Clinical features and bleeding risk factors of angiodysplasia lesions in a Tunisian population.

INTRODUCTION: Gastrointestinal angiodysplasia (GIAD) is the most common vascular anomaly in the gastrointestinal (GI) tract, yet little is known about the factors favoring their bleeding. Our study aim was to determine the characteristics of patients with GIAD lesions in a Tunisian population and identify the risk factors of bleeding. PATIENTS AND METHODS: A retrospective study was carried out from January 2010 to February 2020 at a tertiary care medical center in Tunisia. Clinical and endoscopic data were collected from each patient's medical reports. We divided the patients into two groups: group A, patients with symptomatic GIAD; and group B, patients with incidental lesions. Group A was subsequently divided into two subgroups, according to the presence or absence of recurrent bleeding. The groups were compared by clinical, laboratory, and endoscopic features. RESULTS: GIAD was diagnosed in 114 patients, with a mean age of 70 ±â€¯13.3 years. GIAD lesions were mainly located in the colon (n = 72, 63%). Fifty-four patients (47%) presented with GIAD-related bleeding. The bleeding diagnosis was made during endoscopic procedures by visualizing active bleeding and the stigmata of recent hemorrhage in 10 (18.5%) and 12 (22.2%) cases, respectively. Most of the patients were treated by argon plasma coagulation (93%). Predictive factors of bleeding were age > 75 years, number of lesions >10, chronic kidney disease, diabetes mellitus, and coronary artery disease (p: 0.008; 0.002; 0.016; 0.048; and 0.039, respectively). CONCLUSION: Knowledge of the predictive factors of bleeding aids endoscopists in the decision-making process in cases of angiodysplasia.

Predictive factors of difficult biliary cannulation: An experience of a tunisian tertiary center.

Introduction: Selective biliary cannulation is a prerequisite for a successful endoscopic retrograde cholangiopancreatography (ERCP). However, conventional biliary access can be difficult. The aims of our study were to determine the prevalence of difficult biliary cannulation (DBC) and its associated factors and to describe the efficiency and safety of used standard and advanced cannulation techniques. Methods: We conducted a single-center retrospective study including all patients with naïve papilla who had an ERCP procedure in Gastroenterology department of Mohamed Taher Maamouri Hospital from June 2019 to December 2021. Efficiency was defined as successful selective deep biliary cannulation. DBC was defined based on the presence of one or more of the European Society of Gastrointestinal Endoscopy (ESGE) criteria (5-5-1): more than five cannulation attempts, more than 5 min before cannulation and more than one accidental passage in the wirsung. Prevalence was measured using ESGE 5-5-1 cutoffs and chinese set cutoffs 15-10-2. Predictors of DBC were sought by univariate and multivariate analysis (SPSS software, p significant if < 0.05). Results: We included 664 patients (mean age 62 years and sex ratio M/W = 0.8). Main indication for ERCP was choledocholithiasis (67%, n = 442) followed by malignant biliary stenosis (21%, n = 138). Based on ESGE criteria, prevalence of DBC was 42.62% (n = 283). Prevalence was 21.15% when 15-10-2 cutoffs are applied in trainee-involved procedure. Cumulative biliary success rate was 96.46%. Standard cannulation method achieved access in 98.2% while advanced methods permitted success in 92.2% in fistulotomy, 94.1% in papillotomy and 77.3% in transpancreatic sphincterotomy. Independent predictive factors of DBC in multivariate analysis were: Trainee presence OR 1.80 [1.24-2.65], SOD OR 4.71 [1.11-19.88], biliary stenosis found on imaging examinations (OR 2.53 [1.63-3.92], small papilla OR 4.09 [1.82-9.17] and difficult orientation of the papilla OR 14.90 [3.28-67.62]. Conclusion: DBC is a frequent endoscopic situation. Predictors of DBC can be related to trainee involvement in the procedure, anatomical and clinical factors. A thorough understanding of these factors can actively contribute to ERCP management plans.

[Tunisian version validation of quality life's questionnaire for chronic inflammatory disease of intestine]. / Validation de la version tunisienne du questionnaire de la qualité de vie dans les maladies inflammatoires chroniques de l'intestin.

BACKGROUND: The systematic evaluation of the quality of life is essential in the management of patients with chronic bowel disease ( IBD) inflammatory diseases. AIM: Translate in Tunisian Arabic dialect the English version of «inflammatory bowel disease questionnaire¼ (UK- IBDQ ) and validated by studying its psychometric validity, discriminative ability, reliability and sensitivity to change. METHODS: 80 Tunisian patients with IBD completed the Tunisian version of the IBDQ (T- IBDQ ) , a visual analog scale , the SF- 36, the Harvey- Bradshaw index for Crohn's disease , and the index Simple clinical colitis activity for ulcerative colitis. RESULTS: The T- IBDQ included in the final version 5 fields. The internal validity of the items was satisfactory for all patients. TIBDQ was correlated with scores of SF- 36, visual analog scale scores and indices of activity of IBD. T- IBDQ distinguish between active disease and inactive disease . He was also sensitive to changes in disease activity . CONCLUSION: We validated in this work a Tunisian dialect Arabic version of the IBDQ : T- IBDQ . Its validity, discriminative ability , reliability and sensitivity to change were demonstrated.

Microalgae: a potential source of polyunsaturated fatty acids.

Selected fish oils are the main industrial sources of PUFAs. However, this oil may be insufficient in the future to meet the expected growth in world demand for n-3 fatty acids (Tacon, 1995). Refined oils produced by marine microalgae represent potential sources of supplemental dietary fatty acids. This study examines the lipid and fatty acid composition of three microalgae that were isolated from the costal waters of Tunisia with particular interest on the variability of composition related to the cellular growth stage.

