The Endocrine System

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Link to Image source Pituitary: Macro view of the pituitary gland. This and the following pituitary slides are stained with Masson's trichome wherein nuclei and other basophilic structures (may include cytoplasm) are blue, collagen is green or blue, and cytoplasm (nonbasophilic) are red. Notice the lightly-stained neurohypophysis and darker-stained adenohypophysis.

LABORATORY FINDINGS   Increased plasma PRL (>300 ng/ml) - this finding is more diagnostic than are tests designed to stimulate or suppress PRL secretion Diminished PRL increase following administration of thyrotropin-releasing hormone (TRH) or phenothiazines, such as chlorpromazine or perphenazine

• One or more of the pituitary hormones will be either decreased or in the low-normal range with an attendant decrease in target hormones.  The pituitary hormones do not increase appropriately following stimulation.
• Decreased GH, which does not respond to stimulation by at least two of the following: hypoglycemia, arginine, l-dopa
• Decreased FSH -> decreased estrogens and progesterone
• Decreased LH (ICSH) -> decreased estrogens and progesterone or testosterone
• Decreased FSH and LH do not respond to stimulation by Gn-RH or clomiphene citrate.
• Decreased TSH -> decreased free T₄ index
• Decreased TSH does not respond to stimulation by TRH
• Decreased ACTH -> decreased cortsol
• Decreased ACTH does not respond to stimulation by metyrapone

Click here for enlarged view

LABORATORY FINDINGS Diagnostic Studies   Increased serum GH, which is not suppressed by oral administration of glucose;  there is suppression of GH by glucose in normal persons. GH is increased in response to TRH administration;  there is no such increase in normal persons. Other Laboratory Findings   Increased serum phosphorus due to increased renal tubular phosphate reabsorption Increased serum alkaline phosphatase reflects increased bone formation. Increased serum and urine calcium reflect increased intestinal absorption of calcium. Increased serum and urine creatinine reflect an increased rate of tissue synthesis. Diabetes mellitus occurs in 10% of patients and there is impaired glucose tolerance in 50% of patients;  these occur as a result of the antagonistic effect of GH on insulin.

LABORATORY FINDINGS
 

• Increased urine volume (4 litres/24 hr - 15 litres/24 hr)
• Decreased urine specific gravity (<1.004) - not appreciably increased when fluids are withheld
• Decreased urine osmolality (<200 mOsm/Kg H₂0) in the presence of high-normal or elevated plasma osmolality

• Overnight water deprivation causes an increase in serum osmolality, but urine osmolality is less than 400 mOsm/Kg H₂0, and is usually less than that of serum.  Patients also show weight loss due to continued renal loss of water despite water deprivation.
• If the diagnosis is uncertain after overnight water deprivation, a hypertonic saline infusion test should be performed.  Failure to demonstrate a rise in urine osmolality and a decrease in urine volume indicates diabetes insipidus.
• If concentrated urine is not produced following the infusion of hypertonic saline, aqueous ADH may then be given to determine whether the diabetes insipidus is of renal or pituitary origin.  Following ADH injection, pituitary diabetes insipidus shows increased urine osmolality and decreased urine output;  renal diabetes insipidus shows no change in urine osmolality or urine output.

LABORATORY FINDINGS
 

• Decreased serum sodium due to dilution by retained fluid
• Decreased serum osmolality (<285 mOsm/Kg H₂0) due to fluid retention
• Increased urine osmolality (300 mOsm/Kg H₂0-400 mOsm/Kg H₂0) - reflects decreased fluid excretion
• Increased ratio of urine osmolality to serum osmolality
• Normal urine sodium and creatinine clearance

HYPERTHYROIDISM

Click here for enlarged image

LABORATORY FINDINGS Diagnostic Studies   Increased serum T4 - this may be normal Increased resin T3 uptake - this measures the availability of unbound binding sites for T4 and T3 on T4 - binding proteins;  this may be normal even more often than is T4. Increased free T4 index - this is the product of T4 X resin T3 uptake;  this usually parallels absolute free T4 concentration. Increased serum T3 - measurement of this hormone is indicated when the free T4 index is normal or borderline and clinical suspicion of hyperthyroidism is high. Increased free T3 index - this is the product of T3 X resin T3 uptake;  this usually parallels absolute free T3 concentration. Minimal or absent increase in TSH following IV administration of TRH - this reflects pituitary suppression by increased T4 and T3 and indicates thyroid autonomy.  Autonomy means that thyroid function is independent of pituitary regulation, but does not necessarily imply clinical thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins such as LATS in patients with Graves' disease Other Laboratory Findings   Increased serum glucose due to increased intestinal absorption and gluconeogenesis Decreased serum cholesterol and triglycerides due to increased utilization

