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Biomedical subjects

J Mahoudeau

Publications and source records attributed to J Mahoudeau.

14 recordsLinked to original sources
PubMed1992

Food-dependent Cushing's syndrome mediated by aberrant adrenal sensitivity to gastric inhibitory polypeptide.

BACKGROUND: Some patients with Cushing's syndrome have nodular adrenal hyperplasia. In most the disease is corticotropin-dependent, but in others it is corticotropin-independent. The cause of the adrenal hyperplasia in the latter patients is not known. METHODS: We studied a 49-year-old woman with Cushing's syndrome and nodular adrenal hyperplasia in whom food stimulated cortisol secretion. Plasma cortisol concentrations were measured in response to the ingestion of mixed meals, glucose, protein, and fat and after the administration of various gastrointestinal and other types of hormones. We also studied the ability of the long-acting somatostatin analogue octreotide to prevent the food-induced increase in plasma cortisol concentrations and to ameliorate the clinical manifestations of Cushing's syndrome in this patient. RESULTS: The patient's fasting plasma cortisol concentrations were subnormal, ranging from 3.0 to 7.5 micrograms per deciliter (83 to 207 nmol per liter), and they increased to as high as 16.5 micrograms per deciliter (455 nmol per liter) after a mixed meal. Her urinary cortisol excretion ranged from 164 to 250 micrograms per day (453 to 690 nmol per day) and could not be suppressed by a large dose of dexamethasone. Plasma corticotropin concentrations were virtually undetectable at all times. The ingestion of glucose, protein, and fat increased plasma cortisol concentrations to 3.6, 2.2, and 4 times the base-line value, respectively; the meal-induced and glucose-induced increases were inhibited by octreotide. The infusion of gastric inhibitory polypeptide (GIP) increased the patient's plasma cortisol concentration to 3.7 times the base-line value, but had no effect in normal subjects. The patient's fasting plasma GIP concentrations were normal both before and after a meal, and there was a close correlation between her plasma cortisol and GIP concentrations. Treatment with octreotide decreased urinary cortisol excretion and ameliorated the clinical manifestations of Cushing's syndrome. CONCLUSIONS: The development of aberrant adrenal sensitivity to GIP can result in food-dependent adrenal hyperplasia and therefore in Cushing's syndrome.

Adrenal Glands↗
PubMed1991

Polycythemia and steroid overproduction in a gonadotropin-secreting seminoma of the testis.

While investigating the cause of mild polycythemia in a young man, a testicular seminoma was discovered with unusual and tumor-dependent features: an absolute polycythemia with high plasma erythropoietin (EPO) levels, an overproduction of estradiol and testosterone, and a dramatic Leydig cell hyperplasia surrounding the tumor tissue. The authors attempted to gain insight into the relationship between this testicular tumor and the hormonal overproduction, i.e., of EPO, estradiol, and testosterone. Their results favored the conclusion that the high EPO levels and the polycythemia were an indirect effect secondary to the steroid overproduction rather than a direct EPO-producing activity. Moreover, the steroid overproduction by the testis could be caused by a paracrine mechanism through human chorionic gonadotropin activity on the Leydig cells.

Adult↗
PubMed1991

[Clinical aspects of gonadal dysgenesis].

Gonadal dysgenesis are classified according to the aspect of external genitalia. The group with female genitalia includes Turner's syndrome, and "pure" dysgenesis; the group with male genitalia involves Klinefelter's syndrome, XX males and may be anorchia; the group with ambiguous genitalia includes "mixed" gonadal dysgenesis, true hermaphroditism and Leydig-cell agenesis. An algorythmic approach to patients with ambiguous external genitalia is presented in order to distinguish between gonadal dysgenesis and male or female pseudohermaphroditism.

Algorithms↗
PubMed1990

Stimulation by hCG of ovarian inactive renin synthesis in rabbit preovulatory theca cells.

