – Brief Article Medical Laboratory Observer, April, 2000 by D. Robert Dufour

^ PROOPIOMELANOCORTIN; NCBI –> POMC Retrieved on September 28, 2009

^ a b c Unless else specified in boxes, then ref is: Ashwood, Edward R.; Tietz, Norbert W.; Burtis, Carl A. (1994). Tietz textbook of clinical chemistry (2nd ed.). Philadelphia: Saunders. ISBN 0-7216-4472-4. 

^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg ch ci cj ck cl cm cn co cp cq cr cs ct cu cv cw cx cy cz da db dc dd Last page of Deepak A. Rao; Le, Tao; Bhushan, Vikas (2007). First Aid for the USMLE Step 1 2008 (First Aid for the Usmle Step 1). McGraw-Hill Medical. ISBN 0-07-149868-0. 

^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg ch ci cj ck cl cm cn co cp cq cr cs ct cu cv cw cx cy cz da db dc Normal Reference Range Table from The University of Texas Southwestern Medical Center at Dallas. Used in Interactive Case Study Companion to Pathologic basis of disease.

^ a b c d Derived from molar values using molar mass of 22.99mol1

^ a b Derived from molar values using molar mass of 39.10mol1

^ a b c d e f g h i j k l m n MERCK MANUALS > Common Medical Tests > Blood Tests Last full review/revision February 2003

^ a b Derived from molar values using molar mass of 35.45mol1

^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by Blood Test Results – Normal Ranges Bloodbook.Com

^ a b Gardner MD, Scott R (April 1980). “Age- and sex-related reference ranges for eight plasma constituents derived from randomly selected adults in a Scottish new town”. J. Clin. Pathol. 33 (4): 3805. doi:10.1136/jcp.33.4.380. PMID 7400337. PMC 1146084. http://jcp.bmj.com/cgi/pmidlookup?view=long&pmid=7400337. 

^ a b c d Finney H, Newman DJ, Price CP (January 2000). “Adult reference ranges for serum cystatin C, creatinine and predicted creatinine clearance”. Ann. Clin. Biochem. 37 ( Pt 1): 4959. doi:10.1258/0004563001901524. PMID 10672373. http://acb.rsmjournals.com/cgi/pmidlookup?view=long&pmid=10672373. 

^ a b c d e f g h Derived from molar values by multiplying with the molar mass of 113.118 g/mol, and divided by 10.000 to adapt from g/L to mg/dL

^ a b MedlinePlus Encyclopedia Glucose tolerance test

^ a b c Derived from molar values using molar mass of 180g/mol

^ a b c d e f g h i j k Slon S (2006-09-22). “Serum Iron”. University of Illinois Medical Center. http://uimc.discoveryhospital.com/main.php?t=enc&id=1456. Retrieved 2006-07-06. 

^ a b c d Diagnostic Chemicals Limited > Serum Iron-SL Assay July 15, 2005

^ a b c d e f g h i j k l m Derived from mass values using molar mass of 55.85mol1

^ a b Table 1. Page 133. Clinical Chemistry 45, No. 1, 1999 (stating 1.93.3 g/L)

^ a b Derived by dividing mass values with molar mass

^ a b c d Ferritin by: Mark Levin, MD, Hematologist and Oncologist, Newark, NJ. Review provided by VeriMed Healthcare Network

^ a b c d Derived from mass values using molar mass of 450,000mol1

^ a b Mitchell ML, Filippone MD, Wozniak TF (August 2001). “Metastatic carcinomatous cirrhosis and hepatic hemosiderosis in a patient heterozygous for the H63D genotype”. Arch. Pathol. Lab. Med. 125 (8): 10847. PMID 11473464. http://journals.allenpress.com/jrnlserv/?request=get-abstract&issn=0003-9985&volume=125&page=1084. 

^ a b Diaz J, Tornel PL, Martinez P (July 1995). “Reference intervals for blood ammonia in healthy subjects, determined by microdiffusion”. Clin. Chem. 41 (7): 1048. PMID 7600690. 

^ a b c d Derived from molar values using molar mass of 17.03 g/mol

^ a b Derived from mass values using molar mass of 63.55mol1

^ a b Derived from mass using molar mass of 151kDa

^ a b c d Derived from mass values using molar mass of 90.08 g/mol

^ a b Derived from mass values using molar mass of 88.06 g/mol

^ Middleton P, Kelly AM, Brown J, Robertson M (August 2006). “Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate”. Emerg Med J 23 (8): 6224. doi:10.1136/emj.2006.035915. PMID 16858095. 

^ a b c d e f g h i j k l The Medical Education Division of the Brookside Associates–> ABG (Arterial Blood Gas) Retrieved on Dec 6, 2009

^ a b Derived from molar values using molar mass of 1.01mol1

^ a b c d e f g h Derived from mmHg values using 0.133322 kPa/mmHg

^ a b Derived from molar values using molar mass of 44.010 g/mol

^ a b c d Derived from molar values using molar mass of 61 g/mol

^ Reference range (albumin) at GPnotebook

^ a b Derived from mass using molecular weight of 65kD

^ a b c d e Derived from mass values using molar mass of 585g/mol

^ a b Derived from molar values using molar mass of 585g/mol

^ a b c d e f g h i j k l m n o p q r s Fachwrterbuch Kompakt Medizin E-D/D-E. Author: Fritz-Jrgen Nhring. Edition 2. Publisher:Elsevier, Urban&FischerVerlag, 2004. ISBN 3437151207, 9783437151200. Length: 1288 pages

^ a b c d GPnotebook > reference range (AST) Retrieved on Dec 7, 2009

^ a b Creatine kinase at GPnotebook

^ a b c d e f g h i j South London Healthcare NHS Trust

^ Reference range (amylase) at GPnotebook

^ a b C-reactive protein at GPnotebook

^ a b 2730 Serum C-Reactive Protein values in Diabetics with Periodontal Disease A.R. Choudhury, and S. Rahman, Birdem, Diabetic Association of Bangladesh, Dhaka, Bangladesh. (the diabetics were not used to determine the reference ranges)

^ a b c d Derived from mass using molar mass of 25,106 g/mol

^ Plasma Measurement of D-Dimer Levels for the Early Diagnosis of Ischemic Stroke Subtypes Walter Ageno, MD; Sergio Finazzi, MD; Luigi Steidl, MD; Maria Grazia Biotti, MD; Valentina Mera, MD; GianVico Melzi d’Eril, MD; Achille Venco, MD. Arch Intern Med. 2002;162:2589-2593.

^ Kline JA, Williams GW, Hernandez-Nino J (May 2005). “D-dimer concentrations in normal pregnancy: new diagnostic thresholds are needed”. Clinical chemistry 51 (5): 8259. doi:10.1373/clinchem.2004.044883. PMID 15764641. http://www.clinchem.org/cgi/content/full/51/5/825. 

^ a b Larsson L, Ohman S (November 1978). “Serum ionized calcium and corrected total calcium in borderline hyperparathyroidism”. Clin. Chem. 24 (11): 19625. PMID 709830. http://www.clinchem.org/cgi/pmidlookup?view=long&pmid=709830. 

^ a b c d Derived from molar values using molar mass of 40.08 mol1

^ a b c Derived from mass values using molar mass of 40.08 mol1

^ Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  Page 849

^ Reference range for copper at GPnotebook

^ a b http://www.dlolab.com/PDFs/DLO-OCTOBER-2008-LAB-UPDATE.pdf

^ a b Derived from molar values using molar mass of 65.38 g/mol

^ a b Derived from mass values using molar mass of 65.38 g/mol

^ a b Derived from molar values using molar mass of 24.31/mol

^ a b Derived from mass values using molar mass of 24.31/mol

^ a b c d e f g h i j k l m n o Adeva Nutritionals Canada > Optimal blood test values Retrieved on July 9, 2009

^ a b c d e f Derived from values in mg/dl to mmol/l, by dividing by 89, according to faqs.org: What are mg/dl and mmol/l? How to convert? Glucose? Cholesterol? Last Update July 21, 2009. Retrieved on July 21, 2009

^ a b c Derived from values in mg/dl to mmol/l, by dividing by 39, according to faqs.org: What are mg/dl and mmol/l? How to convert? Glucose? Cholesterol? Last Update July 21, 2009. Retrieved on July 21, 2009

^ a b c Reference range (cholesterol) at GPnotebook

^ a b c d e f g h Royal College of Pathologists of Australasia; Cholesterol (HDL and LDL) – plasma or serum Last Updated: Monday, 6 August 2007

^ What Your Cholesterol Levels Mean. American Heart Association. Retrieved on September 12, 2009

^ a b c d e f g h i Derived from values in mmol/l (to mg/dl), by multiplying by 39, according to faqs.org: What are mg/dl and mmol/l? How to convert? Glucose? Cholesterol? Last Update July 21, 2009. Retrieved on July 21, 2009

^ American Association for Clinical Chemistry; HDL Cholesterol

^ GP Notebook > range (reference, ca-125) Retrieved on Jan 5, 2009

^ ClinLab Navigator > Test Interpretations > CA-125 Retrieved on Jan 5, 2009

^ a b Bjerner J, Hgetveit A, Wold Akselberg K, et al. (June 2008). “Reference intervals for carcinoembryonic antigen (CEA), CA125, MUC1, Alfa-foeto-protein (AFP), neuron-specific enolase (NSE) and CA19.9 from the NORIP study”. Scandinavian journal of clinical and laboratory investigation 68: 112. doi:10.1080/00365510802126836. PMID 18609108. 