Diagnostic Studies   Decreased serum T4, resin T3 uptake, and free T4 index - the degree of depression of these indices depends on the extent of destruction of the thyroid gland. Increased serum TSH - this is the single most important diagnostic laboratory test for primary hypothyroidism.  This might be elevated, even with a normal free T4 index.  TSH is low or undetectable in cases of secondary hypothyroidism. Other Laboratory Findings   Increased serum cholesterol and triglycerides reflect decreased utilization. Increased serum creatinine phosphokinase (CPK), lactate dehydrogenase (LDH), and serum glutamic-oxaloacetic transaminase (SGOT) - myxedema of skeletal muscles causes leakage of these enzymes through the muscle membranes into capillaries Flat glucose tolerance curve due to decreased gastric emptying and diminished cellular utilization of gtlucose Anaemia, usually normocytic due to decreased erythropoietin production, decreased tissue oxygen needs, or impaired marrow function.  Microcytic anaemia might follow increased menstrual blood loss.  The occasional occurrence of macrocytic anaemia is due to vitamin-B12 or folate deficiency. Achlorhydria and parietal cell antibodies occur in up to 40% of patients.

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Link to Image source This slide shows a diffuse lymphocytic and plasma cell infiltrate around the follicular structures of the thyroid gland. The appearances are those of Hashimoto's thyroiditis. This is an autoimmune disease which produces a diffuse goitre. Serum anti-thyroglobulin and anti-microsomal antibodies are raised. The natural history of the disease results in diffused fibrosis and hypothyroidism. The risk of thyroid lymphoma is increased

LABORATORY FINDINGS   Increased serum antithyroglobulin and antimicrosomal antibodies.  Microsomal antibody titers correlate with the degree of lymphocytic infiltrate in the thyroid gland.  Thyroglobulin antibodies correlate with the degree of thyroid fibrosis and occur in the chronic stage of the disorder.  Children often do not have elevated antibody titers. Increased TSH characteristically reflects primary hypothyroidism;  this occurs before the free T4 index decreases. Free T4 index is normal early in the disease but decreases as the disease progresses and more of the thyroid gland is destroyed.

LABORATORY FINDINGS
 

• Increased sedimentation rate is a characteristic finding.
• Free T₄ index and free T₃ index are usually elevated but may be normal early in the course of the disease;  they are often decreased later in the disease;  they are normal after six months.
• Increased antithyroglubulin antibodies - slight elevation, which falls to normal with recovery
• Mild normocytic anaemia

Link to image source Papillary thyroid carcinoma, . The majority of this tumor showed features of the follicular variant of papillary carcinoma. Note the prominent intranuclear inclusions at the center of the field. H&E, x200

LABORATORY FINDINGS   Biopsy of the thyroid gland is required for definitive diagnosis. Increased serum calcitonin - characteristic finding in medulary carcinoma.  An increased level may occur only following stimulation by calcium or pentagastrin infusion.  These stimulation tests should be performed on relatives of patients with medullary carcinoma to facilitate early recognition of the disease at a stage when it might be curable. Increased serum thyroglubulin - this occurs in many patients with untreated papillary and follicular carcinomas;  it might also be elevated in Graves' disease and in subacute thyroiditis.  The major use of this assay is in the follow-up of patients with thyroglobulin-secreting thyroid carcinoma.  Very low or undectable postoperative thyroglobulin levels indicate complete removal of the tumour.  Persistence of elevated thyroglobulin indicates that residual thyroid carcinoma probably remains.  Thyroglobulin is also elevated when metastases develop. Papillary Carcinoma of the Thyroid

LABORATORY FINDINGS

Diagnostic Studies

Low-Dose Dexamethasone Test

• In normal persons, dexamethasone inhibits pituitary ACTH release and consequently suppresses adrenal cortisol secretion.  Patients with Cushing's syndrome, in whom feedback control is abnormal, do not usually show cortisol suppression with low doses of dexamethasone.
• Following a low dose of dexamethasone given over two days, these patients show no suppression of the 24-hour urinary excretion of 17-hydroxycorticosteroids (17-OHCS) and urinary free cortisol.  For outpatient screening, a single bedtime low dose of dexamethasone will not suppress plasma cortisol drawn the next morning.

