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

West syndrome (WS) is an age dependent epileptic syndrome caused by various brain disorders. WS has been frequently classified in two groups, cryptogenic and symptomatic. As symptomatic WS consists of patients with numerous types of brain lesions, the prognosis and evolutional changes may be different among the types of brain lesions. WS is resistant to treatment to most conventional antiepileptic drugs, and only valproic acid, benzodiazepines, adrenocorticotropic hormone (ACTH), corticosteroids and vigabatrin have been found efficacious. Benzodiazepine, notably nitrazepam, and less clonazepam had been effective in bringing spasms under control but emerging tolerance and significant side effects (hypotonia and drowsiness) precluded its wider use. ACTH has been the treatment of choice for infantile spasms ever since Sorel and Dusaucy-Bouloye described its effectiveness in 1958. Despite the empirical approach steroids were capable of controlling the spasms and normalizing EEG in about 60% of cases. Corticotropin (ACTH) was used in doses from 5 to 180 I.U. daily, prednizolone 2-10 mg/kg daily, hydrocortisone 5-10 mg/kg daily and dexamethason 0.3-0.5 mg/kg. However, poor consensus was defined regarding the best steroid molecule to use, the dosage, and the duration of treatment. Also frequent and sometimes serious side effects have occurred during ACTH therapy, notably serious infections and hypertension that promoted continuous search for alternative and safer drugs tolerated outpatient treatment, good tolerance and minor side effects. Recently a specific visual field loss has been reported in treated adults that raised concern about safety of vigabatrin. New reports in children claim that vigabatrin treatment of children and adolescents has a lower risk for visual field defect than in adults, because of reported reversibility. Vigabatrin paediatric advisory group recommend the trial of vigabatrin for 12-14 days as first treatment for WS and in the case of good clinical response continuation of therapy for six months. Other new antiepileptic drugs (lamotrigine, topiramate, felbamate and zonisamide) have shown significant efficacy in the treatment of resistant WS to previous medication. The current task is to determine risk/benefit ratios of these two drugs (vigabatine, ACTH) and to delineate the group of patients with WS where their use would be optimal.
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PMID:[West syndrome--new therapeutic approach]. 1563 97

We present an unusual patient who simultaneously had severe renal artery stenosis RAS and Cushing's syndrome. The case highlights the difficulty of reaching a specific diagnosis of Cushing's syndrome and the possible interaction between Cushing's syndrome and some other concurrent illnesses that this patient had. A 37-year old man presented with severe hypertension HTN and uncontrolled diabetes mellitus DM without clear physical signs of Cushing's syndrome. He was found to have severe osteoporosis, proximal myopathy, several cutaneous warts, tinea versicolor, and chronic viral hepatitis. Captopril-stimulated renal scan and renal artery angiogram revealed severe RAS. Partial balloon dilatation of RAS led to improvement in HTN. Unexpectedly, urine free cortisol 24 hour was found extremely high. Serum adrenocorticotropic hormone ACTH was also elevated and high dose dexamethasone suppression tests were inconclusive. Several imaging studies failed to localize the source of ACTH. Despite normal MRI of the pituitary gland, bilateral inferior petrosal sinus sampling IPSS localized the source of ACTH secretion to the right side of the pituitary gland and right anterior hemihypophysectomy resulted in cure of Cushing's disease, HTN, DM, and tinea versicolor with significant improvement in cutaneous warts, osteoporosis, and chronic hepatitis. In conclusion, RAS and Cushing's syndrome may occur together. Significant hypercortisolemia can occur without clear signs of Cushing's syndrome. Controlling hypercortisolemia is of paramount importance when treating chronic infections in patients with Cushing's syndrome.
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PMID:Severe hypertension secondary to renal artery stenosis and Cushing's syndrome. 1590 Mar 83

Pheochromocytoma (PHEO) occasionally associates with pathological lesions of the adrenal cortex. In most of them, ectopic adrenocorticotropic hormone (ACTH) produced by PHEO resulted in bilateral adrenocortical hyperplasia. The coexistence of PHEO and pre-clinical Cushing's syndrome (PCS) of the same adrenal gland has rarely been reported. We report on a patient and discuss the peculiar diagnostic aspects of this entity. A 52-yr-old Turkish woman was hospitalized at Farabi Hospital for further examinations of a right adrenal mass that was incidentally discovered by abdominal ultrasonography during examinations for abdominal bloating and "gas" in other hospital. The patient had a history of palpitations, nervousness, sweating and heat intolerance. On admission, her blood pressure was 140/90 mmHg. A physical examination revealed no signs of an excessive production of adrenocortical steroids such as in CS. Tension Holter monitoring revealed paroximal hypertension attacks (183/105 mmHg). Urinary catecholamines were markedly increased. Her serum cortisol concentrations ranged from 5 to 17 microg/dl, whereas ACTH levels were undetectable. Cortisol was not suppressed on the overnight 1 mg oral dexamethasone suppression test (DST), 2-day low-dose dexamethasone suppression test (DST). Abdominal computed tomography and magnetic resonance imaging studies revealed a solid round tumor approximately 4 cm in diameter, located in the right adrenal gland. A 131 lodine-metaiodobenzylguanidine (131 I-MIBG) scan revealed uptake within tumor in the right adrenal gland. Right adrenalectomy was performed; the surgical specimen revealed PHEO and adrenocortical hyperplasia. To our knowledge, the present report is a rare case of PHEO combined with PCS in the same adrenal gland.
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PMID:Pheochromocytoma combined with pre-clinical Cushing's syndrome in the same adrenal gland. 1611

