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Biomedical subjects

M Beaugrand

Publications and source records attributed to M Beaugrand.

At least 73 records · Page 4Linked to original sources
PubMed1994

[Hepatocellular carcinoma: treatment with arterial chemo-embolization].

Due to extensive tumoural invasion, less than 10% of the patients with hepatocellular carcinoma can benefit from surgery. A variety of proposed palliative procedures, including general chemotherapy and radiotherapy, have given quite less than satisfactory results. Percutaneous alcoolization and hormone therapy are currently being evaluated. Increased use of intra-arterial embolization has developed over the last 10 years, initially in Asia and now in Europe. The aim of intra-arterial chemotherapy is to increase the concentration of anticancer agents within the tumour. Adding lipiodol with certain agents would increase the duration of cancer cell exposure. Arterial embolization aims at creating tumour necrosis by ischaemia and relies on the fact that the main blood supply from hepatocellular carcinomas comes from arteries while non-tumoural hepatic tissue is supplied by the portal vein. Numerous reports on intra-arterial treatment protocols combining chemotherapy and embolization have demonstrated that this technique can produce partial or total tumour necrosis. However, due to the variable nature of the natural history of hepatocellular carcinoma the clinically beneficial effect in terms of survival rate has not been established and would not appear to be highly significant, probably due to chemoresistance which cannot be overcome by intra-arterial administration. Indeed, the necrotic effect appears to result from hepatic embolization itself. In two randomized studies necrosis was significantly greater in patients who underwent repeated embolizations than in those receiving general or intra-arterial chemotherapy. It is generally accepted that intra-arterial chemoembolization is contraindicated in cases of portal thrombosis or major liver failure. In addition, each procedure requires at least one week hospitalization with the inherent effect on patient comfort and quality of life. Nevertheless, should intra-arterial, chemoembolization be abandoned? Probably not because there is no alternative method, at least for inoperable patients. Efforts should be made to improve the technique which should be reserved for carefully selected patients. New, more liposoluble drugs and possible combinations with glycoprotein inhibitors could be studied. Until an effective treatment for hepatocellular carcinoma has been developed, the role of palliative care must be evaluated in terms of survival rate, cost and quality of life.

Adult↗
PubMed1994

Systemic antibiotic therapy prevents bacterial infection in cirrhotic patients with gastrointestinal hemorrhage.

This randomized prospective study was aimed at assessing the efficiency of a systemic antibiotic therapy for the prevention of bacterial infections in cirrhotic patients with gastrointestinal hemorrhage by ruptured esophageal varices. For 15 mo, all patients hospitalized with no infection on admission, were included in the study. Starting on admission day, patients in group A received ofloxacin (400 mg/day) for 10 days, first intravenously then orally. They also received an intravenous bolus of amoxicillin plus clavulanic acid (1 g) before each endoscopy performed during hemorrhage. Patients in group B received antibiotic therapy only in cases of established or suspected infection. Chest X-ray, blood culture, urine culture and sputum and ascitic fluid culture were performed every day for 7 days, then every other day for the next 7 days. A bronchial sampling was performed with the Wimberley technique on patients with endotracheal intubation. Ninety-one patients (55 men, 54 +/- 11 years, 78% Child Pugh class C) were included in the study (46 in group A, 45 in group B). Group A showed a lower incidence of bacterial infections than group B (20% vs. 66%; p < 0.001). Breakdown of positive bacteriological sampling was as follows: blood (6 vs. 17), ascites (3 vs. 7), lungs (2 vs. 18), urine (1 vs. 10). The 2-wk mortality rate was 24% in group A and 35% in group B.

Adult↗
PubMed1994

Prospective study of screening for hepatocellular carcinoma in Caucasian patients with cirrhosis.