High-Dose Dexamethasone test
 

• This test is performed following an abnormal low-dose dexamethasone test to establish the origin of the hypercortisolism.
• a high dose of dexamethasone is given over a period of 48 hours, or as a single bedtime dose.  A basal blood sample is obtained for ACTH.  Twenty-four-hour urine samples are collected before and after dexamethasone for measurement of urinary free cortisol and 17-OHCS to determine whether there is cortisol suppression.

Other Laboratory Findings
 

• Slightly increased haemoglobin and haematocrit
• Decreased total lymphocyte, monocyte, and eosinophil counts - these cells move out of the circulation into the bone marrow, spleen, and lymph nodes.
• Decreased serum potassium occurs in ectopic ACTH syndrome and adrenocortical carcinoma with markedly elevated cortisol levels;  potassium loss is sue to both increased glomerular filtration rate (GFR) and increased protein catabolism with loss of intracellular potassium.
• Increased blood pH and bicarbonate (metabolic alkalosis) accompanies hypopotassemia.
• Increased serum and urine glucose and decreased glucose tolerance - cortisol is a glucocorticoid that increases hepatic glycogen and glucose production and decreases glucose uptake and utilisation in peripheral tissues.
• Increased urine calcium, in approximately 40% of patients - glucocorticoids decrease renal reabsorption of calcium.

Fig. 1 Hyperpigmentation (adrenocortical insufficiency), sparse head hair and totally absent body hair (hypothyroidism). Link to image (English/German site)

LABORATORY FINDINGS Diagnostic Studies Rapid ACTH Stimulation Test Using Cosyntropin (synthetic ACTH) A lack of increase in plasma cortisol following cosyntropin injection indicates adrenocortical insufficiency. Differentiation of Primary From Secondary Adrenocortical Insufficiency   Increased plasma ACTH indicates primary insufficiency. Normal or low plasma ACTH indicates secondary insufficiency. Other Laboratory Findings Primary Adrenocortical Insufficiency Presence of adrenal antibodies occurs in 50% to 70% of patients with nontuberculous Addison's disease. Effects of mineralcorticoid deficiency:   Decreased serum sodium due to loss in urine;  this finding might be obscured by associated dehydration Increased serum potassium Increased blood urea nitrogen (BUN) and creatinine due to decreased blood volume and dehydration Effects of glucocorticoid deficiency:   Normocytic, normochromic anaemia - this finding might be obscured by associated dehydration Decreased neutrophils, increased lymphocytes, increased eosinophils Secondary Adrenocortical Insufficiency   Adrenal effects are only those of glucocorticoid deficiency (listed above), because the mineralocorticoid, aldosterone, is not effected by diminished ACTH secretion. Decreased GH, gonadotropins, and possibly TSH reflect pituitary insufficiency.

LABORATORY FINDINGS

Diagnostic Studies
 

• Increased urinary and plasma aldosterone - these cannot be reduced with high-sodium diet, with saline infusion, or with administration of fludrocortisone acetate.
• Increased plasma aldosterone; plasma renin activity ratio (>400) occurs in primary aldosteronism. This ratio does not seem to be influenced by variations of sodium intake or diuretic administration.  The ratio seems to separate patients with aldosterone-producing adenomas from other hypertensive patients.
• Decreased plasma renin indicates primary aldosteronism.  Renin is not increased following salt restriction, diuretics, and upright posture.  These mechanisms decrease plasma volume and stimulate the renin-angiotensin system.
• Normal or increased plasma renin indicates seconary aldosteronism.

• Increased urine potassium (> 30 mEq/24 hr) - this degree of urine potassium loss reflecting the aldosterone effect is inappropriately excessive in the presence of hypokalemia.
• Decreased plasma potassium - 20% of patients may have normal plasma potassium, between 3.5 mEq/litre and 4.0 mEq/litre.  In these patients, hypokalemia may be demonstrated by increasing sodium intake.  This will cause a significant fall in plasma potassium and an increase in urine potassium in all patients with aldosteronism.
• Increased serum ppH and C0₂ content (metabolic alkalosis) accompany potassium depletionand urinary hydrogen-ion loss.

