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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe the unusual case of a 52-year-old man with Cushing's syndrome caused by bilateral pigmented micronodular adrenal hyperplasia. The only features of hypercortisolism were hypertension and severe symptomatic osteopenia with vertebral, rib, and scapular fractures. Four years after bilateral adrenalectomy, the bone density had increased slightly, but the patient remained osteopenic and continued to have vertebral compression fractures. This case report emphasizes the importance of an indepth search for secondary causes of osteoporosis, including evaluation of adrenal function in patients who have unexplained osteoporosis. Early diagnosis and treatment is imperative to prevent severe bone loss and associated skeletal morbidity.
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PMID:Severe symptomatic osteopenia in a man with pigmented micronodular adrenal hyperplasia. 764 84

Conn's syndrome due to an adrenal adenoma is very rare in children. This paper reports a 14-year-old boy with primary hyperaldosteronism due to an adrenal adenoma. His biochemistry data were compatible with either bilateral adrenal hyperplasia or an adrenal adenoma. A dexamethasone test did not suppress aldosterone levels. Venous catheter sampling and 75Se-selenomethylcholesterol scanning suggested that the hyperaldosteronism originated at the right adrenal. Computed tomography showed an 8-mm low-density nodule in the right adrenal gland and magnetic resonance imaging confirmed the nodule which had high signal intensity on T2-weighted images consistent with a functioning adenoma. Surgery confirmed the right adrenal adenoma, and the patient was cured by right adrenalectomy. This case illustrates the difficulty of defining the aetiology of primary hyperaldosteronism and we review the biochemical and scanning techniques available to aid in diagnosis. Hypertension is unusual in children and endocrine causes are very rare, but Conn's syndrome should always be considered in the differential diagnosis.
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PMID:Primary hyperaldosteronism due to an adrenal adenoma in a 14-year-old boy. 772 19

A case of adrenocorticotropic hormone independent bilateral adrenocortical macronodular hyperplasia (AIMAH) is reported. A 59 year old male was admitted to hospital because of hypertension. Subsequently, hypercortisolism, low plasma adrenocorticotropic hormone (ACTH), loss of diurnal rhythm of ACTH, lack of suppression with high dose dexamethasone were found and bilateral adrenal enlargement was detected by abdominal computerized tomography and adrenal scintigraphy. Bilateral total adrenalectomy was performed under a diagnosis of bilateral adrenal hyperplasia associated with Cushing's syndrome. Both adrenal glands were enlarged in size and weight. Bulging nodules were found at the cut section. Microscopically, a variegated histologic pattern including trabecular, adenoid and zona glomerulosa-like (ZG-like) structures was revealed in the nodules. Immunohistochemical examination disclosed positive staining of cytochrome P-450 17 alpha, negative of 3 beta-HSD in the ZG-like structure. Ultrastructurally, the cells composing the ZG-like structure were similar to those of the ZG in normal adrenal cortex. The authors agree that AIMAH is one of the entities causing Cushing's syndrome, and advise pathologists to keep this disorder in mind when they examine the adrenals in Cushing's syndrome.
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PMID:Adrenocorticotropic hormone-independent bilateral macronodular adrenocortical hyperplasia associated with Cushing's syndrome. 778 95

Ten cases of adrenal adenomas, one case with unilateral adrenal hyperplasia, and another case with apparent bilateral are reported, in whom an alternative pathway of aldosterone via 21-deoxyaldosterone is operative. They all manifested hypertension, low renin activity, low normal potassium values, as well as high urinary excretion rates of 21-deoxyaldosterone and its related metabolite Kelly's-M1 steroid. In all cases, urinary aldosterone metabolites (aldosterone-18-glucuronide and tetrahydroaldosterone) and aldosterone precursor 18-hydroxycorticosterone levels were normal. Hence, the adrenal lesions give rise to hyper-21-deoxyaldosteronism. 21-Deoxyaldosterone is a weak mineralocorticoid, and its elevated production in the presence of normal aldosterone can induce a pathological state of hypermineralocorticoidism. Adrenalectomy resulted in normalization of hypertension in six of eight and amelioration in two of eight cases. Six of seven adenoma cases examined as well as the case of unilateral adrenal hyperplasia were sensitive to ACTH. One of the seven adenomas and, as expected, the case with apparent bilateral hyperplasia were angiotensin responsive. Histologically and electron microscopically, the operated adenomas consisted predominantly of clear cells, characterized by mitochondria with tubulo-vesicular internal structure similar to those of the zona fasciculata (in contrast, our classical Conn's adenoma with normal 21-deoxyaldosterone excretion exhibited a more heterogenous histological appearance and were, in terms of ultrastructure, more similar to cells of the zona glomerulosa). Ultrastructurally and immunocytochemically, the clear cells of 21-deoxyaldosterone adenomas showed features of both the zona glomerulosa and the zona fasciculata and are, hence, considered to be hybrid cells. We conclude that the determination of 21-deoxyaldosterone and Kelly's-M1 should be considered in the diagnosis of mineralocorticoid-induced forms of hypertension, especially when an adrenal adenoma has been detected with an imaging procedure.
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PMID:A new subset of mineralocorticoid hypertension with excess of 21-deoxyaldosterone and Kelly's-M1 steroid: clinical and morphological findings. 788 25

