Successful treatment by argon plasma coagulation of bleeding radiation-induced gastroduodenal vasculopathy.
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Biomedical subjects
Publications and source records attributed to M Pagenault.
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Over a 12-month period, we diagnosed poorly differentiated infiltrative independent-cell gastric adenocarcinoma in two brothers and one sister aged 41 to 47 years. Their father had died from antral cancer at the age of 34 years. These cancers had two characteristic clinical features: rapid course and distant malignant dissemination. In all three patients, polymerase chain reaction-sequencing of the E-cadherin (CDH1) gene of white blood cells identified a heterozygous nonsense mutation of exon 3, producing a stop codon at position 95 (Q95X), resulting in a truncated protein. The alteration of this protein, which plays a crucial role in epithelial cell adhesion, probably explains the clinical expression in this type of familial diffuse gastric cancer.
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AIM: To evaluate in a prospective study the prognostic factors of recurrent bleeding and mortality in patients presenting with high risk peptic ulcer bleeding routinely treated by endoscopic hemostasis. PATIENTS AND METHODS: A multicenter study was carried out in 8 Western French hospitals in 144 patients with gastrointestinal bleeding peptic from ulcer type I or IIa, b as defined by Forrest classification. Thirty four and 38 parameters were studied respectively in order to predict recurrent bleeding and death. Significant predictive factors (P < 0.1) in univariate analysis were entered in a multivariate logistic regression analysis. RESULTS: Endoscopic hemostasis was performed in 108 of 144 cases (75%). Recurrent bleeding and death occurred in 39 (28%) and 22 cases (15%), respectively. By multivariate analysis, the only predictor of rebleeding was hypovolemia at admission. Predictors of death were ASA score, cardiovascular Goldman score and recurrent bleeding. In this study, prevalence of Helicobacter pylori infection was low (41%) but was not a predictive factor. CONCLUSIONS: In a selected population of peptic ulcer bleeding patients with high risk of rebleeding, prevalence of recurrent bleeding and death remains rather high, despite routine endoscopic hemostasis. In the era of endoscopic hemostasis, clinical parameters remain the best prognostic factors of peptic ulcer bleeding outcome.
OBJECTIVE: One third of subjects who suffer from fecal incontinence are found to have values within the normal range when anal manometry is performed. For these patients, one hypothesis is that impaired rectal adaptation to distension may occur. The aim of our study was to analyze anorectal responses to rectal isobaric distension in this population. METHODS: This was a prospective study conducted in 51 consecutive incontinent patients (45 female, six male) divided into two groups according to their functional anal state: absence (19 patients aged 55 +/- 6 yr) or presence of manometric anal weakness (32 patients aged 59 +/- 2 yr). The subjects were submitted to two randomized modes of rectal isobaric distension (tonic, phasic) with an electronic barostat. Anal pressures, perception, and volumes of the rectum were recorded at six different preselected pressures. RESULTS: As compared with those having anal weakness, patients with no anal weakness retained higher mean pressures at both upper (36.9 +/- 2.2 vs 22.9 +/- 1.4 mm Hg; p = 0.01) and lower parts (41.0 +/- 2.0 vs 23.3 +/- 1.4 mm Hg; p = 0.002) of the anal canal, similar perception scores, but much lower rectal volumes (68.5 +/- 5.5 vs 121.8 +/- 7.0 ml; p = 0.008) in response to rectal isobaric distension. CONCLUSION: A decrease in rectal adaptation could be involved in fecal leakage in patients with no anal manometric weakness.
