ABSTRACT
Drug-induced pancreatitis injury due to celecoxib, a first generation Cox-2 inhibitor, has been rarely reported. We describe one case of severe pancreatitis after treatment with celecoxib for 3 months in a woman. No aetiology has been found for pancreatitis. The role of celecoxib in the etiology of colitis was considered probable. This report and a few other cases in the literature suggest to seek a pancreatitis in the event of pains abdominal when there is a catch of the cyclooxygenase-2 selective non-steroidal anti-inflammatory drug inhibitor.
Subject(s)
Cyclooxygenase Inhibitors/adverse effects , Pancreatitis/chemically induced , Pyrazoles/adverse effects , Sulfonamides/adverse effects , Acute Disease , Celecoxib , Female , Humans , Middle AgedABSTRACT
AIMS: Etiological investigations proposed for patients with acute pancreatitis have been evolving considerably these past few years, significantly limiting the number of cases labeled idiopathic. The aim of this study was to determine the incidence of non alcoholic non biliary pancreatitis and identify causes, comparing severity by etiology. PATIENT AND METHODS: This retrospective analysis included 108 patients managed from October 1996 to April 2005. Standar-dized extensive etiological investigations were performed. The following criteria of severity were recorded: peak CRP value, Ranson score, Balthazar score, duration of hospital stay and pseudocyst occurrence. RESULTS: The cause of acute pancreatitis was alcohol (N=45), gallstones (N=50), obstruction (N=10), unknown (N=10), drugs (N=9), auto-immunity (N=4), infections (N=3), post-operative (N=2), post-ERCP (N=2), trauma (N=1), hypertriglyceridemia (N=1), genetic (N=1). The main criteria of severity were significantly different between non alcoholic non biliary pancreatitis and the other causes (CRP>120 mg/L, Ranson score>3 and Balthazar score > or =D) while other criteria (pseudocyst occurrence and duration of hospitalisation) were similar. Mean peak CRP was 79.5 mg/L for the overall population and varied significantly by etiology: peak CRP for drug-induced acute pancreatitis (4.6 mg/L) was significantly lower than for the other causes (P<10(-6)). CONCLUSION: This study shows that non alcoholic non biliary causes account for one third of the cases of acute pancreatitis, usually with a mild to moderate presentation. As the mean peak CRP value is significantly lower in drug-induced acute pancreatitis, careful search for an adverse drug reaction is appropriate in patients with acute pancreatitis of unknown cause and a low peak CRP level.
Subject(s)
Pancreatitis/epidemiology , Pancreatitis/etiology , Acute Disease , Adult , Aged , Female , Gastroenterology , Hospital Departments , Hospitalization , Humans , Incidence , Male , Middle Aged , Retrospective Studies , Severity of Illness IndexABSTRACT
BACKGROUND: The recurrent microlithiasis represents one of the most frequent clinical forms of lithiasis of the bile ducts. This affection is characterized by the presence of cholesterolic microgallstones on hepatic canaliculars, and belongs to a heterogeneous group of autosomal recessive liver disorders. Radiological diagnosis can be confirmed by analysis of MDR3 gene, coding a protein involved in physiologic translocation of phospholipids in bile. Discovery of MDR3 mutations is of particular interest, since normally associated with good effectiveness of medication by ursodesoxycholic acid. AIM: To review MDR3 mutations in humans associated with recurrent cholesterol microlithiasis and to suggest a practical approach for MDR3 gene analysis. RESULTS: 48 mutations of MDR3 gene have been reported in humans to date, from which 43 (89.5%) in the coding region, and 5 splice site mutations have been associated to cholesterol cholelithiasis. 21 (43.8%) of the 43 precited mutations are located in only 8 exons on 28, near transmembrane or nucleotide binding domains of the protein. From the 22 remaining described mutations, 9 (18.8%) are restricted to exon 14. We suggest therefore to start analysis of MDR3 gene by screening exons 6, 7, 9, 10, 12, 14, 17, 23 and 24 with an appropriate protocol in this diagnosis associated with effective treatment. In conclusion such therapeutic orientation is valuable, since recurrent cholesterolic microlithiasis occurs relatively early in life, and by the fact that recurrence of symptoms may occur despite cholecystectomy, or shock-wave therapy.
Subject(s)
ATP Binding Cassette Transporter, Subfamily B/genetics , ATP-Binding Cassette Transporters/genetics , Cholecystolithiasis/genetics , Choledocholithiasis/genetics , Cholecystolithiasis/metabolism , Choledocholithiasis/metabolism , Cholesterol/metabolism , Gallbladder/metabolism , Humans , Liver/metabolism , Mutation/geneticsABSTRACT
INTRODUCTION: The classical mode of revelation of a coeliac disease is chronic diarrhoea. We report the case of a patient in whom acute diarrhoea revealed the disease. OBSERVATION: In a 40 year-old man with acute diarrhoea with 7 non-bleeding stools per day, upper digestive tract endoscopy showed a villosity atrophy aspect confirmed by the histological examination. The search for specific antibodies of a coeliac disease was positive. A gluten-free diet led to the disappearance of the diarrhoea, followed by the disappearance of the specific antibodies and the regression of the villosity atrophy. COMMENTS: Acute diarrhoea that resists medical treatment must evoke the hypothesis of a coeliac disease and lead to a gastroscopy with duodenal biopsies. The interest of evoking the diagnosis is not only in order to obtain the rapid disappearance of the clinical signs after the introduction of a gluten-free diet but also to avoid an increase in the high risk of malignant lesions of the small intestine.
Subject(s)
Celiac Disease/complications , Celiac Disease/diagnosis , Diarrhea/etiology , Acute Disease , Adult , Celiac Disease/diet therapy , Diagnosis, Differential , Endoscopy, Gastrointestinal , Gastrointestinal Hemorrhage , Glutens , Humans , MaleABSTRACT
P-glycoprotein (P-gp) and MDR1 mRNA expressions were assessed in tumoral and peritumoral specimens from patients with hepatocellular carcinoma (HCC) and in cirrhotic livers without HCC, using immunohistochemistry (C494 monoclonal antibody) and reverse transcription-polymerase chain reaction (RT-PCR) analysis. P-gp overexpression was detected in 24/28 tumoral livers (85%). In the peritumoral liver, staining was strong in cirrhotic nodules, and fainter in non-cirrhotic specimens. P-gp expression was as intense in the cirrhotic specimens free of HCC as in the peritumoral tissue of HCC developing in cirrhotic patients. These results were confirmed by RT-PCR analysis.