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Hormone report – 2007


E: HORMONE REPORT – 2007

LABORATORY REPORT

CLIENT CODE :C000000613

 

CLIENT’S NAME AND ADDRESS :

 

TRIVEDI MAHENDRA KUMAR

SRL Ranbaxy Ltd – Mumbai
113, 15th Street, Andheri (East),
Mumbai – 400 093
Maharashtra, INDIA
Tel. : 022 – 3081 1111 – 99 Fax : 022 – 6692 4717
E-mail: srl.mumbai@srlranbaxy.co.in

Toll Free No.: 1800 222 333. E-mail: srlbom@srlranbaxy.co.in

 

PHN NO : 9869118769/32910208

 

REFERRING DOCTOR : DR. SHRIKANT PATIL

 

PATIENT NAME : MAHENDRA KUMAR TRIVEDI

 

ACCESSION NO.
0002GB012612
AGE: 43 Years
SEX: Male
DATE OF BIRTH: 10/02/1963
PATIENT ID

 

 

CLINICAL INFORMATION
RESULTS

 

TEST REPORT STATUS     FINAL 
 IN RANGE
OUT OF RANGE

 REFERENCE

RANGE

UNITS
GROWTH HORMONE. SERUM

HUMAN GROWTH HORMONE

L < 0.05
0.06 – 5.00
ng/mL
ADRENOCORTICOTROPIC HORMONE, PLASMA

ADRENOCORTICOTROPIC HORMONE

39.9
10.0 -46.0
pg/mL
TSH 3RD GENERATION, SERUM

TSH 3RD GENERATION

4.40
0.35 – 5.50
μlU/mL
FSH & LH EVALUATION, SERUM

LUTEINIZING HORMONE

4.01
1.50 – 9.30
mlU/mL
FOLLICLE STIMULATING HORMONE
L 1.11
1.40 – 18.10
mlU/mL
LH/FSH RATIO
H 3.61
0.00 – 2.00
ANTIDIURETIC HORMONE

ANTIDIURETIC HORMONE

1.75
1.0 – 14.0
pg/ml
TSH RECEPTOR ANTIBODIES, SERUM

TSH RECEPTOR ANTIBODIES

<5.0

< 9.0 (Negative)

9.0 – 14.0 (Indeterminate)

> 14.0 (Positive)

U/L
CORTISOL. SERUM

CORTISOL

17.99

7:00-9:00 a.m.:

4.30 – 22.40

3:00-5:00 p.m.:

3.09 – 16.66

ug/dL
PROGESTERONE. SERUM

PROGESTERONE

1.17
0.28 – 1.22
ng/mL
PARATHYROID HORMONE (INTACT), SERUM
CALCIUM
9.0
8.5 – 10.1
mg/bL
PTH (INTACT)
45.1
14.0 – 72.0
pg/ml
IMMUNOGLOBULIN
TOTAL IgA
2.85
0.90 – 4.50
g/L
TOTAL IgG
13.37
8.00 – 18.00
g/L
TOTAL IgM
0.70
0.60 – 2.50
g/L
COMMENT:
************************************************************************************
NOTE: RECHECKED FOR SERUM FSH.

PLEASE CORRELATE CLINICALLY.

************************************************************************************
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Hormone Bot

LABORATORY REPORT

CLIENT CODE :C000000613

 

CLIENT’S NAME AND ADDRESS :

 

TRIVEDI MAHENDRA KUMAR

SRL

CLINICAL REFERENCE LABORATORIES

113, Street 15, MIDC, Andheri (East),

Mumbai – 400 093 INDIA

Tel. : 022 – 3081 1111 – 99 Fax : 022 – 5692 4717

Toll Free No.: 1800 222 333. E-mail: srlbom@srlranbaxy.co.in

 

PHN NO : 9869118769/32910208

 

REFERRING DOCTOR : DR. SHRIKANT PATIL

 

DRAWN 06/02/2007 09:00
RECEIVED 06/02/2007 09:05
REPORTED 10/02/2007 15:52

 

PATIENT NAME : TRIVEDI MAHENDRA KUMAR

 

ACCESSION NO.
0002GB012612
AGE: 43 Years
SEX: Male
DATE OF BIRTH: 10/02/1963
PATIENT ID

 

 

CLINICAL INFORMATION
RESULTS

 

TEST REPORT STATUS     FINAL 
 IN RANGE
OUT OF RANGE

 REFERENCE

RANGE

UNITS

CORTISOL, SERUM

Cortisol is a primary glucocorticoid hormone synthesized and secreted by the adrenal cortex. Cortisol plays an important role in regulating carbohydrate, protein and lipid metabolism, maintaining normal blood pressure and inhibiting allergic and inflammatory reactions. Cortisol is synthesized and secreted by the cortex of the adrenal gland under the effect of adrenocorticotropic hormone (ACTH).

Circulating Cortisol levels follow a diurnal pattern in healthy individuals. Levels are highest in the morning after waking and lowest in the evening. Disorders of the hypothalamic pituitary adrenal axis override this diurnal pattern.

