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Biomedical subjects

J P Capron

Publications and source records attributed to J P Capron.

At least 19 recordsLinked to original sources
PubMed1992

[Management of asymptomatic lithiasis].

A careful analysis of the series of patients with asymptomatic gallstones suggests that prophylactic cholecystectomy is not necessary. The purpose of this work was to try to detect subgroups of asymptomatic patients with factors predictive of symptoms or of severe complications such as acute cholecystitis, pancreatitis, or gallbladder carcinoma. Among local factors, neither the size, number or nature of gallstones, nor alterations of the walls or contractility of the gallbladder were predictive of symptoms or complications. Among general factors, neither the age or sex of patients nor associated diseases such as diabetes mellitus or recent organ transplantation were predictive of symptoms or complications. Only the few patients with a porcelain gallbladder were at high risk for gallbladder carcinoma requiring prophylactic cholecystectomy. In all other patients treatment of asymptomatic gallbladder stones is unnecessary as well as any surveillance.

Cholelithiasis↗
PubMed1992

Fibrin ring granulomas in hepatitis A.

Fibrin ring granuloma is characterized by a fibrinous ring surrounding a central fat vacuole. It has been found in the liver and bone marrow of patients with Q fever, and occasionally with visceral leishmaniasis, cytomegalovirus, Epstein-Barr virus, Staphylococcus epidermidis infections, Hodgkin's lymphoma, and hypersensitivity to allopurinol. We describe a case of serologically confirmed viral hepatitis A with this lesion in the liver biopsy. A false positive anti-hepatitis A virus IgM result has been excluded. This is, to our knowledge, the second reported case of type A hepatitis with hepatic fibrin ring granulomas. It confirms that hepatitis A should be included in the differential diagnosis of this lesion.

Acute Disease↗
PubMed1992

[The estrogen-androgen profile is unchanged in men with cholelithiasis].

It is well established that cholelithiasis is more frequent in women than in men. This difference is usually explained by the effects of estrogens and progesterone on the metabolism of bile acids, biliary cholesterol secretion and saturation, and gallbladder motility. Another explanation could be a protective effect of androgens against cholelithiasis in men. To test this hypothesis, we determined the hormonal, androgenic and estrogenic, status of 15 male patients with asymptomatic gallstone disease and in 15 control patients with normal gallbladder matched for age and body weight. No significant difference in the plasma concentrations and the urinary excretion rate of sex hormones (testosterone, dihydrotestosterone, androstenedione, testosterone and androstanediol glucuronides, estradiol, estrone, total estrogens), as well as in the plasma sex hormone binding globulin, was found between the 2 groups of patients. The development of cholelithiasis in men, therefore, does not appear to be related to modification of sex steroids.

Adult↗
PubMed1992

[Effect of acute administration of acamprosate on the risk of encephalopathy and on arterial pressure in patients with alcoholic cirrhosis].

To evaluate the risk of hepatic encephalopathy and arterial hypotension in cirrhotic patients after acute administration of acamprosate, a GABA mimetic drug used in the weaned alcoholic, a randomized double-blind trial was conducted in 24 cirrhotic patients with low or moderate hepatic insufficiency (Pugh grade A or B). Twelve patients received 666 mg (2 tablets) of acamprosate and 12 received placebo. The 2 groups were similar before treatment, except for a male predominance in the acamprosate group. Tested parameters were the P100 latency of visual evoked potentials using a checkerboard pattern reversal as stimulus, the number connection test and the arterial blood pressure in upright and recumbent positions. The two first parameters were studied before and 2 hours after treatment. Blood pressure was recorded every half hour during 6 hours. No significant effect on the development of subclinical hepatic encephalopathy was noted. Nevertheless, even if some authors disagree with the GABA hypothesis of hepatic encephalopathy, it is possible that the dose was too low to induce subclinical hepatic encephalopathy. A study with more prolonged treatment could be necessary to be sure of the drug's safety in these patients. On the other hand, a transient decrease of diastolic arterial blood pressure was observed without significant systolic blood pressure modification. These results suggest that a moderate dose of acamprosate does not induce subclinical encephalopathy, but transient diastolic hypotension.

