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Mild adrenal steroidogenic defects common in patients with high BP
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Mild defects of adrenal steroidogenesis occur in nearly half of patients with high blood pressure, according to research published in the International Journal of Endocrinology.
In patients with either essential or secondary high BP, secretion of aldosterone is commonly dependent on adrenocorticotropic hormone (ACTH), according to researchers.
“Besides specific diseases, like Cushing’s syndrome, pheochromocytoma and primary aldosteronism, the adrenals probably play a more general and major role in high BP in general,” João Martin Martins, MD, PhD, of the Hospital Santa Maria and Lisbon Medical School, Lisbon, Portugal, told Endocrine Today.
Martins and colleagues evaluated 100 consecutive patients (66% women; mean age, 46 years) with inappropriate or recent onset high BP. Specific methods were used to confirm the condition and diagnose secondary forms.
The investigators assessed adrenal steroidogenesis with the cosyntropin test, which was modified to include simultaneous measurement of renin and aldosterone in addition to 17-hydroxyprogesterone and 11-deoxycortisol.
Secondary forms of high BP were diagnosed in 32 patients; 14 patients had primary hyperaldosteronism (14%), and 10 patients had pheochromocytoma (10%).
Mild defects of the 21-hydroxylase and 11-hydroxylase enzymes were observed in 42% of patients.
Adrenocorticotropic hormone-dependent aldosterone secretion was seen in 54% of participants; the condition was characteristic of those with mild defects of adrenal steroidogenesis (>60%) or primary hyperaldosteronism (>75%).
“Mild defects of steroidogenesis, namely the 11-hydroxylase defect and the 21-hydroxylase defect, are common in high BP and are probably acquired abnormalities,” Martins said. “On the other hand, ACTH-dependent aldosterone secretion is very common in patients with high BP. This may shed new light on the pathogenesis of essential high BP and on the epidemics of primary aldosteronism.”
Searching for ACTH-dependent aldosterone secretion in patients with high BP using the cosyntropin test could be beneficial, Martin said, and particularly relevant in those with stress-associated forms of the condition.
Determining the frequency at which the abnormalities occur, and whether they are genetic variants or acquired, warrant additional investigation, Martin said.
“Is ACTH the driving stimulus regarding primary hyperaldosteronism? Is it possible to establish a continuum between hyperplasia and adenoma in primary hyperaldosteronism? Is stress-related high BP associated with ACTH-dependent aldosterone secretion?” – by Allegra Tiver
For more information:
João Martin Martins, MD, PhD, can be reached at the Endocrine Department, Hospital Santa Maria and Lisbon Medical School, Professor Egas Moniz Avenue, 1649-028 Lisbon, Portugal; email: jmartinmartins@sapo.pt.
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Robert M. Carey, MD, MACP, FAHA, FRCPI
This preliminary study found that some mild adrenal steroid secretory defects may play a role in hypertension and that ACTH may be stimulating aldersterone to a greater extent than expected.
Although intriguing, confirmatory evidence and more-detailed investigation are needed to accept these findings.
A few things were unusual about this study. The researchers included only participants with hypertension. Without a normotensive control group, they relied for their normal values on preset laboratory reference ranges. Of the 100 patients in the study, researchers identified 32% with secondary hypertension, 14% with primary aldosteronism, and 10% with pheochromocytoma. All of these rates are much higher than those found in the general hypertensive population; pheochromocytoma is a rare condition present in less than 1%.
The finding that aldosterone responses to ACTH were enhanced is interesting and raises the possibility that some patients may be hyper-responsive to ACTH. I might add that if ACTH is totally absent (as in hypopituitarism), it is not necessary to replace aldosterone; so ACTH is a transient stimulant for aldosterone secretion, but would not be expected to contribute to long-term regulation of aldosterone or to long-term blood pressure control.
To put this in perspective, an interesting study published in 2004 in the New England Journal of Medicine from the Framingham group showed that aldersterone levels were mildly elevated in patients with primary hypertension compared with those with normal blood pressure. With increasing severity of hypertension, aldosterone levels rose — although they were far lower than those usually found in patients with primary aldosteronism.
The current study is intriguing and suggests that a mild increase in ACTH-stimulated aldosterone secretion and possibly other mineralocorticoids might be candidate mechanisms for increased blood pressure in some patients with primary hypertension.
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