315 research outputs found
Oral burning with dysphagia and weight loss
Fibromyalgia is a disorder characterized by an abnormal pain regulation. Widespread pain, fatigue, and sleep disturbance are the prevalent symptoms. When unusual symptoms are overbearingly predominant at clinical presentation, the diagnosis becomes challenging. We report on the case of a patient with fibromyalgia, who presented with dysphagia, odynophagia, and glossodynia as prevalent symptoms. Difficulty in swallowing gradually developed over a month prior hospitalization, and worsened progressively so that nourishment and fluid intake were impeded. Because anemia with mild iron deficiency was found, esophagogastroduodenoscopy was performed, but no lesions were seen in the upper digestive tract. Levels of zinc and vitamin B12 were normal. Intense pain at pelvis and the inferior limbs, which was at a first glance referred to as osteoarthrosis, associated with oral symptoms and feeling of being in the clouds allowed us to diagnose fibromyalgia. Amitriptyline was used, with relief of symptoms. Although oropharyngeal symptoms were occasionally reported in fibromyalgia, they are often overlooked. The present case, therefore, testifies the need to consider the diagnosis of fibromyalgia when the patient presents with such symptoms that cannot be readily explained on other grounds
RAndomized Clinical Trial Of NAfamostat Mesylate, A Potent Transmembrane Protease Serine 2 (TMPRSS2) Inhibitor, in patients with Covid-19 pneumonia: Safety SUPPLEMENTAL DATA
The file includes: Protocol of RACONA Study; Table S1: Seven-category ordinal scale; Table S2. Inclusion and ex-clusion criteria; Table S3. Flow-chart of the study; Table S4. Laboratory tests; Table S5. Secondary Outcomes; Table S6. Secondary biomarker endpoints; Table S7. Group-sequential design; Table S8. Completed trials of nafamostat mesylate for treatment of Covid-19 patients; Table S9. Ongoing trials of nafamostat mesylate for treatment of Covid-19 patients; Figure S1. Flow chart of the RACONA Study; Annex 1: CONSORT chart
Treatment of atherosclerotic renovascular hypertension: review of observational studies and a meta-analysis of randomized clinical trials.
open9Atherosclerotic renal artery stenosis can cause ischaemic nephropathy and arterial hypertension. We herein review the observational and randomized clinical trials (RCTs) comparing medical and endovascular treatment for control of hypertension and renal function preservation. Using the Population Intervention Comparison Outcome (PICO) strategy, we identified the relevant studies and performed a novel meta-analysis of all RCTs to determine the efficacy and safety of endovascular treatment when compared with medical therapy. The following outcomes were examined: baseline follow-up difference in mean systolic and diastolic blood pressure (BP), serum creatinine, number of drugs at follow-up, incident events (heart failure, stroke, and worsening renal function), mortality, cumulative relative risk of heart failure, stroke, and worsening renal function. Seven studies comprising a total of 2155 patients (1741 available at follow-up) were considered, including the recently reported CORAL Study. Compared with baseline, diastolic BP fell more at follow-up in patients in the endovascular than in the medical treatment arm (standard difference in means -0.21, 95% confidence interval (CI): -0.342 to -0.078, P = 0.002) despite a greater reduction in the mean number of antihypertensive drugs (standard difference in means -0.201, 95% CI: -0.302 to -0.1, P < 0.001). At variance, follow-up changes (from baseline) of systolic BP, serum creatinine, and incident cardiovascular event rates did not differ between treatment arms. Thus, patients with atherosclerotic renal artery stenosis receiving endovascular treatment required less anti-antihypertensive drugs at follow-up than those medically treated. Notwithstanding this, they evidenced a better control of diastolic BP.openopenCaielli P;Frigo AC;Pengo MF;Rossitto G;Maiolino G;Seccia TM;CalĂČ LA;Miotto D;Rossi GPCaielli, P; Frigo, ANNA CHIARA; Pengo, Mf; Rossitto, G; Maiolino, G; Seccia, TERESA MARIA; CalĂČ, La; Miotto, Diego; Rossi, Gianpaol
Endothelin-1 Drives Epithelial-Mesenchymal Transition In Hypertensive Nephroangiosclerosis
BACKGROUND: Tubulointerstitial fibrosis, the final outcome of most kidney diseases, involves activation of epithelial mesenchymal transition (EMT). Endothelinâ1 (ETâ1) activates EMT in cancer cells, but it is not known whether it drives EMT in the kidney. We therefore tested the hypothesis that tubulointerstitial fibrosis involves EMT driven by ETâ1. METHODS AND RESULTS: Transgenic TG[mRen2]27 (TGRen2) rats developing fulminant angiotensin IIâdependent hypertension with prominent cardiovascular and renal damage were submitted to drug treatments targeted to ETâ1 and/or angiotensin II receptor or left untreated (controls). Expressional changes of Eâcadherin and αâsmooth muscle actin (αSMA) were examined as markers of renal EMT. In human kidney HKâ2 proximal tubular cells expressing the ET(B) receptor subtype, the effects of ETâ1 with or without ETâ1 antagonists were also investigated. The occurrence of renal fibrosis was associated with EMT in control TGRen2 rats, as evidenced by decreased Eâcadherin and increased αSMA expression. Irbesartan and the mixed ETâ1 receptor antagonist bosentan prevented these changes in a blood pressureâindependent fashion (P < 0.001 for both versus controls). In HKâ2 cells ETâ1 blunted Eâcadherin expression, increased αSMA expression (both P < 0.01), collagen synthesis, and metalloproteinase activity (P < 0.005, all versus untreated cells). All changes were prevented by the selective ET(B) receptor antagonist BQâ788. Evidence for involvement of the Rhoâkinase signaling pathway and dephosphorylation of Yesâassociated protein in EMT was also found. CONCLUSIONS: In angiotensin IIâdependent hypertension, ETâ1 acting via ET(B) receptors and the Rhoâkinase and Yesâassociated protein induces EMT and thereby renal fibrosis
