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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Authors evaluated the prevalence of symptoms of the metabolic syndrome and insulin resistance in 25 patients with adrenal incidentalomas (10 men, 15 women) of the mean age 57.9+/-15 years. 15 patients had adrenal adenoma determined by CT or MR scan and 10 had unilateral or bilateral hyperplasia. The prevalence of obesity was 72%, arterial hypertension 60%, diabetes mellitus or impaired glucose tolerance 28%, hyperlipidemia 56% and hyperuricemia 20%, respectively, which is more frequent occurrence than that in normal human population. Patients with adrenal adenomas had mildly but significantly higher body mass index (BMI, p<0.05) and insulin resistance calculated as HOMA IR (p<0.05) and FIRI (p<0.05) and significantly higher values of serum ferritin (p<0.01). Plasma cortisol values were slightly but not significantly higher in the group with adrenal adenomas. Authors conclude that adrenal adenomas are probably more related to the metabolic syndrome than adrenal hyperplasia.
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PMID:Adrenal incidentalomas and the metabolic syndrome--are there any differences between adenoma and hyperplasia? 1683 60

Primary aldosteronism is the most common cause of secondary hypertension, accounting for about 10% of all forms of high blood pressure. Life-time pharmacological therapy is the treatment of choice for primary aldosteronism due to idiopathic adrenal hyperplasia (IHA), while adrenalectomy is effective in curing most patients with an aldosterone producing adenoma (APA). Far from being a benign form of hypertension, primary aldosteronism is characterized by the development of cardiovascular renal and metabolic complications, including left ventricular hypertrophy, myocardial infarction, atrial fibrillation and stroke, microalbuminuria, renal cysts as well as metabolic syndrome, glucose impairment and diabetes mellitus. We review recent clinical experience with the above mentioned complications and long-term outcomes of blood pressure normalization and cardiac, renal and gluco-metabolic complications in patients with primary aldosteronism, after medical treatment with mineralocorticoid receptor antagonists and surgical treatment. We conclude that removal of adrenal adenoma results in normalization of the renin-angiotensin-aldosterone system (RAAS) and of kalaemia and improvement of blood pressure levels in all patients. Complete resolution of hypertension is achieved in nearly half of treated patients. Moreover, unilateral adrenalectomy is the best treatment to have the regression of cardiovascular, renal and metabolic complications in patients with APA. On the other hand, targeted medical treatment with aldosterone antagonists improves blood pressure control and appears able to prevent the progression of cardiac and metabolic complications in patients with IHA.
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PMID:Management of primary aldosteronism: its complications and their outcomes after treatment. 1935 5

Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is one of the most common autosomal recessive hereditary diseases. The impairment of cortisol synthesis leads to excessive stimulation of the adrenal glands by adrenocorticotropic hormone (ACTH), adrenal hyperplasia, and excessive androgen synthesis. The syndrome is characterised by a considerable correlation between the genotype and the phenotype with the type of CYP21A2 gene mutation affecting the severity of 21-hydroxylase deficiency. The clinical manifestations of CAH in adults result from adrenocortical and adrenomedullary insufficiency, hyperandrogenism, and the adverse effects of glucocorticosteroids used for the treatment of the condition. Non-classic CAH may sometimes be asymptomatic. In patients with classic CAH obesity, hyperinsulinaemia, insulin resistance, and hyperleptinaemia are more often seen than in the general population. These abnormalities promote the development of metabolic syndrome and its sequelae, including endothelial dysfunction, and cardiovascular disease. Long-term glucocorticosteroid treatment is also a known risk factor for osteoporosis. Patients with CAH require constant monitoring of biochemical parameters (17a-hydroxyprogesterone [17-OHP] and androstenedione), clinical parameters (body mass, waist circumference, blood pressure, glucose, and lipids), and bone mineral density by densitometry. The principal goal of treatment in adults with CAH is to improve quality of life, ensure that they remain fertile, reduce the manifestations of hyperandrogenisation in females, and minimise the adverse effects of glucocorticosteroid treatment. Patients with classic CAH require treatment with glucocorticosteroids and, in cases of salt wasting, also with a mineralocorticosteroid. Radical measures, such as bilateral adrenalectomy, are very rarely needed. Asymptomatic patients with non-classic CAH require monitoring: treatment is not always necessary. Medical care for patients with CAH should be provided by reference centres, as the management of such patients requires collaboration between an endocrinologist, diabetologist, gynaecologist, andrologist, urologist, and psychologist.
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PMID:Congenital adrenal hyperplasia due to 21-hydroxylase deficiency - management in adults. 2020 17