Link to Image source Pheochromocytoma, Adrenal Pheochromocytoma (Cut Surface) Mottled brown tan mass is the neoplasm filling up the adrenal medulla. Blue arrow points to residual normal medulla. Yellow arrows point to golden yellow adrenal cortex. Black discoloration around the specimen is india ink applied to assess the margins of the specimen. Image Contrib. by: Hartford Hospital Description by: Melinda Sanders, M.D. ( 423-6151)

LABORATORY FINDINGS Diagnostic Studies   Increased 24-hour urine metanephrines - this is the best single screening test; metanephrines might be elevated even between hypertensive attacks. Increased plasma norepinephrine (noradrenalin) - this is not suppressed by clonidine hydrochloride. This is the best definitive test and should be done regardless of urinary metanephrine excretion if the entire clinical picture is strongly suggestive of pheochromocytoma. Increased urine metanephrine - creatinine ratio (> 2.2 mcg/mg) Other Laboratory Findings   Increased serum and urine glucose due to catecholamine - induced suppression of insulin secretion and acceleration of glucose production

LABORATORY FINDINGS
 

• Barr bodies are present in >20% of oral-cavity cells
• Decreased serum free testosterone - does not increase following stimulation by human chorionic gonadotropin (HCG)
• Increased serum and urine FSH and LH - this finding characterises primary hypogonadism and differentiates it from secondary hypogonadism
• Absence of sperm in seminal fluid
• Testicular biopsy shows atrophy with hyalinised tubules and absence of spermatogenesis
• Karyotype is usually 47XXY.

Three sex chromosomes are associated with Klinefelter rather than the expected 2 - XXY. These individuals are males with some development of breast tissue normally seen in females. Little body hair is present, and such person are typically tall, with or without evidence of mental retardation. Males with XXXY, XXXXY, and XXXXXY karyotypes have a more severe presentation, and mental retardation is expected.

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LABORATORY FINDINGS
 

• Decreased or low-normal serum and urine FSH and LH - Failure of increase following stimualtion by clomiphene citrate, along with a strong increase following stimulation by clomiphene citrate, along with a strong increase following Gn-RH stimulation, suggests a hypothalamic lesion.  Failure of increase following stimulation by Gn-RH suggests a pituitary lesion.
• Decreased serum free testosterone, which increases following administration of HCG
• Absence of sperm in seminal fluid
• Testicular biopsy shows atrophy and failure of spermatogenesis.
• Possible increase in GH or prolaction

LABORATORY FINDINGS
 

• Increased urine HCG - this is formed by tumours having chorionic tissue, such as choriocarcinoma and embryonal carcinoma.  The HCG assay should be Beta-subunit specific to avoid a false-positive result due to cross-reaction with LH.
• Increased serum Alpha 1-fetoprotein occurs with embryonal carcinomas and yolk-sac tumours.

Seminomas are radiosensitive Stage I and II disease treated by inguinal orchidectomy plus Radiotherapy to ipsilateral abdominal and pelvic nodes ('Dog leg') or Surveillance Stage IIC and above treated with chemotherapy	Teratomas are not radiosensitive Stage I disease treated by orchidectomy and surveillance Chemotherapy (BEP = Bleomycin, Etopiside, Cisplatin) given to: Stage I patients who relapse Metastatic disease at presentation

LABORATORY FINDINGS
 

• Absence of Barr bodies (approximately 80% of patients) - reflects the presence of only one X chromosome
• Decreased serum and urine oestrogens, which do not increase following administration of HCG
• Increased FSH - this is elevated in early childhood and again prepubertally, but may be normal in mid-childhood
• Increased LH - this usually does not increase until puberty
• Karyotype shows 45XO in typical cases;  other chromosomal abnormalities also occur.

Only 1 sex chromosome is present -X0, or X_. The expected Y chromosome is missing. Turner syndrome is associated with underdeveloped ovaries, short stature, webbed/.bull neck, and broad chest. Individuals are sterile, and lack expected secondary sexual characteristics. Mental retardation typically not evident.

LABORATORY FINDINGS
 

• Increased LH-FSH ratio is a characteristic finding.
• Increased serum free testosterone
• Increased serum androstenedione, which is a testosterone precursor

LABORATORY FINDINGS
 

• Normal or decreased serum and urinary FSH and LH
• Normal or decreased serum and urinary oestrogens - these will increase following administration of gonadotropins.