Screening is widely used to detect early hepatocellular carcinoma in Asian patients with cirrhosis. Its effectiveness in Caucasian patients has been suggested, but remains to be proven. Therefore we prospectively studied 118 French patients (68 males, 50 females, age 55 +/- 12) with Child-Pugh A or B cirrhosis (alcoholic in 82) and without detectable hepatocellular carcinoma. The screening program consisted of ultrasound examination of the liver and determination of blood alpha-fetoprotein and des-gamma-carboxyprothrombin levels every 6 months. The median follow up was 36 months (range 4-48). Only four patients were lost to follow up. Fourteen hepatocellular carcinomas were detected, in six cases by ultrasonography alone, in four by alpha-fetoprotein alone, in three by ultrasonography and alpha-fetoprotein and in one case by ultrasonography and des-gamma-carboxyprothrombin, but never by des-gamma-carboxyprothrombin alone. The tumor presented as a unique nodule in nine patients. The tumor was less than 3 cm in diameter without portal thrombosis or metastasis in three cases. Surgery was performed in only one case. In this study, the annual incidence of hepatocellular carcinoma was high (5.8%), but the screening methods used did not effectively identify potentially resectable tumors in Caucasian patients with cirrhosis.

Biomarkers↗
PubMed1994

[Role of hepatitis C virus in the genesis of hepatic lesions observed in alcoholic patients with liver cirrhosis].

The aim of study was to assess the role of hepatitis C virus (HCV) infection in 164 alcoholic cirrhotic patients. We studied the prevalence of anti-HCV antibodies using ELISA and RIBA first and second generation tests. Twenty-two % of the patients had anti-HCV antibodies detected by ELISA 2, RIBA 2 test was positive in 10% of the patients and indeterminate in 3%. We compared epidemiological, biological and histological characteristics according to the results of the tests. By comparing ELISA 2-RIBA 2 positive patients to ELISA 2 negative patients, we observed, in the former, a) a higher serum aminotransferase activity, b) a lower serum gammaglutamyl transpeptidase activity, and c) a lower histological score of alcoholic hepatitis. In addition, in a group of ELISA 2 positive RIBA 2 negative patients, the values were intermediate between those of the two former groups. However, most of these patients had a negative third generation ELISA test. The whole results suggest that HCV is likely to play a role in the pathogenesis of liver damage in a high number of alcoholic cirrhotic patients.

Adult↗
PubMed1994

[Significance of type III serum N-terminal peptide procollagen assay in chronic viral hepatitis C].

The aim of this study was to evaluate the relationship between the serum N-terminal peptide of type III procollagen (PIIINP), Knodell's score and the response to treatment in 79 patients with viral C chronic hepatitis. Liver biopsy and serum PIIINP was assessed in all patients. Serum PIIINP was correlated with Knodell'score (r = 0.60; P = 10(-4)). Correlation between serum alanine amino-transferase and Knodell'score was smaller than for PIIINP (r = 0.38; P = 0.02). Forty-nine patients were treated with interferon alpha. A second biopsy and serum PIIINP determination were performed one year after treatment discontinuation. Means of serum PIIINP and Knodell'score significantly decreased after treatment (P < 0.01; P < 0.03). Among non-responder patients, serum PIIINP was initially more elevated: 37.5 +/- 12.6 ng/mL versus 22.6 +/- 3.8 (P < 10(-3)). Knodell's score decreased only among responder patients (P < 0.01 vs P < 0.7). Positive and negative predictive value for the response to treatment, evaluated by aminotransferases normalization, of serum PIIINP level < or = 24 ng/mL were 0.6 and 0.9 respectively. These findings suggest that serum PIIINP is a relevant marker of activity in patients with viral C chronic hepatitis and that it might have a predictive value of response to treatment.

Adult↗
PubMed1994

[Secondary sclerosing cholangitis and chemo-embolization with lipiodol].

Two cases of sclerosing cholangitis after oily arterial chemoembolization are reported. In one patient angiocholitis with liver abscesses, in the other patient gradual cholestasis were the main clinical features. In both cases, endoscopic retrograde cholangiogram showed a stricture of the common hepatic bile duct and, in one case, irregularities of intrahepatic biliary tree. Histologic examination of the liver in the two patients pointed out the involvement of small bile ducts and arteriolar endarteritis obliterans. Ischaemia is likely to be the main mechanism of these two cases of sclerosing cholangitis as well as in those described after FUDR intra-arterial chemotherapy. The prevalence of sclerosing cholangitis after arterial oily chemoembolization is probably underestimated because of a non specific clinical presentation and need to be precise by further study.

Carcinoma, Hepatocellular↗
PubMed1993

[Comparison of six potential serum markers of hepatic fibrosis in alcoholic disease of the liver].