^ Carcinoembryonic Antigen(CEA) at MedicineNet

^ The TSH Reference Range Wars: What’s “Normal?”, Who is Wrong, Who is Right… By Mary Shomon, About.com. Updated: June 19, 2006. About.com Health’s Disease and Condition

^ a b 2006 Press releases: Thyroid Imbalance? Target Your Numbers Contacts: Bryan Campbell American] Association of Clinical Endocrinologists

^ a b The TSH Reference Range Wars: What’s “Normal?”, Who is Wrong, Who is Right… By Mary Shomon, About.com. Updated: June 19, 2006

^ a b Demers, Laurence M.; Carole A. Spencer (2002). “LMPG: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease”. National Academy of Clinical Biochemistry (USA). http://www.nacb.org/lmpg/thyroid_LMPG_PDF.stm. Retrieved 2007-04-13.  – see Section 2. Pre-analytic factors

^ a b c d e f g h i j Free T4; Thyroxine, Free; T4, Free UNC Health Care System

^ a b c d e f g h i j Derived from mass values using molar mass of 776.87 g/mol

^ a b c d e f g h i j k l m n o Table 4: Typical reference ranges for serum assays – Thyroid Disease Manager

^ a b c d Euthyroid Patient with Elevated Serum Free Thyroxine George van der Watt1,a, David Haarburger1 and Peter Berman

^ a b c d Derived from mass values using molar mass of 650.98 g/mol

^ a b Serum concentration of free T3, free T4 and TSH in healthy children Cioffi Michele; Gazzerro Patrizia; Vietri Maria Teresa; Magnetta Rosa; Durante Adriana; D’Auria Annamaria; Puca Giovanni Alfredo; Molinari Anna Maria ;

^ a b Andrology Australia: Your Health > Low Testosterone > Diagnosis

^ a b c d Derived from mass values using molar mass of 288.42g/mol

^ a b c d e f g Derived from molar values using molar mass of 288.42g/mol

^ a b c d MedlinePlus > Testosterone Update Date: 3/18/2008. Updated by: Elizabeth H. Holt, MD, PhD, Yale University. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director

^ a b c d e f g h i j reference range (FSH) GPnotebook. Retrieved on September 27, 2009

^ a b c d e f g h Values taken from day 1 after LH surge in: Establishment of detailed reference values for luteinizing hormone, follicle stimulating hormone, estradiol, and progesterone during different phases of the menstrual cycle on the Abbott ARCHITECT analyzer. Reto Stricker, Raphael Eberhart, Marie-Christine Chevailler, Frank A. Quinn, Paul Bischof and Rene Stricker. Clin Chem Lab Med 2006;44(7):883887 PMID: 16776638

^ a b c d e f New York Hospital Queens > Services and Facilities > Patient Testing > Pathology > New York Hospital Queens Diagnostic Laboratories > Test Directory > Reference Ranges Retrieved on Nov 8, 2009

^ a b c d e f g h i j GPNotebook – reference range (oestradiol) Retrieved on September 27, 2009

^ a b c d e f g h i j k l Derived from molar values using molar mass of 272.38g/mol

^ a b Derived from molar values using molar mass of 314.46 g/mol

^ a b Derived from mass values using molar mass of 4540g/mol according to PROOPIOMELANOCORTIN; NCBI –> POMC Retrieved on September 28, 2009

^ “Adrenocorticotropic Hormone:Normal”. WebMD. 09-03-2006. http://children.webmd.com/adrenocorticotropic-hormone?page=2. Retrieved 2008-11-09. 

^ Derived from molar values using molar mass of 4540g/mol according to PROOPIOMELANOCORTIN; NCBI –> POMC Retrieved on September 28, 2009

^ a b c d Biochemistry Reference Ranges at Good Hope Hospital Retrieved on Nov 8, 2009

^ a b c d Derived from molar values using molar mass of 362 g/mol

^ a b Derived from molar values using molar mass of 9.4 kDa

^ a b Table 2 in: Aloia JF, Feuerman M, Yeh JK (2006). “Reference range for serum parathyroid hormone”. Endocr Pract 12 (2): 13744. PMID 16690460. 

^ a b Derived from mass values using molar mass of 9.4 kDa

^ a b c d e f Derived from molar values using molar mass 400.6 g/mol

^ a b c d Bender, David A. (2003). “Vitamin D”. Nutritional biochemistry of the vitamins. Cambridge: Cambridge University Press. ISBN 0-521-80388-8. http://books.google.com.br/books?id=pxEJNs0IUo4C.  Retrieved December 10, 2008 through Google Book Search.

^ a b c d Bischoff-Ferrari, H.A., Dietrich, T., Orav, J.E., Hu, F.B., Zhang, Y., Karlson, E., Dawson-Hughes, B. 2004. Higher 25-hydroxyvitamin D levels are associated with better lower extremity function in both active and inactive adults 60+ years of age. American Journal of Clinical Nutrition. 80:752-758.

^ a b c d Reusch J, Ackermann H, Badenhoop K (May 2009). “Cyclic changes of vitamin D and PTH are primarily regulated by solar radiation: 5-year analysis of a German (50 degrees N) population”. Horm. Metab. Res. 41 (5): 4027. doi:10.1055/s-0028-1128131. PMID 19241329. 

^ a b c d e f g h Letter: Calcium and vitamin D in preventing fractures. Data are not sufficient to show inefficacy Alex Vasquez, researcher. BMJ 2005;331:108-109 (9 July), doi:10.1136/bmj.331.7508.108-b.

^ a b c d e f g h The Doctor’s Doctor: Homocysteine

^ a b c d e f g h Derived from molar values using molar massof 135 g/mol

^ a b c d e f Central Manchester University Hospitals –> Reference ranges Retrieved on July 9, 2009

^ University of Kentucky Chandler Medical Center > Clinical Lab Reference Range Guide Retrieved on April 28, 2009

^ a b c d e Derived from mass values using molar mass of 441 mol1

^ a b c d e f g GPnotebook > B12 Retrieved on April 28, 2009

^ a b Derived form molar values using molar mass of 1355g/mol

^ a b Derived from mass values using molar mass of 1355g/mol

^ a b Derived from mass values using molar mass of 176 grams per mol

^ a b c For Driving under the influence by country, see Drunk driving law by country

^ Derived from mass values using molar mass of 46g/mol

^ a b c d e Derived from mass values using 64,500 g/mol, according to Van Beekvelt MC, Colier WN, Wevers RA, Van Engelen BG (2001). “Performance of near-infrared spectroscopy in measuring local O2 consumption and blood flow in skeletal muscle”. J Appl Physiol 90 (2): 511519. PMID 11160049. 

^ a b c d Derived from mass concentration, using molar mass of 64,458 g/mol (Van Beekvelt MC, Colier WN, Wevers RA, Van Engelen BG (2001). “Performance of near-infrared spectroscopy in measuring local O2 consumption and blood flow in skeletal muscle”. J Appl Physiol 90 (2): 511519. PMID 11160049. ). 1 g/dL = 0.1551 mmol/L

^ a b c d e f g h lymphomation.org > Tests & Imaging > Labs > Complete Blood Count Retrieved on May 14, 2009

^ a b c d e f g h i j k l m n o p q r s t u Clinical Laboratory Medicine. By Kenneth D. McClatchey. Page 807.

^ Determination of monocyte count by hematological analyzers, manual method and flow cytometry in polish population Central European Journal of Immunology 1-2/2006. (Centr Eur J Immunol 2006; 31 (1-2): 1-5) authors: Elbieta Grska, Urszula Demkow, Roman Pikowski, Barbara Jakubczak, Dorota Matuszewicz, Jolanta Gawda, Wioletta Rzeszotarska, Maria Wsik,

^ a b MedlinePlus Encyclopedia 003652

^ a b Retrieved on November 20, 2009

^ a b Miller A, Green M, Robinson D (1983). “Simple rule for calculating normal erythrocyte sedimentation rate”. Br Med J (Clin Res Ed) 286 (6361): 266. doi:10.1136/bmj.286.6361.266. PMID 6402065. 

^ Bttiger LE, Svedberg CA (1967). “Normal erythrocyte sedimentation rate and age”. Br Med J 2 (5544): 857. doi:10.1136/bmj.2.5544.85. PMID 6020854. 

^ a b Sipahi T, Kara C, Tavil B, Inci A, Oksal A (March 2003). “Alpha-1 antitrypsin deficiency: an overlooked cause of late hemorrhagic disease of the newborn”. J. Pediatr. Hematol. Oncol. 25 (3): 2745. doi:10.1097/00043426-200303000-00019. PMID 12621252. http://www.jpho-online.com/pt/re/jpho/fulltext.00043426-200303000-00019.htm. 

^ a b Derived from mass values using molar mass of 44324.5 g/mol

^ a b Derived from molar values using molar mass of 44324.5 g/mol

^ a b c d e f g h i j The Society for American Clinical Laboratory Science > Chemistry Tests > Immunoglobulins Retrieved on Nov 26, 2009

External links

biochemical reference values at GPnotebook

Values at lymphomation.org

Descriptions at amarillomed.com

v  d  e

Medical test: Serology, reference range: blood tests

Clinical biochemistry

Metabolic panel

BMP: electrolytes (Na+/K+, Cl-/HCO3-)  renal function, BUN-to-creatinine ratio (BUN/Creatinine)  Glucose  Ca

CMP: BMP + protein tests (Human serum albumin, Serum total protein)  liver function tests (ALP, ALT, AST, Bilirubin)

derived values: Plasma osmolality  Serum osmolal gap

Acid-base homeostasis

Arterial blood gas  Base excess  Anion gap  CO2 content

Iron tests

Transferrin saturation = Serum iron / Total iron-binding capacity

Ferritin  Transferrin  Transferrin receptor

Blood sugar

Glucose test  Glucose tolerance test  Noninvasive glucose  C-peptide  Fructosamine  Glycated hemoglobin

Endocrine

ACTH stimulation test  Thyroid function tests

Cardiac marker

Troponin test  CPK-MB test  Glycogen phosphorylase isoenzyme BB

Other

Beutler test  Blood lipids  Tumor marker

Hematology/CBC

Clotting

Platelet count  Mean platelet volume  vWF: Ristocetin induced platelet agglutination

clotting factors: Prothrombin time  Partial thromboplastin time  Thrombin time

other/general coagulation: Bleeding time  animal enzyme (Reptilase time, Ecarin clotting time, Dilute Russell’s viper venom time)  Thromboelastography

fibrinolysis: Euglobulin lysis time  D-dimer

Red blood cell indices

Hematocrit  Hemoglobin  RBC count

ratios: Mean corpuscular hemoglobin  Mean corpuscular hemoglobin concentration  Mean corpuscular volume

Fetal hemoglobin: Apt-Downey test  Kleihauer-Betke test  Red blood cell distribution width

Reticulocyte index  Haptoglobin

Other

Blood film  Blood viscosity  Absolute neutrophil count

Immunology

Infections

viral infection: HIV (HIV test, BDNA test)  Epstein-Barr virus (Monospot test)

bacterial infection: syphilis (VDRL, Rapid plasma reagin, Wassermann test, FTA-ABS)  rickettsia (Weil-Felix test)  helicobacter (HelicoCARE direct)  streptococcus (Antistreptolysin O titre)

protozoan infection: toxoplasmosis (Sabin-Feldman dye test)

Inflammation

C-reactive protein  Erythrocyte sedimentation rate  MELISA  RAST test

see also reference ranges for blood tests

Categories: Blood tests

Due to insatiable demands, oil prices in the global market are continuously rising. In effect, gasoline prices in the local or domestic market are also high. Despite this, a good thing arises. Because of new technology, diesels are now more acceptable by the consuming public.

According to J.D. Power of J.D. Power and Associates, from today’s 3.2 percent share of first-time registrants, diesel will rise to make up 15 percent in the United States by 2015. One determinant of this prediction is Mercedes-Benz’s make up of three models, namely E-, ML- and GL-Class, which will have a 3.0-liter, turbocharged, six-cylinder diesel.

