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[PMID]:28552621
[Au] Autor:Wellman AS; Metukuri MR; Kazgan N; Xu X; Xu Q; Ren NSX; Czopik A; Shanahan MT; Kang A; Chen W; Azcarate-Peril MA; Gulati AS; Fargo DC; Guarente L; Li X
[Ad] Endereço:Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
[Ti] Título:Intestinal Epithelial Sirtuin 1 Regulates Intestinal Inflammation During Aging in Mice by Altering the Intestinal Microbiota.
[So] Source:Gastroenterology;153(3):772-786, 2017 Sep.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Intestinal epithelial homeostasis is maintained by complex interactions among epithelial cells, commensal gut microorganisms, and immune cells. Disruption of this homeostasis is associated with disorders such as inflammatory bowel disease (IBD), but the mechanisms of this process are not clear. We investigated how Sirtuin 1 (SIRT1), a conserved mammalian NAD -dependent protein deacetylase, senses environmental stress to alter intestinal integrity. METHODS: We performed studies of mice with disruption of Sirt1 specifically in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1 mice) and control mice (villin-Cre-, Sirt1 ) on a C57BL/6 background. Acute colitis was induced in some mice by addition of 2.5% dextran sodium sulfate to drinking water for 5-9 consecutive days. Some mice were given antibiotics via their drinking water for 4 weeks to deplete their microbiota. Some mice were fed with a cholestyramine-containing diet for 7 days to sequester their bile acids. Feces were collected and proportions of microbiota were analyzed by 16S rRNA amplicon sequencing and quantitative PCR. Intestines were collected from mice and gene expression profiles were compared by microarray and quantitative PCR analyses. We compared levels of specific mRNAs between colon tissues from age-matched patients with ulcerative colitis (n=10) vs without IBD (n=8, controls). RESULTS: Mice with intestinal deletion of SIRT1 (SIRT1 iKO) had abnormal activation of Paneth cells starting at the age of 5-8 months, with increased activation of NF-κB, stress pathways, and spontaneous inflammation at 22-24 months of age, compared with control mice. SIRT1 iKO mice also had altered fecal microbiota starting at 4-6 months of age compared with control mice, in part because of altered bile acid metabolism. Moreover, SIRT1 iKO mice with defective gut microbiota developed more severe colitis than control mice. Intestinal tissues from patients with ulcerative colitis expressed significantly lower levels of SIRT1 mRNA than controls. Intestinal tissues from SIRT1 iKO mice given antibiotics, however, did not have signs of inflammation at 22-24 months of age, and did not develop more severe colitis than control mice at 4-6 months. CONCLUSIONS: In analyses of intestinal tissues, colitis induction, and gut microbiota in mice with intestinal epithelial disruption of SIRT1, we found this protein to prevent intestinal inflammation by regulating the gut microbiota. SIRT1 might therefore be an important mediator of host-microbiome interactions. Agents designed to activate SIRT1 might be developed as treatments for IBDs.
[Mh] Termos MeSH primário: Envelhecimento/genética
Envelhecimento/metabolismo
Colite/genética
Microbioma Gastrointestinal
Sirtuína 1/genética
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Animais
Antibacterianos/administração & dosagem
Anticolesterolemiantes/administração & dosagem
Ácidos e Sais Biliares/metabolismo
Resina de Colestiramina/administração & dosagem
Colite/induzido quimicamente
Colite Ulcerativa/genética
Sulfato de Dextrana
Fezes/microbiologia
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
NF-kappa B/metabolismo
Celulas de Paneth/metabolismo
RNA Mensageiro/análise
Transdução de Sinais
Sirtuína 1/deficiência
Estresse Fisiológico
Transcriptoma
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Anticholesteremic Agents); 0 (Bile Acids and Salts); 0 (NF-kappa B); 0 (RNA, Messenger); 11041-12-6 (Cholestyramine Resin); 9042-14-2 (Dextran Sulfate); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


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[PMID]:28521862
[Au] Autor:Kusumoto Y; Irie J; Iwabu K; Tagawa H; Itoh A; Kato M; Kobayashi N; Tanaka K; Kikuchi R; Fujita M; Nakajima Y; Morimoto K; Sugizaki T; Yamada S; Kawai T; Watanabe M; Oike Y; Itoh H
[Ad] Endereço:Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan.
