Biomedical subjects
Publications and source records attributed to B Rueff.
We report the case of a patient with primary sclerosing cholangitis associated with systemic lupus erythematosus. Only one similar case has been previously reported. The relationship between the two diseases is discussed.
Among 61 patients admitted for non-A, non-B fulminant viral hepatitis to Hôpital Beaujon, 10 had returned from Asia or Africa, and 51 had not been outside France, within the month preceding jaundice. This suggests that hepatitis might have been contracted in Asia or Africa in the former, and in France in the latter. The interval between the onset of jaundice and the onset of hepatic encephalopathy was 10 days in the former and 26 days in the latter (P less than 0.03). The serum of the patient returning from Asia contained, and the sera of the nine patients returning from Africa did not contain, antibodies to a virus isolated from the stools of patients suffering from an epidemic fecal-oral non-A, non-B viral hepatitis in Central Asia. It is concluded that infection with Asian-African non-A, non-B viruses can be the cause of fulminant hepatitis in persons returning from these countries, that the course of this type of non-A, non-B fulminant viral hepatitis is shorter than that of non-A, non-B fulminant hepatitis contracted in France, and that different viruses might be responsible for non-A, non-B hepatitis in Asia and Africa.
We report a case of chronic active hepatitis caused by benzarone, a benzofuran derivative used in Europe for the treatment of peripheral venous disorders. Jaundice and serum alanine aminotransferase activity increased while drug administration was continued, but promptly decreased when it was eventually interrupted. Liver lesions were those of chronic active hepatitis. Anti-smooth muscle antibodies were present at a titer of 1:500 and disappeared 8 months after withdrawal of benzarone.
We investigated hepatitis B virus (HBV) DNA in liver samples from 22 patients with acute benign hepatitis (AH) and 26 with acute fulminant hepatitis (FH) and compared the results with those obtained by detection of serum HBV DNA and HBV serological markers. Free HBV DNA forms were detected in 11 patients with AH and one with FH, a reflection of active HBV DNA replication in three patients and the end of viral multiplication in nine. Free monomeric HBV DNA was present in three patients with AH and six with FH, and free oligomers were identified in three patients with AH. Results from two patients with AH and seven with FH suggested the presence of dimeric or multimeric HBV DNA. Thus, the various forms of HBV DNA previously described in chronic HBV carriers may be observed at the acute stage of the viral infection. After comparing serological and hybridization data, we found that nine of 19 patients (one with AH and eight with FH) lacking serum HBV surface antigen might have had acute hepatitis related to infection with HBV or HBV variants.
We report the cases of one patient with the acquired immunodeficiency syndrome as a result of human immunodeficiency virus type 1/lymphadenopathy associated virus type 1/human T-cell lymphotrophic virus type III (HIV-1/LAV-1/HTLV-III) infection and of another patient with AIDS related complex caused by human immunodeficiency virus type 2/lymphadenopathy associated virus type 2 (HIV-2/LAV-2) infection, who were suffering from cholangitis. The manifestations and possible mechanisms for cholangitis in these patients and in 10 previously reported similar cases are reviewed.
Orthotopic liver transplantation was done in 17 patients with fulminant hepatitis. The cause of the liver disease was infection with hepatitis B virus, or co-infection with hepatitis B virus and hepatitis D virus, or infection with hepatitis A virus in 6 patients; drug hepatotoxicity in 5; and indeterminate in 6. Grafts from incompatible blood groups, steatotic grafts, or reduced-size grafts were used in 5, 4, and 4 patients, respectively. Of the 17 patients, 5 died: 2 of early liver failure due to the poor quality of the graft, 1 presumably of accidentally transmitted acute infection with the human immunodeficiency virus, and 2 of decerebration occurring during or immediately after surgery. The 12 other patients were alive 2 to 15 months after transplantation.