Quantitative Value of Aldosterone-Renin Ratio for Detection of Aldosterone-Producing Adenoma: The Aldosterone-Renin Ratio for Primary Aldosteronism (AQUARR) Study
Current guidelines recommend use of the aldosterone-renin ratio (ARR) for the case detection of primary aldosteronism followed by confirmatory tests to exclude false-positive results from further diagnostic workup. We investigated the hypothesis that this could be unnecessary in patients with a high ARR value if the quantitative information carried by the ARR is taken into due consideration
Angiotensin peptides in the regulation of adrenal cortical function
The adrenal cortex plays a key role in the regulation of metabolism, salt and water homeostasis and sex differentiation by synthesizing glucocorticoid, mineralocorticoid and androgen hormones. Evidence exists that angiotensin II regulates adrenocortical function and it has been contended that angiotensin peptides of the non-canonical branch of the renin angiotensin system (RAS) might also modulate steroidogenesis in adrenals. Thus, the aim of this review is to examine the role of the RAS, and particularly of the angiotensin peptides and their receptors, in the regulation of adrenocortical hormones with particular focus on aldosterone production
Endothelin-1 (ET-1) modulates epithelial-mesenchymal transition (EMT), which contributes to kidney tubulo-interstitial fibrosis in angiotensin II-dependent hypertension
The origin of myofibroblasts remains uncertain, but studies suggest that the epithelial cells may acquire a fibroblast-like phenotype via epithelial-mesenchymal transition (EMT). Objective of the study was to investigate whether EMT may contribute to the development of kidney fibrosis in a model of angiotensin II-dependent hypertension and to identify the role of ET-1 via ETA/ETB receptors. Transgenic rats TGRen2 (n=35) received for 4 weeks one of the following treatments a) irbesartan, b) bosentan, non selective ETA /ETB receptor antagonist, c) BMS-182874, selective ETA,antagonist, d) BMS+irbesartan, e) placebo. EMT was assessed by investigating coexpression of a marker of epithelial cell (E-cadherin) and one of myofibroblast (S100A4 or alfa-SMA) with double immunofluorescence. Specific immunoreactivity was measured using QWinStandard Leica ImageTMsoftware. A reduction in blood pressure was found only with irbesartan, whereas both bosentan and irbesartan significantly lowered tubulo-interstitial fibrosis. Coexpression of E-cadherin and S100A4, or E-cadherin and alfa-SMA, markedly decreased in the tubular cells of TGRen2 treated with irbesartan or bosentan. Alfa-SMA expression decreased after irbesartan, bosentan and BMS+irbesartan, but not after BMS. S100A4 expression was reduced after irbesartan, bosentan and BMS+irbesartan. E-cadherin increased only after irbesartan. Coexpression of the markers of myofibroblasts and kidney epithelial cells, by demonstrating the development of EMT during the onset of kidney hypertension-induced damage, suggests a crucial role of EMT in the pathogenesis of Ang II-mediated fibrosis. The reduction of myofibroblast markers not only after irbesartan, but also after blockade of ETA/ETB receptors, suggests an involvement of ET-1 in the development of Ang II-mediated EMT
Endothelin-1 (ET-1) modulates epithelial-mesenchymal transition (EMT), which contributes to kidney tubulo-interstitial fibrosis in angiotensin II-dependent hypertension
The origin of myofibroblasts remains uncertain, but studies suggest that the epithelial cells may acquire a fibroblast-like phenotype via epithelial-mesenchymal transition (EMT). Objective of the study was to investigate whether EMT may contribute to the development of kidney fibrosis in a model of angiotensin II-dependent hypertension and to identify the role of ET-1 via ETA/ETB receptors. Transgenic rats TGRen2 (n=35) received for 4 weeks one of the following treatments a) irbesartan, b) bosentan, non selective ETA /ETB receptor antagonist, c) BMS-182874, selective ETA,antagonist, d) BMS+irbesartan, e) placebo. EMT was assessed by investigating coexpression of a marker of epithelial cell (E-cadherin) and one of myofibroblast (S100A4 or alfa-SMA) with double immunofluorescence. Specific immunoreactivity was measured using QWinStandard Leica ImageTMsoftware. A reduction in blood pressure was found only with irbesartan, whereas both bosentan and irbesartan significantly lowered tubulo-interstitial fibrosis. Coexpression of E-cadherin and S100A4, or E-cadherin and alfa-SMA, markedly decreased in the tubular cells of TGRen2 treated with irbesartan or bosentan. Alfa-SMA expression decreased after irbesartan, bosentan and BMS+irbesartan, but not after BMS. S100A4 expression was reduced after irbesartan, bosentan and BMS+irbesartan. E-cadherin increased only after irbesartan. Coexpression of the markers of myofibroblasts and kidney epithelial cells, by demonstrating the development of EMT during the onset of kidney hypertension-induced damage, suggests a crucial role of EMT in the pathogenesis of Ang II-mediated fibrosis. The reduction of myofibroblast markers not only after irbesartan, but also after blockade of ETA/ETB receptors, suggests an involvement of ET-1 in the development of Ang II-mediated EMT
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