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A 37-year-old man developed generalized medium-brown hyperpigmentation in the course of progressive systemic scleroderma. Histologically there were numerous Melanin granules in the basal epidermis, but also in the upper Malpighian layer and in corneocytes. An allergic rash developed on administration of spironolactone given for the scleroderma. After healing there remained slate-grey spots. As a consequence of the drug rash the already present hyperpigmentation was aggravated by marked pigment deposition in the upper corium. At the same time there were numerous melanophages as sign of an absorptive removal of the melanin granules. The drug allergy was thus the occasion for the persisting pigment deposition with circumscribed spotty pigmentation of the skin.
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Gonadal dysfunction is common in chronic liver disease, but most of the previous studies have been restricted to men with alcohol-induced liver disease. We have evaluated hypothalamic-pituitary-testicular function in patients with end-stage non-alcoholic liver disease before and at 6 and 12 months after hepatic transplantation.
All pertinent clinical trials, retrospective studies, and case reports in human subjects published in the English language were identified and evaluated for the safety and efficacy of pharmacologic and nonpharmacologic treatments of PMS/PMDD. Data from these studies and information from review articles were included in this review.
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This study confirms the beneficial effects of metformin in PCOS patients. It also indicates that the addition of low-dose spironolactone induces a more marked reduction of clinical and biochemical hyperandrogenism as compared to metformin alone.
Although uterine leiomyomas are the most common gynaecological benign tumour and greatly affect reproductive health and well being, the pathophysiology and epidemiology of uterine leiomyomas are not well known. Elevated blood pressure has an independent, positive association with risk for clinically detected uterine leiomyomas. Aldosterone is a key biological peptide in the renin-angiotensin-aldosterone system that regulates blood pressure. In this study, we investigated the siginificant stimulatory effect of aldosterone on leiomyoma cells proliferation.
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Patients with obstructive sleep apnea (OSA) often have hypertension that is difficult to control. We review the causes of OSA hypertension and evidence supporting specific therapies.
A patient with chronic kidney disease (CKD) due to membranous nephropathy with daily urinary protein excretion exceeding 5 g did not respond well to dual therapy with an angiotensin converting enzyme inhibitor (ACE-I) and angiotensin II receptor blocker (ARB). Addition of the mineralocorticoid receptor blocker (MRB), spironolactone, led to moderate reduction in daily urinary protein excretion. However, spironolactone had to be inevitably discontinued due to gynecomastia. Replacement of spironolactone with the selective MRB, eplerenone, added to the preceding treatment with ACE-I and ARB, resulted in remarkable reduction of daily urinary protein excretion to less than 0.2 g. This case suggests that triple blockade of renin-angiotensin-aldosterone (RAA) system with ACE-I, ARB, and MRB could be useful for CKD patients with massive proteinuria.
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The EMPHASIS-HF trial compared eplerenone with placebo added to standard therapy in 2737 patients with New York Heart Association class II HF and left ventricular ejection fraction ≤35%. We conducted a post hoc analysis in the 2338 patients randomized within 180 days of a CVH. The interaction between the time from the qualifying CVH to randomization and the primary outcome of CV death or hospitalization for HF (HHF), as well as other secondary outcomes, was assessed in Cox survival models. Most of the qualifying CVHs were HHF (N = 1496, 64.0%), acute coronary syndromes (N = 390, 16.7%), and arrhythmias (N = 197, 7.2%). The median time of study drug initiation from qualifying CVH was 42 days. The relative rate reductions in CV death/HHF, HHF, and all-cause mortality were similar (P for interaction = 0.65, 0.44, and 0.40, respectively) whether the treatment was initiated <42 or 42+ days after qualifying CVH. Absolute rate reductions were -5.61 [-8.67, -2.55] events per 100 patient × years in the <42 days group and -3.58 [-6.37, -0.79] in the 42+ days group. The adverse effects of eplerenone were also unaffected by the time from the qualifying CVH.