This strategy is not the first for Mercedes. Daimler-Benz AG, the owner of Mercedes-Benz has sold diesels in the US since 1960. During that period, a very significant 80 percent of its U.S. sales were diesels. However, gasoline prices were cheap then. Consequently, demand for diesels diminished so the company, in 1999, stopped selling them.

Mercedes returned back its commitment to diesel in 2004. And in 2008, the car brand will roll out its Blue Tec line of clean diesels. Glad to say, those power plants will be legal in all 50 states.

The new diesel has a particulate filter. Only low-sulfur fuel must be burned by the engine. The diesels really aim to help its customers as they will have a system that augments urea to the exhaust in 2008 to further clean up emissions. This, in effect, makes diesel engines as clean as gasoline engines.

This generation’s diesels really drive away diesel misinterpretation. Diesel’s image is noisy and smelly. But in the case of the 2007 Mercedes-Benz ML 320 CDI, the engine was not noisy, nor does it smell bad. You will experience something that sounds like a dragon under the hood only at start-up or initial throttle tip-in. This is what makes it different from a gasoline burner.

And because of the seven-speed transmission (a five-speed with two overdrives), the ML 320 CDI purrs at 65 mph and turns less than 2000 revolutions.

The 2007 Mercedes-Benz ML 320 CDI earned several praises when it was evaluated for two weeks. It does not have a low range. Rather, it has hill-descent control and an air-ride suspension that helps remove obstacles on the road.

Benz, which comes with Mercedes relays, charges ,000 for the diesel. This is a small amount to forego I return for an efficient performance, cleaner exhausts, and an effective alternative for gasoline.

In the competitive environment of San Diego Real Estate corporation where tasting victory can be a difficult feat to attain, depending on the Proper medium for delivery of a message is quite integral to experience triumph. With technology being constantly enhanced to New realms, Reality Businesses and San Diego Realtors are utilizing this chance to promote themselves efficiently. With the Proper advertising tool on hand marketing Premises might Obtain fairly straightforward besides reducing costs significantly.

One of the direct lines of communication towards prospective clientele is Through organization cards. For a San Diego Real Estate agent carrying a professional corporation card might support matters immensely as it is one most successful advertising medium accessible. Well designed business cards can provide you every information you need to have besides, it also forms an impression with the consumer that will stay with him/her for as long as the card is with them. Other than company cards, Magnetic signs are ever so popular among San Diego Realtors and estate agents as they may be stuck almost wherever. The perfect part concerning them is that they could be readily noticed and are quite versatile in nature. But what makes this advertising medium so effective is it is eye catching. They could go onto almost anything and interestingly can be removed at any given moment. This feature comes in handy specifically when you really don’t want to promote.

Most time’s, San Diego Real Estate investors are on the move as Asset locations tend to differ among each other. generating usage of this advantage could be an ingenious thought. The very best way to do it is Through side walk signs. They are just the Right size, not so extravagant in fact more practical. Not only do you reach the average Asset customer you also let them know about your organization or your Property status.

On the extreme side, you could also adopt vinyl banners to accomplish Tremendous exposure without incurring much of an expense. Besides you may precisely identify the exact size that you might be comfortable with. Vinyl banners also offer the chance of brilliant paint jobs therefore you might now present your message in a colorful way. With San Diego Realtors jostling for the top spot in the San Diego Real Estate market, advertising is a key medium which allows you to present and market yourself in an successful manner.

Have you been thinking about investing in real estate but weren’t sure whether or not it was worth the time, effort, and money to do so? The truth is that there are quite a few benefits to be gained from realestate investment Here are a few of the biggest benefits of all.

1. Owning property raises your credibility, your credit rating, and your equity portfolio by a substantial margin. People are more inclined to trust and want to do business with property owners and, if you make your property payments on time every month, your credit score will shoot through the roof.

2. Unlike other types of property, realestate investments usually only appreciate as time passes on. Look at the housing market. The cost of housing today is more than four times what it was as little as two decades ago. A lot of real estate moguls got their start by a realestate investment technique called “house flipping.”

3. There is more leverage allowed with realestate investment than with other types of investments. Real estate property owners are allowed to borrow against the value of their properties while other types of property owners are not. Think about it: how many banks allow you to put up your stereo system as collateral for a loan?

4. Two words: tax benefits. Realestate investment experts will tell you that the tax advantages involved in owning real estate property far outweigh any initial cost in purchasing the property. Home owners are given a wide array of tax incentives and credits every year!

These are just four of the most important benefits of realestate investment Many people are afraid of investing in real estate because the initial cost (and risk) is so large. The experts will tell you, though, that the many benefits far outweigh the expenses!

When it comes to remodeling your home, no remodeling task is quite as daunting as the kitchen. The kitchen, according to most realtors, is the most important room in the house and can singlehandedly determine whether you get a good offer on your home if you decide to sell it. The cabinets are of obvious importance to the kitchen because they are prominently featured in most kitchens. So, when remodeling your kitchen, it makes sense to think primarily of the cabinets. Cabinet refacing in San Francisco is one of the best ways to remodel your kitchen. The subsequent paragraphs will summarize everything you need to know about cabinet refacing in San Francisco.

Cabinet refacing in San Francisco is a process where existing cabinets are redone with a new coating such as laminate, thermo-foil, or wood veneer. It typically involves replacing the cabinet doors and the drawer fronts. In essence, you are getting a completely new look to your cabinets without having to complete tear them out and replace them.

Cost savings of cabinet refacing in San Francisco can be upwards of 60 percent when compared to the cost of buying new cabinets. To summarize, it is a practical, economical, and relatively easy way to enhance the appearance of your kitchen.

You will also be interested in the types of coating used in cabinet refacing in San Francisco. As mentioned earlier, the three most common types of coating used in cabinet refacing are wood veneer, laminate, and thermo-foil.

Wood veneer is a thin slice of wood cut from a log with a machine. The slice will be applied to the surface to give the cabinets a wood grain appearance. You have many options when looking at wood veneer. For example, you can find a style of wood veneer that matches your wood floors. To make the wisest selection, it would be a good idea to talk with an expert on cabinet refacing in San Francisco.

Laminate is the cheapest coating material used in cabinet refacing. It is made of plastic film. It is cheap because it isn’t as visually appealing as the other options, but it is very durable.

With wood veneer being the most expensive and laminate being the cheapest, thermo-foil falls somewhere in between. It is a relatively new coating material and is being heralded as revolutionary for those that work with cabinets. It has a thick vinyl film that is bonded permanently to a wood core that is not subject to warping.

The last thing to know about cabinet refacing is how it’s actually done. The process of refacing requires the existing cabinet doors and drawer fronts to be disassembled from the existing structure. Afterwards, you need to install the new cabinet doors and drawer fronts in place of the old ones.

This is a very basic explanation of how the cabinet refacing will take place. To get the best idea of how to do it and what to look for, consult a professional that has experience with cabinet refacing in San Francisco. He or she can help you with selection of materials and with the actual installation.
Cabinet Refacing San Francisco

Authors:Bhurgri Ghulam Rasool,Momina Taki Muhammad,Shamim-Ur-Rehman,ShahMurad,RajKumar Chohan,DahriGhulam Mustafa, Shaikh zulfikar,

INTRODUCTION:

TUBERCULOSIS:

Tuberculosis, one of the oldest diseases known to affect human, is caused by bacteria belonging to mycobacterium tuberculosis complex. The disease usually affects the lungs, although in up to one third of cases other organs are involved. If properly treated, tuberculosis caused by drug susceptible strains is curable in virtually all cases. If untreated, the disease may be fatal within 5 years in more than half of cases. Transmission usually takes place through airborne spread of droplet nuclei produced by patients with infectious pulmonary tuberculosis (Mario C Raviglione, Richard JO Brein, 2003).

Tuberculosis is a disease of great antiquity. Today, tuberculosis gas become the most important communicable disease in the world, with over 8 millions cases of pulmonary tuberculosis occurring each year 95% which are in developing countries (A Gordon Leitch, 2000).

Tuberculosis is chronic granulomatous disease of human and other mammals caused by a group of closely related obligate pathogens, the mycobacterium tuberculosis complex, and comprising M. tuberculosis. The human tubercle bacillus – M. bovis – the bovine tubercle bacillus, -agricanum – a heterogeneous type found principally in effuational Africa with properties intermediate between the former two species and M-microti-a rare cause of disease involves and other small mammals but attenuated for humans. (PDO D awis et al, 2003).

Annual risk of infection

Areas

Current

Level

Annual decline

Trend (%)

Health resource

Availability

Industrialized

0.04-0.1

>10

Excellent

Middle income Latin America

West Asia

0.5-1.5

5-10

Good

Middle income East and South

Eest Asia

1.0-2.5

<5

Good

Sub-Saharan Africa

Indian Subcontinent

1.0-2.5

0-3

Poor

                                                                                                                                (A Gordon Leitch, 2000)

In 1994 World Health Organization (WHO) declared that tuberculosis (TB) constituted a global emergency. It developed a five point strategy known as direct observe treatment strategy (DOTS) in order to combat the increasing incidence of the disease. The main aim was to detect 70% of smear positive tuberculosis (TB) cases and to treat85% of smear positive new cases successfully. This strategy has improved worldwide cure rates. Tuberculosis is an increasingly important cause of morbidity and mortality in refugees and displaced populations, particularly during the post acute phase of complex emergencies (Alison H Rodger et al., 2002).

EPIDEMIOLOGY:

In Pakistan, only limited data is available, however, the prevalence of tuberculosis is estimated to be as high as 250,000 cases annually. According to official estimates, the rate of open bacillary cases among adult population (15 years and above), was 17% and among children 5 to 9 years of age, 13% were infected with tuberculosis. It is thought to be the fourth major cause of all deaths in Pakistan (Shamim A Qazi et al., 1998).

PATHOLOGY OF TUBERCULOSIS:

CASE WITH INFECTOUS TUBERCULOSIS

Cough and generate droplet nuclei which are ingaled by a contact

Primary

Onset of CMI response

Bacillimia                                                   Apical Implant

Sterilization of the primary complex

Immunosuppressive event

Multiple of tubercle bacilli

Restoration of CMI

Caseation of necrosis

        Infectous tuberculosis

Figure: Schematic representation of the basic events in the pathogenesis of tuberculosis.

CMI: Cell mediated immune.

(VB Balasurbramanian et al., 1994).

DRUG TREATMENT OF TUBERCULOSIS

Tuberculosis is among the top ten cause of global mortality and affects low icome countries in particular. The treatment of smear positive tuberculosis using World Health Organizzation (WHO) directly  observed treatment, short course, Direct observe treatment strategy (DOTS) has far highest impact while BC immunization recuces childhood tuberculosis mortality (Martien W Borgdorff et al.m 2002).

