Nodular adrenal hyperplasia and Cushing's syndrome may be food-dependent as a result of abnormal responsiveness of adrenal cells to physiologic secretion of GIP. "Illicit" (ectopic) expression of GIP receptors on adrenal cells presumably underlies this disorder.

Adrenalectomy is usually performed via transabdominal or posterior approaches. Unfortunately, both approaches are associated with painful postoperative syndromes. Recently, laparoscopic surgery was applied to organ removal. During a period of 12 months, we performed a series of successful laparoscopic adrenalectomies (10 of the right and 11 of the left gland). The pathologies were medullary cyst (1), angiomyolipoma (1), DHEAS hyperplasia (1), primary aldosteronism (2), Cushing's adenoma (3), pheochromocytoma (4), Cushing's syndrome (4), and nonfunctional adenoma (5). A flank approach was taken with four 11-mm trocars. Electrocautery and blunt forceps were used for dissection. The vessels were secured with medium-large titanium clips, and the adrenal was removed in a sterile plastic bag. The average operating time was 2.3 h, and median postoperative stay was 4 days. Two patients required blood transfusion of 2 units postoperatively. We believe this technique is adequate for the surgical removal of adrenal tissue, resulting in less postoperative pain and in rapid recovery. It may also change the surgical management of asymptomatic adrenal lesions.

In 15 cases of therapeutic abortion by laparotomy the placenta was disconnected from the foetus and perfused in situ with tracer amounts of radioactive dehydroepiandrosterone (DHA), dehydroepiandrosterone sulphate (DHAS), androst-4-ene-3,17-dione (A), testosterone (T) and 17β-oestradiol (OE2). Analysis of the placentas, perfusates and urine samples revealed an extensive aromatisation of DHA, A and T; more than 70% of the radioactive material recovered was phenolic, and at least 80 % of this phenolic material was identified as oestrone (OE1), 17β-oestradiol (OE2) and oestriol (OE3), the latter being detected only in the urine. Comparative studies indicated that A and T were aromatised somewhat better than DHA and that all three unconjugated steroids were aromatised to a much greater extent than DHAS. Radioactive OE1 and OE2 were isolated and identified in the placentas and perfusates, but no OE3, epimeric oestriols, or ring D ketols could be detected in these sources, not even when human chorionic gonadotrophin (HCG) was added to the blood prior to perfusion. Lack of placental 16-hydroxylation was also apparent when OE2 was perfused. Regardless of the precursor perfused, there was three times more OE2 than OE1 in the placenta and three times more OE1 than OE2 in the perfusate. This was also the case following perfusion with OE2. The results are interpreted as suggesting the existence in the pregnant human of a placental »barrier« limiting the passage of circulating androgen. The barrier consists of a) limited ability to transfer directly DHAS and b) an enzymic mechanism resulting in the rapid and extensive aromatisation of the important androgens DHA, A and T.

No abstract

Four previable foetuses (18th to 20th week of gestation) were perfused with a combination of 14C-labelled dehydroepiandrosterone (DHA) and 3H-labelled dehydroepiandrosterone sulphate (DHAS). Approximately 80% of the radioactive material administered was recovered from the various foetal tissues and perfusates. With the exception of the liver, which exhibited an approximately equal concentration of the two isotopes, all foetal tissues contained more 14C-than 3H-labelled material. On an average, 27% of the 14C-, and 8% of the 3H-labelled material administered was retained by the foetal organism. Approximately 80% of the 14C-labelled material recovered from the foetal tissues was in a conjugated form; very little, if any of the 3H-labelled material was recovered as unconjugated (free) material. More than 90% of the conjugated radioactive material present in the different foetal tissues, except the liver and residual foetus, was isolated and identified as DHAS. The 3H- to 14C-ratio of the DHAS isolated from various tissues showed marked differences; it was lowest in the lungs and adrenals, indicating that these organs are active sites of sulpho-conjugation of DHA. In addition to DHAS, androst-5-ene-3β,17β-diol 3-sulphate (Δ5-DIOLS) and androst-5-ene-3β,16α,17β-triol 3-sulphate (Δ5-TRIOLS) were isolated from the liver and a smaller amount of Δ5-TRIOLS from the residual foetal tissues. From the perfusates, 3β,16α-dihydroxyandrost-5-en-17-one 3 sulphate (16αHO-DHAS) was isolated. The 3H- to 14C-ratio of the Δ5-TRIOLS isolated from the liver was considerably lower than those of Δ5-DIOLS and DHAS isolated from the same organ. It is concluded that DHA is extensively sulphurylated by a variety of foetal tissues, very little, if any DHAS is hydrolysed by the foetal organism, DHAS and also some DHA is 16α-hydroxylated by the previable foetus, the foetal liver is the principal site of 16α-hydroxylation of the DHAS circulating in the foeto-placental unit.

Tixocortol pivalate is a corticosteroid with topical anti-inflammatory activity equal to that of hydrocortisone. It was evaluated in a group of 18 normal subjects to determine whether it exerted any systemic glucocorticoid activity after single oral or intrarectal doses and after short-term dosing by the intranasal route. Effects of tixocortol pivalate were compared to those of oral dexamethasone and intrarectal betamethasone 21-phosphate. By the three routes, tixocortol pivalate does not induce any changes in plasma cortisol, leukocyte counts (neutrophils, lymphocytes, monocytes, eosinophils), blood glucose, or 24-hr urinary excretion of sodium and potassium, whereas there were changes after dexamethasone and betamethasone. Tixocortol pivalate, however, increased urinary free cortisol-like substances. It is concluded that tixocortol pivalate given for short periods by nonparenteral routes does not induce a measurable systemic glucocorticoid effect.

Yearly episodes of edema, hypokalemia, anxiety, and depression were found to be due to cortisol and deoxycorticosterone surges secondary to a pituitary adenoma in a woman without any of the usual clinical features of Cushing's syndrome. During the long clinical remissions, she had no recognizable laboratory abnormality. She had two episodes in the year following incomplete transphenoidal pituitary tumor resection, but has had none in 2 yr since receiving radiotherapy. The episodes were caused by mineralocorticoid actions of large ACTH-induced increases in cortisol and deoxycorticosterone secretion. A history of episodic edema and hypokalemia, often attributed in women to surreptitious diuretic abuse, requires a careful search for hypercorticism even in the absence of clinical Cushing's syndrome.

A case of fertile eunuchoidism is presented. The diagnosis was established on the basis of low androgen secretion in the presence of active spermatogenesis, increase in testosterone output after gonadotrophin stimulation, and adequate peripheral response to exogenous testosterone. Resistance to clomiphene stimulation but normal pituitary response to LH-RH was elicited indicating a suprasellar disturbance as the cause of the disorder.