Decreased Cortisol levels are induced by either primary or secondary adrenal insufficiency. Addison’s disease is caused by primary adrenal insufficiency due to metabolic errors or destruction of the adrenal cortex. Secondary adrenal insufficiency is caused by pituitary destruction or failure, resulting in loss of ACTH stimulation of the adrenal gland.

Increased levels of Cortisol due to either primary or secondary adrenal hyper function cause Cushing’s syndrome. Causes of primary adrenal hyper function are adrenal tumors and nodular adrenal hyperplasia. Secondary adrenal hyper function is caused by pituitary overproduction of ACTH or ectopic production of ACTH by a tumor. Increased Cortisol levels are induced by pregnancy and by stress due to depression, trauma, surgery, hypoglycemia, alcoholism, uncontrolled diabetes and starvation.

Due to the diurnal pattern of secretion, an assessment of serum Cortisol at a single time-point is of little diagnostic value. The ACTH stimulation test is used to evaluate Addison’s disease. The dexamethasone suppression test is used to diagnose Cushing’s syndrome or depression due to neuroendocrine disorders.

Test method: Chemiluminescence.

GROWTH HORMONE, SERUM

Human growth hormone (hGH, somatotropin) is a polypeptide originating in the anterior pituitary. It is 191 amino acids in length and has a molecular mass of approximately 22,000 daltons. Its metabolic effects are primarily anabolic. It promotes protein conservation and engages a wide range of mechanisms for protein synthesis. It also enhances glucose transport and facilitates the buildup of glycogen stores.

Measurement of hGH is primarily of interest in the diagnosis and treatment of various forms of inappropriate growth hormone secretion. Clinical disorders of hyposecretion include dwarfism and unattained growth potential. Hypersecretion is associated with gigantism and acromegaly.

Caution must be exercised in the clinical interpretation of growth hormone levels. These vary throughout the day, making it difficult to define a reference range or to judge an individual’s status based on single determinations. Many factors are known to influence the rate of growth hormone secretion, including periods of sleep and wakefulness, exercise, stress, hypoglycemia, estrogens, corticosteroids, L-dopa, and others.

Growth hormone-deficient individuals have fasting/resting levels similar to those found in healthy individuals. Various challenge tests have therefore been devised to differentiate these groups. Thus with the onset of deep sleep or after 15 to 20 minutes of vigorous exercise, growth hormone levels normally show a rise. Other tests of growth hormone responsiveness are based on the administration of L-dopa, arginine and insulin. Propanolol and estrogen are sometimes given in conjuction with the primary stimulus to accentuate the response.

A small number of cases of dwarfism have been documented in which both the basal level and the response to challenge testing were normal. Such cases may involve tissue insensitivity to either growth hormone or somatomedins, or the presence of antibodies or immunoreactive but biologically inactive growth hormone.

REFERENCE RANGE FOR GROWTH HORNOME STIMULATION TEST

Post- stimulation normal peak levels or gh are 10 ng/ml or more. In children, gh levels 7.0 ng/ml or less and in adults gh levels of 5.0 ng/ml or less indicate gh deficency . Gh levels between normal and deficient states are considered as indeterminate.

 

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directly stimulates TSH production. TSH interacts with specific cell receptors on the thyroid cell surface and exerts two main actions. The first action is to stimulate cell reproduction and hypertrophy. Secondly, TSH stimulates the thyroid gland to synthesize and secrete T3 and T4.

 

The ability of quantitate circulating levels of TSH is important in evaluating thyroid function. It is especially useful in the differential diagnosis of primary (thyroid) from secondary (pituitary) and tertiary (hypothalamic) hypothyroidism. In primary hypothyroidism, TSH levels are significantly elevated, while in secondary and tertiary hypothyroidism, TSH levels are low. TRH stimulation differentiates secondary and tertiary hypothyroidism by observing the change in patient TSH levels. Typically, the TSH response to TRH stimulation is absent in cases of secondary hypothyroidism and normal to exaggerated in tertiary hypothyroidism. Historically, TRH stimulation has been used to confirm primary hyperthyroidism, indicated by elevated T3 and T4 levels and low or undetectable TSH levels. TSH assays with increased sensitivity and specificity provide a primary diagnostic tool to differentiate hyperthyroid from euthyroid patients.

Below mentioned are the guidelines for age related reference ranges of TSH:

 

Age Reference Range Units
Cord Blood 2.0 – 40.0 μIU/mL
1 – 6 days 0.4 – 15.0 μIU/mL
1 – 3 weeks 0.4 – 10.0 μIU/mL
1 month & over 0.4 – 5.0 μIU/mL

Test method: Chemiluminescence

FSH & LH EVALUATION, SERUM

Circulating FSH levels vary throughout the menstrual cycle in response to Estradiol and Progesterone. A small but significant increase in circulating FSH accompanies the mid- cycle LH surge. FSH declines in the luteal phase in response to Estradiol and Progesterone production by the developing Corpus Luteum. FSH is elevated and gonadal steroids are depressed include Menopause, Premature Ovarian Failure, and Ovariactomy, while with Polycystic Ovarian Syndrome the LH / FSH ratio may be increased. At Menopause, FSH and LH increase sufficiently in response to diminished feed back mechanism of Gonadotropin release. Elevated concentration of LH may indicate Primary Amenorrhea, Menopause, Premature Ovarian Failure, Polycystic Ovarian Syndrome, or Hypergonadotropic Hypogonadism. The levels of LH & FSH in women are to be correlated with the day of the menstrual cycle.