We have reviewed the clinical, histological and hemodynamic features of sarcoidosis complicated by portal hypertension in seven patients and in 40 previously reported cases. Young black patients of either sex and white females over 40 years were selectively affected. In 12 of these 47 patients, portal hypertension appeared to be a consequence of cirrhosis due to longstanding intrahepatic cholestasis; in white patients, this condition was clinically, histologically, and serologically indistinguishable from primary biliary cirrhosis. In most of the other patients, portal hypertension was the predominant and often the presenting symptom of hepatic sarcoidosis; in these patients portal hypertension was due to a presinusoidal block probably determined by portal granulomas, with or without superimposed sinusoidal block determined by fibrosis. Corticosteroids did not prevent the development of portal hypertension.
Alcoholic foamy degeneration is a recently recognized type of alcohol related liver disease. We report 3 cases occurring in men aged 40, 51 and 38 years. All 3 patients had marked elevation of serum aminotransferases which decreased rapidly after withdrawal of alcohol intake. In each case, the diagnosis of alcoholic foamy degeneration was made on microscopic examination of a liver specimen. The lesion is similar to that found in other diseases in which microvesicular steatosis is a main finding, such as acute fatty liver of pregnancy and Reye's syndrome. This condition, when isolated, is a rare form of alcoholic liver disease. A milder form probably exists, more commonly associated with other alcoholic liver injuries. The diagnosis of alcoholic foamy degeneration must be suspected when marked elevation of serum aminotransferases is observed in alcoholic patients, and it must be confirmed by microscopic examination.
Explore the source record for details and available documents.
In a series of 40 patients with Budd-Chiari syndrome, 5 (12%) were found to be afflicted with paroxysmal nocturnal hemoglobinuria. The clinico-pathological features in these 5 patients and in 26 well-documented previously reported cases could be ascribed to three groups of increasing severity: thrombosis limited to small-sized hepatic veins with no or transient ascites, partial thrombosis of large-sized hepatic veins with chronic ascites, and complete thrombosis of large-sized hepatic veins with a life-threatening course. These three groups did not differ with regard to sex, age, and duration and characteristics of paroxysmal nocturnal hemoglobinuria. In view of the relationship between prognosis and the extent of hepatic vein obstruction, we suggest that early therapy directed toward limiting the extension of thrombosis, or toward dissolving formed thrombi, should improve the prognosis of this severe complication of paroxysmal nocturnal hemoglobinuria.
In a case-control study, we evaluated the relative risk of hepatic vein thrombosis among recent oral contraceptive users as compared with nonusers. Thirty-three cases of hepatic vein thrombosis affecting women aged 15-45 yr were collected between 1970 and 1983, and individually matched to 3 or 4 controls interviewed in 1982-1984. There were 18 recent oral contraceptive users among the 33 cases, and 44 recent oral contraceptive users among the 128 case-matched controls. The relative risk of hepatic vein thrombosis was 2.37 (95% confidence interval: 1.05-5.34, p less than 0.02). The relative risk of hepatic vein thrombosis is close to that of stroke, myocardial infarction, and venous thromboembolism among oral contraceptive users as compared with nonusers.
Fulminant or subfulminant liver failure, complicated by encephalopathy and in many cases by death is seen to be a syndrome that may result from numerous causes. Although viral hepatitis, drug-induced hepatitis, and hepatitis due to various types of poisonings, in decreasing frequency, account for 90% of all cases, a variety of miscellaneous conditions account for the remainder. Consideration of the possibility of these less common etiologies by the clinician is of considerable importance, since some, including massive malignant involvement (such as leukemia) or acute fulminant Wilson's disease, may respond to specific treatment measures. Thus, unless hepatic transplantation proves to be applicable in FHF of many etiologic diagnosis may continue to have important therapeutic indications in at least some cases with this syndrome.