The Na,K-ATPase contains a binding site for cardiac glycosides, such as ouabain, digoxin, and digitoxin, which is highly conserved among species ranging from Drosophila to humans. Although advantage has been taken of this site to treat congestive heart failure with drugs such as digoxin, it is unknown whether this site has a natural function in vivo. Here we show that this site plays an important role in the regulation of blood pressure, and it specifically mediates adrenocorticotropic hormone (ACTH)-induced hypertension in mice. We used genetically engineered mice in which the Na,K-ATPase alpha2 isoform, which is normally sensitive to cardiac glycosides, was made resistant to these compounds. Chronic administration of ACTH caused hypertension in WT mice but not in mice with an ouabain-resistant alpha2 isoform of Na,K-ATPase. This finding demonstrates that the cardiac glycoside binding site of the Na,K-ATPase plays an important role in blood pressure regulation, most likely by responding to a naturally occurring ligand. Because the alpha1 isoform is sensitive to cardiac glycosides in humans, we developed mice in which the naturally occurring ouabain-resistant alpha1 isoform was made ouabain-sensitive. Mice with the ouabain-sensitive "human-like" alpha1 isoform and an ouabain-resistant alpha2 isoform developed ACTH-induced hypertension to greater extent than WT animals. This result indicates that the cardiac glycoside binding site of the alpha1 isoform can also mediate ACTH-induced hypertension. Taken together these results demonstrate that the cardiac glycoside binding site of the alpha isoforms of the Na,K-ATPase have a physiological function and supports the hypothesis for a role of the endogenous cardiac glycosides.
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PMID:The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation. 1624 2

Aldosterone is the principal circulating mineralocorticoid in humans, and aldosterone synthesis normally occurs in the face of volume depletion and renin stimulation. In primary and secondary aldosteronism, aldosterone synthesis continues despite volume expansion and causes hypertension. Other steroid hormones that are aldosterone and cortisol precursors also activate the mineralocorticoid receptor and cause hypertension when overproduced. Mineralocorticoid synthesis in these pathologic states can be constitutive or driven by pituitary adrenocorticotropic hormone (ACTH), due to genetic defects that cause disordered steroid synthesis or catabolism. This review focuses on uncommon forms of ACTH-dependent mineralocorticoid excess states associated with hypertension.
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PMID:Miscellaneous endocrine causes of hypertension. 1625 10

We investigated the effect of antioxidant N-acetylcysteine (NAC) on adrenocorticotropic hormone (ACTH)-hypertension. Male Sprague-Dawley rats received NAC (10 mg/L) or water 4 days before ACTH/saline treatment for 13 days (prevention study). In a reversal study, NAC commenced on day 8 of ACTH/saline treatment and continued for 5 days. ACTH increased systolic blood pressure (SBP) in water drinking rats (111 +/- 1 to 131 +/- 3 mmHg, p < 0.001). In the prevention study, NAC + ACTH increased SBP (108 +/- 2 to 120 +/- 2 mmHg, p < 0.001) but less than ACTH alone (p' < 0.05). In the reversal study, NAC had no significant effect (132 +/- 4 to 124 +/- 3 mmHg, ns). Thus, NAC partially prevented but did not reverse ACTH-induced hypertension.
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PMID:N-acetylcysteine antagonizes the development but does not reverse ACTH-induced hypertension in the rat. 1654 35

Essential hypertension is associated with changes in central catecholaminergic pathways which might also be reflected in the pituitary response to stress stimuli. The aim of this study was to determine whether the response of pituitary hormones, cortisol, plasma renin activity, aldosterone and catecholamines to insulin-induced hypoglycaemia is changed in hypertension. We studied 22 young lean male patients with newly diagnosed untreated essential hypertension and 19 healthy normotensive, age- and body mass index (BMI)-matched controls. All subjects underwent an insulin tolerance test (0.1 IU insulin/kg body weight intravenously) with blood sampling before and 15, 30, 45, 60 and 90 min after insulin administration. Increased baseline levels of norepinephrine (P<0.05), increased response of norepinephrine (P<0.001) and decreased response of growth hormone (P<0.001), prolactin (P<0.001), adrenocorticotropic hormone (P<0.05) and cortisol (P<0.001) were found in hypertensive patients when compared to normotensive controls. Increased norepinephrine levels and a decreased pituitary response to metabolic stress stimuli may represent another manifestation of chronically increased sympathetic tone in early hypertension.
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PMID:Decreased pituitary response to insulin-induced hypoglycaemia in young lean male patients with essential hypertension. 1661 9

