[Reninoma: a rare but curable cause of high blood pressure, a case report]. / Réninome: une cause rare mais curable d'HTA. A propos d'un cas.

We report a case of a renin secreting tumor, which is a very rare cause of secondary high blood pressure. A 22-year-old woman was hospitalised for exploration of high blood pressure (160/110 mmHg) with severe hypokaliemia (2,7 mmol/l) and secondary hyperaldosteronism. Physical examination was normal except the high blood pressure. Bioassays show increased kaliuresis (66 mmol/24h), plasma renin (89 pg/ml in clinostastism--108 pg/ml in orthostatism), pro-renin (1207 pg/ml in clinostastism--1412 pg/ml in orthostatism) and aldosterone (210 pg/ml in clinostastism--566 pg/ml in orthostatism). The rest of the endocrine tests were normal (cortisol and ACTH at 8:00 am, urinary free cortisol, overnight 1 mg dexamethasone suppression test). Doppler ultrasound method, performed by an experienced radiologist, did not show renal artery stenosis. Abdominal computerized tomography showed a nodular formation at the upper pole of the right kidney, isodense to renal medullary. The size tumor was 15 mm. The renal vein sampling shows high values of renin on both sides whereas, for the pro-renin, the values were higher on the tumor side. In spite of treatment with CEI (Converting Enzyme Inhibitors) and calcium antagonists, the blood pressure was not controlled. Hypokaliemia persisted (3 mmol/l) in spite of high daily potassium intake (64 mmol/l of potassium chloride). After tumor resection, reninoma was diagnosed by the pathology examination and blood pressure, plasma rennin, plasma aldosterone level returned to normal.

Food-dependent Cushing's syndrome: characterization and functional role of gastric inhibitory polypeptide receptor in the adrenals of three patients.

In the present work, the presence of gastric inhibitory polypeptide (GIP) receptors and their functional role in the adrenal cells of three patients with food-dependent Cushing's syndrome were studied. RT-PCR and in situ hybridization studies demonstrated the presence of GIP receptor in the adrenals of the three patients. The presence of this receptor was also demonstrated in two human fetal adrenals, but not in two normal adult human adrenals or in the adrenals of one patient with nonfood-dependent Cushing's syndrome. Freshly isolated cells from patient adrenals responded in a dose-dependent manner to the steroidogenic action of both ACTH and GIP, whereas cells from normal adrenals responded only to ACTH. Treatment of cultured normal adrenal cells with ACTH, but not with GIP, increased the messenger ribonucleic acid (mRNA) levels of cholesterol side-chain cleavage cytochrome P-450, P450c17, and 3beta-hydroxysteroid dehydrogenase, whereas both hormones enhanced these mRNAs in patients' adrenal cells, although the effects of ACTH were greater than those of GIP. Moreover, pretreatment with ACTH enhanced the steroidogenic responsiveness of both normal and patient adrenal cells, whereas GIP caused homologous desensitization, and this was associated with a marked reduction of GIP receptor mRNA levels, as demonstrated by RT-PCR and in situ hybridization. Finally, both ACTH and GIP inhibited DNA synthesis in one patient's adrenal cells, whereas in normal adrenal cells only ACTH had this effect. In conclusion, the present data demonstrate that ectopic expression of functional GIP receptors is the main cause of food-dependent Cushing's syndrome.

[Amyloid goiter. Report of two cases]. / Le goitre amyloïde. A propos de deux observations.

We report two cases of amyloid goiter which clinical appearance had evoked a neoplastic lesion. The diagnosis was made by histologic examination. The nature of the amyloid precursor, determined by immunohistochemistry, has allowed to evoke primitive amyloidosis in one case and to attribute amyloid goiter to renal insufficiency in the second case.

[Congenital generalized lipodystrophy. Lipid changes. Therapeutic trials]. / Lipodystrophie généralisée congénitale. Perturbations lipidiques. Essais thérapeutiques.

On the occasion of a new case of congenital generalized lipodystrophy the clinical features of this disease are reviewed. Furthermore, the frequent association of type V hypertriglyceridemia is emphasized. Various pathogenic hypotheses guide the therapeutic attempts, which are often unsuccessful.

[Hyperlipidemia aggravated or induced by combined oral contraceptives: preliminary results of a decision-making scheme for the prevention of cardiovascular episodes]. / Hyperlipidemies revelees ou induites par les contraceptifs estroprogestatifs. Attitudes adoptees--resultats preliminaires.

PIP: This article outlines a systematic treatment for patients on combined oral contraceptives (OCs) in whom hyperlipidism is induced or aggravated by the OCs. 36 women aged 20-40 years who used OCs containing 50 mcg of ethinyl estradiol (EE) and Norgestrel were treated by the same team of physicians with an identical protocol. 9 of the 36 women had elevated triglyceride (TG) levels, 5 had elevated total cholesterol (TC) levels, and 22 had both. The average level of TG was 1.56 and of TC 2.88 g/l. When the EE dosage of the 1st group was reduced to 30 mcg, the average TG level fell from 1.44 to l g/l. In a 2nd group, in which either lipid levels were very high or predisposing factors were present, the use of combined OCs was discontinued; the average level of TG declined from 1.64 to .95. Some patients were treated successively in both groups. In patients receiving reduced dosages of EE, the average TC level declined from 2.80 to 2.22. The average TC level for those discontinuing OC therapy declined form 2.89 to 2.40. Despite high initial values in those for whom OC therapy was stopped, most cases were normalized with these procedures. In 2 cases of elevated TG, 5 of TC, and 5 of both, the levels were not normalized within 3 months of discontinuing OC therapy. In 9 of 10 cases of elevated TC or TC and TG, predisposing factors were present. The experience suggests the existence of 2 categories of lipid anomales, those induced by the OCs, which tend to be moderate and subject to improvement or disappearance with reduced dosage of EE or discontinuation of OCs, and probably preexisting cases which are aggravated by the OCs. Such cases are of greater significance and are likely to persist longer. In cases of preexisting lipid anomalies when genetic factors are involved, OCs should be stopped to avoid the risk of vascular accidents.^ieng

Causes of death in adults with acute leukemia.

The causes of death were investigated in 315 adults with acute leukemia during a 7-year period (1966-1972). Infection alone or in combination was the most common cause (75%), followed by hemorrhage (24%) and organ failure (9%). Most of the infections were either systemic or pulmonary. Seventy-five percent of the systemic infections and 72% of the pneumonias were caused by bacteria. Klebsiella pneumoniae, Escherichia coli and Pseudomonas aeruginosa were the most frequent organisms isolated. After 1968, there was a sharp decrease in the number of fatal infections caused by Pseudomonas aeruginosa and a marked increase in the incidence of fatal infections caused by Klebsiella spp. and E. coli. Infections caused by Gram-positive cocci occurred in only 3% of the cases. The incidence of systemic fungal infections was 13%; most common fungi causing infection were Candida spp. and Aspergillus spp. Eighty-five percent of 159 patients with a terminal neutrophil count of less than 100/mm3 died of infection, compared to 48% of 62 patients with a terminal neutrophil count of greater than 1000/mm3. Hemorrhage was mostly due to thrombocytopenia (61%) and disseminated intravascular coagulation (12%). This study indicates that infection continues to be the most common cause of death in patients with acute leukemia. Although advances in antibiotic therapy have changed the distribution of causative organisms, ultimate control of infection requires further improvements in supportive care measures which rectify impairments in the patients' host defense mechanisms.