[Ti] Título:Bile acid binding resin prevents fat accumulation through intestinal microbiota in high-fat diet-induced obesity in mice.
[So] Source:Metabolism;71:1-6, 2017 Jun.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bile acid binding resin (BAR) absorbs intestinal bile acids, and improves obesity and metabolic disorders, but the precise mechanism remains to be clarified. Recent findings reveal that obesity is associated with skewed intestinal microbiota. Thus, we investigated the effect of BAR on intestinal microbiota and the role of microbiota in the prevention of obesity in high-fat diet-induced obesity in mice. PROCEDURES: Male Balb/c mice were fed a low-fat diet (LFD), high-fat diet (HFD), or HFD with BAR (HFD+BAR), and then metabolic parameters, caecal microbiota, and metabolites were investigated. The same interventions were conducted in germ-free and antibiotic-treated mice. MAIN FINDINGS: The frequency of Clostridium leptum subgroup was higher in both HFD-fed and HFD+BAR-fed mice than in LFD-fed mice. The frequency of Bacteroides-Prevotella group was lower in HFD-fed mice than in LFD-fed mice, but the frequency was higher in HFD+BAR-fed mice than in HFD-fed mice. Caecal propionate was lower in HFD-fed mice than in LFD-fed mice, and higher in HFD+BAR-fed mice than in HFD-fed mice. HFD+BAR-fed mice showed lower adiposity than HFD-fed mice, and the reduction was not observed in germ-free or antibiotic-treated mice. Colonized germ-free mice showed a reduction in adiposity by BAR administration. Energy expenditure was lower in HFD-fed mice and higher in HFD+BAR-fed mice, but the increments induced by administration of BAR were not observed in antibiotic-treated mice. CONCLUSIONS: Modulation of intestinal microbiota by BAR could be a novel therapeutic approach for obesity.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/metabolismo
Resina de Colestiramina/farmacologia
Gorduras na Dieta/metabolismo
Microbioma Gastrointestinal/efeitos dos fármacos
Obesidade/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Bacteroides/efeitos dos fármacos
Ceco/microbiologia
Clostridium/efeitos dos fármacos
Dieta Hiperlipídica
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Prevotella/efeitos dos fármacos
Ganho de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Dietary Fats); 11041-12-6 (Cholestyramine Resin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE


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[PMID]:28487440
[Au] Autor:Sjöberg BG; Straniero S; Angelin B; Rudling M
[Ad] Endereço:Metabolism Unit C2:94 and KI/AZ Integrated CardioMetabolic Center, Department of Medicine, and Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.
[Ti] Título:Cholestyramine treatment of healthy humans rapidly induces transient hypertriglyceridemia when treatment is initiated.
[So] Source:Am J Physiol Endocrinol Metab;313(2):E167-E174, 2017 Aug 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bile acid (BA) production in mice is regulated by hepatic farnesoid X receptors and by intestinal fibroblast growth factor (FGF)-15 (in humans, FGF-19), a suppressor of BA synthesis that also reduces serum triglycerides and glucose. Cholestyramine treatment reduces FGF-19 and induces BA synthesis, whereas plasma triglycerides may increase from unclear reasons. We explored whether FGF-19 may suppress BA synthesis and plasma triglycerides in humans by modulation of FGF-19 levels through long-term cholestyramine treatment at increasing doses. In a second acute experiment, metabolic responses from 1 day of cholestyramine treatment were monitored. Long-term treatment reduced serum FGF-19 by >90%; BA synthesis increased up to 17-fold, whereas serum BAs, triglycerides, glucose, and insulin were stable. After long-term treatment, serum BAs and FGF-19 displayed rebound increases above baseline levels, and BA and cholesterol syntheses normalized after 1 wk without rebound reductions. Acute cholestyramine treatment decreased FGF-19 by 95% overnight and serum BAs by 60%, while BA synthesis increased fourfold and triglycerides doubled. The results support that FGF-19 represses BA synthesis but not serum triglycerides. However, after cessation of both long-term and 1-day cholestyramine treatment, circulating FGF-19 levels were normalized within 2 days, whereas BA synthesis remained significantly induced in both situations, indicating that also other mechanisms than the FGF-19 pathway are responsible for stimulation of BA synthesis elicited by cholestyramine. Several of the responses during cholestyramine treatment persisted at least 6 days after treatment, highlighting the importance of removing such treatment well before evaluating dynamics of the enterohepatic circulation in humans.