The relationship between fulminant viral hepatitis (FVH) and pregnancy was compared in Algeria and France. This comparison was based on the study of 22 Algerian and 77 French pregnant and non-pregnant women, aged 15 to 49 years, consecutively admitted for FVH to the Centre Hospitalier Universitaire, Constantine, Algeria, or to Hôpital Beaujon, Clichy, France. The observed and expected (calculated from demographic data) percentage of pregnant women was significantly different among the Algerian patients with FVH (45.5% v. 24.9%, P less than 0.03), but not among the French patients (3.9% v. 5.8%). Hepatitis A was the cause of FVH in none of the Algerian patients, but in eight French patients, none of whom was pregnant. Hepatitis B was the cause of FVH in one non-pregnant Algerian patient and in 49 French patients, two of whom (4.1%) were pregnant. Hepatitis non-A, non-B was the cause of FVH in 21 Algerian patients, ten of whom (47.6%, a percentage significantly higher than expected, P less than 0.04) were pregnant, and in 19 French patients, one of whom (5.3%, a percentage similar to that expected) was pregnant. In conclusion, (1) there is a relationship between FVH and pregnancy in Algeria, but not in France, and (2) this difference is mainly or exclusively attributable to infection with a non-A, non-B virus affecting the Algerian population, but which is much less common or absent in France.
To compare the effect of diet, cirrhotic patients with ascites were randomised into two treatment groups: (1) a low sodium diet (21 mmol) per day or (2) an unrestricted sodium intake. Both groups received effective doses of diuretics (spironolactone or, if necessary, spironolactone and furosemide. One hundred and forty patients from 12 liver units were included according to well defined criteria (group 1: 76; group 2: 64). After an initial four to seven day period of bed rest and salt restriction (21 mmol sodium pd), randomisation was done in each centre. We saw no significant difference between the two groups with respect to clinical and biochemical data; mortality or withdrawal (definitive or temporary) because of biochemical disturbances (group 1: 34%, group 2: 22%); the time for complete disappearance of ascites was significantly shorter (p = 0.014) for the salt restricted patients actuarial survival (curves plotted up to the 120th day) was not statistically different (p = 0.18), but division into subgroups using various prognostic factors showed that survival was significantly better for salt restricted patients without previous gastrointestinal bleeding (p = 0.02); hospitalisation time and costs were identical in both groups. We conclude that the advantage of a normal salt diet was not shown in this study.
Cross hepatotoxicity between drugs in very uncommon. We report the case of a patient in whom acute hepatitis was induced by a tricyclic antidepressant, amineptine, and recurred early after administration of another tricyclic antidepressant, clomipramine. This observation suggests that the tricyclic ring is involved in the mechanism of the deleterious effect of both drugs to the liver.
Seven patients developed hepatitis after receiving amodiaquine for malaria prophylaxis for 4 to 15 weeks. Four patients had a minor form of hepatitis: jaundice was mild or absent, serum aminotransferase levels were moderately increased, and recovery was prompt. Three patients had a severe form: jaundice was intense, serum aminotransferase levels were markedly increased, jaundice persisted for 3 to 6 months, and liver tests were still abnormal 7 to 27 months after the onset of hepatitis. In two patients, serum aminotransferase levels increased promptly after readministration of the drug, which is consistent with an immunoallergic mechanism for amodiaquine-induced hepatitis.
Explore the source record for details and available documents.
We report the cases of 2 female patients aged 69 and 61 yr, suffering from fulminant hepatitis induced by pirprofen, a new nonsteroidal antiinflammatory drug. The duration of pirprofen administration before the onset of hepatitis was long, 7 and 9 mo, respectively. Hepatitis was not preceded or accompanied by hypersensitivity manifestations. The liver lesion consisted of massive, predominantly centrilobular hepatic cell necrosis and microvesicular steatosis. One patient died of liver failure. Although the risk of fulminant hepatitis is very low, we recommend that, in patients taking pirprofen for more than 2 mo and complaining of asthenia, nausea, or vomiting, serum aminotransferase levels should be measured and administration of the drug should be interrupted as soon as an increased level is noted.