Drugs used in the treatment of tuberculosis can be divided into two major categories. First line after combined the greatest level of efficacy with unacceptable degree of toxicity. These include isoniazid, rifampin, ethambutol, streptomycin and pyrazinamide. Excellent results for patients with non drug resistant tuberculosis can be treated with 6 month course of treatment, for the first 2 months, isoniazid, rifampin and pyrazinamide are given, followed by isoniazid and rifampin for remaining 4 months (William A Petri Jr, 2001).

RIFAMPIN

Rifampin is a semisynthetic broad spectrum bactericidal antibiotic derived from streptomyces mediaterani.The introduction of this antibiotic that permitted the development of the first effective short course of 9 month chemotherapy for tuberculosis.

It is an addition of antituberculosis activity, it has wide range of activity against other bacteria including staphylococcus, Streptococcus, Clostridium, Coliforms, Pseudomonas, Proteus,Shigella and Legionella. Rifampin is almost completely absorbed from gastrointestinal tract after an oral dose. When it is taken is an empty stomach the plasma levels of 6-7 ug/ml are reached at 3 hours and its half-life of about 5 hours (A Gordon Leitch, 2000).

Adverse effects:

Rifampin dependent antibodies are considered responsible for most of immunological side effects in which hepatotoxicity, thrombocytopenia and allergic reactions are important (Mehta YS et al., 1996). Rifampin causes anorexia, nausea, vomiting, diarrhea, fever, dizziness, bone pain, shortness of breath, urine and saliva are colored orange red (Cheema MA, 2000).

ISONIAZID

Since its  introduction in 1952 isoniazid has been widely recognized as a safe and effective chemotherapeutic agent against tuberculosis. Numerous studies of isoniazid in combination with other tuberculous drugs have repeatedly demonstrated its therapeutic efficacy (Richard et al.,1972).

Isoniazid is the most widely used antituberculosis agent. It is an ideal in many aspects, being bactericidal, relatively non-toxic easily administered and inexpensive. It is readily absorbed from the gastrointestinal tract, with peak concentration of approximately 5ug/ml occurring about 2 hour after administration. It penetrates to all tissues including cerebrospinal fluids (C.S.F.) some part of drug excreted in urine in unchanged form but proportion is acetylated by hepatic acetyl transferase to an inactive form. Drug is usually given orally with combination of rifampin and pyrazinamide are available (A Gordon Leitch, 2000). Isoniazid is still most important drug world wide for the treatment of all types of tuberculosis. The commonly usual dose is 10-50 mg/kg/day with maximum of 300 mg (William A Petri Jr, 2001).

The incidence of adverse effects of isoniazid are skin rash, fever , jaundice hypersensitivity to isoniazid may result in fever, various skin eruption occurs (William A Petri Jr, 2001).

Isoniazid preventive therapy is contraindicated in persons with chronic active hepatitis should be given caution to person who consumes alcohol daily (M Suess, 1994).

ETHAMBUTOL

Ethambutol is a synthetic, water soluble, heat stable compound. Susceptible strains of Mycobacterium tuberculosis and other mycobacteria are inhibited in vitro by ethambutol. Ethambutol is an ingibitor of mycobacterial arabinosyl transferases, which are encoded by the embCAB operon. Arabinosy1 transferases are involved in the polymerization reaction of arbinoglycan, an essential component of the mycobacterial cell wall (Henry FC, 2001). It is rapidly absorbed from intestine. It is excreted in urine. It should not be given in renal disease (MA Cheema, 2000). The most important side effect is optic neuritis, resulting decrease of visual acuity and loss of ability to differentiate red from green (William A Petri Jr, 2001).

Hypersensitivity to ethambutol is rare. The most common serious adverse event is retrobulbar neuritis causing loss of visual acuity and red green color blindness. The dose related side effect is more likely to occur at a dosage of 25 mg/kg/day continued for several months. The peripheral neuropathy owing to demyelinization. Other less common adverse effects include gastrointestinal intolerance, hyperurecemia, and hypersensitivity reactions including rash, and rarely thrombocytopenia. It is safe during pregnancy with no known teratological effects (Edwards D,Chan,2003).

PYRAZINAMIDE

Pyrazinamide is bactericidal in an acid environment and as sterilizing effect on intracellular mycobacteria. It is well absorbed from gastrointestinal tract, with peak concentration of about 50ug/mloccurring 1.5-2 gour after ingestion. It penetrates well into tissues including cerebrospinal fluid (A Gordon Leitch, 2000).

Pyrazinamide is synthetic orally effective bactericidal ant tubercular agent used along with isoniazid and rifampin (William A Petri Jr, 2001).

The reasons for this increased incidence of hepatotoxicity reactions in developing countries are unclear, Perhaps poor nutrition, increased age, wide spread parasitism, chronic infections, indiscriminate use of various drugs without prescription may play a role individually or collectively (H Turktas et al.,1994).

Gastrointestinal reactions, cutaneous reactions, sidiroblastic anemia (A Harries, 2003). Moreover pyrazinamide is considered to be significantly less hepatotoxic than isoniazid and rifampin. Less common adverse reactions to pyrazinamide include rhabdomyolysis with myoglobinuric renal failure, gouty arthritis, photosensitivity, maculopapular raxh, thrombocytopenia, increased serum iron, urticaria, and other hypersinsitivity reactions (Edward DE Ehan et al., 2004).

STREPTOMYCIN

Streptomycin is tuberculocidal, but less effective than isoniazid or rifampin, acts only on extracellular bacilli (because of poor penetration into cells). Thus, host defense mechanisms are needed to eradicate the disease. It penetrates tubercular cavities, but does not cross to the cerebrospinal fluid (CSF), and has poor action in acidic medium. Resistance developed rapidly when streptomycin was used alone in tuberculosis most patients had a relapse (Tripathi, 2003). Streptomycin is bactericidal for tubercle bacillus in vitro. Concentration as low as 0.4 mg/ml may inhibit the growth. Vast majority of strains of mycobacterium tuberculosis are sensitive to 10mg/ml (William A Petri Jr, 2001)

Untoward effects include rash and fever, auditory and vestibular function of eighth cranial nerve is affected (William A Petri Jr, 2001).

BCG

Unfortunately, the protective efficacy of BCG, the most widely used vaccine against pulmonary tuberculosis varies from 0% to 80%. BCG gives good protection (75-80%) against disseminated tuberculosis includes tuberculous meningitis, in childhood, BCG is given at birth or as soon as possible, therefore after and although the duration of protection is uncertain, it may not be longer than 15 years, this limiting protection against infectious pulmonary tuberculosis, which may occur mainly in adults (Martein W Borgdorff et al., 2002).

Today over, 70 years of BCG development, it is still the only tuberculosis vaccine availed, and the achievements of tuberculosis vaccine research have been largely operational, such as expanding delivery of BCG through the expanded programe on immunization and holding field trials in different geographical locations (Ann M Ginberg,2002).

MATERIAL AND METHODS

This study was carried out in the department of Pharmacology and Therapeutics, Basic Medical Sciences Institute (BMSI), Jinnah Postgraduate Medical Centre, Karachi, from January 2005 to June 2005.

The 100 newly diagnosed patients of pulmonary tuberculosis, enrolled is this study after taking informed and written consent.

The patients were selected as diagnosed cases of pulmonary tuberculosis from medical chest OPD and chest ward of Jinnah Postgraduate Medical Center, Karachi. Out of these 97 patients were associated through out the study period. Out of remaining three have not come for follow up.

                                     

All patients, in this study, were selected according to following criteria:

INCLUSION CRITERIA:

Diagnosed cases of pulmonary tuberculosis.
Age between 2o to 70 years.
Sex either male or female.

EXCLUSION CRITERIA:

Patients suffering from liver disease.
Patients suffering from cardiac disease.
Patients suffering from renal disease.
Patients suffering from diabetes mellitus.
Patients suffering from other respiratory disease.
Patients suffering from HIV infections.
Pregnant or nursing women.
Patients with previous multiple drug resistance.

The study period extended up to 24 weeks and 12 follow up visits of patients were taken. The required information such as name, age, sex, occupation, address, details of follow up visits and laboratory investigations etc, of each patients were recorded on proforma especially designed for this study.

The selected patients were divided according to untoward effects of drugs during study period.

Group1:                 In this group those patients were included who manifested the hepatitis in different age groups

Group2:                 In this group those patients were included who manifested the peripheral neuropathy inh defferent age groups

Group3:                 In this group those patients were included who manifested the skin rashes in different age groups

Group4:                 In this group those patients were included who manifested the joint pain in different age group

Group5:                 In this group those patients were included who manifested the optic neuritis in different age group

Group6:                 In this group those patients were included who manifested the thrombocytopenia in different age group

Group7:                 In this group those patients were included who manifested the nephrotoxicity in different age group

Group 8:                In this group those patients were included who manifested the ototoxicity in different age group

MATERIALS

Isoniazid—adult 5 mg/kg -maximum 300 mg
Rifampin—-adult 10 mg/kg -maximum 450 mg
pyrazinamide 15-30 mg/kg
Ethambutol 15-25 mg/kg-maximum 300 mg
Streptomycin — 15 mg/kg – maximum 1 gm
Disposable syringes.
C.P. bottles.
Kits for the liver function test, measurement of urea, creatinine

Ninety seven patients were studied after medications with anti tuberculosis therapy and divided in eight groups after the manifestation of untoward effects of therapy.

The observations of all the treatment groups were recorded on day 0, day 30 and day 80.

Table 1 and figure 1 show hepatitis after taking the anti tuberculosis drugs. The hepatitis was manifested more in combined therapy during medication of pulmonary tuberculosis. The hepatitis found significant different with p < 0.01 among anti tuberculosis therapy. Out of 97 patients, there were 15 patients were affected by this untoward effect. The highest proportion of hepatitis in isoniazid (10.3%) followed by pyrazinamide (3.1%) and rifampin (2.1%

 The hepatitis in different age groups. The decade between 20-29 of age has shown maximum number of hepatitis (5.1 & followed by the extreme age 60-69 years (P<0.05), keeping the high proportion of isoniazid as compared to pyrazinamice (1.03%) and rifampin (2.06%) in different age groups. Isoniazid manifested 4 cases of hepatitis in age group 20-29 years, pyrazinamide 1 respectively. Four patients produced hepatitis in age between 60 to 69. Pyrazinamide produced hepatitis in age between 60 to 69. Pyrazinamide produced hepatitis (2.66%). INH and rifampin affected with equal percentage (1.03%). Two patients were produced hepatitis in age between 30-39 years. The INH and rifampin affected with equal (1.03%) in this age group respectively. It was non significant statistically. One patient was affected by isoniazid in the age group of 50-59 years. It was non significant statistically

 The peripheral neuropathy in 25 patients out of 97 patients. The isoniazid produced more peripheral neuropathy than other causative drugs. The isoniazid affected 11.3% patients. The pyrazinamide and ethambutol produced the peripheral neuropathy in same percentage (7.2%). It was non significant statistically.

