Efficacy of a 7-day course of furazolidone, levofloxacin, and lansoprazole after failed Helicobacter pylori eradication

<p>Abstract</p> <p>Background</p> <p>Increasing resistance to clarithromycin and nitroimidazole is the main cause of failure in the <it>Helicobacter pylori </it>eradication. The ideal retreatment regimen remains unclear, especially in developing countries, where the infection presents high prevalence and resistance to antibiotics. The study aimed at determining the efficacy, compliance and adverse effects of a regimen that included furazolidone, levofloxacin and lansoprazole in patients with persistent <it>Helicobacter pylori </it>infection, who had failed to respond to at least one prior eradication treatment regimen.</p> <p>Methods</p> <p>This study included 48 patients with peptic ulcer disease. <it>Helicobacter pylori </it>infection was confirmed by a rapid urease test and histological examination of samples obtained from the antrum and corpus during endoscopy. The eradication therapy consisted of a 7-day twice daily oral administration of lansoprazole 30 mg, furazolidone 200 mg and levofloxacin 250 mg. Therapeutic success was confirmed by a negative rapid urease test, histological examination and 14C- urea breath test, performed 12 weeks after treatment completion. The Chi-square method was used for comparisons among eradication rates, previous treatments and previous furazolidone use.</p> <p>Results</p> <p>Only one of the 48 patients failed to take all medications, which was due to adverse effects (vomiting). Per-protocol and intention-to-treat eradication rates were 89% (95% CI- 89%–99%) and 88% (88–92%), respectively. Mild and moderate adverse effects were reported by 41 patients (85%). For patients with one previous treatment failure, the eradication rate was 100%. Compared to furazolidone-naïve patients, eradication rates were lower in those who had failed prior furazolidone-containing regimen(s) (74% vs. 100%, p = 0.002).</p> <p>Conclusion</p> <p>An empiric salvage-regimen including levofloxacin, furazolidone and lansoprazole is very effective in the eradication of <it>Helicobacter pylori</it>, particularly in patients that have failed one prior eradication therapy.</p

Expression regulatory chemokines and Natural Killer T-regulatory cells in patients with severe endometriosis

Introdução: A endometriose, condição inflamatória prevalente, associa-se a alterações da reposta imune na cavidade peritoneal e no útero. Evidências sugerem participação de mediadores inflamatórios, como as células Natural Killer e T-reguladoras na patogênese desta doença. A resposta destas células pode ser controlada pela atividade de algumas quimiocinas. O objetivo deste estudo foi avaliar a expressão gênica das quimiocinas reguladoras das células Natural Killer e T-reguladoras em endométrio tópico em lesões endometrióticas de pacientes com endometriose. Pacientes e Métodos: A expressão gênica das quimiocinas reguladoras da atividade das células Natural Killer (CXCL9, 10, 11, CXCL12, XCL1 e CX3CL1) e T reguladoras (CCL17 e CCL21) foi avaliada por meio de RTPCR no endométrio tópico e lesão endometriótica de 22 pacientes com endometriose de retossigmóide; 10 pacientes com endometriose retrocervical e no endométrio tópico de 32 mulheres sem endometriose comprovada por laparoscopia para laqueadura tubária. Resultados: Dentre as quimiocinas relacionadas às células Natural Killer, encontramos diferença estatística significativa na CX3CL1 e CXCL12, as quais foram mais expressas no foco de endometriose intestinal e retrocervical, quando comparadas ao endométrio tópico das pacientes e controles (p < 0,05). Das relacionadas às células T-reguladoras, a CCL17 foi mais expressa no endométrio tópico de pacientes com lesão em retossigmóide quando comparada aos demais grupos (p < 0,05). Conclusões: As quimiocinas CX3CL1 e CXCL12 foram mais expressas nos focos de endometriose intestinal e a CCL17 foi mais expressa no endométrio tópico de pacientes com lesão de retossigmóide. Estes resultados sugerem que as quimiocinas CX3CL1, CXCL12 e CXCL17 participam da resposta inflamatória que ocorre na endometriose pélvicaObjective: Endometriosis is a highly prevalent inflammatory condition associated with an altered immune response in the peritoneal cavity and uterus. Evidence suggests a participation of inflammatory mediators such as natural killer (NK) and T-regulatory (T-reg) cells in the pathogenesis of this disease while the response of these cells may be controlled by the activity of some chemokines. Patients and Methods: Gene expressions of the chemokines that regulate the activity of NK (CXCL9, CXCL10, CXCL11, CXCL12, XCL1 and CX3CL1) and T-reg cells (CCL17 and CCL21) were evaluated using real time polymerase chain reaction (PCR) in the eutopic and ectopic endometrium of 22 patients with bowel endometriosis, 10 patients with retrocervical endometriosis and 32 controls. Results: Of the chemokines associated with NK cells, the expression of CX3CL1 and CXCL12 was significantly greater in the foci of endometriosis (p < 0.05). Of those associated with T-reg cells, significant differences between groups were found in CCL17. In addition, CCL17 was expressed to a higher degree in the eutopic endometrium of the patients with rectosigmoid lesions when compared to the other groups (p < 0.05). Conclusions: Chemokines CX3CL1 and CXCL12 were more expressed in intestinal endometriosis and CCL17 expression was higher in eutopic endometrium of the patients with rectosigmoid lesions. These results suggest that those chemokines participate in the inflammatory response that occurs in pelvic endometriosi