[Mh] Termos MeSH primário: Resina de Colestiramina/efeitos adversos
Hipertrigliceridemia/induzido quimicamente
[Mh] Termos MeSH secundário: Adulto
Ácidos e Sais Biliares/metabolismo
Resina de Colestiramina/administração & dosagem
Relação Dose-Resposta a Droga
Feminino
Fatores de Crescimento de Fibroblastos/sangue
Voluntários Saudáveis
Seres Humanos
Hipertrigliceridemia/metabolismo
Fígado/metabolismo
Masculino
Fatores de Tempo
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (FGF19 protein, human); 0 (Triglycerides); 11041-12-6 (Cholestyramine Resin); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00416.2016


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[PMID]:27897155
[Au] Autor:Pardi DS
[Ad] Endereço:Inflammatory Bowel Disease Clinic, Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
[Ti] Título:Diagnosis and Management of Microscopic Colitis.
[So] Source:Am J Gastroenterol;112(1):78-85, 2017 Jan.
[Is] ISSN:1572-0241
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microscopic colitis (MC) is a relatively common cause of chronic watery diarrhea, especially in older persons. Associated symptoms, including abdominal pain and arthralgias, are common. The diagnosis is based upon characteristic histological findings in the presence of diarrhea. The two types of MC, collagenous and lymphocytic colitis, share similar clinical features, with the main difference being the presence or absence of a thickened subepithelial collagen band. There are several treatment options for patients with MC, although only budesonide has been well studied in multiple controlled clinical trials. This review will describe the clinical features, epidemiology, pathophysiology, diagnostic criteria, and treatment of patients with MC.
[Mh] Termos MeSH primário: Colite Colagenosa/diagnóstico
Colite Linfocítica/diagnóstico
[Mh] Termos MeSH secundário: Resinas de Troca de Ânions/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Antidiarreicos/uso terapêutico
Autoimunidade/imunologia
Ácidos e Sais Biliares/metabolismo
Budesonida/uso terapêutico
Resina de Colestiramina/uso terapêutico
Colite Colagenosa/tratamento farmacológico
Colite Colagenosa/imunologia
Colite Colagenosa/patologia
Colite Linfocítica/tratamento farmacológico
Colite Linfocítica/imunologia
Colite Linfocítica/patologia
Colite Microscópica/diagnóstico
Colite Microscópica/tratamento farmacológico
Colite Microscópica/imunologia
Colite Microscópica/patologia
Colágeno/metabolismo
Colo/patologia
Predisposição Genética para Doença
Glucocorticoides/uso terapêutico
Antígenos HLA/genética
Antígenos HLA/imunologia
Seres Humanos
Mesalamina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anion Exchange Resins); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antidiarrheals); 0 (Bile Acids and Salts); 0 (Glucocorticoids); 0 (HLA Antigens); 11041-12-6 (Cholestyramine Resin); 4Q81I59GXC (Mesalamine); 51333-22-3 (Budesonide); 9007-34-5 (Collagen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1038/ajg.2016.477


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[PMID]:27800600
[Au] Autor:Hilmer AJ; Jeffrey RB; Park WG; Khosla C
[Ad] Endereço:Departments of Chemistry, Chemical Engineering, and Biochemistry, Stanford University, Stanford 94305, California.
[Ti] Título:Cholestyramine as a promising, strong anion exchange resin for direct capture of genetic biomarkers from raw pancreatic fluids.
