[Lithiasis of the common bile duct during pregnancy. Treatment by endoscopic sphincterostomy].
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Biomedical subjects
Publications and source records attributed to J P Capron.
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Thirty-one patients with primary biliary cirrhosis were observed in Picardy during the decade 1975-1984. Mean annual incidence was 2.6 per 10(6), and point prevalence, 13 per 10(6) inhabitants in 1984. Asymptomatic cases (without clinical manifestations of cholestasis) constituted 32% of all patients. In five of the 21 symptomatic patients, ascites and/or digestive hemorrhage due to ruptured esophageal varices revealed the disease. Nine patients (2 with initially asymptomatic PBC) died during the follow-up period. Cholelithiasis was present in 10 patients (32%) and one case of hepatocellular carcinoma was found at autopsy.
We report on the observation of a 26-year-old woman with portal vein obstruction, diagnosed at the age of 3, and liver iron overload. Celiac and superior mesenteric angiography showed large and multiple venous collaterals between the portal and caval systems. Liver biopsy demonstrated, on Perl's staining, an important hemosiderin deposition, confirmed by an increased hepatic iron concentration (15.6 mumol/100 mg dry weight). No other histologic abnormality was found. This report suggests that large spontaneous portosystemic shunting may stimulate hepatic iron deposition in an otherwise normal liver. This mechanism could, at least in part, explain the significant hepatic siderosis observed in some cirrhotic patients.
Fatal hemoperitoneum due to liver capsule perforation has been reported after transvenous liver biopsy. We report 2 cases of prophylactic embolization of such capsular gap. We propose the following techniques for embolization: detection of liver capsule puncture if the liver biopsy is difficult to perform because the liver is small or moves in ascites; and therapeutic embolization of detected capsular gap.
A multi-centre random trial of 57 cases of alcoholic cirrhosis with refractory ascites was carried out; 29 patients received a LeVeen shunt and 28 were treated by conventional medical therapy. The effectiveness of the LeVeen shunt in reducing ascites was good in the first month, but was not different from conventional medical therapy by the end of one year. Complications were significantly more frequent in the surgical group. Of the 29 patients fitted with a LeVeen shunt, 25 developed one or more complications. Of the 28 patients in the medical control group, only 8 developed complications. The mortality rate of the two groups also differed significantly. Twelve patients in the surgical group (41%) died in the course of the first month against only 5 (18%) in the medical control group. By the end of one year, the mortality rate of the two groups was almost identical: 23 (79%) and 21 (75%) respectively. These observations confirm the poor prognosis for refractory ascites in cases of alcoholic cirrhosis and the inadvisability of attempting to treat it by implanting a LeVeen shunt.
The endoscopic features of the gastric mucosa in patients with cirrhosis have not been systematically investigated. In these patients, we observed an endoscopic aspect, consisting of multiple small erythematous areas, outlined by a subtle yellowish network (resembling a mosaic), mainly located in the proximal part of the stomach. We tested the value of this sign by comparing two groups: 100 patients with portal hypertension due to cirrhosis, and 300 control patients without signs of liver disease or portal hypertension. This endoscopic pattern was observed in 94 of the patients with cirrhosis, whereas oesophageal varices were seen in 78 only. In contrast, only one patient of the control group had this aspect. Moreover, this sign was also found in seven of eight patients with non cirrhotic portal hypertension, but was seen neither in 100 patients with chronic alcoholism but without liver disease, nor in 10 cirrhotic patients with end-to-side portacaval shunts. These endoscopic changes might be because of mucosal and/or submucosal oedema and congestion highlighting the normal areae gastricae pattern and related to raised portal pressure. We conclude that the mosaic pattern of the gastric mucosa is a sensible and specific sign for diagnosis of portal hypertension, whatever the cause.
An increase in lower oesophageal sphincter pressure induced by domperidone has previously been reported to decrease superior portosystemic collateral flow in patients with portal hypertension owing to cirrhosis. Although a 10-mg intravenous dose of domperidone was effective in increasing lower oesophageal sphincter tone in a group of six patients with cirrhosis, the same dose failed to affect azygos blood flow in a matched group of six patients. The results do not support the hypothesis that an increase in lower oesophageal sphincter tone can decrease flow through oesophageal varices in patients with cirrhosis.
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We describe two patients with myeloid metaplasia in whom portal hypertension resulted, not from infiltration of the liver sinusoids by myeloid cells, but from perisinusoidal fibrosis and nodular regenerative hyperplasia of the liver. We hypothesize that myeloid metaplasia induced the development of perisinusoidal fibrosis, which resulted in heterogeneous hepatic tissue blood perfusion, with atrophy of the liver cells in the underperfused areas and nodular regenerative hyperplasia in the normally perfused areas.
We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: O (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.
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A number of studies have demonstrated a high incidence of synchronous or metachronous esophageal carcinoma in association with carcinoma of head and neck. Carcinoma of the esophagus must be systematically looked for before the treatment of head-neck carcinomas and during follow-up. The aim of this study was to determine the incidence of synchronous esophageal carcinoma in patients with head and neck carcinoma and to evaluate the advantages of lugol and toluidine blue vital staining in fiberoptic endoscopy. One hundred patients (97 males and 3 females, mean age 54.9 years) were studied. A fiberoptic esophagoscopy was performed in all patients. Vital staining was realized with 5 p. 100 lugol in 40 cases and with 1 p. 100 toluidine blue e in 20 cases. Squamous cell carcinoma of the esophagus was observed in 12 patients, typical grossly in 5 cases and occult in 7 cases. In these latter cases, lugol (2 cases) or toluidine blue (5 cases) stain facilitated the forceps biopsies. Histological examination was positive in all cases. The incidence of esophageal carcinoma synchronous to carcinoma of the mouth was high (35.3 p. 100). Lugol vital staining seems to be sensitive, non-specific and easy to realize. Toluidine blue staining calls for a more difficult and prolonged technique. Although it can reveal occult carcinoma, false positive or negative results may be observed.
We encountered a case of primary biliary cirrhosis in a nonalcoholic man who had been operated on for idiopathic retroperitoneal fibrosis 20 years previously. Chronic pancreatitis was also detected on endoscopic retrograde examination. After several episodes of digestive bleeding due to ruptured esophageal varixes, the patient died of massive hemorrhage. Postmortem examination showed stage 3 primary biliary cirrhosis and a thick retroperitoneal fibrous plaque, consisting of densely fibrotic areas of collagen with rare vessels and mononuclear cells. We suggest that idiopathic retroperitoneal fibrosis may be a new autoimmune disorder associated with primary biliary cirrhosis and that primary biliary cirrhosis is a potential cause of portal hypertension, cholestasis, or both in the course of idiopathic retroperitoneal fibrosis.
The authors report a case of xanthogranulomatous cholecystitis in a 63-year-old woman hospitalized because of a right hypochondrium mass. Ultrasonography, computed tomography, and celiac arteriogram showed a gallbladder tumour. Surgical management allowed subtotal tumour resection. Diagnosis of xanthogranulomatous cholecystitis was established by histological examination. Twenty-two months later, patient is in good health. From this observation and a world-wide literature review (90 previously reported cases), the authors analyse the clinical, pathological, and pathophysiological features of this very unusual entity.
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