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

Transcatheter arterial embolization (TAE) was performed in 2 patients with Cushing's syndrome caused by adrenal adenoma by using a mixture of absolute ethanol and iohexol. In 1 patient successful suppression of the hypersecretion of cortisol has continued for 9 months after TAE without complications. However, in the other patient, TAE was discontinued due to marked hypertension and tachycardia induced by a massive release of catecholamines from the embolized "normal" part of the tumor-bearing adrenal gland during the procedure. These results suggest that it is important to perform TAE of only the arterial branches feeding the tumor.
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PMID:Transcatheter adrenal arterial embolization of cortisol-producing tumors. Two cases of Cushing's syndrome. 997 12

We report a case of preclinical Cushing's syndrome in a 54-year-old male associated with bilateral adrenocortical tumours. Physical findings and general laboratory data were unremarkable except for mild hypertension (158/90 mmHg) and impaired glucose tolerance. Endocrinological evaluation revealed the presence of autonomous cortisol secretion including unsuppressible serum cortisol by 8 mg dexamethasone test (11 microg/dl), high serum DHEA-S (3580 ng/ml, normal: 400-3500) and increased urinary 17-KS excretion (31.0-35.8 mg/day, normal: 5.8-21.3). CT scan demonstrated the presence of tumours in both adrenals and bilateral adrenalectomy was subsequently performed. Histological examination of the resected specimens revealed an adrenocortical carcinoma on the right side and an adenoma on the left side with noticeable cortical atrophy in non-neoplastic adrenals. Immunohistochemical study of steroidogenic enzymes demonstrated that all the steroidogenic enzymes involved in cortisol biosynthesis were expressed in both right and left adrenal tumours. Enzymatic activities of 21, 17alpha, 18, 11beta-hydroxylases were detected in both right and left adrenals except for the absence of 11beta-hydroxylase activity in the left adrenal adenoma. Results of in vitro tissue steroidogenesis examined in short-term tissue culture of the specimens revealed no significant differences between carcinoma and adenoma in cortisol production, but the production of adrenal androgens in carcinoma was significantly higher than that in adenoma, which may indicate the importance of evaluating adrenal androgen levels in patients with adrenocortical neoplasms.
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PMID:A patient with preclinical Cushing's syndrome and excessive DHEA-S secretion having unilateral adrenal carcinoma and contralateral adenoma. 1042 68

We determined the factors for postoperative persistent hypertension in the patients with aldosterone-producing adrenal adenoma (APA) in 53 patients with APA who were followed up for average 3.1 years. All had normal serum potassium concentration postoperatively. Blood pressure was normal in 37 patients (69.8%) but 18.7/12.7 kPa or more in 16 patients (30.2%) with persistent hypertension. Also compared were sex, age, history of hypertension, effect of reducing blood pressure to antisterone, preoperative blood pressure, time of persistent hypertension, serum potassium concentration, aldosterone concentration in 24 hour urine, amount of PRA, and the type of operation. The results showed that an APA patient aged 50 years or more appears to have a great chance of persistent hypertension than an APA patient under age of 40 years, and the odds ratio is 3:1. There was a significant difference between the mean age for persistent hypertension and for normal blood pressure, and varioas response of reducing blood pressure to antisterone (P < 0.05). It is suggested that for an older APA patient and the patient without of reducing blood pressure to antisterone, there are other factors for hypertension such as renal veinlet change or renal interstitial lesions except for hyperaldosteronism. We recommend renal biopsy (using kidney puncture) at the operating table for those patients in order to understand pathological change and guide treatment after operation.
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PMID:[Factors for postoperative persistent hypertension in patients with aldosterone-producing adenoma]. 1067 82

Adrenal myelolipoma is an uncommon benign tumor usually discovered by chance in patients with hypertension, obesity, atherosclerosis, cancer or endocrine disorders. The association with adrenal endocrine dysfunctions appears to be the most frequent. Myelolipoma has been found in patients affected by Cushing's syndrome, hyperaldosteronism, Addison's disease, virilization. We report herein a case of association, based on clinical and radiological signs, between myelolipoma and adrenal adenoma in a patient with Conn's disease. The myelolipoma was localized in the opposite adrenal gland to that of adenoma, at difference with the other cases described.
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PMID:[Adrenal adenoma and myelolipoma in an elderly patient with Conn's syndrome]. 1076 42