The peripheral neuropathy in different age groups. The age between 60 and above was more affected than other age groups. Isoniazid produced 602% peripheral neuropathy in this age group. Ethambutol produced 1.03% peripheral neuropathy. The age group between 20-29 developed peripheral neuropathy by isoniazid 301%, pyrazinamide 2.01% and ethambutol 1.03% respectively. The total patients were 6 with this age group. The age between 30-39 manifested peripheral neuropathy by isoniazid 1.03% and ethambutol 1.03% respectively. The age between 40-49 was affected by peripheral neuropathy by pyrazinamide 3.1% and ethambutol 3.1%                                                                                                  

Therapy produced, 3 patients, thrombocytopenia. The rifampin produced thrombocytopenia in 3.1% males.

 Thrombocytopenia according to age groups. The combined therapy affected in age between 40-49, 1.03%, 50-59, 1.03% and 60 and above 1.03% respectively. The rifampin produced this side effects with same percentages i.e. 1.03% in age groups 40-49, 50-59 and above.

            Table 10 and figure 10 show the joint pain as an adverse effect of anti tuberculosis drugs. The combined therapy affected 8 patients out of 97. pyrazinamide produced joint pain in 8.24% patients.

Table 12 and figure 12 show the joint pain according to age groups. The pyrazinamide affected 3.09% in age between 60 and above, 2.06% in age between 20-29 and 1.03% in further age groups respectively.

 The optic neuritis. The combined therapy produced optic neuritis in 7 patients out of 97. ethambutol produced 7.2% optic neuritis

 The optic neuritis according to age groups. The combined therapy produced the optic neuritis in 3 in 6o to69, 2 in 50-59 and one in 30-39 and 40-49 years respectively. The ethambutol produced the optic neuritis in 3.09 in age between 60-69, 2.06% in 50-59 and 1.03% in 40-49 and 30-39 tears.

 Skin rashes as an adverse effect of anti tuberculosis drugs. The skin rashes found significant (P<0.01) by combined therapy. The combined therapy produced skin rashes in 6 patients out of 91 patients. The pyrazinamide produced skin rashes (4.12%) and rifampin produced 2.1% respectively.

Skin rashes in age groups. The combined therapy produced skin rashes in 2 from 20-29 years age group, 1 from 40-49 years, 1 from 60-69 respectively. The pyrazinamide produced skin rashes 2.06% in age between 20-29 years, 1.03% in 50-59 years, 1.03% in 60-69 years age group, 1.03% in 50-59 years respective

 Nephrotoicity as an adverse effect. Streptocomycin was main drug to manifest the nephrotoxicity in combined therapy during treatment of pulmonary tuberculosis in combined therapy during treatment of pulmonary tuberculosis patients. Out 97 patients, there were 3 reactions documented in this study.   Nephrotoxicity in gender after taking the anti tuberculosis drugs. Two males and one female was affected during the study

The nephrotoxicity in different age group. In the age group 30-39 1, 40-49 1, and 50-59 1 reaction was documented in this study.

 The ototoxicity after taking anti tuberculosis drugs. There were 2 reactions recorded in this study.

Adverse effect

Pyrazinamide

Isoniazid

Ethambutol

Rifampin

Streptomycin

Total

%

95% CI

Peripheral neuropathy

7 (7.2%)

11 (11.3%)

7 (7.2%)

-

-

25

25.8

17.80-35.1

Hepatitis

3 (3.1%)

10 (10.3%)

-

2 (2.1%)

-

15

15.5

9.2-23.7

Joint pain

8 (8.2%)

-

-

-

-

8

8.20

3.9-15.0

Optic neuritis

-

-

7 (7.2%)

-

-

7

7.20

3.2-13.7

Skin rashes

4 (4.2%)

-

-

2 (2.1%)

-

6

6.20

2.5-12.4

Table show overall side effects of ATT in this study.

FIGURES:

Overall Frequency of Adverse Effect

(n=69)

DISCUSSION:

This study observed the untoward the untoward effects of antituberculous drugs in pulmonary tuberculosis patients. The selected patients were divided into two groups according to the age and sex. In this study the following reaction i.e., hepatitis, peripheral neuropathy, thrombocytopenia, joint pain, optic neuritis, ototoxicity and nephrotoxicity were recorded in the first line antituberculous drugs used in pulmonary tuberculosis patients.

The adverse effects of antituberculous drugs i.e., isoniazid (INH), pyrazinamide, rifampin, ethambutol and streptomycin were observed during this study, discussed here.

Isoniazid (INH) 300 mg per day was started in selected 97 tuberculosis patients. The major side effects were recorded after two weeks of medication, which included hepatitis and peripheral neuropathy.

Hepatitis – there were 10 reactions of hepatitis were documented in this study. In a group of gender, there were 7 reactions in male and 3 reactions in female. According to age group between 20-29, the isoniazid produced 4 reactions, 3 reactions in 40-49, 1 reaction in other age groups. Isoniazid was stopped but remaining other drugs rifampin, pyrazinamide, ethambutol and streptomycin were continued in these patients.

After the stoppage of isoniazid, the liver function test was normal in 6 cases, isoniazid was reintroduced after 2-3 weeks with dose of 50 mg per day and was increased subsequently to 300 mg per day. There were 4 cases referred to the Medical Outpatient Department (OPD) for management of liver disease.

Peripheral neuropathy – isoniazid produced 11 reactions of  peripheral neuropathy out of 25 reactions in this study. According to gender, 4 reactions were produced in male and 7 reactions in female. According to age group the peripheral neuropathy produced in age group 30-39 and 40-49 respectively. This showed the higher side effect of isoniazid in older age group.

Pyrazinamide (1-2 g/day) – the major side effect of this drug were produced after 3-4 weeks of medication. The hepatitis 3, peripheral neuropathy 7, joint pain 8, and skin rashes were documented in this study.

Hepatitis – the pyrazinamide produced 3 reactions of hepatitis in this study. According to gender, 1 male and 2 female reactions were recorded in this study. According to age, pyrazinamide produced 2 reactions in age group of 60-69 and 1 reaction 20-29 of age group. The 1 reaction of pyrazinamide was subsided when drug was stopped. But 2 reactions in older age group, the liver function test did improved and they were referred to the Medical Outpatient Department (OPD) for the management of liver disease.

Peripheral neuropathy – there were 7 reactions caused by pyrazinamide were documented in this study, according to gender, 2 reactions in male and 5 reactions in female according to age group, age between 50-59 3 reactions and 1 reaction in age group 20-29 and 40-49 respectively. These reactions were reversible after decreasing dose of pyrazinamide.

Skin rashes – the pyrazinamide produced 4 reactions out of 6 reactions of antituberculous drugs in this study. According to gender, in female 3 reactions and 1 reaction in male were recorded in this study. According to age group, 2 reactions were recorded in age group of 20-29 and 1 reaction in 50-59, 60-69 respectively. Skin rashes were subsided after stoppage of pyrazinamide for 3 weeks.

Joint Pain – there were 8 reactions of joint pain documented in this study. This study showed that pyrazinamide was only causative drug for joint involvement, the uric acid level was done before and after the start of drug. A remarkable increase level of uric acid was noted after the pyrazinamide treatment. Thus the drug was stopped in these 8 patients and later the level of uric acid significantly decreased and joint involvement clinically improve.

                Ethambutol was administered at dose of 15-30 mg/Kg/Day. The side effects of this drug were manifested after 2-3 weeks of treatment. The peripheral neuropathy and optic neuritis were recorded as main side effects.

Peripheral neuropathy – there were 7 reactions of peripheral neuropathy recorded in this study. The ethambutol produced these reactions in 2-4 weeks after starting of treatment. According to gender, 5 in female and 2 reactions in male, were observed in this study. According to age group, 3 reactions in 50-59 and 1 reaction in each age group respectively. These reactions were reversible after stoppage of the drug.

Optic neuritis – the ethambutol produced the 7 side effects of optic neuritis in this study. According to gender, male manifested 4 and female 3 reactions of optic neuritis in this study. According to age group 3 reactions in 60-69 age group and 2 in 50-59 group and 1 reaction in 50-59, 30-39 age group respectively in this study. Drug was discontinued in these 7 cases of optic neuritis but the remaining four other drugs were continued. They were referred to Eye Outpatient Department for the management of optic neuritis. Only in two patients drug was reintroduced with low dose 15-20 mg/Kg/Day.

Rifampin (450 mg/day) – after 2-3 weeks of starting with combined therapy, the major side effects were manifested. When this drug was hold, the hepatitis 2 and skin rashes 3 were improved and reactions of thrombocytopenia were documented in this study.

Hepatitis – according to gender, 1 reaction of hepatitis in male and 1 in female produced by rifampin. According to age group, 1 reaction in 30-39 and 60-69 were produced by rifampin. One side effect of hepatitis was improved when drug was stopped after one week and other patient was referred to Medical out patient department for further management.

                Skin Rashes – the rifampin developed the skin rashes in two patients; one in male and one in female in this study. According to age group, 1 adverse effect in 40-49 and 50-59 were observed respectively. These skin rashes were reversible after stoppage of drug.

Thrombocytopenia – after 5-11 weeks of treatment of tuberculosis patients, the level of platelets were decreased and clinically the patients were complaint epistaxis, bruises, and petechial rashes. Rifampin was stopped in 3 patients but the remaining other four drugs were continued.

Streptomycin (1 g per day) – it was started with other drugs. After 3-7 weeks of medication, 3 patients complaint of oliguria and 2 patients presented during follow up with hearing deficit. These reactions proved clinically and laboratory investigations.

Nephrotoxicity was recorded in these patients two in male and 1 in female. According to age group 1 in 30-39, 2 40-49 and 1 50-59 side effects were documented in this study. Drug was stopped for 3 weeks and found that blood urea nitrogen and creatinine levels were decreased, therefore this drug was permanently stopped and the remaining four drugs were continued.

The proximal renal tubule cells may accumulate aminoglycoside, accounting for nephrotoxicity associated with aminoglycosides. The mechanism of renal toxicity is hypothesized to by the inhibition of intracellular phospholipase in the proximal tubule. The renal insufficiency is typically characterized by the nonoligouric decrease in glomerular filtrate rate occurring after at least taking a week therapy. Baseline and periodic surveillance of analysis blood urea nitrogen levels, creatinine values is indicated (Edward et al., 2004).

Streptomycin is nephrotoxic and should used with caution in patients with renal impairment. If reaction is trouble some which is an infrequent occurrence, the dose may be reduced (NCG,2002).

Ototoxicity – there were 2 reactions recorded in this study. According to gender, 1reaction was in male and 1 in female was documented in this study. Side effects of streptomycin were recorded. One in age group 20-29 and one in 40-49. The drug was a stopped and patients were advised to consult in Ear Nose and Throat OPD. Remaining other drugs were continued.

