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PubMedDate not supplied

[Recurrent hyperaldosteronism and hypertension post adrenalectomy (author's transl)].

Primary Aldosteronism may be due to adenoma or hyperplastic adrenals. Such a distinction can be obtained from biochemical studies. In our observation, a man with recurrent aldosteronism after right adrenalectomy was studied. Radiological and surgical data might indicate an adenoma. This opinion was modified by pathological studies. This absence of capsule and the presence of microadenomatous hyperplastic lesions indicated pseudo-adenomatous hyperplastic glands. On the other hand, high blood pressure remained after adrenalectomy. A treatment with beta-blocking substances corrected this hypertension.

Adenoma↗
PubMed1999

Ventricular fibrillation: an extreme presentation of primary hyperaldosteronism.

Patients with primary aldosteronism often present with hypokalemia and hypertension. Primary aldosteronism presenting as sudden death due to ventricular fibrillation is described in an otherwise healthy 37-year-old woman. After successful direct current cardioversion, serum potassium was 1.4 mmol/L. Investigations revealed a suppressed renin level, elevated serum aldosterone and a right adrenal nodule found on imaging. Ventricular fibrillation has not previously been described as a presention of a biochemically and surgically proven aldosterone-producing adenoma. This case highlights the importance of early detection and proper diagnosis of secondary hypertension before serious sequelae occur.

Adrenal Cortex Neoplasms↗
PubMed1999

[Remediable glucocorticoid hyperaldosteronism: molecular diagnosis].

BACKGROUND: The first family diagnosed in Spain of glucocorticoid remediable aldosteronism (GRA) is reported. SUBJECTS AND METHODS: We described the phenotype, biochemical values and genetic diagnosis of a GRA pedigree. DNA analysis was performed by using Southern-blot and polymerase chain reaction. RESULTS: We reported a 14-year-old boy who presented with severe hypertension, and strong family history of early-onset hypertension. His suppressed plasmatic renin activity, family history and failure to respond to conventional antihypertensive therapy raised GRA as a potential etiology. The diagnosis was confirmed by genetic testing, in the index case and in one of family members, which demonstrated the chimeric gene duplication, which was a resultant of a crossing-over between the proximal portion of 11 beta-hydroxylase gen, CYP11B1, and the distal portion of aldosterone synthetase gene CYP11B2. Two other family members, who died, suffered hyporeninemic severe hypertension. The cause of death in one of them was hemorrhagic stroke. Amiloride, which blocks sodium transport in the distal nephron, plus hydroclorothiazide was an effective treatment option. CONCLUSIONS: The role of molecular diagnosis techniques is essential for the rapid diagnosis of cases of arterial hypertension secondary to familial glucocorticoid remediable aldosteronism.

Adolescent↗
PubMedDate not supplied

[Hyperaldosteronism in thyrotoxicosis].

In 30 patients with a moderately severe and severe form of thyrotoxicosis a study was made of urinary aldosterone excretion following acid hydrolysis, by thin-layer chromatography. During decompensation the majority of the patients displayed an increased aldosterone excretion. Medicinal compesation of the disease did no lead to normalization of the mineralocorticoid function of the adrenal glands, whereas aldosterone excretion remained high in many of the patients. To ascertain the mechanisms of increase of aldosterone excretion in thyrotoxicosis a correlative analysis was carried out of associations between the aldosterone excretion and the circulating blood and plasma volume, potassium blood plasma content, catecholamine and 17-oxycorticoid excretion. On the basis of the results obtained and literature data it was supposed that intensified beta-adrenergic activity of the nervous system and increased catecholamine production participated in increase in the mineralocorticoid function of the adrenal glands during thyrotoxicosis.

Adult↗