[So] Source:Biotechnol Bioeng;114(4):934-938, 2017 Apr.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability to capture cell-free DNA from the gastrointestinal tract, in a minimally invasive manner, could enhance our ability to diagnose gastrointestinal disease, or gain a better understanding of the spatial mapping of the intestinal microbiota. We, therefore, sought to identify a class of capture agents that could directly and efficiently sequester genetic material from intestinal fluids. As a particular case study, we examined the ability to capture DNA from pancreatic secretions, for potential application in enabling the sequestration of early, genetic biomarkers of pancreatic disease. We hypothesized that the cholestyramine series of strong cation exchange resins, which are FDA approved for the treatment of high cholesterol, may be capable of capturing DNA from pancreatic secretions. We identified a particular cholestyramine resin, DOWEX 1 × 2 100-200 mesh, which is able to efficiently capture and purify DNA from pancreatic fluid. Using only 200 µL of pancreatic secretions, we are able to recover 247 ± 182 ng of amplifiable human DNA, giving an estimated pancreatic fluid DNA content of 1.23 ± 0.91 ng/µL. To our knowledge, this is the first demonstration of a material that can effectively capture and purify DNA directly from untreated pancreatic fluids. Thus, our approach could hold high utility for the in vivo capture of DNA and disease biomarkers if incorporated into an appropriate sampling device. Biotechnol. Bioeng. 2017;114: 934-938. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Resinas de Troca de Ânions/química
Resina de Colestiramina/química
DNA/isolamento & purificação
Marcadores Genéticos/genética
Suco Pancreático/química
[Mh] Termos MeSH secundário: Resinas de Troca de Ânions/metabolismo
Linhagem Celular
Resina de Colestiramina/metabolismo
DNA/análise
DNA/genética
DNA/metabolismo
Seres Humanos
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anion Exchange Resins); 0 (Genetic Markers); 11041-12-6 (Cholestyramine Resin); 9007-49-2 (DNA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26207


  6 / 2540 MEDLINE  
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[PMID]:27884451
[Au] Autor:Masuda Y; Yamaguchi S; Nishizawa T
[Ad] Endereço:End-Organ Disease Laboratories, Daiichi Sankyo Co., Ltd., Tokyo, Japan. Electronic address: masuda.yusuke.z8@daiichisankyo.co.jp.
[Ti] Título:Cholesterol-lowering pattern affects the progression of atherosclerosis in apolipoprotein E deficient mice.
[So] Source:J Pharmacol Sci;132(4):271-274, 2016 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Although the importance of LDL cholesterol lowering is widely recognized, the impact of the cholesterol-lowering pattern on the atherosclerosis remains unclear. Here, we used cholestyramine in apolipoprotein E deficient mice in two different regimens to induce a see-saw shaped or a sustained cholesterol reduction, with the trough of cholesterol comparable. After 12 weeks-treatment, a sustained cholesterol reduction exhibited a smaller atherosclerotic area. Moreover, we observed a correlation between the area under the curve of plasma cholesterol and the atherosclerotic area. These results suggest that the sustained cholesterol reduction is beneficial for preventing the progression of atherosclerosis in cholesterol lowering therapy.
[Mh] Termos MeSH primário: Apolipoproteínas E/deficiência
Aterosclerose/sangue
LDL-Colesterol/sangue
[Mh] Termos MeSH secundário: Animais
Anticolesterolemiantes/farmacologia
Aterosclerose/patologia
Resina de Colestiramina/farmacologia
Dieta Ocidental
Masculino
Camundongos
Camundongos Knockout
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Apolipoproteins E); 0 (Cholesterol, LDL); 0 (Triglycerides); 11041-12-6 (Cholestyramine Resin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  7 / 2540 MEDLINE  
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[PMID]:27872940
[Au] Autor:Er C; Sule AA
[Ad] Endereço:Department of General Medicine, Tan Tock Seng Hospital, Singapore.
[Ti] Título:Cholestyramine as monotherapy for Graves' hyperthyroidism.
[So] Source:Singapore Med J;57(11):644-645, 2016 Nov.
[Is] ISSN:0037-5675
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Mh] Termos MeSH primário: Resina de Colestiramina/uso terapêutico
Doença de Graves/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Carbimazol/uso terapêutico
China
Feminino
Seres Humanos
Hipertireoidismo/tratamento farmacológico
Admissão do Paciente
Sepse/complicações
Glândula Tireoide/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
11041-12-6 (Cholestyramine Resin); 8KQ660G60G (Carbimazole)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.11622/smedj.2016177


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[PMID]:27784958
[Au] Autor:Guagnozzi D; Landolfi S; Vicario M
[Ad] Endereço:Danila Guagnozzi, Department of Gastroenterology, Hospital Universitario Vall d'Hebron, 08035 Barcelona, Spain.