Lack of somatic mutation in the coding sequence of SIAH1 in tumors hemizygous for this candidate tumor suppressor gene.

The human homolog of the Drosophila seven in absentia gene (SIAH1) may play an important role in apoptosis and tumor suppression. Transcription of SIAH1 is up-regulated in non-tumorigenic clonal populations of cells derived from 2 different tumorigenic parental cell lines. Intracellular SIAH1 mRNA concentration increases in intestinal cells as they migrate from the bottom of the crypt to the lumen, where they undergo apoptosis. Finally, SIAH1 is located on chromosome 16q12-q13, a region that is frequently deleted in a large variety of human tumors. These observations suggest SIAH1 as a candidate tumor suppressor gene that may be inactivated during tumorigenesis. To test this hypothesis, a search for mutation in the coding sequence of this gene was initiated in tumors exhibiting loss of heterozygosity (LOH) at 16q12-q13. No difference was found in 12 hepatocellular carcinomas, 19 breast carcinomas, 9 prostate carcinomas, 7 colon carcinomas and 5 human cell lines derived from colon cancer. One silent sequence variant (C to T transition at amino acid 270) was observed in the FET colon carcinoma cell line. It was subsequently found once in a group of 100 unrelated individuals from the CEPH families. A rapid real-time quantitative RT-PCR fluorescent method shows that SIAH1 remained transcriptionally active in the 6 colon cancer-derived cell lines, and the expression is comparable to the normal colon tissue. Taken together, these observations suggest that although many tumors may have lost one SIAH1 allele, the second allele would not be the site of frequent somatic mutations and may even remain functional.

Activation of the human homologue of the Drosophila sina gene in apoptosis and tumor suppression.

Developmentally regulated genes in Drosophila, which are conserved through evolution, are potential candidates for key functions in biological processes such as cell cycle, programmed cell death, and cancer. We report cloning and characterization of the human homologue of the Drosophila seven in absentia gene (HUMSIAH), which codes for a 282 amino acids putative zinc finger protein. HUMSIAH is localized on human chromosome 16q12-q13. This gene is activated during the physiological program of cell death in the intestinal epithelium. Moreover, human cancer-derived cells selected for suppression of their tumorigenic phenotype exhibit constitutively elevated levels of HUMSIAH mRNA. A similar pattern of expression is also displayed by the p21waf1. These results suggest that mammalian seven in absentia gene, which is a target for activation by p53, may play a role in apoptosis and tumor suppression.

Isolation of 10 differentially expressed cDNAs in p53-induced apoptosis: activation of the vertebrate homologue of the drosophila seven in absentia gene.

We report the isolation of 10 differentially expressed cDNAs in the process of apoptosis induced by the p53 tamor suppressor. As a global analytical method, we performed a differential display of mRNA between mouse M1 myeloid leukemia cells and derived clone LTR6 cells, which contain a stably transfected temperature-sensitive mutant of p53. At 32 degrees C wild-type p53 function is activated in LTR6 cells, resulting in programmed cell death. Eight genes are activated (TSAP; tumor suppressor activated pathway), and two are inhibited (TSIP, tumor suppressor inhibited pathway) in their expression. None of the 10 sequences has hitherto been recognized as part of the p53 signaling pathway. Three TSAPs are homologous to known genes. TSAP1 corresponds to phospholipase C beta 4. TSAP2 has a conserved domain homologous to a multiple endocrine neoplasia I (ZFM1) candidate gene. TSAP3 is the mouse homologue of the Drosophila seven in absentia gene. These data provide novel molecules involved in the pathway of wild-type p53 activation. They establish a functional link between a homologue of a conserved developmental Drosophila gene and signal transduction in tumor suppression leading to programmed cell death.

Refined mapping of a gene (NPH1) causing familial juvenile nephronophthisis and evidence for genetic heterogeneity.

Familial juvenile nephronophthisis (NPH) is an autosomal recessive progressive tubulo-interstitial kidney disorder, responsible for 6-10% of end-stage renal failure in children, and is frequently associated with Leber amaurosis (termed Senior-Løken syndrome). The biochemical basis of NPH is unknown. We recently reported linkage of the purely renal form of NPH to three markers on chromosome 2. Our results also suggested the existence of genetic heterogeneity between NPH and SLS. To map this NPH gene more precisely, we have now tested the segregation of six new microsatellite markers and five additional families. Haplotype analyses show unequivocally that four NPH families are not linked to the chromosome 2 markers, although there are no clinical or pathological features discernible in these families that could separate them from the families linked to the chromosome 2 NPH locus (NPH1). This reveals genetic heterogeneity in the purely renal form of NPH. In situ hybridization of YAC clones isolated with two closely linked markers assigned the NPH1 region to 2q13. Furthermore, based on haplotype analysis and specific recombination events, the NPH1 gene has been placed between D2S293/D2S340 and D2S121, a genetic interval of about 5-7 cM.

A gene for familial juvenile nephronophthisis (recessive medullary cystic kidney disease) maps to chromosome 2p.

Familial juvenile nephronophthisis (NPH) is a chronic autosomal recessive kidney disease responsible for 15% of end stage renal failure in children. NPH is frequently (16% of cases) associated with Leber amaurosis (termed Senior-Løken syndrome, SLS). Linkage analyses, performed in 22 multiplex NPH families (18 without and 4 with ocular abnormalities), have localized the gene to a region between D2S48 and D2S51 on chromosome 2p. This was confirmed using adjacent microsatellite markers, one of which (AFM220ze3 at the D2S160 locus) gave a lod score of 4.78 at theta = 0.05 in the 18 families with isolated NPH, whereas the same marker excluded linkage with SLS. These results demonstrate linkage of the purely renal form of NPH to chromosome 2p, and suggest that there may be genetic heterogeneity between NPH and SLS.