The origin of ovarian renin and its regulation by hCG were investigated in rabbit periovulatory follicles and cultured preovulatory follicular cells. Intracellular content of renin in thecal cells was 8-fold greater than of granulosa cells. In vivo, administration of hCG increased intracellular content of renin in thecal but not granulosa cells. Similar results were obtained for cultured follicular cells, from which renin was partly released into the medium. In vitro, hCG increased intracellular renin content of thecal but not granulosa cells, without obvious effect on release. Approximately 95% of ovarian renin was inactive, but could be activated by trypsin. Thecal renin was antagonized in vitro by renin antiserum, indicating a specific renin activity. Our study establishes in the rabbit the thecal cell origin of ovarian inactive renin and demonstrates hCG regulation of its synthesis.

Animals↗
PubMed1979

[Prostatic carcinoma: metabolic effect of percutaneous beta-estradiol (author's transl)].

Twenty one patients suffering from carcinoma of the prostate, confirmed histologically and previously untreated, received treatment in the form of 17 beta-estradiol administered percutaneously. At a dose of 6 mg of estradiol per day, testosterone levels fell to a mean of 1 ng/ml. No change in lipids, lipoproteins nor cholinesterase were detected.

Administration, Topical↗
PubMed1979

[Sipple's syndrome: type II endocrine polyneoplasia (author's transl)].

Sipple's syndrome is a generally familial polyneoplastic affection associating a medullary thyroid cancer and a pheochromocytoma. The overall picture of the syndrome has, in fact, become larger now that it is known that there is previous hyperplasia of thyroid C cells and chromaffin cells in relation to neoplasms. Increase in plasma thyrocalcitonin levels is the best indicator of medullary cancer, and the discovery of this hormone in pheochromocytomas has shown the secretory origin of the two tumors, the cells of which have a common embryological origin in the neural crest. Sipple's syndrome is often associated with hyperparathyroidism, hyperplasia without adenoma (endocrine polyneoplasia type II a), or phacomatosis and a dystrophic condition (type II b or III). The authors discuss the nosology of the syndrome and its relation to the diffuse endocrine and APUD systems.

Adrenal Gland Neoplasms↗
PubMed1975

Antiandrogenic effect of spirolactones: mechanism of action.

Spirolactones are aldosterone antagonists which inhibit the binding of aldosterone to the renal mineralocorticoid receptor. These molecules also possess an antiandrogenic effect which could be due, among other possibilities, to a peripheral antagonism of androgens. This hypothesis has been tested in the present study. From in vivo experiments, spironolactone K+ canrenoate appear to inhibit the binding of [3H]5alpha-dihydrotestosterone [3H]DHT to the cytosolic and nuclear receptor of the rat ventral prostate. The doses used are in the same range as those used for demonstrating the antimineralocorticoid effect of these molecules. In vitro incubations and in vitro displacement studies show that spironolactone and K+ canrenoate are respectively about 20 and 100 times less effective than DHT in displacing 50 percent of 5 times 10- minus 10 M [3H]DHT from its receptor. Spirolactones are also able to compete with [3H]DHT for the specific 8 S cytosolic receptor. Neither spironolactone nor K+ canrenoate decreases prostatic 5alpha-reductase activity, even at a concentration as high as 10- minus 5 M. It seems likely that spirolactones, besides their action on testosterone biosynthesis, exert their antiandrogenic activity via a peripheral androgen antagonism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMedDate not supplied

[Gonadotropic function in female Cushing syndrome (author's transl)].

A study of 38 female Cushing syndromes showed decreased levels of FSH and LH, with normal LH-RH stimulation in most adrenal hyperplasia and benign adenoma, and absent stimulation in carcinoma. The levels were normalized by suppression of hypercorticism. This suggests a blunted gonadotropic function, in female Cushing syndrome, probably at the hypothalamic level. The predominant respective roles of hyperandrogeny in carcinoma and of hypercortisolism in adrenal hyperplasia and benign adenoma seem probable.

Adenoma↗
PubMedDate not supplied

[Gonadotropic function in female Cushing's syndrome (author's transl)].

Gonadotropic function has been studied without selection in 38 female patients with Cushing's syndrome followed during four years. The level of gonadotropins FSH and LH was low in all etiologies of the syndrome. LH-RH stimulation is normal in adrenal hyperplasia and adenoma, and very low in carcinoma. These abnormalities are cured after reduction of hypercorticism. The share of either cortisol or androgens is discussed. A predominant hypercortisolism blunting action on gonadotropic function is possible, cortisol being the common factor of Cushing's syndrome.

Adenoma↗