Incidentally discovered adrenal masses are mostly benign, asymptomatic lesions, often arbitrarily considered as nonfunctioning tumors. Recent studies, however, have reported increasing evidence that subtle cortisol production and abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis are more frequent than previously thought. The purpose of this study was to investigate the clinical and hormonal features of patients with incidentally discovered adrenal adenomas, in relation to their clinical outcome. Fifty consecutive patients with incidentally detected adrenal adenomas, selected from a total of 65 cases of adrenal incidentalomas, were prospectively evaluated. All of them underwent abdominal computed tomography scan and hormonal assays of the HPA axis function: circadian rhythm of plasma cortisol and ACTH, urinary cortisol excretion, 17-hydroxyprogesterone, androgens, corticotropin stimulation test and low-dose (2 mg) dexamethasone test. The patients were reevaluated at regular intervals (6, 12, and 24 months) for a median period of 38 months. Subtle hypercortisolism, defined as abnormal response to at least 2 standard tests of the HPA axis function in the absence of clinical signs of Cushing's syndrome (CS), was defined as subclinical CS. Mild-to-severe hypertension was found in 24 of 50 (48%) patients, type-2 diabetes in 12 of 50 (24%), and glucose intolerance in 6 of 50 (12%) patients. Moreover, 18 of 50 patients (36%) were diffusely obese (body mass index, determined as weight/height2, > 25), and 14 patients (28%) had serum lipid concentration abnormalities (cholesterol > or = 6.21 mmol/L, low-density lipoprotein cholesterol > or = 4.14 mmol/L and/or triglycerides > or = 1.8 mmol/L). Compared with a healthy population, bone mineral density Z-score, determined by the DEXA technique, tended to be slightly (but not significantly) lower in patients with adrenal adenoma (-0.41 SD). Endocrine data were compared with 107 sex- and age-matched controls, and patients with adenomas were found to have heterogeneous hormonal abnormalities. In particular, significantly higher serum cortisol values (P < 0.001), lower ACTH concentration (P < 0.05), and impaired cortisol suppression by dexamethasone (P < 0.001) were observed. Moreover, in patients with adenomas, cortisol, 17-OH progesterone, and androstenedione responses to corticotropin were significantly increased (P < 0.001, all), whereas dehydroepiandrosterone sulfate levels were significantly lower at baseline, with blunted response to corticotropin (P < 0.001, both). However, the criteria for subclinical CS were met by 12 of 50 (24%) patients. Of these, 6 (50%) were diffusely obese, 11 (91.6%) had mild-to-severe hypertension, 5 (41.6%) had type-2 diabetes mellitus, and 6 (50%) had abnormal serum lipids. The clinical and hormonal features improved in all patients treated by adrenalectomy, but seemed unchanged in all those who did not undergo surgery (follow-up, 9 to 73 months), except for one, who was previously found as having nonfunctioning adenoma and then revealed to have subclinical CS. In conclusion, an unexpectedly high prevalence of subtle autonomous cortisol secretion, associated with high occurrence of hypertension, diabetes mellitus, elevated lipids, and diffuse obesity, was found in incidentally discovered adrenal adenomas. Although the pathological entity of a subclinical hypercortisolism state remained mostly stable in time during follow-up, hypertension, metabolic disorders, and hormonal abnormalities improved in all patients treated by adrenalectomy. These findings support the hypothesis that clinically silent hypercortisolism is probably not completely asymptomatic.
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PMID:Subclinical Cushing's syndrome in patients with adrenal incidentaloma: clinical and biochemical features. 1115 83

Primary aldosteronism (PA) was thought to be rare but recent evidence from Australia suggests that it may be more common. As this has important implications in terms of hypertension management, we undertook to screen for this treatable condition in our hypertension clinic. We obtained blood samples in sequential patients referred for assessment in our hypertension clinic in Tayside for plasma renin activity (PRA) and aldosterone. The aldosterone to PRA ratio (ARR) was used as an initial screening test to identify potential patients with PA. Those patients with an elevated ratio (> or =750) were admitted for the salt loading and fludrocortisone suppression test. These patients also underwent adrenal CT scanning, and in selected patients, adrenal scintigraphy. Between May 1995 and January 1997 (21 months), we screened a total of 495 patients. ARR was available in 465 (93.9%) patients. Out of that number, 77 (16. 6%) had an elevated ratio of > or =750, five of whom had an adrenal adenoma (one had previous adrenalectomy). Forty-five of these patients were admitted for the salt loading and fludrocortisone suppression test with 41 positive test results suggesting PA. One patient with a negative salt loading test result however had an adenoma proven on histology. A total of 43 cases of PA were identified, giving a minimum prevalence of 9.2% (43/465). Potentially the prevalence may be up to 15% assuming that the ARR has a sensitivity of 93% (42/45) in predicting PA. In conclusion, about one in 10 patients attending a hypertension clinic may have PA. This suggests that the prevalence of PA in Tayside is as high as that in the Australian hypertensive population, and this is likely to be true elsewhere, with obvious important implications for hypertension management.
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PMID:High prevalence of primary aldosteronism in the Tayside hypertension clinic population. 1082 17

