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PubMed1987

[Influence of angiotensin on the secretion of aldosterone in idiopathic hyperaldosteronism].

The purpose of study was to investigate the role of angiotensin II in idiopathic primary aldosteronism (IPA) and to evaluate the interest of angiotensin converting enzyme inhibitors (ACEI) in its management. The study concerned 10 hypertensive patients, mean 49 +/- 11 years with idiopathic primary aldosteronism due to bilateral adrenal hyperplasia: plasma renin activity (PRA) less than 1.5 ng/ml/h and plasma aldosterone (PA) greater than 25 ng/100 ml. Adrenal venography and adrenal vein aldosterone levels demonstrated bilateral hyperplasia. PRA and PA were evaluated in recumbent position, then after 4 hours in upright posture. The next day, a "captopril screening test" was performed with PA assays before and three hours after a single oral administration of captopril (1 mg/kg). Upright PRA and PA were slightly increased and acute administration of captopril reduced significantly PA levels in all patients. Blood pressure (BP was unmodified under captopril. These hormonal results demonstrated that adrenal glomerulosa remained sensitive to low concentrations of angiotensin II, and underlined the potential interest of ACEI in the management of IPA. Brown R. demonstrated already an increase of adrenal sensitivity to angiotensin II infusions, and isolated an aldosterone-stimulating factor (ASF). Plasma aldosterone levels were related to increased ASF concentrations but there was no link between PRA and ASF. Carey R. suggested that ASF acts through an increase of the sensitivity of aldosterone production to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1988

[Malignant adrenal cortex carcinoma revealed by an isolated picture of primary hyperaldosteronism].

Adrenocortical carcinoma (ACC) is a rare disorder with an estimated incidence of only 0.023 percent of all malignancies. In most cases, Cushing's syndrome and virilization or feminization due to abnormal steroid production by the tumor rapidly lead to the diagnosis. Occasionally, the tumor produces an excessive amount of mineralocorticoids only and ACC can be revealed by an isolated syndrome of primary aldosteronism. Out of 100 cases of tumoral primary aldosteronism studied from 1977 to 1987, we observed 4 ACC and 96 Conn's adenomas (CONN). When primary aldosteronism was diagnosed, ACC and CONN had same clinical features, although hypokalemia in ACC was more profound: 2.2 +/- 0.76 mmol/l (1.4 to 3.2) compared to 2.9 +/- 0.5 (1.6 to 4.2) in CONN. Mean supine plasma aldosterone levels, plasma renin and aldosterone responses to the upright posture or to serum saline infusion, cortisol at 8 a.m. were not different in patients with ACC from those observed in patients with CONN. 24 hours urinary cortisol excretion and 17-ketosteroids excretion were highly increased in three out four patients with ACC. Clinical, biological and hormonal investigations were therefore not sufficient to diagnose malignant tumoral primary aldosteronism. Systematic computed tomographic scanning allowed to differentiate carcinomas from adenomas on the following criteria: ACC showed enlarged tumor size that was always above 30 mm in diameter, whereas the largest CONN measured 20 mm.ACC appeared as an heterogeneous tumor with the presence of internal calcifications in each case of ACC, that were diagnosed both on ultrasound and CT scan, whereas none of the CONN showed any calcification, using the same screening procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

17-Ketosteroids↗
PubMed1988

[Localization of primary hyperaldosteronism].

After diagnosis of primary aldosteronism on the basis of biochemical evidence, the detection of the tumour is of crucial importance in the management of the disease. We reviewed the efficacy of CT-Scan, Iodo-Cholesterol Scintigraphy, digitalized phlebography, adrenal vein sampling for steroid measurements (AVS), and Nuclear Magnetic Resonance (NMR) in 160 hypertensive patients with primary aldosteronism. Diagnosis of Conn's adenoma (n = 96) or Adrenal Hyperplasia (n = 40) was confirmed by surgery or at least two concordant tumour localization tests. Scintigraphy gave a correct diagnosis in 53% of the 51 exams, CT-Scan in 82% of the 85 exams, and phlebography in 79% of 61 exams. Plasma Aldosterone/Cortisol ratio was 5 times higher on the side of adenoma in 55% of the 47 cases but this ratio was also present in 23% of 22 patients with adrenal hyperplasia. Each procedure exhibited few false positive and false negative cases. NMR performed in 15 patients with Conn's adenoma identified all the cases. But tumours displayed a signal close to the liver signal and identical to the normal adrenal. These results and the risk of invasive procedure (failure of catheterization of the right adrenal vein (n = 6) and adrenal haematoma (n = 2) lead us to propose a schema of exploration of patients with primary aldosteronism. The CT-Scan could be performed at the first step once the biological diagnosis confirmed. Phlebography and AVS will be performed only if tumour was less than 1 cm at the CT-Scan despite important biological abnormalities. This schema requires to be validated by a prospective evaluation.

Adenoma↗