Interestingly, the damage may be fairly isolated to either the choclear or vestibular component, or rarely both. The mechanism for the cochlear toxicity is unclear, although the target site is considered to the outer hair cells of the organ of corti.

Aminoglycoside induced cochlear dysfunction is generally considered to be irreversible. Injury to the hair cells of the ampullar cristae by aminoglycosides is the mechanism of the vestibular toxicity. Sign and symptoms of vestibular toxicity include nausea, vomiting, vertigo and nystagmus (Edward et al., 2004).

Our study matches with study of Menzies et al (2005), who observed the side effects of antituberculous therapy. They reported that at least monthly a nurse, a case manager, a treating physician saw the 430 test patients who had active tuberculosis therapy . At the time of their visit patients were questioned specifically about the occurrence of common side effects of their tuberculosis drugs. Liver enzyme levels were checked routinely in all patients after one month of treatment. Patients were encouraged to return at any time if symptoms or problems arose during therapy.

The striking observation is that pyrazinamide was association with rate of toxicity that was threefold higher than isoniazid and rifampin and 20-fold higher than ethambutol. The rate of toxicity with pyrazinamide was 1.5 per 100 person – months compared with 0.5 per 100 person – months for isoniazid. Pyrazinamide rashes attributed to pyrazinamide may have led to in appropriate drug discontinuation. It seems that pyrazinamide-related rashes usually resolve spontaneously and not considered a reason to stop therapy. While in this study the rate of toxicity of pyrazinamide was higher than isoniazid and rifampin. Therefore, causative drugs like pyrazinamide, isoniazid and rifampin was stopped, because they induced hepatitis, which increase risk of liver damage. However, ethambutol and streptomycin were continued in this study.

In case of skin rashes, pyrazinamide was responsible drug but it was discontinued from therapy, skin rashes were improved after three weeks.

                There was a difference between this study and Menzies study may be due to short duration of study period, difference in number of patients studied. Moreover, his study conducted in United States of America. In this study there was a short duration of study and small selected number of patient and many environmental factors were involved. The patients selected in this study belong to poor socioeconomic class and they could not repeatedly visit Doctors for their checkup the occurrence of side effects of antituberculous drugs.

The British Thoracic Society (1998) guides that if the aspartate aminotransferase and alanine transferase are two or more times normal, liver function should be monitored for two weeds, then two weekly until normal. If the aspartate aminotransferase and alanine transferase under two times normal, liver function should be repeated at two weeks. If the aspartate aminotransferase and alanine transferase level rises to five times normal or bilirubin level rises, rifampin, isoniazid and pyrazinamide should be stopped. Alternative treatment will need to be considered if the patient is unwell or is smear positive and within two weeks of starting treatment.

Reactions most frequently observed with intermittent regimens of rifampin are cutaneous syndrome consisting of flushing and/or pruritus, with or without rash, involving particular face, and scalp, often with redness and watering of eye (Fried et al., 2004). Pyrazinamide produce GIT reactions, cutaneous reactions and sidero blastic anaema (Harries, 2004).

The results of this study matches with the study of Pelletier et al (2003), who observed the side effect of antituberculous drugs in 4.30 patients between 1990-99. They stated that the major adverse reaction of first line antituberculous drug, which results in discontinuation of that drug, has severely implication. They may be considerable morbidity even mortality particular may drug-induced hepatitis. Alternative agents may gave greater problems with toxicity and often less effective so that treatment must be prolonged, with attendant challenged to ensure complains as a risk of treatment failure and relapse are higher. In their results, only 37 patients had major side effects on six occasions. Severe hepatitis resulted in discontinuation of the isoniazid and pyrazinamide and neither were restarted. In three instances (two of rash and one of the severe gastrointestinal intolerance). Rifampin and pyrazinamide were stopped not rechallenged. They observed the rifampin did not commonly cause the drug-induced hepatitis. The drug mostly responsible for occurrence of hepatitis or rash during therapy of antituberculosis in tuberculosis hepatitis or rash during therapy of antituberculosis in tuberculosis patients was pyrazinamide.

                In this study, pyrazinamide manifested more side effects than other antituberculous drugs were documented according to age and gender. But incidence of drug-induced hepatitis was observed more in isoniazid than other antituberculous drugs. The rifampin had shown less side effects than other antituberculous drugs.

                The occurrence of side effects in the present study was noted to be much higher than the study done by Pelletier and colleagues. In this study there is a short duration of study and small selected number of patient and many environmental factors were involved. The patients selected in this study belong to poor socio-economical class and they could not repeatedly visit Doctors for their checkup the occurrence of side effects of antituberculous drugs.

Hepatotoxicity is one of the most serious adverse effects of anti tuberculosis drugs (ATD). Although many risk factors gave been associated with antituberculosis drugs induced hepatotoxicity, their influence on hepatitis severity has not been studied systematically. This study evaluated whether the presence of hepatotoxicity risk factors (advanced age, chronic liver diseases, abuse of alcohol or other drugs or malnutrition) influences the severity of ATD induced hepatotoxicity (Villar et al., 2004).

The results of present study match with the study of Fernanoted it al (2004). Their prospective cohort study of 471 active tuberculosis diseased patients treated with isoniazid, rifampicin and pyrazinamide were followed in tuberculosis clinic between January 1998 and July 2002. The incidence of antituberculous drug induced hepatitis was 18.2% patients in a risk group and 5.8% patients in non-risk group. Antituberculous drug-induced hepatitis is a significant and more severe in patients with risk factors. Our study correlates with this study because our big part of population live in a risk factor i.e., poverty, malnutrition, lack of clean water, combine family structure, high prevalence of viral hepatitis. So in our study there were more cases of hepatitis due to pyrazinamide, isonaizid and rifampin gave been responsible for drug-induced hepatitis.

Manifestations of hepatotoxicity include a symptomatic elevation in serum aminotransferase, jaundice and liver tenderness. One recommendation for monitoring for rifampin and pyrazinamide induced hepatitis is to determine the levels of aminotransferase at baseline and at 2, 4 and 6 weeks of treatment and to discontinue rifampin/pyrazinamide when there is (a) serum aminotransferase level that exceeds five times the upper limit of normal in an a symptomatic individual (b) any elevation of serum aminotransferase that accompanied by symptoms of hepatitis (c) any elevation in serum bilirubin (Edward et al., 2004).

The results of this study also match with the results of study carried out by Dossing et al (1996). They observed 61 patients out of 127 patients had elevated aspartate aminiotranferase after the treatment of antituberculous drug. Most of these were men with daily alcohol consumption of 60 g. Hepatitis were confirmed by challenged with pyrazinamide 7 and isoniazid 6 cases.

In the present study, we monitored that occurrence of untoward effects of antituberculous drugs. There was a difference between two studies due to short duration of study and small selected patients. In this study, the cases of hepatitis were recorded more than the study done my Dossing et al.

                This study also matched with the study of Ferner (1990). He observed that ethambutol dose related toxicity. He reported sub clinically impairment of color discrimination relatively common in 54 patients received about 15 mg/Kg/Day of ethambutol as a part of antituberculous therapy. In the present study, the ethambutol produced the opticneurites in high percentage than the Ferner’s study. But similar results were observed in old age patients group who were affected more in both studies. The peripheral neuropathy has been reported in 3 tubercular patients who had receiving the athambutol by 13 to 50 mg/Kg/day.

Peripheral neuropathy was manifested by ethambutol in our study. There were 7 reactions of peripheral neuropathy produced by ethambutol but these reactions were reversible after stoppage of ethambutol.

                In patients prescribed ethambutol it is recommended that after obtaining baseline visual acuity and color perception tests, these tests be repeated every 4 to 6 weeks, especially with new visual symptoms (Chan et, 2004).

                Zinc is found in high concentration in choroids, retina, and ganglion cells and is used by retinal dehydrogenase for transformation of retinal. This last step is important for color vision. Most case of color toxicity are bilateral and result from a dose related retro bulbar optic neuritis that can either axial or peripheral. Axial neuritis involves the papillomacular bundle. It reduces visual acuity and causes central scotomas and color vision deficits. The peripheral visual field deficits but stable visual acuity and color vision (DorothyNahm Friedberg et al.,2004).

                Ellard et al (1976) in their study observed the occurrence of joint pain on a reduction of renal elimination of urate in man caused by administration of pyrazinamide.

                The urinary excretion of pyrazinamide, pyrazinoic acid, 5-hydroxypyrazinoic acid and uric were determined in healthy subjects after giving single or multiple doses of pyrazinamide or its metabolites pyrazinoic acid. The results obtained demonstrated that 5-hydroxypyrazinoic acid is major metabolite of pyrazinoic acid in man and supported previous evidence under that retention of uric acid caused by the administration of pyrazinamide is mediated by pyrazinoic acid. After giving 3 g pyrazinamide the urinary excretion of uric acid was maximally suppressed for 24 hours. Prolonged exposure to pyrazinoic acid resulted in a net reduction in the urinary excretion of uric acid. The finding suggested that the degree of uric acid retention in patients treated with pyrazinamide containing regimens could be reduced by giving pyrazinamide intermittently (Ellard et al., 1976).

This study matched with study conducted by Ellard and coworkers. Pyrazinamide was responsible for joint pain for different age group and gender in the present study. The old age group was commonly affected by pyrazinamide.

                In a study of Hussain et al (2003), ocular reaction and toxic neuropathy were produced by ethambutol in patient’s age between 11 to 80 years. The defected color vision was fouced in 76% of eyes and 27% of eyes had defect in color vision inspite having visual acuity of 6/9 or 6/6. Dilated fundus examination revealed normal optic disc in 66 (67%) of eyes, disc pallor in 27 (28%) of eyes and 4 (4%) eyes had swollen by hyperemic disc.

                The results of present study matched with the results of study conducted by Hussain and coworkers because the ethambutol was effected in the same pathogeneses in old age group.

                Ethambutol is an effective treatment for tuberculosis. It can cause a multitude of dose and time dependent ocular side effects including color changes, visual field defects, and either unilateral or bilateral optic neuritis. Gradual decreases in central visual acuity and green red color vision problem (or less commonly blue yellow color vision defects) have been reported. These defects continue to progress for 1 to 2 months after drug is discontinued (Katherine, 2002).

                This study was also correlated with the study of Mehta (1996). He observed thrombocytopenia in three patients of pulmonary tuberculosis during therapy. Rifampicin was causative drug. The immunological studies in all three patients showed the presence of antiplatelets antibodies reaction resulting in thrombocytopenia.

Moreover, binding of these antibodies to platelet membrane was more avid in presence of rifampicin. In present study, thrombocytopenia was major side effect of rifampin in different age and gender groups. These three patients were separated on the bases of blood complete picture and clinically showed bleeding from nose, petechial rashes and bruises. The pyrazinamide was stopped and it did not reintroduced in these cases.