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BACKGROUND: Early evaluation of the severity of acute pancreatitis (AP) requires measurement of many variables within 48 h after admission. Septic complications (SC) are frequent, and preliminary studies have highlighted the value of prophylactic antibiotherapy; however, single and reliable predictive markers of sepsis are not yet available. The aim of this study was to assess the value of determining early blood Th-1 cytokines and their natural antagonists (interleukin-6 (IL-6), IL-1, IL-1ra, and the soluble form of tumor necrosis factor (sTNF) receptors RI and RII) to predict the severity and SC during AP. METHODS: Thirty-seven patients with AP were prospectively included; 25 of them had severe AP, including 8 with SC. Serum cytokines were measured 48 h and 72 h after the onset of AP with an enzyme-linked immunosorbent assay. The optimal severity or SC diagnostic thresholds was determined using receiver operative curves. RESULTS: Severe AP in accordance with the Atlanta criteria were better predicted by C-reactive protein and IL-6 serum determination, albeit these levels could not predict absolutely the death of two patients. In severe AP cases (n = 25) the IL-1 to IL-1-ra ratio was lower in cases further complicated by sepsis ((6+/-4) 10(-3) versus (34+/-13) 10(-3), P < 0.05); moreover, sTNF RI (2497+/-270 pg/ml versus 2133+/-611 pg/ml, P < 0.05) and RII (3751+/-400 pg/ml versus 3045+/-509 pg/ml, P < 0.05) were higher in AP characterized by further SC. The IL-1 to IL-1-ra ratio and IL-1 concentration were dramatically decreased within the first 48 h ((0.4+/-0.4) 10(-3) versus (30+/-11) 10(-3), P < 0.05, and 0.3+/-0.3 versus 15+/-3 ng/l, P < 0.05) in patients with further infection of the pancreatic necrosis (n = 3). The SC diagnosis was better anticipated by an IL-1 to IL-1-ra ratio lower than 5 x 10(-3) or by an sTNF RI higher than 1750 pg/ml and sTNF RII higher than 2750 pg/ml, and the infection of the pancreatic necrosis by an IL-1 concentration <2 ng/l or an IL-1 to IL-1-ra ratio <2 x 10(-3). CONCLUSION: Besides severity markers, IL-1, IL-1-ra, and sTNF RI and RII should be considered in base-line AP assays and, if confirmed by larger studies, could help to screen patients at risk for SC and candidates for prophylactic antibiotherapy with a good negative predictive value.
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The Leiden factor V mutation is observed in 20% of unexplained lower limb venous thromboses and involves substitution of the arginine residue at position 506 by glutamine (R506Q). It is known to decrease the anticoagulant activity of activated protein C. This case report describes 4 cases of small bowel infarction (SBI) associated with the presence of this mutation. Two cases of arterial and 2 cases of venous SBI were observed. Extensive assessment excluded the usual causes of SBI and plasma hypercoagulation syndrome (antithrombin III, protein C, and protein S deficiency and myeloproliferative syndrome). An abnormal resistance to activated protein C was observed. Molecular analysis consisting of polymerase chain reaction amplification and digestion with MnlI showed that 2 patients were heterozygous and 2 were homozygous for the R506Q mutation. Despite familial history of thrombosis in only 1 patient, first- and second-degree relatives of 2 patients also had the presence of the mutation. Examination for the presence of abnormal resistance to activated protein C should be part of the etiological assessment of SBI. Its presence may warrant consideration of long-term anticoagulant therapy, especially for patients with shortened small bowel who are treated by home parenteral nutrition with deep venous access.
BACKGROUND: Many studies suggest the implication of genetic factors in inflammatory bowel diseases. Despite some associations with HLA genes, the lack of definite data may be due to ethnic variations, clinical heterogeneity, or the involvement of additional susceptibility genes beside or within the major histocompatibility complex (MHC), such as TAP genes. The aim of this study was to analyze in patients with ulcerative colitis (UC) or Crohn's disease (CD) the polymorphism of TAP genes that encode the proteins necessary for the transfer of antigenic peptides through the endoplasmic reticulum membrane. METHODS: One hundred and one UC and 148 CD patients were compared with 173 unrelated healthy controls. Dimorphisms within the TAP1 and TAP2 alleles were analyzed by sequence-specific oligonucleotide typing. RESULTS: No difference was found between patient groups and controls. However, when CD patients were classified on the basis of their responsiveness to steroid therapy, a significant decrease of TAP2 AA (*0101/*0101) genotype was found in CD patients who did not respond to steroid therapy (22.9% versus 43.7% in steroid responder group; Pc < 0.05; odds ratio = 2.6; 95% confidence limits (CL) = 1.2-5.9). These data appear independent of the distribution of HLA DRB1*01 or DRB1*03 alleles despite a significant linkage disequilibrium between these alleles and TAP2A. CONCLUSIONS: This result suggests, despite the absence of arguments favoring a genetic susceptibility to CD, that the TAP2 gene or other genes located on chromosome 6 may be involved in the genetic heterogeneity of CD.
