RESUMEN
BACKGROUND: Appendicectomy reduces the risk of having ulcerative colitis. However, its effect on the natural history of ulcerative colitis remains uncertain. AIM: To determine whether appendicectomy reduces the overall severity of ulcerative colitis. PATIENTS AND METHODS: Appendicectomy status and smoking habits were specified by direct interview in 638 patients seen consecutively between 1997 and 2000. Severity of ulcerative colitis was assessed by reviewing therapeutic needs from the onset of colitis. Additionally, the annual incidence of flare up was assessed prospectively between 1997 and 2000 in patients who had not been colectomised. RESULTS: The 10 year risk of colectomy was 16 (7)% in previously appendicectomised patients (n=49) compared with 33 (2)% in non-appendicectomised patients (n=589, p=0.05). Cox regression showed that previous appendicectomy and current smoking were independent factors protecting against colectomy (adjusted hazard ratio and 95% confidence intervals: 0.40 (0.20-0.78) and 0.60 (0.40-0.95), respectively). The respective proportions of appendicectomised and non-appendicectomised patients who required oral steroids and immunosuppressive therapy were not significantly different (67% v 70% and 27% v 19%, respectively). Between 1997 and 2000, ulcerative colitis was active for 48% of the time in appendicectomised patients (47 of 98 patient years) and for 62% of the time in non-appendicectomised patients (631 of 1024 patient years; p<0.01). CONCLUSION: Previous appendicectomy is associated with a less severe course of ulcerative colitis. The beneficial effect of appendicectomy on the risk of colectomy is additive to that of current smoking.
Asunto(s)
Apendicectomía , Colitis Ulcerosa/prevención & control , Adulto , Distribución de Chi-Cuadrado , Colectomía , Colitis Ulcerosa/patología , Colitis Ulcerosa/cirugía , Colon/patología , Femenino , Humanos , Masculino , Estudios Prospectivos , Recto/patología , Estudios Retrospectivos , Riesgo , Fumar/efectos adversosRESUMEN
Graft-versus-host disease (GVHD) can be acute or chronic. The pathogenesis of chronic GVHD is unclear. Chronic GVHD affects mainly skin, liver and digestive tract. Intestinal involvement is uncommon and histological features are poorly described. We report here the clinical, histological and immunohistochemical features of chronic GVHD with intestinal involvement. Intestinal biopsies from children with chronic GVHD (n=17) were compared to control children (n=21: 10 non-transplant cases, four non-GVHD transplant cases, seven acute GVHD). We evaluated clinical outcome, histological features and characterized immunohistochemically the immune cells involved locally. Chronic GVHD with intestinal involvement was usually multisystemic (88.2%) and preceded by acute GVHD in 88.2% of cases. The outcome was severe with complete recovery in only 58.8% of cases, and death related to chronic GVHD in 17.6% of cases. Histological features were characterized by (1) villous atrophy and (2) glandular lesions, mainly apoptotic with variable intensity and (3) lamina propria infiltrate with cytotoxic T lymphocytes (CD3+, CD8+, TiA1+, granzyme B-) which were significantly (P<0.001) increased compared to non-GVHD transplant and non-transplant controls. Therefore in chronic intestinal GVHD, the apoptotic process could be related to cytotoxic T lymphocytes.
