Urinary excretion of aldosterone metabolite Kelly-M1 in patients with adrenal dysfunction

Lewicka, Sabina; Vecsei, P.; Bige, K; Fisher, Tamas; Winter, J.; Abdelhamid, S.; Heinrich, U.; Vd, Bokkenheuser

doi:10.1016/0022-4731(88)90035-0

Cited by 4 publications

(2 citation statements)

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“…Among the several other metabolites isolated was one described as 11β:18(S),18:.20α − diepoxy-5β-pregnan-3αol [48] and called the Kelly M1 metabolite. It was found in normal individuals and in higher concentrations in patients with 21-hydroxylase deficiency [50]. Aldosterone in the gut is deoxygenated to 21-deoxyaldosterone and other metabolites by gut bacteria [51] and is probably the origin of the Kelly M-1 metabolite.…”

Section: Metabolism Of Aldosteronementioning

confidence: 99%

An Abbreviated History of Aldosterone Metabolism, Current and Future Challenges

Gómez-Sánchez

2023

Exp Clin Endocrinol Diabetes

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The initial isolation of adrenal steroids from large quantities of animal adrenals resulted in an amorphous fraction resistant to crystallization and identification that had potent effects on electrolyte transport. Aldosterone was eventually isolated and identified in the fraction and was soon shown to cause hypertension when in excess. The autonomous and excessive production of aldosterone, primary aldosteronism, is the most common cause of secondary hypertension. Aldosterone is metabolized in the liver and kidney and its metabolites conjugated with glucuronic acid for excretion. The most common liver metabolite is 3,5-tetrahydroaldosterone-3-glucuronide; that of the kidney is aldosterone-18-oxo-glucuronide. Their values, especially the aldosterone-18-oxo-glucuronide, are commonly used for the diagnosis of primary aldosteronism because they provide and integrated value of the total daily production of aldosterone. Conversion of aldosterone to 18-oxo-glucuronide is impeded by drugs, like some common NSAIDS that compete for UGT2B7, the most important glucuronosyltransferase for aldosterone metabolism. Tetrahydroaldosterone is the most abundant metabolite and most reliable for the diagnosis of primary aldosteronism, but is not commonly measured.

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Section: Metabolism Of Aldosteronementioning

confidence: 99%

An Abbreviated History of Aldosterone Metabolism, Current and Future Challenges

Gómez-Sánchez

2023

Exp Clin Endocrinol Diabetes

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“…vereinzelten Beobachtungen vergleichbare Ergebnisse (1,23). Eine normale 18-OH-Corticosteron-Ausscheidung bei Patienten mit Nebennierenrinden-Adenom kann Ausdruck einer veränderten Metabolisierung sein, derart, daß genügend Enzyme vorhanden sein müssen, die 18-OH-Corticosteron in Aldpsteron umwandeln, oder aber, daß Adenome zum Teil auch über alternative Biosynthesewege Aldosteron bilden können unter Umgehung von 18-OH-Corticosteron (24). Unsere Ergebnisse zeigen, daß Hyperplasie-Fälle auch erhöhte 18-OH-Corticosteron-Werte aufweisen können.…”

Section: Tab 3b: Varianzanalyse Zur Ermittlung Der Trenneigenschafteunclassified

Untersuchungen zum diagnostischen Stellenwert der Aldosteron-Vorstufe 18-Hydroxycorticosteron in der Diagnose und Differentialdiagnose des primären Hyperaldosteronismus

Abdelhamid¹,

Thomas²,

Nensel³

et al. 1994

LaboratoriumsMedizin

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Lab.med. 18:275(1994) 275 Brought to you by | University of Arizona Authenticated Download Date | 7/13/15 5:36 AM Orlginalie Schlüsselwörter: 18-Hydroxycorticosteron -Tetrahydro-Aldosteron -primärer Hyperaldosteronismus -Nebennierenrinden-Adenom -Nebennierenrinden-Hyperplasie Summary:18 is considered to be the immediate precursor o f aldosterone. In vitro studies and few clinical observations show that adrenal adenomas (associated with primary aldosteronism), in contrast to adrenal hyperplasia, produce increased amounts of 18 OH-B. In this study the diagnostic value of 18 OH-B was compared with that ofthe aldosterone metabolites aldosterone-18-glucuronide (ALD-18-G) and tetrahydroaldosterone (TH-ALD) in regard to recognition of primary aldosteronism and differential diagnosis of adenomas and hyperplasia. 1,272 outpatients with hypertension were studied, whereby the diagnosis of primary aldosteronism could be confirmed, in 84 patients due to adrenal adenomas and in 1 10 patients due to adrenal hyperplasia. A diagnostic sensitivity of 99.2% and a diagnostic specificity of 95.2% was calculated for 18 OH-B when differentiating primary aldosteronism due to adenomas from essential hypertension. This was markedly Iower when differentiating between primary aldosteronism due to hyperplasia and essential hypertension; the diagnostic sensitivity here was 79.7% and the diagnostic specificity 60.9% Furthermore, in 1 1 ofthe 84 adenoma cases and in 5 ofthe 1 10 hyperplasia cases 18 OH-B was at first the only elevated steroid. Only over an observation period of up to two years could a slow increase in the aldosterone metabolites be observed in these patients. Thus, 18 OH-B is an "early maker" for primary aldosteronism.

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