Low-renin hypertension is common and usually implies increased retention of sodium (Na(+)). In every case of known etiology, there is a mineralocorticoid-induced increase in number of epithelial Na(+) channels (ENaCs) in the collecting duct of the kidney, leading to a state of "hyperENaCactivity." In primary aldosteronism, a result of either an adrenal adenoma or bilateral adrenal hyperplasia, aldosterone itself mediates the increase in ENaC function. A severe form of low-renin hypertension in which a molecular mutation in ENaC prevents removal of the channel from the cell surface, known as Liddle's syndrome, results in increased net ENaC activity but, in this case, independently of an increase in aldosterone. Glucocorticoid remedial aldosteronism, an autosomal dominant form of primary aldosteronism, results from a "new" or chimeric gene for aldosterone synthase. Adrenocorticotropic hormone stimulates its expression as well as secretion of aldosterone. Apparent mineralocorticoid excess results from a molecular mutation that allows cortisol to bind to the mineralocorticoid receptor. Both glucocorticoid remedial aldosteronism and apparent mineralocorticoid excess result in an increase in the number of ENaCs. The question remains whether low-renin essential hypertension is related to an increase in ENaC activity. Low-renin hypertension is most common in black patients, who tend to have lower levels of aldosterone as well as renin, which are features that resemble those found in Liddle's syndrome. Preliminary findings suggest that black patients with low-renin hypertension who are resistant to standard antihypertensive therapy respond favorably to the addition of spironolactone, a mineralocorticoid receptor antagonist that reduces ENaC activity.
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PMID:Low-renin hypertension: more common than we think? 1117 96

Surgical treatment of adrenal disorders is increasingly performed under laparascopic approach. Both pneumoperitoneum and adrenal tumour manipulation may induce haemodynamic variations. The aim of this study was to compare the inhalational and intravenous anaesthetic management for laparascopic adrenalectomy. Between 1977 and 1999 there were performed 28 laparascopic adrenalectomies. At patients with functioning adenoma and hypertension the anaesthesia was maintained with isoflurane in 8 cases and sevoflurane in 6 cases, et 14 patients with non-functioning adrenal masses with propofol and fentanyl (TIVA). In addition to the circulatory and respiratory monitoring there were made serial laboratory determinations (acid-base state, serum potassium, blood glucose) during the operation. On the basis of measured parameters isoflurane and sevoflurane anaesthesia proved to be favourable in case of functioning adrenal adenoma and TIVA with propofol and fentanyl in case of non-functioning adenoma.
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PMID:General anaesthesia for laparascopic adrenalectomy. 1120 70

The traditional workup for primary aldosteronism is cumbersome and requires discontinuing antihypertensive medications, which is inconvenient and potentially dangerous. A simple and accurate screening test that can be used without modifying medications is needed. The plasma aldosterone-renin ratio (ARR) is a valid screening assay for primary aldosteronism, but antihypertensives are usually discontinued before obtaining this ratio, limiting its utility. The present prospective study is designed to examine the validity of the ARR as a screening test for primary aldosteronism if the ratio is measured randomly while patients continue antihypertensive therapy. During the 18-month study period, 90 patients were referred to the hypertension clinic with poorly controlled hypertension. ARR was measured in random blood samples in all 90 patients while maintaining their prescribed antihypertensive medications. Those with elevated ARRs (>100 ng/dL / ng/mL/h) underwent further diagnostic workup, including adrenal computed tomography and/or magnetic resonance imaging and adrenal iodine 131 norcholesterol uptake scan. Fifteen patients (17%) had elevated ARRs greater than 100:1. Ten of 15 patients were found to have adrenal adenoma on diagnostic workup, and adenoma was later confirmed by histological examination after surgical removal in these 10 patients. Five patients were found to have adrenal hyperplasia; all 5 patients responded to antialdosterone treatment. Thus, all 15 patients had good control of blood pressure after surgery and/or antialdosterone medications. No patient showed a falsely elevated ARR. Data suggest that the ARR is a valid screening assay for primary aldosteronism in patients with poorly controlled blood pressure, and discontinuation of antihypertensive medications is not needed for this test.
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PMID:Screening for primary aldosteronism without discontinuing hypertensive medications: plasma aldosterone-renin ratio. 1127 68

Primary hyperaldosteronism is a potential cause of hypertension. Unilateral adrenal adenoma and bilateral adrenal cortical hyperplasia are the most common causes of primary hyperaldosteronism. Adrenal venous sampling is employed as the gold standard test to differentiate between these two different causes when the results of other studies in the work-up protocol are non-diagnostic or ambiguous. Adrenal venous sampling can be a challenging procedure, especially in the presence of anomalous venous drainage patterns. Knowledge of normal adrenal venous anatomy, as well as possible variants, is therefore important to ensure a successful procedure. The authors describe an unusual variant of left adrenal venous drainage directly into the IVC.
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PMID:Anomalous left adrenal venous drainage directly into the inferior vena cava. 1128 20


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