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

The content of total metabolizing sodium was studied in 74 patients with hypertension of different genesis, using the Na24-isotope dilution technique. Among these patients 31 had essential hypertension, 43--symptomatic hypertension (40--renal, and 3--adrenal). In Stage IB and IIA hypertension, a reduction of the level of total metabolizing sodium and its increased urine excretion were found. At late stages of essential hypertension, like in symptomatic renal hypertension, normal levels of total metabolizing sodium were found, or a slight tendency towards its elevation. In cases of adrenal hypertension (Conn's syndrome, pheochromocytoma) the level of total metabolizing sodium is significantly elevated. No correlation was seen between the levels of total metabolizing sodium, and plasma and erythrocytes sodium. The decrease of total metabolizing sodium at early stages of essential hypertension must be an adaptative reaction of the body, which is proved by the increased urine excretion of sodium.
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PMID:[Content of total metabolic sodium in arterial hypertension of varying origin]. 97 79

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.
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PMID:Scintigraphic studies in adrenal hypertension. 265 11

We describe an unusual patient presenting with a history of refractory hypertension and hypokalemia. Initial screening tests for adrenal hypertension were consistent with primary aldosteronism and an abdominal computed tomography scan showed an 8-mm left adrenal mass. However, adrenal venous sampling revealed markedly suppressed plasma aldosterone in the left adrenal vein but increased plasma aldosterone in the right adrenal vein. Therefore, on the basis of the clinical, radiographic, and laboratory findings, we concluded that the patient had a nonfunctioning adrenocortical adenoma on the left and an aldosterone-producing adrenocortical adenoma on the right, with the aldosteronoma resulting in hypertension and hypokalemia. Right adrenalectomy decreased the hypertension and corrected the hypokalemia. The right adrenal contained a 7-mm nodule microscopically consistent with the diagnosis of a cortical adenoma. The case highlights key steps and potential pitfalls in the evaluation of adrenal hypertension.
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PMID:Primary aldosteronism in a patient with an aldosterone-producing adenoma. 835 64

The aim of the study was to evaluate possible changes of plasma endothelin-1 levels (ET-1) in patients with hypertension secondary to primary aldosteronism and pheochromocytoma. We enrolled in the study: 12 patients affected by aldosterone-producing adenoma (5 M and 7 W; mean age 42.1 +/- 17.2 years); 8 patients with pheochromocytoma (5 M, 3 W; mean age 36.2 +/- 17.1 years); 15 patients with essential hypertension (9 M, 6 W; mean age 48.5 +/- 10 years). We also enrolled a normal control group (8 M, 12 W; mean age 34.2 +/- 11 years). The mean plasma ET-1 concentrations in patients with pheochromocytoma were significantly higher (23.9 +/- 5.2 pg/ml) than those in normal subjects (7.3 +/- 1.9 pg/ml), in patients with primary aldosteronism (12.1 +/- 3.8 pg/ml) and in patients with essential hypertension (9.2 +/- 3 pg/ml); p < 0.001, respectively. The present investigation demonstrates that in human adrenal hypertension patients with pheochromocytoma have increased circulating ET-1 levels respect to patients with aldosterone-producing adenoma.
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PMID:Plasma endothelin-1 levels in patients with aldosterone-producing adenoma and pheochromocytoma. 888 76

162 patients with adrenal hypertension have been examined. 48 of them had Cushing's syndrome, 10--aldosteromas, 85 --icenko--Cushing disease. The examination of patients with endocrine hypertension included hormonal background study, computer and MR tomography thin-needle biopsy and made it possible to make valid clinical and topical diagnosis in all cases. Magnetic-resonance tomography appeared to be the most efficient diagnostic method in the syndrome of hypercorticoidism. Ultrasound examination is the most available and highly informative method of revealing hormonally active adrenal tumors when they are more than 1 cm in size. An adequate preoperative preparation equally with an optimal scope of surgery and efficient postoperative substitution hormonal therapy are key factors in treatment of endocrine adrenal hypertension.
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PMID:[Diagnosis, surgical treatment and prognosis in endocrine hypertension of adrenal origin]. 896 39

Hypertension affects 20% to 25% of the adult population. Most patients are diagnosed as having essential or primary hypertension. Up to 10% to 15% have an identifiable cause and many of those have an adrenal basis. The identification of an adrenal cause of hypertension provides an opportunity for a targeted therapeutic intervention. Mineralocorticoid hypertension refers to hypertension caused by increased sodium and water retention by the kidney, expansion of the extracellular fluid compartment, and direct effects on the vasculature and circumventricular areas of the central nervous system (CNS), which result in elevation of blood pressure. The most common form of mineralocorticoid hypertension (MCH) is primary hyperaldosteronism (PA). In the past decade, significant advances have been made in our understanding of the pathogenesis of low-renin hypertension with the elucidation of the genetic basis and characterization of 3 forms of monogenic hypertension: glucocorticoid-remediable aldosteronism, syndrome of apparent mineralocorticoid excess, and Liddle's syndrome. This article focuses attention on the role of steroid hormones in the pathogenesis of hypertension and outlines the pathophysiology of the different forms of adrenal hypertension.
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PMID:Pathophysiology of adrenal hypertension. 1178 68