                Tuberculosis is a granulomatous disease, caused by mycobacterium tuberculosis. As world Health Organization estimates more than 300,000 new cases of tuberculosis develop in Pakistan every year. Cure of infectious cases of tuberculosis is the key to effective control of the disease. Treatment of tuberculosis patients reduces suffering and, if adequately, prevents death from tuberculosis. The first tine of drugs used in the treatment of tuberculosis consists of isoniazid, pyrazinamide, rifampin, streptomycin, and ethambutol. The major side effects are those giving rise to serious health hazards, and require discontinuation of the drug and referral to chest physician. Minor side effects cause relatively little discomfort; they often respond to symptomatic or simple treatment but occasionally persist for the duration of drug treatment. Chemotherapy should be stopped or temporarily interrupted only of severe drug intolerance or toxicity occurs. In fact tuberculosis drugs are relatively toxic and mild side effects are not uncommon but most do not warrant drug withdrawal.

REFERENCES:

A Harries. What are the most common adverse drug events to first line tuberculosis drugs, and what is procedure for reintroduction of drugs. Bulletin of WHO 2004; 154-158.

AD          Harries, NJ Hargreaves, F Gause, JH Kwanjama and FM Salaniponi. “Preventing tuberculosis among health workers in Malawi”. Bulletin of WHO 2002; 526.

Afficial Ammerican Statement. American thoracic society. Treatment of TB and TB infection in adults and children. Am Jr Respiratory Int Car Med 1994; 1359-1374.

Agordon Leitch. “Management of Tuberculosis”, Crofton and Douglas’s Respiratory Disease 5th edition 2000; 444-564.

Agordon Leitch. “Tuberculosis”, Crofton and Douglas’s Respiratory Disease 5th edition, 2000; 476-505.

Alison J Rodger Mice Toole, Babyinuntlvangi, Vmuana and Peter Duts Schmann. “Dots-based tuberculosis treatment and control during civil conflict and HIV epidemic. Church and Pur District, India WHO Bullin 2002; 451-456.

Ann M Ginsberg. What new in TB vaccine? Bulletin of WHO 2002; pp. 483-488.

Arther C Guyton, John D. Pulmonary ventilation In: “Hall Medical Physiology” 10th edition Philadelphia WB Saunder Company 2000; pp.432.

Balasubramanian V CH, Weigeshaus BT Taylor and Smith DW. Pathogeneses of tuberculosis pathway to apical localization. Tubercle and Lung Disease 1994; 75:168-178.

BTS “Adverse reactions to tuberculosis therapy”. Joint Tuberculosis Committee of British Thoracic Society. Thorax 1998; 3:536-548.

Chan KL, Chan HS, Lui SF, Lai KN. Recurrent acute pancreatitis induced by isoniazid. Tubercle and Lung Disease 1994; 75:383-385.

Cheema MA. “Anti Tubercular drugs” Multi author test book of pharmacology and therapeutics” Vol. II, Lahore, National Medical Publication, 2000; pp. 368-370.

Czent. Study of the effect of concomitant food on the bioavability of rifampin. Tubercle and Lung Disease 1995; 76:109-113.

D Marsh, B Hashim, F Hassany and L Hussain. Front line management of pulmonary tuberculosis: analysis of tuberculosis and treatment practices in urban Sindh, Pakistan. Tubercle and Lung Disease 1996; 77:86-92.

David Guwatudde, Sarah Zalwango, Mosses R Kamya, Sara M Debanne, Mireyal J Diaz, Alphonse Okqera, Roy D Muqerova, Charles King and Christopher C Whaten. Burden of tuberculosis in Kampla Uganda. Bulletin of WHO 2003; 799-805.

Dick Menzies. Respiratory epidemiology unit, side effects of common anti-tuberculosis drugs. Am J resp Crit Care Med 2003.

Dorthy Nahm, Friedberg it al. Ocular complications of ethambutol In: Tuberculosis. 2nd Edition. Philadelphia Lipincott William and Wilkins 2004.

Edward D Chan, Celphi Chaterjee, Michael D Iseman. Pyrazinamide, ethambutol, Aminoglycosides 2nd edition, Philadelphia, Lippincott William and Wilkins 2004; 573-589.

Fernandez villar A, Sopina, B Fernandez villar, Luro. Influence of rixk factors on the severity of anti tuberculosis and induced hepatotoxicity. International J Tuber Dis 2004; 8(12):499-505.

Frieden and M Espinal What is the therapeutic effect and what is the toxicity of antituberculosid drug? Toman’s Tuberculosis WHO 2004; 110-121.

GA Ellard and Ruth M hastam. Observation on the reduction of the renal elimination of urate in man caused by the administration of pyrazinamide. Tubercle Lung Dis 1976;57:97-103..

H Turktas, M Unsal, N Tuled, O Uruc. Hepatotoxicity of antituberculous therapy (rifampin, isonizid and pyrazinamide) or viral hepatitis. Tubercle and Lung Disease 1994; 75:58-60.

Henry F, Chambers. “Antimycobacterial drugs”. In: Basic and Clinical Pharmacology, eight edition ,edited by Bertram G Katzung International edition Lame Medical books New York 2001; pp. 803-8114.

Intizar Hussain, Kamran Khalid, M Tayy B. Ocular manifestation of ethambutol toxic optic neuropathy in patients with pulmonary tuberculosis. Pak Postgrad Med J 2003; 14.

M Dossing, JTR Wilikes, DS Askgard, B Liver infury during anti tuberculosis treatment : an 11 year study. Tubercle Lung Dis 1996; 77:335-340.

M Suess. Tuberculosis preventive therapy in HIV infected individuals. Division of communicable disease. Bulletin WHO 1211 Geneva 27, Switzerland 1994.

Martein W Borgdorf. “ Annual risk of tuberculosis infection time for an up date” . Bullentin of WHO 2002; 501-503.

MD isman. What’s in aname… TB or not TB? Tubercle and Lubh Disease 1996; 77:102.

Megan Muray and Edward Nardell. Global epidemiology of tuberculosis: achievements and challenge to current knowledge. Crofton and Douglas’s Respiratory Disease 5th edition, 2004; 80(6):477-483.

Mario C, Raviglione/Richard O’Brain, “Tuberculosis” In: Harrison’s Principles of Internal Medicine, Stephen L, Hauser Dan L. Longo et al . 15th edition vol I, New York MC Graw hill Medical publication division 2001; pp. 1024-35.

      Nizami SQ. Childhood TB. J Pak Med Assoc 1998;48:88.

Ormerod IP and Horfield. N. “Frequency and type of reactions to antituberculosis drugs: observations in routine treatment. Tubercle and Lung Disease 1996; 77:37-42.

Perveen Kumar. Tuberculosis. In: Clinical Medicine 5th edition, Edinburg, WB saunder 2002; pp. 892-897.

PaulNunn, Anthony Harries, PeterGodfrey, Rajgupta, Dermot Maher, Masio Raviglone. The research agenda for improving health, systems performance, and service delivery for tuberculosis control. A WHO perspective World Health Organization 2002; 471-476.

PDO Dawis, DJ uirling and JM Grange. Pulmonary disease IN: Infectious desease 6th edition, Lippincott Williams and Wilkins, Philadelphia 2003; pp. 1644-657.

Pelletier, Yee et al. Incidence of serious side effects from first line antituberculosis drugs among patients treated for active tuberculosis. AJP and Crit care Med 2003.

Philip C Hopwell. Tuberculosis control how the world has changed since 1990. Bulletin of WHO 2002; 427-728.

R Ferner. P. “Ethambutol” New castle upon tyne. Peer Review Strasbourg, France, April 1990.

Richard A Garibaldo, Ronald #E and H Febrebee. Isoniazid associated hepatitis. Am Rev Resp Dis 1972; 1-6:356-367.

Shamim A Qazi, A. KIhan, m. Ak Khan “Epidemiology of childhood of tuberculosis in hospital setting”. J Pak Med Assoc 48:1998.

Tripathi KD. “Antitubercular drugs” In: Essentials of Medical Pharmacology 5th edition, New Dehli, Japee Brothers 2003; pp.698-708.

W Levinson. “Mycobacteria” IN: Medical Microbiology and Immunology. Examination and Board Review 5th edition, New York, Lous Medical Books 200; p.157.

William AP Jr. “Anticicrobial agents” Goodman and Gilmans the Pharmacological bases of therapeutics 10th edition, (Joe1 G Hardman, Ph.D. Lee E. Limbird et a1). McGraw Hill Medical Publishing Division, New York 2001, pp.1273-1295.

YS Mehta EE Jinina, SS Badakere, D M obanty. Rifampin induced ummune thrombocytopenia. Tubercle and lung Disease 1996; 77:558-562.

 

Welcome to www.BrowardHomesForSale954.com.You will find every Broward home for sale listed on the Florida MLS including homes, condos, town homes, foreclosures, bank owned homes. We can show you any Broward home listed on the Broward MLS and provide you with detailed information. Best of all our services are provided to Broward home buyers at NO COST. Broward MLS listings are generated from the Broward MLS and are updated in real time.

 

SEARCH THE ENTIRE BROWARD MLS PORTAL - EVERY BROWARD HOME FOR SALE LISTED BY EVERY BROWARD REALTOR - To Receive a Complete list of Broward Homes that meet your specifications. www.BrowardMLS954.com

 Search the entire Broward MLS, or Broward Multiple Listing Service at http://www.browardhomesforsale954.com/ for the most comprehensive database of Broward Homes for sale in Broward County Florida. Regardless of which Broward home type you are looking for you will find it at BrowardHomes954.com including but not limited to single family homes Condos, coops, villas, townhomes, income property, bank owned homes Broward foreclosures or other Broward home type for sale you will find it all on the Broward MLS at Browardhomes954.com All Broward county FL real estate agents who are members of their local Broward FL Board of Realtors can show and sell any Broward FL home or Broward condo, townhouse, Foreclosure or any other home on the Broward MLS, including properties listed by other Broward FL real estate brokers. For example, the Broward County MLS (which is actually part of one or more regional Florida MLS) includes nearly every Broward FL home for sale in Broward County and nearly every Broward condo for sale in Broward County as well as Broward Foreclosures, Bank owned Homes other Broward Florida properties for sale are listed on the Broward MLS. BrowardHomes954.com is a member of the local Broward multiple listing service (Broward MLS), which provides our Broward homebuyers with full access to any Broward home for sale or condo, townhouses or another Broward FL home listed in the local MLS. Broward FL MLS rules allow us to display nearly every Broward home and Townhouse, Foreclosure and all home types listed for sale in the Broward MLS on our website so our customers can search the Broward MLS right from their personal computers. While the Broward MLS may confuse some the good news is that because Browardhomes954.com is a member of the local Broward MLS in the areas we serve, Broward homebuyers have access to nearly every Broward home for sale in Broward County Florida.