FSH, LH and Testosterone regulate spermatogenesis by the Sertoli cells in seminiferous tubules of the testes. FSH may also be elevated in Klinefelter’s Syndrome (Seminiferous Tubule Dysgenesis) or as a consequence of Sertoli cell Failure. Elevated concentration of LH and FSH accompanied by low concentration of gonadal steroids may result in infertility due to Gonadal Failure. Elevated concentration of LH may result in Primary Testicular Failure, Seminiferous Tubule Dysgenesis. (Klinefelter’s Syndrome), Sertoli cell Failure & Hypergonadotropic Hypogonadism.

Hormone assay values are to be correlated with the age and clinical status of the patient irrespective of whether the values are appearing in the ‘In Range’ or ‘Out of Range’ columns.

Test method: Chemiluminescence.

PARATHYROID HORMONE (INTACT), SERUM

Parathyroid hormone (PTH) produced by the parathyroid gland is the major circulating factor regulating extra cellular calcium concentration.

The intact PTH peptide (MW~9425) consists of 84 amino acids that are sequenced and designated according to reactivity. The N-terminal or amino-terminal 1-34 region of the intact PTH modecule is biologically active. This region of the molecule contains the amino acid sequence that enables PTH to bind to the parathyroid hormone receptors in target tissues and regulates extra cellular calcium concentration. The middle and carboxy terninal 35-84 region of the intact PTH molecule is biologically inert but possesses immunological reactivity.

 

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Quantification of circulating intact PTH assists in the differential diagnosis of hypercalecmia. In conjunction with the measurement of ionized calcium, intact PTH evaluations can be used to distinguish between patients with hypoparathyroidism, hypoparathyroidism or hypercalcemia of malignancy.

 

The diagnosis of primary hyperparathyroidism, a common cause of hyper calcemia is confirmed by elevated ionized calcium concentrations and elevated parathyroid hormone concentrations. Intact PTH levels are also used to assess and manage other metabolic bone disorders including osteoporosis and renal osteodystrophy. The measurement of intact PTH using two site immunoassays provides a more accurate assessment of parathyroid tissue secretary status, especially in patients with renal impairment.

Interpretation of intact PTH values should always take into account serum Calcium results and inter-relationship between these two elements in various disorders involving PTH & Calcium. It is recommended that the intact PTH results should always be interpreted with caution & with consideration of the overall manifestations even when used in conjunction with calcium values.

Measurement of intact PTH is useful in differentiation between hypercalcemia due to hyperparathyroidism & hypercalcemia of malignancy. However the assay is not intended as and should not be relied upon as a diagnostic indicator of malignancy.

Heterophilic antibodies in human serum can react with reagent immunoglobulins, interfering with in vitro immunoassays. Patients routinely exposed to animals or to animal serum products can be prone to this interference and anomalous values may be observed. Additional information may be required for diagnosis.

Test method: Chemiluminescence.

Total Immunoglobulin

Serum IgG levels are decreased in several immunodeficiencies. In congenital hypogammaglobulinemia IgG is less than 200 MG/DL by 6 months of age. Acquired hypogammaglobulinemia may occur at any age and has IgG levels less than 500 MG/DL. IgG levels may also be decreased in combined cell-mediated and antibody immunodeficiencies. Lymphocyte phenotype and function studies may be helpful in evaluation of immunodeficiencies. Suspected paraproteinemias should be screened for with immuno electro phoresis. Selective deficiency of one or more IgG subclasses is associated with a variety of recurrent infections or asthma.

Total IgM evaluates humoral immunity; establishes the diagnosis and monitors therapy in Macroglobulinemia of Waldenstrom & Plasma Cell Myeloma. IgM levels are used to evaluate likehood of in utero infections or acuteness of infections.

IgA deficiency is the most common of the primary immunodeficiency diseases. It can be induced by drug such as penicillamine, phenytoin, sulfasalzine & captoril. IgA deficiency is also seen in autoimmune diseases.

Polymeric IgA is found in conditions resulting in parenchymal liver damage, IgA Nephropathy, utreated Coeliac Disease, Chronic bronchial suppurative disorders, herpes Simplex, Encephalites, Herpes zoster, Mumps & Meningitis.

Test method: Immunoturbidimetric assay.

** End Of Report **

Harmones Report Bot

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Spine MRI

" The Augmentation and Aortic reflection show the amount of stiffness seen in a person 20-25 years younger"
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" The pituitary fossa is the largest ever found in a healthy subject with fully functioning body having excellent health"
–Dr Shailendra Patil, India