Hyperaldosteronism is associated with elevated cardiovascular risk. Using mineralocorticoid receptor antagonists a significant reduction in mortality was archived in patients with heart failure. In addition, in refractory hypertension and in patients with metabolic syndrome aldosterone seems to play an important role. Therapy with mineralocorticoidreceptor (MR) antagonists is feasible when aldosterone levels are elevated, in particular in patients with aldosterone-escape. Of particular interest is primary aldosteronism (PA). PA is one of the major causes of secondary hypertension. Since most patients with PA present with normokalemia screening has to be performed using the aldosterone renin ratio, in particular patients with refractory hypertension, young hypertensive patients and patients with incidentaloma. One has to point out that drugs that interfere with the aldosterone-renin-aldosterone-system need to be discontinued or changed. After successful screening, confirmatory testing (e.g. i.v. salt suppression test) has to follow. In order to differentiate between unilateral and bilateral disease computed tomography and adrenal vein sampling are performed. While unilateral adenomas can be cured surgically, bilateral adrenal hyperplasia is treated with MR-antagonists. In case of positive family history for PA one should consider familiar hyperaldosteronism (FH). Three forms are currently defined--FH type I, type II and type III. A hybrid gene consisting of CYP11B1 and CYP11B2 that produces aldosterone in an ACTH dependant manner can be found in FH type I. Diagnosis is verified by long range PCR. No underlying monogenetic cause for FH II and FH II could be detected so far. Through mechanisms way more than water and salt regulation, hyperaldosteronism can negatively influence cardiovascular mortality and morbidity and should therefore play an important part in diagnosis and therapy of arterial hypertension.
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PMID:[The role of aldosterone in hypertension]. 2021 71

Primary aldosteronism (PA) has a prevalence in the general hypertensive population from 5 to 10%, and is widely recognized as the most frequent form of secondary hypertension. The 2 main PA subtypes are aldosterone producing adenoma (APA) and bilateral adrenal hyperplasia (BAH) that account for 95% of all PA cases. The diagnosis of PA is a 3-step process that comprises screening, confirmatory testing, and subtype differentiation. The different categories of patients at an increased risk of PA who should thus undergo a screening test were described in the first Endocrine Society (ES) Practice Guidelines for diagnosis and treatment of PA published in 2008. These categories include patients with Joint National Committee Stage 2, Stage 3, or drug-resistant hypertension; hypertension, and spontaneous or diuretic-induced hypokalemia; hypertension with adrenal incidentaloma; hypertension and a family history of early-onset hypertension or cerebrovascular accident at a young age and all hypertensive first degree relatives of patients with PA. Recently, a growing number of studies have linked PA with the metabolic syndrome, diabetes, and obstructive sleep apnea that may be partly responsible for the higher rate of cardio and cerobrovascular accidents in PA patients. The aim of this review is to discuss, which patients should be screened for PA, focusing not only on the well-established categories of the ES Guidelines, but also on additional other group of patients with a potentially high prevalence of PA that has emerged from recent research.
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PMID:Primary aldosteronism: who should be screened? 2212 Jan 35

Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is one of the most common autosomal recessive hereditary diseases. The impairment of cortisol synthesis leads to excessive stimulation of the adrenal glands by adrenocorticotropic hormone (ACTH), adrenal hyperplasia, and excessive androgen synthesis. The syndrome is characterised by a considerable correlation between the genotype and the phenotype with the type of CYP21A2 gene mutation affecting the severity of 21-hydroxylase deficiency. The clinical manifestations of CAH in adults result from adrenocortical and adrenomedullary insufficiency, hyperandrogenism, and the adverse effects of glucocorticosteroids used for the treatment of the condition. Non-classic CAH may sometimes be asymptomatic. In patients with classic CAH obesity, hyperinsulinaemia, insulin resistance, and hyperleptinaemia are more often seen than in the general population. These abnormalities promote the development of metabolic syndrome and its sequelae, including endothelial dysfunction, and cardiovascular disease. Long-term glucocorticosteroid treatment is also a known risk factor for osteoporosis. Patients with CAH require constant monitoring of biochemical parameters (17a-hydroxyprogesterone and androstenedione), clinical parameters (body mass, waist circumference, blood pressure, glucose, and lipids), and bone mineral density by densitometry. The principal goal of treatment in adults with CAH is to improve quality of life, ensure that they remain fertile, reduce the manifestations of hyperandrogenisation in females, and minimise the adverse effects of glucocorticosteroid treatment. Patients with classic CAH require treatment with glucocorticosteroids and, in cases of salt wasting, also with a mineralocorticosteroid. Radical measures, such as bilateral adrenalectomy, are very rarely needed. Asymptomatic patients with non-classic CAH require monitoring: treatment is not always necessary. Medical care for patients with CAH should be provided by reference centres, as the management of such patients requires collaboration between an endocrinologist, diabetologist, gynaecologist, andrologist, urologist, and psychologist.
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PMID:[Congenital adrenal hyperplasia due to 21-hydroxylase deficiency--management in adults]. 2212 31