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Spironolactone use in ESRD patients on hemodialysis may not lead to greater incidence of hyperkalemia.
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Blood pressure increased similarly among strains after clipping and was unaffected by spironolactone. Hypertension caused the greatest renal fibrosis in BN rats (p < 0.001 by ANOVA compared to other strains). Real-time PCR analysis showed greater renal collagen type I and MR gene expression in untreated, hypertensive BN rats (both p < 0.05 compared to other strains). Spironolactone attenuated fibrosis, with similar fibrosis among strains of spironolactone-treated rats.
Clinical profile and prescribed medications of patients with diagnosis of HF who were admitted in the cardiology department of College of Medical Sciences & Teaching Hospital (CMS-TH), Bharatpur, Nepal, April 2010 to May 2012, were analyzed. A total of 255 patients presented with HF during the studied period were included.
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We used routinely collected therapeutic drug monitoring data (n=544), derived from the steady-state serum concentrations of digoxin in 181 hospitalized paediatric patients.
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The advent of angiotensin-converting enzyme inhibitors, beta-blockers, and spironolactone has revolutionized the management of heart failure. Randomized double-blind studies have demonstrated survival benefits of these drugs in heart failure patients. Nevertheless, in spite of these advances, heart failure continues to be a syndrome of poor outcomes.1-4 There is also evidence that a significant portion of heart failure patients does not receive this evidence-based therapy that reduces morbidity and mortality.5-7 Various disease-management programs have been proposed and tested to improve the quality of heart failure care. Most of these programs are specialized multidisciplinary heart failure clinics lead by cardiologists or heart failure specialists and conducted by nurses or nurse practitioners. Similar to the Department of Veterans Affairs (VA) multidisciplinary geriatric assessment clinics, these clinics also use many other services, including pharmacists, dietitians, physical therapists, and social workers. Some of these programs also have an affiliated home health service. Several observation studies, using mostly pre- and postcomparison designs, have demonstrated the effectiveness of these programs in the process of care, resource use, healthcare costs, and clinical outcomes in patients with heart failure.8 Risk of hospitalization was reduced by 50% to 85% in six of the studies.8 Subsequently, several randomized trials were conducted to determine the effectiveness of these programs. The purpose of this systematic review was to determine the effectiveness of these programs on mortality and hospitalization rates of heart failure patients.
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Studies were obtained by performing a systematic review of the literature on hypertension and diabetes, from which management recommendations were developed, reviewed, and voted on by a group of experts selected by the Canadian Hypertension Education Program and the Canadian Diabetes Association; authors' expert opinions on optimal pharmacologic management were also considered during this process.
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Hypothalamic-pituitary-adrenal (HPA) axis dysregulation may underlie disorders including obesity, depression, cognitive decline, and the metabolic syndrome. Conventional tests of HPA axis negative feedback rely on glucocorticoid receptor (GR) agonists such as dexamethasone but do not test feedback by endogenous cortisol, potentially mediated by both GR and mineralocorticoid receptors (MR).
Five-year cumulative survival was 44.5%. The mean annual medical admission rate was 204/100 000; 54.84% of which were readmissions in the same year. Prescription rates for angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers, beta-blockers and spironolactone were 68.3%, 74.2% and 24.9%, respectively, with only 17.6%, 19.0% and 16.4% on maximum recommended doses. implantable cardioverter-defibrillator devices were inserted in 11.5% of eligible patients. Quality of life was impaired in patients <70 years relative to the age-approximated New Zealand index population. Mean EQ-5D visual analogue score was 72.6 ± 0.032 and self-reported New York Heart Association class 2.09 ± 0.107
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Patients were eligible for breast augmentation after 2 yr of estrogen treatment, were Tanner IV or higher breast development, and reported psychological distress due to small breasts. One hundred sixty-five subjects and 165 age-matched controls were identified.