The -344 C/T and intron 2 conversion variants in the CYP11B2 gene, encoding aldosterone synthase, have been associated with markers of impaired 11beta-hydroxylase activity. We hypothesize that this association is because of variations in the adjacent 11beta-hydroxylase gene (CYP11B1) and arises through linkage disequilibrium between CYP11B1 and CYP11B2. The pattern of variation across the entire CYP11B locus was determined by sequencing 26 normotensive subjects stratified by and homozygous for the -344 and intron conversion variants. Eighty-three variants associated with -344 and intron conversion were identified. Haplotype analysis revealed 4 common haplotypes, accounting for 68% of chromosomes, confirming strong linkage disequilibrium across the region. Two novel CYP11B1 polymorphisms upstream of the coding region (-1889 G/T and -1859 A/G) were identified as contributing to the common haplotypes. Given the potential for such mutations to affect transcriptional regulation of CYP11B1, these were analyzed further. A total of 512 hypertensive subjects from the British Genetics of Hypertension Study population were genotyped for these polymorphisms. A significant association was identified between the -1889 polymorphism and urinary tetrahydrodeoxycortisol/total cortisol metabolite ratio, indicating reduced 11beta-hydroxylase efficiency. A similar pattern was observed for the -1859 polymorphism, but this did not achieve statistical significance. Functional studies in vitro using luciferase reporter gene constructs show that these polymorphisms significantly alter the transcriptional response of CYP11B1 to stimulation by adrenocorticotropic hormone or forskolin. This study strongly suggests that the impaired 11beta-hydroxylase efficiency associated previously with the CYP11B2 -344 and intron conversion variants is because of linkage with these newly identified polymorphisms in CYP11B1.
Hypertension 2007 Jan
PMID:Polymorphic variation in the 11beta-hydroxylase gene associates with reduced 11-hydroxylase efficiency. 1707 29

Primary aldosteronism is defined as secondary hypertension accompanied by aldosterone hypersecretion that leads to suppressed plasma renin, hypokaremia and hypertension. Primary aldosteronism occurs in 3-15% of hypertensive patients and is commonly caused by aldosterone-producing adenoma (APA) or bilateral idiopathic hyperaldosteronism (IHA). APA is usually treated by adrenalectomy, whereas IHA is best managed medically. Therefore, it is important to distinguish between unilateral and bilateral disease. Computed tomography (CT) is used to differentiate the subtypes. Even when multidetector CT is used, the detection rate of APAs of 1 cm or less is lower than 60% for the following reasons: (a) aldosterone secretion does not depend on tumor size, (b) a tumor may exist without lipid-rich cells, and (c) non-functioning unilateral adenomas are not uncommon, especially in older patients. Adrenal venous sampling is the gold standard for the differentiation of unilateral from bilateral disease in patients with primary aldosteronism. It is important to compare the laterality of aldosterone secretion by performing simultaneous bilateral blood collection 15 min following adrenocorticotropic hormone stimulation. The value of (aldosterone/cortisol)(side)/(aldosterone/cortisol)(contralateral side) provides the best discrimination between patients with and without APA.
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PMID:Primary aldosteronism: a pictorial essay. 1715 4

Gout, a common inflammatory arthritis, can be diagnosed with absolute certainty. Gout results from the body's reaction to urate crystals deposited in tissues, and this pathophysiology is well understood. If used appropriately, available therapies can be entirely effective in not only treating the symptoms of gout, but also in eliminating the excess urate from the body, thereby eradicating the disease. Because of these facts, management of patients with gout should be successful. However, management of gout is particularly challenging in the elderly, even though the principles of management are the same for all age groups. The purpose of this article is to review these principles and discuss them as they pertain to the elderly. The classic gout attack is acute in onset, extremely painful and associated with marked swelling, warmth, erythema and tenderness of a single joint. However, the diagnosis of gout may be challenging in the elderly because atypical presentations are more common in this group. Treatment of acute gout involves the use of NSAIDs, colchicine, corticosteroids or corticotropin (adrenocorticotropic hormone). Unfortunately, co-morbid conditions such as chronic kidney disease, peptic ulcer disease and congestive heart failure may make the use of these agents dangerous or contraindicated. Thus, it is important to try to treat an acute flare of gout at the earliest sign, because the sooner treatment is initiated, the faster the inflammation will resolve. Urate-lowering agents include allopurinol and uricosuric agents. These also must be used judiciously in the elderly. However, if used at the lowest dose that maintains the serum urate level below 5.0-6.0 mg/dL, the excess urate in the body will be eliminated, acute flares will no longer occur and tophi will resolve. Gout is often seen in association with hypertension, excessive alcohol consumption, obesity and hypertriglyceridaemia. These conditions and the medications used to treat them may contribute to the hyperuricaemia. Treating these conditions and using medications that do not promote hyperuricaemia will aid in the management of gout. Despite the challenges that often complicate the management of gout in the elderly, an understanding of the pathophysiology of the disease and both the indications and limitations of the medications used should allow successful treatment.
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PMID:Management of gout in older adults: barriers to optimal control. 1723 45


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