[Ti] Título:Towards a new paradigm of microscopic colitis: Incomplete and variant forms.
[So] Source:World J Gastroenterol;22(38):8459-8471, 2016 Oct 14.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microscopic colitis (MC) is a chronic inflammatory bowel disease that has emerged in the last three decades as a leading cause of chronic watery diarrhoea. MC classically includes two main subtypes: lymphocytic colitis (LC) and collagenous colitis (CC). Other types of histopathological changes in the colonic mucosa have been described in patients with chronic diarrhoea, without fulfilling the conventional histopathological criteria for MC diagnosis. Whereas those unclassified alterations remained orphan for a long time, the use of the term incomplete MC (MCi) is nowadays universally accepted. However, it is still unresolved whether CC, LC and MCi should be considered as one clinical entity or if they represent three related conditions. In contrast to classical MC, the real epidemiological impact of MCi remains unknown, because only few epidemiological studies and case reports have been described. MCi presents clinical characteristics indistinguishable from complete MC with a good response to budesonide and cholestiramine. Although a number of medical treatments have been assayed in MC patients, currently, there is no causal treatment approach for MC and MCi, and only empirical strategies have been performed. Further studies are needed in order to identify their etiopathogenic mechanisms, and to better classify and treat MC.
[Mh] Termos MeSH primário: Colite Colagenosa/diagnóstico
Colite Linfocítica/diagnóstico
Colo/patologia
Mucosa Intestinal/patologia
[Mh] Termos MeSH secundário: Biópsia/efeitos adversos
Budesonida/uso terapêutico
Resina de Colestiramina/uso terapêutico
Colite Colagenosa/classificação
Colite Colagenosa/epidemiologia
Colite Linfocítica/classificação
Colite Linfocítica/epidemiologia
Colágeno/química
Diagnóstico Diferencial
Diarreia/diagnóstico
Seres Humanos
Imuno-Histoquímica
Doenças Inflamatórias Intestinais/diagnóstico
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
11041-12-6 (Cholestyramine Resin); 51333-22-3 (Budesonide); 9007-34-5 (Collagen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE


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[PMID]:27578083
[Au] Autor:Mittal A
[Ad] Endereço:Department of Dermatology, RNT Medical College and Associate Hospitals, Udaipur, India.
[Ti] Título:Cholestatic Itch Management.
[So] Source:Curr Probl Dermatol;50:142-8, 2016.
[Is] ISSN:1662-2944
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Cholestatic itch is a feature of numerous hepatobiliary disorders such as primary biliary cirrhosis, primary sclerosing cholangitis, the inherited form of cholestasis, and intrahepatic cholestasis of pregnancy. Although undervalued by physicians, cholestatic itch can be a source of great discomfort to the patient and significantly affects quality of life. Many pruritogens such as bile salts, opioids, serotonin, and histamine have been implicated in the pathogenesis of cholestatic itch, but no causative link has ever been established. Recent findings indicate that the potent neuronal activator lysophosphatidic acid and autotaxin, the enzyme forming lysophosphatidic acid, may be key elements in its pathogenesis. Treatment options for patients with cholestatic itch include the anion exchange resin cholestyramine, bile acid ursodeoxycholic acid, PXR agonist rifampicin, opioid antagonist naltrexone, and the serotonin inhibitor sertraline. These drugs can be used as a stepwise therapeutic approach. The body of evidence for many of these options, however, is not very robust. Patients who do not respond to medical therapy can be candidates for interventional measures, such as albumin dialysis, plasmapheresis, or nasobiliary drainage, or certain experimental approaches such as UVB phototherapy. Research over the past decade has elucidated many of the receptors and neuropeptides involved in itch sensation and transmission; it is hoped that in the future this will lead to the development of novel antipruritic medication for cholestatic itch.