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HF was produced in 12 dogs by intracoronary microembolizations. Dogs were randomized to 3 months oral therapy with eplerenone (10 mg/kg twice daily, n = 6) or to no therapy at all (HF-control, n = 6). LV tissue from six normal dogs was used for comparison. mRNA expression was measured using reverse-transcriptase polymerase chain reaction (RT-PCR) and protein expression using Western blots.
Aldosterone-producing adenomas in patients who have not been given spironolactone are more responsive to ACTH than to angiotensin II. In vitro, adenomas respond to ACTH, but their response to angiotensin II has not been clearly defined. Treatment with spironolactone has been given before the removal of some of the adenomas studied in vitro, and it can blunt increases in plasma aldosterone concentrations that occur in response to increases in renin activity. To assess the effect of preoperative spironolactone therapy on the responsiveness of aldosterone-producing adenomas in vitro, tissue from five patients with adenomas was incubated for 4 hours with and without angiotensin II and ACTH, 10(-7) to 10(-5) mol/L. The responsiveness of the adenomas was then related to the duration of preoperative spironolactone therapy. The serum potassium concentration was normal in the patients before the operations. Adenoma tissue from a patient given spironolactone for 4 days was responsive to angiotensin II and to ACTH. Treatment of longer duration with spironolactone appeared to be associated with a pattern of decreasing responsiveness to ACTH and an absence of response to angiotensin II in vitro. Aldosterone production by nonadenomatous adrenal tissue did not respond to angiotensin II or to ACTH. Our results suggest that preoperative spironolactone therapy might decrease the responsiveness of aldosterone-producing adenomas to angiotensin II and ACTH in vitro. Therefore, studies of aldosterone-producing adenomas in vitro should consider the possible effects of preoperative treatment with spironolactone on the responsiveness of the adenomas to angiotensin II and ACTH.
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Experimental animal studies indicate that exposure to increased aldosterone levels might result in renal damage, but the clinical evidence supporting this role of aldosterone is preliminary.
Elevation of C-reactive protein (CRP) in human blood accompanies inflammatory processes, including cardiovascular diseases. There is increasing evidence that the acute-phase reactant CRP is not only a passive marker protein for systemic inflammation but also affects the vascular system. Further, CRP is an independent risk factor for atherosclerosis and the development of hypertension. Another crucial player in atherosclerotic processes is the mineralocorticoid hormone aldosterone. Even in low physiological concentrations, it stimulates the expression and membrane insertion of the epithelial sodium channel, thereby increasing the mechanical stiffness of endothelial cells. This contributes to the progression of endothelial dysfunction. In the present study, the hypothesis was tested that the acute application of CRP (25 mg/L), in presence of aldosterone (0.5 nmol/L; 24 hour incubation), modifies the mechanical stiffness and permeability of the endothelium. We found that endothelial cells stiffen in response to CRP. In parallel, endothelial epithelial sodium channel is inserted into the plasma membrane, while, surprisingly, the endothelial permeability decreases. CRP actions are prevented either by the inhibition of the intracellular aldosterone receptors using spironolactone (5 nmol/L) or by the inactivation of epithelial sodium channel using specific blockers. In contrast, inhibition of the release of the vasodilating gas nitric oxide via blockade of the phosphoinositide 3-kinase/Akt pathway has no effect on the CRP-induced stiffening of endothelial cells. The data indicate that CRP enhances the effects of aldosterone on the mechanical properties of the endothelium. Thus, CRP could counteract any decrease in arterial blood pressure that accompanies severe acute inflammatory processes.
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Adult Sprague Dawley rats were randomized into four groups; controls, spironolactone-treated rats (Spir), diabetic rats (DM), and diabetic rats treated with spironolactone (DM+Spir) for 4 weeks. Blood pressure and cardiac levels of aldosterone and oxidants/antioxidants were measured.
In connection with the total synthesis of naphthospironone A, a model study has revealed a promising approach to construct a benzobicyclo[3.2.1]octene skeleton possessing an oxaspirocycle by employing an intramolecular aldol cyclization.