An unusual cause of lower gastrointestinal bleeding.
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Biomedical subjects
Publications and source records attributed to G Lesur.
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Recent data have confirmed that non-steroidal anti-inflammatory drugs can cause serious damage to the gastrointestinal tract involving localizations other than the well-known gastroduodenal complications. Perforation and hemorrhage of the small bowel have been reported as well as ulcerations, stenoses and diaphragm disease. The same type of lesions can occur in the large bowel in addition to ischemia and collagen colitis. Diverticular diseases of the colon can be complicated by use of non-steroidal anti-inflammatory drugs which may also trigger flare-ups of inflammatory diseases. Use in suppository form can complicate rectitis and rectal stenosis. Non-steroidal anti-inflammatory drugs apparently increase intestinal permeability by inhibiting the cyto-protective effect of prostaglandins. The exact frequency of such complications remains to be determined, but prolonged treatment in elderly subjects appears to increase risk. Current data have not shown greater or lesser toxicity for any specific drug. Non-steroidal anti-inflammatory drugs should be entertained as the cause of intestinal disorders in patients under long-term treatment.
Pseudocysts of the pancreas are collections of liquid more or less completely composed of pancreatic secretions. Patients with acute pancreatitis without underlying chronic pancreatitis may develop necrotic pseudocysts while those with chronic pancreatitis may develop either necrotic or retention pseudocysts. The prevalence and localization are largely dictated by the cause of the pancreatitis. Ultrasonography and computed tomography give the diagnosis and reveal the size, localization and relations of the pseudocyst. Some pseudocysts may regress spontaneously, usually within a few weeks, especially necrotic pseudocysts measuring less than 6 cm. In others, complications include acute infection, intracystic bleeding, rupture, fistulization and compression of neighboring organs. Surgery was classically proposed for all pseudocysts, but puncture-evacuation and percutaneous or endoscopic drainage have also been successful. The risk of recurrence is higher with puncture-evacuation. Today, complicated forms and unsuccessful medical treatment are good indications for surgery. Cystodigestive drainage is preferred although exeresis may be required in specific cases.
We report a case of tuberculous peritonitis in a patient with concomitant HIV infection and liver cirrhosis. A 50-year-old man with viral B and delta liver cirrhosis and AIDS was diagnosed with spontaneous Escherichia coli peritonitis and successfully treated with beta-lactamins. Three months later, ascites reappeared and Mycobacterium tuberculosis was identified in peritoneal fluid cultures. The triple antituberculosis regimen was adjusted to his level of liver failure but the patient died of hepatic encephalopathy. Concomitant HIV infection and liver cirrhosis favour tuberculous peritonitis but they also make its diagnosis extremely difficult. Considering the poor prognosis of this infection when untreated, tuberculous peritonitis should be systematically suspected in such patients.
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We report two cases of metastatic non-functioning pancreatic endocrine tumour with very elevated plasma levels of alpha-fetoprotein. In these two cases, serial plasma levels of alpha-fetoprotein, initially normal, correlated well with hepatic tumour progression and were associated with fatal outcome. These results suggest that elevated plasma concentration of alpha-fetoprotein may be caused by metastatic pancreatic endocrine tumour and than alpha-fetoprotein serial measurement may be useful in prognostic evaluation.
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The oesophagus is a rare localization of extrapulmonary tuberculosis. We report 2 cases of tuberculous mediastinal lymph nodes revealed by dysphagia and fever in immunocompetent subjects. With the actual outbreak of tuberculosis, this localization is worth mentioning, as the precocity of the diagnosis and the therapeutic handling is an important prognostic factor.
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The authors have studied the natural history of duodenal ulcer from published data, in an attempt to determine precisely the evolutive potential of this disease both spontaneously and during its treatment. They deal successively with the risk of complication and the short- or long-term influence of medical and surgical treatment on the occurrence of exacerbations and complications. The role played by Helicobacter pylori in healing of the ulcer and in the long-term course of the ulcerous disease, as well as the problems concerning its duration and mortality, are discussed. The data clearly show that the medical and surgical treatment of duodenal ulcer can slow down, at least temporarily, the course of the disease. Other studies are needed before drawing firm conclusions concerning the relationship between H. pylori and duodenal ulcer, even though numerous studies seem to have demonstrated that eradication of this micro-organism is associated with a substantial decrease in the risk of recurrent ulcer.
The aim of this study was to assess the prevalence, presentation, cause, and location of symptomatic duodenal stenosis, and its relation to the natural course of chronic pancreatitis in a medical-surgical series of 306 patients (86% alcoholics). Mean follow-up of the series was 7.9 years. Symptomatic duodenal stenosis occurred in 17 patients (5.6%). Diagnosis was confirmed by a barium series. The cause of stenosis was compression by the pancreatic head in all patients, associated with a pancreatic abscess in two. No pseudocysts were found at the time of diagnosis. The location was the 1st and 2nd part of the duodenum or the entire duodenal loop in 4, 6, and 7 patients, respectively. Cholestasis due to common bile duct stenosis occurred in association with duodenal stenosis in 9 patients. Fifteen patients were treated surgically; 11 for gastroenterostomy, and 4 for duodenopancreatectomy. Two patients were not treated surgically. We conclude that during the course of chronic pancreatitis, symptomatic duodenal stenosis occurred in 5.6% of patients, mainly during the first years of the clinical course of chronic pancreatitis, was due to pancreatic head compression and not pseudocysts, usually involved the 2nd part of the duodenum and, was associated with biliary stenosis in half of the cases. Since these two complications require surgery, common bile duct stenosis should be investigated when symptomatic duodenal stenosis is diagnosed.
In the course of alcoholic chronic pancreatitis, increased serum alkaline phosphatase level is usually caused by common bile duct stenosis but may also be due to alcoholic liver disease. The aims of this prospective study were to investigate whether clinical, biochemical and radiological factors could predict liver histopathological appearance. The study comprised 48 patients with chronic alcoholic pancreatitis, common bile duct stenosis and increased serum alkaline phosphatase levels; clinical, biochemical, radiological and histological data were recorded in all cases. Liver biopsy examination (surgical [n = 45] or intercostal [n = 3]) showed (a) biliary obstructive liver abnormalities (n = 33), which were severe in 20 cases (biliary fibrosis in 15, secondary biliary cirrhosis in 3, secondary sclerosing cholangitis in 2) and moderate in 13 cases; (b) alcoholic liver disease in 9; and (c) normal liver in 6. Clinical, biochemical and radiological data were not statistically different between patients with biliary obstructive liver disease and those with alcoholic liver disease. Forty-five patients underwent surgery; two patients with alcoholic hepatitis died after surgery, at the beginning of this study. We conclude that in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase levels, clinical, biochemical and radiological data cannot be used to predict the type of liver lesions. Therefore liver biopsy is warranted to identify (a) alcoholic hepatitis, which increases operative risk; and (b) biliary obstructive liver disease, frequent and often severe, in which surgical biliary decompression should be considered.