ABSTRACT
Macronodular liver cirrhosis and hepatocellular carcinoma were found in a 61-year-old male who had been exposed for 35 years to Trinitrotoluene (TNT). The question whether TNT had induced these pathological processes is raised.
Subject(s)
Carcinoma, Hepatocellular/chemically induced , Liver Cirrhosis/chemically induced , Liver Neoplasms/chemically induced , Trinitrotoluene/toxicity , Carcinoma, Hepatocellular/pathology , Chronic Disease , Humans , Liver/drug effects , Liver/pathology , Liver Cirrhosis/pathology , Liver Neoplasms/pathology , Lymphatic Metastasis , Male , Middle AgedABSTRACT
A 45-year-old man, was admitted for investigation of severe sexual impairment. During 20 years of marriage, he had had no normal sexual intercourse and the couple was childless. Physical examination disclosed a severely obese man (weight 300 kg, height 1.75 m), with a relatively small and invaginated penis and small (5 ml) soft testes. Laboratory examinations disclosed the following: low serum testosterone (1 ng/ml), with a reduced response to HCG (3.8 ng/ml). Sex hormone binding globulin was at the lower limit of normal (0.38 microgram/dl), serum free testosterone was low (0.98% of total testosterone) as well as non-SHBG bound testosterone (22% of total testosterone). Daily total urinary estrogen excretion was increased (107 micrograms), the plasma estrone (78 pg/ml) and estradiol (74 pg/ml) were elevated. The gonadotropins were normal and responded adequately to LRH. Plasma growth hormone was decreased, prolactin, T4 and adrenal steroids were normal and responded normally to stimuli and inhibitors. Chromosomal constitution was 46XY. Thus, in this man the marked obesity produced a significant increase in estrogens which subsequently induced a severe decrease in testosterone and its free counterpart in excessive impairment of sexual function.
Subject(s)
Hypogonadism/etiology , Obesity, Morbid/complications , Hormones/metabolism , Humans , Male , Middle Aged , Obesity, Morbid/metabolismABSTRACT
A premenopausal woman with soft tissue metastases from a carcinoma of the breast developed hypercalcemia with hypophosphatemia, reduced tubular reabsorption of phosphate, elevated urinary cyclic AMP levels and normal serum PTH levels was observed. Hormonal therapy with testosterone followed by tamoxifen induced normalization of her serum calcium concomitant with the disappearance of the pleural effusion and reduction in the size of her lung metastases. The correlation between the efficacy of antitumor treatment on pleural effusion, lung metastases, and normalization of serum calcium, as well as the elevated PTH level in the pleural effusion, suggest that this breast carcinoma secreted a PTH-like substance.
Subject(s)
Breast Neoplasms/metabolism , Hypercalcemia/etiology , Parathyroid Hormone/metabolism , Testosterone/therapeutic use , Adult , Breast Neoplasms/complications , Female , Hormones, Ectopic/biosynthesis , Humans , Hypercalcemia/drug therapy , Lung Neoplasms/drug therapy , Lung Neoplasms/secondary , Pleural Effusion/drug therapy , Pleural Effusion/etiology , Tamoxifen/therapeutic useABSTRACT
An eleven-year-old boy was diagnosed to have Addison's disease with an ACTH level of over 4500 pg/ml after a short episode of fever and dehydration. From the age of 6 years his skin and buccal mucosa had been hyperpigmented but there were no other subjective complaints. The clinical examination also revealed signs of advanced puberty for his age (3rd--4th stage according to Tanner's criteria), with advanced bone age (13 years). The elevated levels of plasma testosterone and gonadotropins and their response to LH-RH stimulation were appropriate for his clinical stage of puberty and supported the diagnosis of true precocious puberty. It is proposed that the concomitant appearance of Addison's disease and precocious puberty is due to a "drift" phenomenon of LH-RH and/or gonadotropins following the prolonged elevation of ACTH secretion.
Subject(s)
Addison Disease/complications , Puberty, Precocious/complications , Child , Humans , Hypothalamo-Hypophyseal System/physiopathology , Male , Pituitary-Adrenal Function Tests , Testis/physiopathologyABSTRACT
Marked improvement in the severe hypertension (250/150 mmHg) and hirsutism of a patient suffering from polycystic ovary syndrome was quickly achieved by the use of spironolactone 200 mg per day. Substitution of spironolactone with bromocriptine induced further amelioration of these symptoms and renewal of ovulatory cycles. These drugs may afford another mode of therapy in patients with polycystic ovary syndrome.
Subject(s)
Bromocriptine/therapeutic use , Polycystic Ovary Syndrome/drug therapy , Spironolactone/therapeutic use , Adult , Female , Hirsutism/drug therapy , Hirsutism/etiology , Hormones/analysis , Humans , Hypertension/drug therapy , Hypertension/etiology , Polycystic Ovary Syndrome/complicationsABSTRACT
A 62-year-old man was admitted to hospital 10 times over 12 years because of pyrexia of unknown origin. Hypothalamic hypopituitarism was diagnosed by dynamic tests including clomiphene, LRH, TRH and chlorpromazine stimulation. Lack of ACTH was demonstrated by long and short tetracosactrin tests. The aetiology of the disorder was believed to be previous encephalitis. Following substitution therapy with adrenal and gonadal steroids there were no further episodes of fever.
Subject(s)
Fever of Unknown Origin/etiology , Hypopituitarism/complications , Hypothalamic Diseases/complications , Humans , Hypopituitarism/diagnosis , Hypothalamic Diseases/diagnosis , Male , Middle AgedABSTRACT
Hypertension and hypokalemia were found in a 60-yr-old woman suffering from primary hyperparathyroidism. Laboratory investigations in this patient disclosed 1) elevated levels of plasma aldosterone (PA) which could not be suppressed by a high sodium diet alone or in combination with fludrocortisone (Florinef); 2) a decline of the elevated PA levels after 4 h of ambulation; and 3) low PRA which was unresponsive to stimulation by a low sodium diet coupled with diuretic-induced volume depletion and 4 h of ambulation. These findings were consistent with the diagnosis of primary hyperaldosteronism. Extirpation of a parathyroid adenoma reduced the patient's serum calcium level to normal, and subsequently, a normalization of her blood pressure, serum electrolytes, PA, and PRA were observed. On the basis of these data is is suggested that in this case hyperaldosteronism may have been caused directly or indirectly by primary hyperparathyroidism.