1. Aldosterone levels in patients with unilateral aldosterone-producing adenomas may be responsive or unresponsive to the renin-angiotensin system, with the former often previously misdiagnosed as bilateral adrenal hyperplasia. 2. In tumours from patients in the responsive subgroup, renin mRNA is expressed in greater amounts than in tumours from patients in the unresponsive subgroup, or in normal adrenals. 3. We compared the frequency of four renin gene polymorphisms in peripheral blood DNA from the two subgroups and found significant associations between BglI, TaqI and HinfI restriction fragment length polymorphisms (RFLP) and aldosterone responsiveness. 4. Allelic variation in the constitutive renin gene was associated with a specific cause of hypertension.
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PMID:Renin gene polymorphism associated with aldosterone responsiveness to the renin-angiotensin system in patients with aldosterone-producing adenomas. 791 44

This study evaluated the assessment of plasma endothelin-1 (ET-1) levels in primary aldosteronism and its correlation with other vasoactive hormones such as renin, aldosterone, catecholamines, arginine-vasopressin, and atrial natriuretic peptide. Plasma ET-1 was measured in 12 patients with primary aldosteronism (five adenomas and seven primary hyperplasia) and in 15 normal subjects. No significant differences were found in plasma ET-1 between controls and hypertensive patients both in adenoma and primary adrenal hyperplasia (8.8 + 1.6 pg/mL v 6.2 + 1.4 pg/mL v 6.5 + 1.0 pg/mL, P = NS, respectively). Further, no significant correlations were found among ET-1 and vasoactive hormones. In conclusion, these findings show that there are no differences in ET-1 levels between primary aldosteronism patients and healthy subjects. Circulating ET-1 is not involved in the hypertension in primary aldosteronism.
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PMID:Plasma immunoreactive endothelin-1 in primary hyperaldosteronism. 791 56

Abnormalities of adrenal cortical and medullary function are important causes of hypertension in adults. Mineralocorticoid hypertension, characterized by spontaneous hypokalemia with excessive kaliuresis and low plasma renin activity, is most commonly caused by aldosterone-producing adenoma or, less frequently, by nonadenomatous adrenal hyperplasia. However, recent evidence indicates that this classification oversimplifies the pathophysiologic diversity of this syndrome. Advances in steroid biochemistry and molecular biology have improved our ability to identify patients with various forms of mineralocorticoid hypertension and also provide evidence that they are underdiagnosed. Pheochromocytomas are most commonly located in the adrenal medulla, where they may overproduce norepinephrine or epinephrine. Appropriate screening of norepinephrine, epinephrine, and their metabolites is essential because tumors that secrete epinephrine exclusively may not present with hypertension and, thus, can be overlooked. Extra-adrenal pheochromocytomas are more prevalent than previously considered and pose special problems because they may be multicentric, difficult to locate, and more likely to be malignant than are adrenal pheochromocytomas.
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PMID:Hypertension and adrenal disorders. 792 87

1. Normokalaemic primary aldosteronism (PA) masquerades as 'essential hypertension', and 50% of patients with aldosterone-producing adenoma (APA) are normokalaemic at presentation to this unit. 2. Angiotensin-responsive (AII-R) APA is as common as angiotensin-unresponsive (AII-U) APA, and requires adrenal venous sampling for differentiation from bilateral adrenal hyperplasia (BAH). 3. From 1981 to 1992, 55 patients with APA underwent unilateral adrenalectomy and were followed up for at least 12 months postoperatively. Hypertension was cured in 55% and improved in the remainder. 4. Cure rate was lower (P < 0.001) in males (11/32, 34%) vs females (19/23, 83%), lower (P < 0.005) in patients over 45 years of age (13/33, 39%) vs those 45 years or younger (17/22, 77%), lower (P < 0.05) in AII-R APA (11/28, 39%) vs AII-U APA (19/27, 70%) and tended to be lower (not significant) in normokalaemic APA (7/17, 41%) vs hypokalaemic APA (23/38, 61%). 5. A higher proportion (P <0.001) of AII-R APA patients were males (23/28, 82%) vs AII-U APA (9/27, 33%), and a higher proportion were from the older age group AII-U APA 13/27, 48%; P < 0.05). Females with AII-U APA who were hypokalaemic had a very high cure rate (16/17, 94%). 6. Since unilateral adrenalectomy cures or improves blood pressure in normokalaemic and AII-R as well as in hypokalaemic and AII-U patients, all hypertensives should be screened for PA, and AII-R APA differentiated from BAH in proven PA.
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PMID:Response to unilateral adrenalectomy for aldosterone-producing adenoma: effect of potassium levels and angiotensin responsiveness. 792 99

A patient who presents with refractory hypertension may have a curable underlying cause, such as Conn's syndrome. Because hypertension may be the only presenting sign of this disorder, a high index of suspicion is required. Detection of elevated aldosterone levels after salt loading and of abnormally suppressed plasma renin activity aids in the diagnosis. Conn's syndrome is caused by unilateral adrenal adenoma, which can be removed surgically. Aldosteronism due to bilateral adrenal hyperplasia can be managed with sodium restriction and use of potassium-sparing diuretics.
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PMID:Refractory hypertension due to Conn's syndrome. 812 54

Adrenal arterial embolization with absolute ethanol was performed for the treatment of Cushing's syndrome. A 55-year-old woman was admitted to our hospital with complaints of obesity, hypertension, and back pain caused by left adrenal hyperplasia after surgical resection of the right adrenal gland. Therapeutic adrenal arterial embolization was performed by the coaxial technique using absolute ethanol (AE) as an embolic material. No severe complications were encountered during the procedure, and the patient was discharged without symptoms or abnormalities on laboratory tests.
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PMID:A case with Cushing's syndrome treated with arterial ablation of adrenal gland by absolute ethanol. 815 65


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