OVARIAN TUMOURS

LABORATORY FINDINGS

Feminising Ovarian Tumours
 

• Increased serum and urinary oestrogens
• Decreased urinary FSH as a result of suppression by increased ovarian oestrogens
• Lack of serum progesterone and urinary pregnanediol

• Markedly increased serum free testosterone
• Decreased urinary FSH as a result of suppression by increased ovarian testosterone
• Increased cortisol and other laboratory findings of Cushing's syndrome in adrenal rest tumours
• Increased 17-ketosteroids (17-KS) produced by adrenal rest tumours
• Pap smear shows decreased oestrogen effect

LABORATORY FINDINGS

Diagnostic Studies
 

• Fasting venous plasma glucose > 140 mg/dl on more than one occasion.
• Oral glucose tolerance test utilizing 75-g carbohydrate solution - 2 hr, and one other sample, plasma glucose above 200 mg/dl

• Increased urine glucose when blood glucose is above the renal threshold
• Increased urine volume and osmolality - glucose in the urine acts as an osmotic diuretic
• Decreased serum phosphorus - insulin causes phosphate to enter cells; there is also increased phosphate loss in urine
• Decreased serum sodium - this is inversely related to increased blood sugar;  osmotic diuresis accounts for increased sodium loss in the urine.

• Increased plasma glucose
• Plasma acetone is usually present;  increased Beta-hydroxybutyrate.
• Increased BUN and creatinine - prerenal azotemia reflects dehydration and fall in blood pressure
• Increased urine glucose, ketones, protein, and casts
• Decreased blood pH, C0₂ content (metabolic acidosis) - reflects increased formation of ketoacids and diminished bicarbonate consequent to buffering of acids;  increased anion gap
• Decreased PC02 reflects increased ventilation as compensation for metabolic acidosis.
• Increased serum potassium - acidosis causes potassium to shift from within the cells into the extracellular space.  Potassium may be normal or low, particularly after therapy has been started.
• Leukocytosis may be >20,000/µl, even without infection.

HYPOGLYCEMIA

LABORATORY FINDINGS

Insulin-Producing Islet Cell Tumour

Symptoms of hypoglycemia occur while fasting and are accompanied by plasma glucose <45 mg/dl and an inappropriately high plasma insulin level (>10 µU/ml).  In about 50% of patients, overnight fasting produces the characteristic findings.  Some patients require as much as a 72-hour fast, followed by exercise, to demonstrate hypoglycemia and hyperinsulinemia and establish the diagnosis.

Postprandial (Reactive) Hypoglycemia

Plasma glucose below 45 mg/dl and appropriate symptoms occur 2-4 hours after eating but not during fasting.  The glucose frequently returns to normal spontaneously.  The 5-hour glucose tolerance test is an artificial situation and is not recommended for establishing the diagnosis.  A standard meal may be used in an attempt to produce postprandial hypoglycemia.  Blood sugar should be drawn at the time symptoms occur.  It is not necessary to measure serum insulin levels.

Other Laboratory Findings
 

• Laboratory findings of Cushing's syndrome, hypothyroidism, hypopituitarism, hepatic failure, von Gierke's disease - if hyopoglycemia is secondary to any of these disorders

LABORATORY FINDINGS

Diagnostic Studies
 

• Increased fasting serum gastrin (>500 pg/ml) - borderline levels (250 pg/ml-500 pg/ml) will be markedly increased following stimulation by IV secretin

• Increased volume of highly acid gastric juice; baseline acidity is > 60% of the maximally stimulated level.  A recent report revealed that gastric analysis does not improve on the diagnostic ability of the gfasting serum gastrin test.
• Increased stool lipids - duodenal hyperacidity inactivates pancreatic enzymes and causes maldigestion and malabsorption of lipids and consequent diaorrhea and steatorrhea
• Decreased serum potassium secondary to severe diaorrhea, which often accompanies this syndrome
• Decreased serum albumin - possibly due to protein malabsorption or protein-losing enteropathy

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LABORATORY FINDINGS

Diagnostic Studies
 

• Increased serum calcium (11 mg/dl - 13 mg/dl) is the single most important test in the diagnosis of primary hyperparathyroidism.  It should be elvated on at least three occasions.  Levels > 13 mg/dl suggest nonparathyroid causes of hypercalcemia (e.g., malignant tumours, multiple myeloma, and hypervitaminosis D).
• Decreased serum phosphate (<3.8 mg/dl).  This is lower in hyperparathyroidism than in nonparathyroid hypercalcemia.
• Increased serum chloride - levels above 103 mEq/litre strongly suggest hyperparathyroidism in the absence of thyrotoxicosis; levels below 103 mEq/litre suggest nonparathyroid hypercalcemia in the absence of diuretic administration of vomiting.
• Normal haemotocrit is characteristic of primary hyperparathyroidism; haemotocrit <37% is often found in nonparathyroid hypercalcemia because this is most frequently associated with malignant tumours.
• Lafferty uses the above parameters in the following parameters in the following discriminant formula, constructed so that a positive score indicates hyperparathyroid hypercalcemia and a negative score suggests nonparathyroid hypercalcemia:

*HCT    =    haematocrit
 Cl    =        chloride
 Caex    =    the difference between the total serum calcium and the upper limits of normal in a given laboratory
 P        =    phosphorus
 ±     The formula is not useful in separating hyperparathyroid patients from normal patients.  Patients who are vomiting or using diuretics might be misclassified using
        this formala.
 