DEVELOPPEMENT D'UN SITE INTERNET AU SEIN D'UNE ENTREPRISE DE REPARTITION PHARMACEUTIQUE (L'EXEMPLE D'OCP POINT)

CHATENAY M.-PARIS 11-BU Pharma. (920192101) / SudocSudocFranceF

Fatores ambientais e endometriose

A endometriose representa uma afec&#231;&#227;o ginecol&#243;gica comum, atingindo de 5%-15% das mulheres no per&#237;odo reprodutivo e at&#233; 3%-5% na fase p&#243;s-menopausa. Essa doen&#231;a &#233; definida pelo implante de estroma e/ou epit&#233;lio glandular endometrial em localiza&#231;&#227;o extrauterina, podendo comprometer diversos locais. Humanos e animais s&#227;o expostos diariamente a poluentes qu&#237;micos que t&#234;m a capacidade de influenciar negativamente processos fisiol&#243;gicos e, potencialmente, causar doen&#231;as, dentre elas a endometriose. Com esta revis&#227;o tivemos por objetivo relacionar a influ&#234;ncia dos fatores ambientais e diet&#233;ticos na g&#234;nese da endometriose. O mecanismo pelo qual a dioxina e seus s&#237;miles (TCDD/PCBs) atuam na altera&#231;&#227;o da fisiologia endometrial permanence incerta e &#233; especulativa devido à dificuldade em se avaliar a exposi&#231;&#227;o na vida intraútero, inf&#226;ncia e vida adulta e suas reais consequ&#234;ncias, al&#233;m das limita&#231;&#245;es de sua reprodu&#231;&#227;o in vitro. Devemos entender melhor o mecanismo de a&#231;&#227;o desses poluentes amibentais n&#227;o s&#243; na saúde reprodutiva, mas na saúde em geral do indiv&#237;duo, para se promover estrat&#233;gias de preven&#231;&#227;o que devem incluir n&#227;o s&#243; a educa&#231;&#227;o populacional, mas o estabelecimento de limites de exposi&#231;&#227;o, t&#233;cnicas menos poluentes e melhor aproveitamento dos nossos recursos naturais

Environmental factors and endometriosis

SummaryEndometriosis represents a common gynecological condition affecting 5%–15% of child-bearing age women and up to 3%–5% of post-menopausal women. This disease is defined by the presence of stromal and/or endometrial glandular epithelium implants in extra-uterine locations possibly compromising several sites. Humans and animals are daily exposed to chemical pollutants that could adversely influence physiological processes and potentially cause diseases, including endometriosis. In this review, the authors aimed at settling the influence of environmental and dietary factors on endometriosis pathogenesis. The mechanism by which dioxin and its similes (TCDD/PCBs) act changing the endometrial physiology remains uncertain and is speculative due to the difficulty in assessing the exposure over intrauterine life, childhood and adulthood and its actual consequences, in addition to the limitations to its in vitro reproducibility. We need to better understand the mechanism of action of these environmental pollutants, not only on reproductive health, but also on overall health of individuals and so prevention strategies, including not only population education, but setting exposure limits, less polluting techniques and a better use of our natural resources, could be promoted