OBJECTIVES: The aim of the study was to determine the incidence and the main clinical data of inflammatory bowel disease in Brittany. METHODS: According to EPIMAD registry's methodology, private and public gastroenterologists (n = 139) of Brittany (2836418 inhabitants) referred all patients consulting for the first time, in 1994 and 1995 with clinical symptoms compatible with inflammatory bowel disease. An interviewer practitioner completed at the gastroenterologist's consulting room a standard questionnaire for each patient. Each case was reviewed separately by four experts to assign a diagnosis of definite, probable, possible Crohn's disease, ulcerative colitis, unclassifiable chronic colitis, or acute colitis (onset of symptoms < 6 weeks). RESULTS: 657 cases were recorded: 205 Crohn's disease (31%), 165 ulcerative colitis (25%) including 75 ulcerative proctitis (46%), 42 unclassifiable chronic colitis (7%), 245 acute colitis (37%). The crude mean annual incidence (per 10(5) inhabitants) based on definite and probable cases only was 2.8 for Crohn's disease and 2.9 for ulcerative colitis. The female/male ratio was 0.9 for Crohn's disease and 0.5 for ulcerative colitis. The median age at time of diagnosis was 27 for Crohn's disease and 36 for ulcerative colitis. The median time between onset of symptoms and diagnosis was equal to 3 months for Crohn's disease and ulcerative colitis. CONCLUSION: In Brittany the observed incidence of ulcerative colitis is similar to that of Crohn's disease and close to that observed in northern France. The incidence of Crohn's disease is lower. However, the real incidence of inflammatory bowel disease is currently underestimated due to the large number of acute colitis requiring a follow up and the cases of Crohn's disease classified as possible not taken into account.
OBJECTIVES: Multiplex family studies have excluded chromosome 6 as a candidate gene of susceptibility to inflammatory bowel disease. However, one recent study suggested that a gene involved in the pathogenesis of Crohn's disease is located on chromosome 6 confering to a microsatellite allelic combination (a2, b1, c2, d4, e1) a strong genetic risk factor in Crohn's disease. The aim of our study was to determine simultaneously the polymorphisms of the TNF microsatellites and of the genes coding for TNF synthesis in patients with inflammatory bowel disease. PATIENTS AND METHODS: Sixty patients with ulcerative colitis, 100 patients with Crohn's disease were compared to 64 healthy ethnically matched controls. Five TNF microsatellite loci (a, b, c, d, e) were typed using polymerase chain reaction PCR, and two dimorphisms of TNF alpha and TNF beta (intron 1) were studied by restriction fragment length polymorphism (RFLP). RESULTS: Allelic frequencies of TNF microsatellites and of TNF alpha and beta genes were similar in Crohn's disease, ulcerative colitis and controls. Five loci microsatellite haplotypes, especially a2 b1 c2 d4 e1 allelic combination, were not more frequent in Crohn's disease (25%) compared to ulcerative colitis (27%) or controls (20%). Subgroups stratification according to clinical characteristics did not modify haplotype frequencies. Analysis of our data taking simultaneously into account the MHC alleles (DRB*01 or DRB1*04) did not modify our data; however, it suggested that extended haplotype on short arm of chromosome 6 differed between patients and controls. Linkage disequilibrium (delta = -360.10(-4); P < 0.01) between a2, b1, c2, d4, e1 allelic combination and DRB1*04 allele was observed only in Crohn's disease. CONCLUSION: Percentages of patients with Crohn's disease or ulcerative colitis carrying TNF microsatellite or TNF alpha and beta gene haplotypes were similar to those of healthy controls. These data argue against involvement of the TNF locus without exclusion of short arm of chromosome 6 implication in Crohn's disease pathogenesis.
Hyperplastic polyps are the most common type of colorectal polyps. They are usually multiple and localized in the rectosigmoid area. They are easily recognized by their small size (< 10 mm), sessile form, smooth-surface and translucid appearance. Typically, these polyps have no malignant potential. We report the case of a 68-year-old man who had multiple rectosigmoid polyps, some of them having macroscopic features of adenomatous polyps. Because of the occurrence of bleeding after endoscopic polypectomy of two polyps corresponding to adenomas at examination, because of the multiplicity of these polyps and their localization in diverticulosis, a left colectomy followed by coloanal anastomosis was performed. Histologic examination of the surgical specimen revealed the hyperplastic nature of all polyps with, in two of them, a focus of adenomatous tissue.
Involvement of the gastrointestinal tract is frequently reported among the extranodal sites of non-Hodgkin's lymphoma, but primary lymphoma of the common bile duct is extremely rare. We report the case of a 29-year-old man who presented with obstructive jaundice, leading to the diagnosis of high-grade primary non Hodgkin's T-cell lymphoma, originating from the extrahepatic biliary tract, and confirmed by endosonography and magnetic resonance cholangiography. This patient was treated by sequential chemotherapy without resection and remained in complete remission after one year.