Asunto(s)
Enfermedad Injerto contra Huésped/etiología , Enfermedades Intestinales/inmunología , Adolescente , Adulto , Apoptosis , Biopsia , Trasplante de Médula Ósea , Estudios de Casos y Controles , Niño , Preescolar , Enfermedad Crónica , Femenino , Enfermedad Injerto contra Huésped/mortalidad , Enfermedad Injerto contra Huésped/patología , Humanos , Inmunohistoquímica , Lactante , Recién Nacido , Enfermedades Intestinales/mortalidad , Enfermedades Intestinales/patología , Masculino , Estudios Retrospectivos , Tasa de Supervivencia , Linfocitos T Citotóxicos , Trasplante Homólogo/efectos adversos , Trasplante Homólogo/inmunología , Trasplante Homólogo/estadística & datos numéricos , Resultado del TratamientoRESUMEN
BACKGROUND/AIMS: It is not known how enteric cryptosporidiosis induces severe intestinal impairment despite minimal invasion by the parasite. The aim of this study was to analyse the histological features and locally implicated immune cells in colonic biopsies of AIDS related cryptosporidiosis. PATIENTS/METHODS: Colonic biopsies from patients with AIDS related cryptosporidiosis (n = 10, group I), patients with AIDS but without intestinal infection (n = 9, group II), and human seronegative controls (n = 9, group III) were studied. Using immunohistochemistry the infiltrating mononuclear cells were analysed in both the epithelium and lamina propria for the expression of CD3, CD8, TiA1, granzyme B, and CD68 and for glandular expression of human major histocompatibility complex DR antigen (HLA-DR). RESULTS: Severe histological changes, resulting in abundant crypt epithelial apoptosis and inflammatory infiltrate in the lamina propria, were seen in all biopsies from group I. A significant increase of CD8+, TiA1+, and granzyme B+ T cells in the lamina propria and HLA-DR glandular expression was noted in group I compared with groups II and III. However, the number of intraepithelial lymphocytes, lamina propria CD3+ T cells, and macrophages was not significantly increased in cryptosporidiosis specimens compared with controls. CONCLUSION: Epithelial apoptosis mediated by granzyme B+ cytotoxic host T cells might play a major role in the development of colonic lesions in AIDS related cryptosporidiosis.
Asunto(s)
Infecciones Oportunistas Relacionadas con el SIDA/inmunología , Linfocitos T CD8-positivos/inmunología , Colon/inmunología , Criptosporidiosis/inmunología , Infecciones Oportunistas Relacionadas con el SIDA/parasitología , Adolescente , Adulto , Apoptosis , Estudios de Casos y Controles , Niño , Colon/parasitología , Femenino , Granzimas , Histocitoquímica , Humanos , Masculino , Estudios Retrospectivos , Serina Endopeptidasas/metabolismoAsunto(s)
Colangiopancreatografia Retrógrada Endoscópica/métodos , Colangitis/diagnóstico , Cálculos Biliares/diagnóstico , Anciano , Biopsia , Colangitis/etiología , Colecistectomía , Colecistitis/diagnóstico , Colecistitis/etiología , Colecistitis/cirugía , Conducto Colédoco/diagnóstico por imagen , Conducto Colédoco/patología , Femenino , Estudios de Seguimiento , Cálculos Biliares/complicaciones , Cálculos Biliares/cirugía , Humanos , Masculino , Persona de Mediana Edad , Recurrencia , Estudios RetrospectivosRESUMEN
The distribution and kinetics of hepatitis C virus (HCV) genotypes and the prevalence of mixed infections were studied in a group of 45 French patients with haemophilia A or B or von Willebrand's disease, 21 of them being anti-human immunodeficiency virus (HIV) positive; genotyping was carried out by three methods based on the core, 5' untranslated region (5'UTR), and the detection of type-specific NS4 antibodies. Genotyping of the 5'UTR revealed genotypes 1a (n = 10), 1b (n = 13), 2a (n = 3), 2b (n = 4), 2NC (n = 3), 3a (n = 10), and two mixed infections (1a + 1b and 3a + 2). Five of 33 patients showed a change from one HCV genotype to another. The core genotyping assay showed 8 of 45 mixed infections: 6/8 1a + 1b and 2/8 3a + 2. Sequencing of core polymerase chain reaction (PCR) products showed that mixed infection 1a + 1b could be explained by nonspecific annealing of the 1b primer to type 1a sequence. By designing new primers whose sequence was more specific to HCV types 1a and 1b, we could confirm 1a + 1b mixed infection in only one of six cases. Serotyping assay showed for 17 of 21 anti-HIV negative patients a concordance with the 5'UTR genotype; however, only 6 of 19 anti-HIV positive patients showed detectable serological reactivity. In summary, we have observed a similar HCV genotype distribution between our haemophilic group and the French anti-HCV positive patients. The study demonstrates the difficulties of assessing with the presently available genotyping and serotyping assays the real prevalence of mixed infections in multiply transfused patients.