Other Laboratory Findings
 

• Increased urine phosphate due to decreased renal tubular reabsorption
• Increased urine calcium due to increased intestinal absorption, increased renal tubular reabsorption, and increased mobilisation from bone

• Increased urine volume due to increased urinary phosphate and calcium
• Decreased and fixed urine specific gravity - result of hypercalcemic interference with renal concentrating ability
• Decreased serum pH and bicarbonate (metabolic acidosis) due to renal loss of bicarbonate

• High serum calcium - primary hyperparathyroidism
• Low serum calcium - secondary hyperparathyroidism, as in chronic renal disease
• In patients with hypercalcemia due to malignant disease, PTH values are generally lower than those seen with hyperparathyroidism, but with significant overlap.

A major cause of variability of PTH might help in the patient with borderline elevation of serum calcium, unresolved metabolic bone disease, or recurrent calcium stone formation, but is not usually needed to diagnose hyperparathyroidism.

A major cause of variability in PTH determinations is that the available immunoassays measure different portions of the PTH.  Some assays measure carboxy-terminal fragments and intact PTH, whereas others measure the amino-terminal portion of the PTH molecule.  The latter is the biologically active region of the molecule.  In a study of 29 patients with hypercalcemia.  Raisz et al had serum PTH assaays done by four commercial laboratories and observed, "....we found considerable variation in the frequency of elevated values (of PTH) in hyperparathyroidism and the degree to which the assay discriminated between primary hyperparathyroidism and hypercalcemia of malignancy......it is still necessary to use multiple tests in the different diagnosis of hypercalcemia."

HYPOPARATHYROIDISM

LABORATORY FINDINGS
 

• Increased serum phosphorus, which reflects increased renal reabsorption of phosphorus
• Decreased serum calcium - decreased PTH and 1,25-dihydroxyvitamin D3 result in decreased calcium entry into the blood from bones, GI tract, and renal tubules
• Decreased urine calcium and phosphorus
• Decreased or undetectable serum parathyroid hormone; increased PTH occurs in pseudohypoparathyroidism
• Increased serum pH, bicarbonate (metabolic alkalosis) - due to renal retention of bicarbonate

PRECOCIOUS PUBERTY

LABORATORY FINDINGS
 

• Increased pituitary gonadotropins in true precocious puberty
• Decreased or low-normal pituitary gonadotropins in pseudoprecocious puberty

• Oestrogen effect seen on Pap smear
• Increased oestrogens due to granulosa cell tumour of the ovary

• Increased HCG in choriocarcinoma of the testis
• Increased urinary pregnanetriol or serum 17-hydroxyprogesterone in congenital adrenal hyperplasia
• Increased serum free testosterone in interstitial cell tumour of the testis

LABORATORY FINDINGS

• The most commonly produced hormones that are formed at ectopic sites are listed below.  For the laboratory findings see the disorder indicated.
• ACTH - small-cell (oat cell) carcinoma of lung, epithelial thymoma, pancreatic islet-cell tumour, medullary carcinoma of thyroid, bronchial carcinoid tumour (see Cushing's Syndrome)
• ADH (vasopressin) - small-cell (oat cell) carcinoma of lung (see Syndrome of inappropriate ADH Secretion)
• PTH - squamous cell carcinoma of lung, adenocarcinoma of kidney (see Hyperparathyroidism)
• Non-islet-cell tumours producing hypoglycemia - fibrosarcoma, liposarcoma, mesothelioma, leiomyosarcoma, hepatoma, adrenocortical carcinoma (see Hypoglycemia)
• Erythropoietin - cerebellar haemangioblastoma, uterine fibromas, liver carcinoma (see Seconary Erythrocytosis, Chap. 8)
• HCG - carcinoma of lung, kidney, liver, adrenal gland
• Calcitonin - small cell (oat cell) carcinoma of the lung, breast cancer (see Carcinoma of the Thyroid)

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