ABSTRACT
UNLABELLED: Crohn's disease is a chronic inflammatory bowel disease, with multifactorial traits, that can involve any part of the gastrointestinal tract. In recent years, a dozen genome-wide association scan and meta-analysis were published bringing the number of susceptibility alleles to more than 30 variations. However, the major susceptibility gene for Crohn's disease is NOD2, located on proximal 16q, which is involved in the innate immune response. Three main variants of this gene: two single nucleotide polymorphisms p.Arg702Trp and p.Gly908Arg substitutions and frameshift polymorphism p.Leu1007fsinsC are involved in susceptibility to Crohn's disease. There is no data about the frequency of these allelic variants in Moroccan patients with Crohn's disease. The aim of our study is to genotype the NOD2 gene to assess the involvement of these three variants in susceptibility to Crohn's disease for Moroccans. METHODS: We carried out genotyping for the three variants p.Arg702Trp, p.Gly908Arg and p.Leu1007fsinsC of NOD2 gene using PCR-sequencing among 101 Moroccan patients with Crohn's disease and 107 healthy controls. RESULTS: The three main variants of NOD2 gene were present in Moroccan patients with no significant difference compared to controls. CONCLUSION: This preliminary study shows no evidence association of NOD2 gene with Crohn's disease in the Moroccan population.
Subject(s)
Crohn Disease/genetics , Nod2 Signaling Adaptor Protein/genetics , Adolescent , Adult , Case-Control Studies , Crohn Disease/epidemiology , Female , Genetic Association Studies , Genetics, Population , Humans , Male , Middle Aged , Morocco/epidemiology , Pilot Projects , Polymorphism, Genetic/physiology , Young AdultSubject(s)
Esophageal Motility Disorders/complications , Gastroesophageal Reflux/complications , Aged , Anti-Ulcer Agents/therapeutic use , Deglutition Disorders/drug therapy , Deglutition Disorders/etiology , Esophageal Motility Disorders/diagnosis , Esophageal Motility Disorders/drug therapy , Gastroesophageal Reflux/diagnosis , Gastroesophageal Reflux/drug therapy , Humans , Male , Omeprazole/therapeutic use , Vomiting/drug therapy , Vomiting/etiologySubject(s)
Carcinoma, Squamous Cell/complications , Celiac Disease/complications , Esophageal Neoplasms/complications , Adult , Carcinoma, Squamous Cell/diagnosis , Carcinoma, Squamous Cell/therapy , Celiac Disease/diet therapy , Esophageal Neoplasms/diagnosis , Esophageal Neoplasms/therapy , Esophageal Stenosis/etiology , Esophagoscopy , Fatal Outcome , Female , Humans , Patient ComplianceSubject(s)
Alstrom Syndrome/diagnosis , Adolescent , Cell Cycle Proteins , Consanguinity , Female , Humans , Proteins/geneticsABSTRACT
INTRODUCTION: Neurological manifestations of celiac disease are rare and polymorphic. Similar to lesions of the digestive tract, the standard treatment includes steroids. CASE REPORT: A 41-year-old woman, followed up for celiac disease resistant to gluten-free diet, developed rapidly spastic paraparesis, cerebellar syndrome, horizontal diplopia and decline of visual acuity. The diagnosis of neurological complications of celiac disease was established and the patient was treated with methylprednisolone, followed by oral prednisone. For 9 years, the patient's neurological status remained stabilized with a prednisone dose at 20mg per day. The patient relapsed when progressive reduction of prednisone dose was attempted; neurological and gastrointestinal signs worsening at 15mg per day; increasing the dose to 30mg improved the clinical status. DISCUSSION: The mechanism of onset of neurological disease remains unknown. Immunological, nutritional, toxic or metabolic factors could be involved. The positive response to corticosteroids observed in this patient suggest an immunological mechanism.
Subject(s)
Adrenal Cortex Hormones/therapeutic use , Celiac Disease/complications , Celiac Disease/drug therapy , Nervous System Diseases/diagnosis , Prednisone/therapeutic use , Adult , Diarrhea/etiology , Diplopia/etiology , Female , Humans , Nervous System Diseases/drug therapy , Nervous System Diseases/etiology , Vision Disorders/etiology , Visual AcuityABSTRACT
UNLABELLED: The prevalence of diabetes mellitus is higher in chronic hepatitis C than in hepatitis B, even without cirrhosis. OBJECTIVE: To study the host, specific viral factors associated with diabetes mellitus and the influence of diabetes mellitus on the intensity of steatosis and the severity of fibrosis. MATERIAL AND METHODS: The following data were collected in a cohort of 1249 patients with chronic hepatitis C established between December 1991 and June 2004: age, gender, body mass index (BMI). None of the patients were under treatment for their liver disease. Serum transaminase level and hepatitis C serology with search for viral RNA, viral load and genotype were obtained. The Metavir score, iron overload using the Perls score (0-4) and steatosis class (0-3) were determined on liver biopsies. RESULTS: Mean patient age was 52.5+/-10 years (56% male). Mean BMI was 24.6+/-24 kg/m2. Forty-three patients (17.2%) presented diabetes mellitus. The mean duration of their diabetes was 8.9 years. Genotype 1 predominated (60.4%) and mean viral load was 7.7x10(6) eq.v/ml. Steatosis was present in 69.7% of the diabetic patients versus 17% of the non-diabetic patients. Grade 2 fibrosis (F2) was observed in 32.5% of diabetic patients versus 29% in non-diabetic patients and F3, F4 in 73% of the diabetic patients versus 57% of the non-diabetic patients. Comparison between diabetic and non-diabetic patients demonstrated an absence of statistically significant difference (at 5%) between the groups for gender, viral load and genotype. Diabetic persons were older (58.7 years against 51 years) and liver biopsy revealed steatosis and fibrosis (F3, F4) more often in diabetic patients (69.7% versus 49.5%). CONCLUSION: These findings suggest that steatosis could favor progression of fibrosis in diabetics with chronic hepatitis C.