EXTENSIVE AND COSTLY INVESTIGATIONS: Are not warranted in the vast majority of hypertensive patients. Characteristics identifying the patients at risk for secondary hypertension can be used to define the small percentage of patients with hypertension who require more extensive diagnostic testing and management of their condition. Exposure to certain medicines, foods or drugs may cause reversible rises in blood pressure. Renovascular and adrenal diseases cause curable forms of hypertension. IN MANY CASES, THE PATIENT'S HISTORY: Examination and simple tests can detect such exposures and disorders. Checking for secondary hypertension is therefore an early step required for the management of all patients with hypertension, provided it is based on clinical signs and inexpensive tests. This primary screening cannot exclude the possibility of renovascular or adrenal disease in a small number of asymptomatic patients. The risk of missing a diagnosis is acceptable provided that blood pressure is normalized by non-specific antihypertensive treatment. However, more extensive etiologic investigation is required in patients who subsequently develop resistant hypertension. This secondary screening requires imaging and biochemical tests that are not required for primary screening. CORRECTION OF THE CAUSES: Of secondary forms of hypertension may restore blood pressure to normal. The patient's age affects the reversibility of renovascular and adrenal hypertension after etiologic treatment: the younger the patient, the higher the probability of blood pressure normalization.
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PMID:[Arterial hypertension secondary to curable causes in adults]. 1191 83

Hypertension is one of the most important public health problems, affecting 15-20% of the adult population. The so-called "essential" hypertension includes the majority of cases; however, endocrine hypertension should always be suspected and excluded by physicians for at least 2 important reasons: prevalence rates of primary aldosteronism (the most common cause of mineralocorticoid-based hypertension) among hypertensives seem to be much higher than < 1% of initial studies, and treatment of endocrine hypertension relies on specific drugs (1) or on surgery. Endocrine hypertension comprises a spectrum of diseases (Table 1).
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PMID:Does dynamic testing have a place in the modern assessment of endocrine hypertension? 1460 71

We examined circadian blood pressure (BP) variation (expressed as a relative night-time BP decline) in subjects with primary aldosteronism (78 patients), pheochromocytoma (n=45) and Cushing's syndrome (n=18). Subjects with aldosterone-producing adenoma (n=21) and pheochromocytoma (n=27) were also investigated after the tumour removal. In all, 65 patients with essential hypertension served as a control group. The night-time BP decline was significantly attenuated in all three forms of endocrine hypertension compared to the control group (primary aldosteronism P<0.0001, pheochromocytoma P<0.0001 for systolic and diastolic BP and Cushing's syndrome P<0.0001/<0.001 vs essential hypertension). In the case of pheochromocytoma, the absence of the night-time BP decrease was more prominent compared to the primary aldosteronism group (P=0.003/0.001) and for the diastolic BP also in comparison with the Cushing's syndrome group (P=0.03). Tumour removal led in both groups to the restoration of the previously altered circadian rhythm (aldosterone-producing adenoma: P=0.0005/0.0009; pheochromocytoma: P=0.001/0.0007). Our study demonstrates a blunted circadian BP variation in all forms of adrenal hypertension in comparison with essential hypertension. This reduction of the night-time BP decrease was more prominent in pheochromocytoma than in primary aldosteronism or Cushing's syndrome.
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PMID:Diurnal blood pressure variation in pheochromocytoma, primary aldosteronism and Cushing's syndrome. 1473 Mar 25

Once the diagnosis of hypertension is established, secondary forms should be considered. Especially hormonally active adrenal tumors may allow specific treatment. For primary hyperaldosteronism plasma aldosterone to active renin concentration ratio in patients with plasma aldosterone levels > or = 200 ng/l is a reliable screening method under random conditions. A salt loading test may confirm a primary aldosteronism. A unilateral adrenal adenoma has to be separated from bilateral adrenal hyperplasia. To exclude Cushing's syndrome, the dexamethasone challenge is a reliable screening parameter. Patients with Cushing's syndrome may have an elevated urinary free cortisol and the circadian rhythm may be abolished resulting in an elevated 23:00 h serum cortisol. Alternatively, cortisol may be measured in saliva using specific cutoffs. Determinations of 24-h urinary epinephrine and norepinephrine levels are established diagnostic tools for the diagnosis of pheochromocytoma. Metanephrines, which are metabolites of catecholamines, have been suggested as an alternative more sensitive and specific diagnostic tool. In conclusion, recently established biochemical methods are reliable screening parameters for the diagnosis of adrenal hypertension. Endocrine hypertension due to adrenal tumors may be treated by minimally invasive surgery or specific antihypertensive treatment.
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PMID:[Diagnosis and therapy of endocrine hypertension]. 1680 47


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