[Adrenocortical hypertension].
| Autor: | Kostić N; Klinika za internu medicinu, Klinicko-bolnicki centar Dr Dragisa Misović, Beograd., Milosević M, Jelić S, Nesović M |
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| Jazyk: | srbština |
| Zdroj: | Medicinski pregled [Med Pregl] 2003 Jul-Aug; Vol. 56 (7-8), pp. 346-50. |
| DOI: | 10.2298/mpns0308346k |
| Abstrakt: | Introduction: Endocrine hypertension is almost exclusively adrenal hypertension which includes syndromes of mineralocorticoid, glucocorticoid and amine excess. Aldosteronism: Although primary aldosteronism accounts for less than 1% of hypertensive population, it is the most common form of endocrine hypertension and the second most common form of curable hypertension. It is possible that load in type 2 diabetes mellitus and cardiovascular fibrosis is related to aldosteronism. Diagnosis of Primary Aldosteronism: The conventional approach to low plasma potassium level in hypertensive patients suggests mineralocorticoid excess, whereas high aldosterone level and chronically suppressed plasma renin activity (PRA) are basic for the diagnosis of primary aldosteronism. However, recent studies use the ratio of plasma aldosterone to plasma renin activity (ARR) in plasma. Differential Diagnosis: Differential diagnosis between idiopathic aldosteronism (IHA) and aldosterone--producing adenoma (APA) can be performed using postural testing, 18-hydro- xycorticosterone levels, adrenal computed tomograms, iodocholesterol scans and adrenal venous sampling. Glucocorticoid Hypertension: However, association between glucocorticoid excess and hypertension is complex and still poorly understood. Hypothesized mechanisms include: increased hepatic angiotensinogen synthesis, inhibition of vasodilator and stimulation of vasoconstrictor systems in vascular tissue, enhanced glucocorticoid-mediated vascular reactivity to noradrenaline, shifting of sodium and fluid from intracellular to extracellular compartment, and increase of local endothelial growth factor activity. |
| Databáze: | MEDLINE |
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