Search the Entire Broward County MLS AT www.BrowardMLS954.com provides Broward homes sellers and Broward home buyers with an innovative real estate solution. By using the efficiencies of the Broward MLS, we have streamlined the real estate process and are able to pass significant savings on to our clients.

Get email notifications of Broward homes that fit your criteria. Save your search criteria and you’ll get houses for sale listings that meet such search criteria as they come on the market.

For Yucatan Real Estate buyers, several factors serve as the most important considerations in their Yucatan MLS property search. One of these is the unique choice offered in this area of beautiful, more traditionally Mexican style real estate in the colonial heart of Merida, Yucatan’s capital, or beachfront properties in the nearby communities, such as Progreso. Merida MLS listings will provide property searchers with broad options of these and many other property types, ranging from quaint homes, to colonial estates (“haciendas”) to luxury beachfront condos. While MLS property listings can show buyers the kind of properties available, another important factor is the quality of roads and infrastructure in the area.

Merida is continuously developing its infrastructure system, and investing the maintenance of the beauty which the city can already boast. Recently, the second forum by an organization call the “Strategic Plan for Merida” was held to discuss improvement issues for real estate infrastructure in Merida and related issues. The continued improvement of colonial Historic Center and traffic improvements were among the proposals raised.

The main programs related to these issues are expected to be low cost and, at the same time, highly effective. The first meeting of “Strategic Plan for Merida” presented the project “Mobility in 2035″, which proposes, among other items, to develop four strategic lines to generate a model of mobility, which includes: sustainable urban development, urban transportation, and road infrastructure. The specific actions outlined include modernization of urban transportation, an integrated traffic light system, improved road signs for visitor activities, special improvements for busy intersections, maintenance and continued beautification of the Historical Center, and a considerable repaving project.

A new Transport Act for the State of Yucatan is also being analyzed by State Congress. This bill would improve the already well developed transportation infrastructure and system in Yucatan. Along with Merida’s “Stratigic Planning,” the state government invests ongoing funds into keeping Merida’s city center beautiful, maintaining the “stepping into the past” feeling created the colonial streets and buildings. For real estate buyers, whether they choose to buy a home near the city center, or any of the many other options, Merida’s colonial charm is a key ingredient in the lifestyle that Yucatan real estate buyers enjoy. The traffic and road infrastructure improvements complement the combination of this charm and luxury beachfront with easy access to shopping, restaurants, and the many activities and attractions which Merida and the surrounding area of Yucatan have to offer.

In addition to those already mentioned, Yucatan also includes a rich choice of Mayan pyramid sites, including the world famous Chichen Itza – one of the new Seven Wonders of the Ancient World. Yucatan also includes many ways to enjoy its natural beauty, including “cenotes,” which are calm, cool pools at the entrances to the regions extensive underground cave and river system. Swimming in these pools is a refreshing way to balance the area’s year-round warm weather. Merida and Yucatan also offer real estate owners many eco-parks, where they can enjoy an interactive visit to nature, ancient Mayan history and Yucatan’s rich culture.

For Sale By Owner is gaining popularity for last three years with home owners looking to save as much they can with MLS listing. Not all of the home owners list as For Sale By Owner resulting in time and money loss. But what exactly is “For Sale By Owner” and how does this works? If we look at traditional way of selling a home you will come to know of loss one makes both in terms of money and time. When you list as For Sale By Owner you are your own boss in deciding the price you want to sell you property at. MLS listing provides the best supportive platform to For Sale By Owner listing which is required to sell in quick time and at good price.

Flat fee MLShas made an easy task for home owners who have not enough time to dedicate in selling process. Everyone these days look to save both money and time and Flat fee MLS is the best option to go with. MLS listinghas not been an easy task which many of you might think, but when you experience the same your opinion on this will be totally change. Some of you might also think MLS listing is a costly affair, but Flat fee MLShas changed the way of thinking and the way of selling a home. As the term Flat fee MLS suggest you pay a small flat fees upfront (one-time) to the listing broker for the services you want.

When you list as For Sale By Owner you are one to decide the price for your property and not the real estate broker. Do a bit of desk research to understand the market price prevailing in your area and reach a MLS listing agent to list your property as For Sale By Owner. Home owner either looking to sell or buy can list as For Sale By Ownerand save huge sum of money paid as sales commission. If you look at traditional way of selling process, you were required to contact a traditional broker who would let you know the price you can sell your property at. You had to totally depend on that broker to get the buyer and make yourself available all the time to show the property.

This has totally changed in MLS listing as For Sale By Owner which is widely preferred way of selling a property. Flat fee MLS has incredibly decreased the MLS listing fees when you list as For Sale By Owner. For MLS listing you might pay a flat fee depending on the MLS listing package you go with, that may start from 9. To list as For Sale By Owner you are offered different listing options to choose from depending on the term you want For Sale By Owner listing to appear. MLS listing has proved a boon to people looking to list as For Sale By Owner saving those thousands of dollars in sales commission.Flat fee MLS agents are there to help you in listing as For Sale By Owner and let you experience the best-selling experience.

 

Real estate professionals who do not provide a consumer content solution will become irrelevant.  — Allen Dalton, President of Top4 in Real Estate Network

It has been said that some people have forgotten more (information) than others have ever known to begin with.  Such may be the case in today’s real estate industry, especially when it comes to reminding brokers and agents that the roots of social media are firmly buried in the soil of their very own industry.

Early Realtor Experience Led to Social Media Birthing

According to the U.S. National Association of Realtors®, in the late 1800s real estate brokers met at local association offices to match properties they were trying to sell with customers their colleagues were representing.  The brokers agreed to compensate each other by bringing sellers and buyers together to close sales.  These arrangements led to the birth of the Multiple Listing Service (MLS), which still remains the backbone of the real estate industry.  Of course, the MLS is now a web-based system and is shared by every subscribed US Realtor® from New York to California.

As innovative as the MLS must have seemed to people back in 1890; in 2010 it has proven to be a double-edge sword for an industry that is supposed to be customer centered, but has not been living up to that charge in recent years.  Why is that?

By design, a person selling his/her own property cannot put a listing for his home directly into the MLS. In fact, most MLS systems still restrict membership and access to real estate brokers and their agents.  These restrictions have created a closed society for Realtors® and have shut out John Q. Public, who is searching the web for more and more detailed information to factor into his home buying decisions. They cannot access the specific information contained in the MLS.

Homebuyers Demand Realtor “Access” on the Net

In fact, the National Association of Realtors® reports that 84% of home sales start with the Internet.  So, by not having access to the MLS (in addition to a lack of other information Realtors® are not making available to them) one could make the case that consumers are not being communicated with by brokers and agents the way they want to be communicated with.  In the age of social media, where customer expectations have gained the upper hand, real estate agencies must either re-adjust their customer focus or prepare to fail.

Allen Dalton, President of Top4 in Real Estate Network coined the term “content-sequences,” which represents the threat that “real estate professionals who do not provide a consumer content solution will become irrelevant.”   He goes on to proclaim the death of calendars and magnets as token ways to buy the affection of consumers.  “Agents,” he says, “are not endearing themselves to consumers, which ultimately results in consumers trusting friends or non-industry professionals to advise them on important real estate matters rather than turning to brokers and agents.”

This is unfortunate because Realtors® have always played a critical role in providing expert knowledge to buyers and sellers on changing government regulations, REOs, short sales, negotiations, financing and submarkets.  In some ways, they have taken themselves out of the game by losing touch with the changing expectations of today’s customers.

Realtors Must Become More Customer Focused Using Social Media

Dalton further explains that the real estate industry cannot afford to resist social networking the way they once resisted the Internet, IDX, agency representation and “every single thing in the interest of consumers.”   He asserts that “everything about social media has to solve a problem for consumers. Everything we write, the information, the content; we have to think, ‘how is this solving a problem for consumers?”

While the real estate industry battles with the ghosts of the past, individual real estate agencies can provide actionable and relevant content for customers on their own. There are many social media outlets on the web for this purpose.  Whether you choose Facebook, MySpace, Twitter, YouTube, Flicker, Digg, LinkedIn, Bebo, Orkut or a similar networking platform, the rules still remain the same.  The consumer is looking for great content.  Great content attracts customers – people looking for information and solutions for their needs.

Social Media Success Begins When Your Website Meets Customer Needs

What better place is there to offer useful and valid content than a well designed website?  Allen Dalton puts it this way, “information share equals market share and VOI (value of information) equals ROI (return on investment). ” I have never heard this expressed as powerfully by anyone else.

So, what should an effective Real Estate Agency website include?   The short answer is a well- thought out strategy that takes the consumer through the entire buying cycle from search engine discovery to E-commerce checkout or customer inquiry.

Your website is only effective if:

1.  It is easily found.

2.  Simply navigated

3.  Content rich.  

4.  It leads to some positive action from the customer.

Web analytics will confirm your website’s effectiveness or signal its failure. The day your website launches, Google Analytics or a similar tool should be in place to begin constant measurement.

Always keep an eye on the following metrics: 

1. Hits

2. Visits

3. Unique visitors

4. Page views

5. Top entry and exit (bounces) pages

6. Referrers

7. Search keywords

8. Visitor information

9. Click paths

10. Conversions 

11. Tracking registered users. 

These are the key indicators that need your ongoing attention.  If they are pointing downward, you need to make some changes in content and/or layout wherever they may be indicated.

You Either Have It Or You Don’t…

Site look and design are important factors in making a good first impression, so your website should have a professional look and be pleasing to the eye of its beholder.  Warm colors and cool graphics that complement one another may entice your visitors to visit and stay awhile.

A successful website has intuitive navigation, which makes it easy to find the information one is looking for in only a click or two.  Site maps and the proper naming of links and buttons are especially helpful.

And, I can’t say enough about content.  In real estate, consumers are interested in statistics about the community and its schools.  They also want to know about area businesses and where shopping is located.  Employment and recreational opportunities are also of importance to many homebuyers; as is the types and locations of community places of worship.

In real estate “widgets” are also effective tools.  These are small programs you can import into your site to make it more helpful and memorable.   Including a mortgage payment calculator and/or one for loan qualification might be wise.  Providing a widget that shows off your most desirable listings can be priceless.

Be sure to also include ways for potential customers to contact you through your website. Response forms and E-mail links are just as important as phone and fax numbers on your website and need to be included.

The Payoff (ROI) is There If You Invest in Value of Information (VOI).

When things are working well you’ll receive customer testimonials like the one agent Bill Gassert of Re/Max Executive Realty received from Bruce & Yvonne Rogers of Franklin Massachusetts:

“I wanted to let you know that I think your Metrowest Real Estate website was an excellent tool in finding our 1st home. It was great to be able to see the homes with addresses as soon as they came on the market. You made finding our dream home in Franklin easy! Thanks!”

Once you have an effective website validated by web analytics you will be proud to go out and meet your customers in social media and invite them back to your own home sweet home….PAGE.