[Mh] Termos MeSH primário: Resinas de Troca de Ânions/uso terapêutico
Colagogos e Coleréticos/uso terapêutico
Colestase/terapia
Antagonistas de Entorpecentes/uso terapêutico
Prurido/terapia
Inibidores da Captação de Serotonina/uso terapêutico
Terapia Ultravioleta
[Mh] Termos MeSH secundário: Colestase/complicações
Colestase/metabolismo
Resina de Colestiramina/uso terapêutico
Seres Humanos
Lisofosfolipídeos/metabolismo
Naltrexona/uso terapêutico
Plasmaferese
Prurido/etiologia
Receptores de Esteroides/agonistas
Rifampina/uso terapêutico
Sertralina/uso terapêutico
Ácido Ursodesoxicólico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anion Exchange Resins); 0 (Cholagogues and Choleretics); 0 (Lysophospholipids); 0 (Narcotic Antagonists); 0 (Receptors, Steroid); 0 (Serotonin Uptake Inhibitors); 0 (pregnane X receptor); 11041-12-6 (Cholestyramine Resin); 5S6W795CQM (Naltrexone); 724L30Y2QR (Ursodeoxycholic Acid); PG6M3969SG (lysophosphatidic acid); QUC7NX6WMB (Sertraline); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.1159/000446057


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[PMID]:27578071
[Au] Autor:Pongcharoen P; Fleischer AB
[Ti] Título:Itch Management: Systemic Agents.
[So] Source:Curr Probl Dermatol;50:46-53, 2016.
[Is] ISSN:1662-2944
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Itch is a global clinical problem and finding effective treatment remains a therapeutic challenge because of the complex pathophysiology of itch. The key component of treating itch should be directed at the underlying etiologies when possible. However, without eradication of the underlying diseases, treatment is often palliative at best. Treatment with systemic therapies can vary according to the etiology of the chronic itch. The aim of this article is to review the major systemic anti-itch agents and give a summary on the possible systemic treatments for different types of itch.
[Mh] Termos MeSH primário: Analgésicos Opioides/uso terapêutico
Analgésicos/uso terapêutico
Antagonistas dos Receptores Histamínicos/uso terapêutico
Antagonistas de Entorpecentes/uso terapêutico
Prurido/tratamento farmacológico
[Mh] Termos MeSH secundário: Aminas/uso terapêutico
Resinas de Troca de Ânions/uso terapêutico
Antidepressivos/uso terapêutico
Colagogos e Coleréticos/uso terapêutico
Colestase/complicações
Colestase/tratamento farmacológico
Resina de Colestiramina/uso terapêutico
Ácidos Cicloexanocarboxílicos/uso terapêutico
Seres Humanos
Morfolinas/uso terapêutico
Antagonistas do Receptor de Neuroquinina-1/uso terapêutico
Síndromes Paraneoplásicas/complicações
Síndromes Paraneoplásicas/tratamento farmacológico
Doenças do Sistema Nervoso Periférico/complicações
Doenças do Sistema Nervoso Periférico/tratamento farmacológico
Pregabalina/uso terapêutico
Prurido/etiologia
Receptores Opioides kappa/agonistas
Receptores Opioides mu/antagonistas & inibidores
Rifampina/uso terapêutico
Talidomida/uso terapêutico
Uremia/complicações
Uremia/tratamento farmacológico
Ácido Ursodesoxicólico/uso terapêutico
Ácido gama-Aminobutírico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Amines); 0 (Analgesics); 0 (Analgesics, Opioid); 0 (Anion Exchange Resins); 0 (Antidepressive Agents); 0 (Cholagogues and Choleretics); 0 (Cyclohexanecarboxylic Acids); 0 (Histamine Antagonists); 0 (Morpholines); 0 (Narcotic Antagonists); 0 (Neurokinin-1 Receptor Antagonists); 0 (Receptors, Opioid, kappa); 0 (Receptors, Opioid, mu); 11041-12-6 (Cholestyramine Resin); 1NF15YR6UY (aprepitant); 4Z8R6ORS6L (Thalidomide); 55JG375S6M (Pregabalin); 56-12-2 (gamma-Aminobutyric Acid); 6CW7F3G59X (gabapentin); 724L30Y2QR (Ursodeoxycholic Acid); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.1159/000446041



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