Acamprosate↗
PubMed1991

[Hepatoid adenocarcinoma of the stomach].

One year after gastric resection for cancer, a 67 year old patient was hospitalized because of a large hepatic tumor with extremely high serum alpha-foetoprotein levels (13,245 ng/ml). Histological and immunohistochemical studies of the gastric tumor revealed hepatoid foci with alpha-foetoprotein and protease inhibitor-producing cells. Histopathological and immunohistochemical features of this and the 8 previously reported cases of hepatoid adenocarcinoma of the stomach are analyzed.

Adenocarcinoma↗
PubMed1991

[Increased fasting gallbladder volume: a new ultrasonic sign of cirrhosis?].

Ultrasound was used to calculate fasting gallbladder volume in three groups of patients: 90 with cirrhosis (alcoholic in 75 cases), 41 with non cirrhotic liver disease (alcoholic in 14 cases), and 38 controls. Gallbladder volume was evaluated according to sex, age, alcoholism, presence of gallstones, time of diagnosis, and biological tests of hepatocellular function. Mean fasting gallbladder volume was significantly higher in cirrhotic patients (45.89 +/- 32.65 ml, m +/- 1 SD) than in patients with non cirrhotic liver disease (25.31 +/- 14.08 ml) and in control subjects (21.28 +/- 10.30 ml) (P less than 0.001), but there was a great overlap between individual results in each group. No relationship was found between gallbladder volume and all clinical and biological tested parameters, except for decreased prothrombin time (P less than 0.02). Further studies are necessary to consider this ultrasound sign as an useful diagnostic tool in cirrhosis.

Fasting↗
PubMed1979

Gastrointestinal bleeding due to chronic portal vein thrombosis in ulcerative colitis.

The authors report the case of a patient suffering from ulcerative colitis, who had several episodes of digestive hemorrhage due to portal hypertension. Portal hypertension was secondary to chronic portal vein thrombosis. This diagnosis was made on the venous phase of celiac and mesenteric angiography. The authors review the published cases of ulcerative colitis with portal vein thrombosis and discuss the possible etiologic factors: hypercoagulability, thrombocytosis, and intraabdominal sepsis.

Angiography↗
PubMed1979

Fibrosing alveolitis and hepatitis B surface antigen-associated chronic active hepatitis in a patient with immunoglobulin A deficiency.

Fibrosing alveolitis is described in a 22 year old woman with immunoglobulin A (IgA) deficiency and hepatitis B surface antigen (HBsAg)-associated chronic active hepatitis. At lung biopsy HBsAg was detected by indirect immunofluorescence in the alveolar space but not in the septal fibrosis. We discuss the possible relationships between IgA deficiency on the one hand, and HBsAg-associated lung and liver diseases on the other hand.

Adult↗
PubMed1979

Pulmonary hypertension complicating portal hypertension.

We report 9 patients with pulmonary hypertension complicating portal hypertension. The cause of portal hypertension was cirrhosis in 7 patients, nodular regenerative hyperplasia of the liver in 1, and portal vein obstruction in 1. Six patients had been treated by portal-systemic shunting before the clinical onset of pulmonary hypertension. The interval between the first manifestation of portal hypertension and the recognition of pulmonary hypertension ranged from 2 to 15 years. Histologic examination in 1 of these patients revealed medial hypertrophy, concentric intimal proliferation, and plexiform lesions affecting the small pulmonary arteries. Pulmonary hypertension might result from the effect of a vasoconstrictive agent on the small pulmonary arteries or of a substance toxic to the walls of these vessels that is produced in the splanchnic territory, destroyed by the liver in normal subjects, and reaches the pulmonary arteries through portal-systemic shunts in these patients.

Adult↗