The aim of this study was to compare 6 potential serum markers for hepatic fibrosis in patients with alcoholic liver disease. Ninety-three patients (50 +/- 11 years old, 62 males) with biopsy-proven alcoholic liver disease were included in the study. A liver biopsy and serum assays of type I, type III and type IV collagens, N-terminal peptide of type III procollagen, laminin (by radioimmunoassays) and apolipoprotein A1 (by nephelometry) were performed in all patients. A histological score of hepatic fibrosis was established. Alcoholic hepatitis lesions and perisinusoidal fibrosis were assessed separately. A significant correlation was found between the score of hepatic fibrosis and serum levels of type I collagen (r = 0.44, P < 10(-3)), type III collagen (r = 0.36, P < 10(-2)), N-terminal peptide of type III procollagen (r = 0.50, P < 10(-3)), type IV collagen (r = 0.44, P < 10(-3)), laminin (r = 0.50, P < 10(-3)), and apolipoprotein A1 (r = 0.21, P < 0.05). After adjustment for the presence of lesions of alcoholic hepatitis and perisinusoidal fibrosis (partial correlation), serum levels of type I collagen, type III collagen, N-terminal peptide of type III procollagen, type IV collagen, and laminin remained significantly correlated with the score of hepatic fibrosis; in contrast, correlation with serum apolipoprotein A1 was no longer significant. Serum levels of N-terminal peptide of type III procollagen, type IV collagen and laminin were significantly higher in patients with perisinusoidal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Lymphocytic sialadenitis of Sjögren's syndrome associated with chronic hepatitis C virus liver disease.

Viral infection has often been suggested as a possible cause of Sjögren's syndrome or chronic lymphocytic sialadenitis, and Epstein-Barr virus has been found in the salivary glands of patients with this condition. After we had noted Sjögren's syndrome in several patients infected with hepatitis C virus (HCV), a virus also excreted in saliva, we set up a prospective study to investigate the association of chronic lymphocytic sialadenitis, with or without symptoms, to chronic HCV liver disease. The histological appearances of labial salivary glands in patients with proven HCV hepatitis or cirrhosis were compared with those in dead controls. Histological changes characteristic of Sjögren's syndrome were significantly more common in HCV-infected patients (16 of 28, 57%) compared with controls (1 of 20, 5%). Focal lymphocytic sialadenitis characteristic of Sjögren's syndrome (though only 10 patients had xerostomia and none complained of xerophthalmia) appears to be common in patients with chronic HCV liver disease; if this association is confirmed, identification of the underlying mechanism may improve our understanding of both disorders.

Adult↗
PubMed1992

Multiple nuclear dots antinuclear antibodies are not specific for primary biliary cirrhosis.

Multiple nuclear dots antinuclear antibodies display a specific immunofluorescence pattern on HEp-2 cells. They have been reported to be strongly associated with primary biliary cirrhosis, especially when sicca syndrome was present. To determine whether multiple nuclear dots antinuclear antibodies are specific for primary biliary cirrhosis, we studied the clinical, biochemical, immunological and morphological features of 38 patients between December 1983 and September 1990 who had serum multiple nuclear dots antinuclear antibodies detected in an immunology laboratory of a large medical center. Sufficient information was reliable in 36 patients; the group included 31 women and 5 men (mean age = 57.6 +/- 14.5, range = 30 to 87). Fifteen patients (42%) had primary biliary cirrhosis, 5 patients (14%) had type 1 autoimmune chronic active hepatitis, 4 patients (11%) had liver disease of unknown cause and 12 patients (33%) had various immunological disorders but no liver disease. Two of the patients with primary biliary cirrhosis (13%) had clinical sicca syndrome. Our study demonstrates the following: (a) serum multiple nuclear dots antinuclear antibodies are not specific for liver disease because they can be observed in one third of patients with various immunological disorders without liver involvement, and (b) serum multiple nuclear dots antinuclear antibodies are not specific for PBC because they can also be observed in type 1 autoimmune chronic active hepatitis. Our results also suggest that patent sicca syndrome is abnormally present in patients with primary biliary cirrhosis and multiple nuclear dots antinuclear antibodies.

Adult↗
PubMed1992

Serum type I collagen and N-terminal peptide of type III procollagen in patients with alcoholic liver disease: relationship to liver histology.

This study compared, in patients with alcoholic liver disease, the serum concentration of N-terminal peptide of type III procollagen and of a novel serum marker, type I collagen, with liver histological data and assessed the role of these markers in the diagnosis and follow-up of liver changes. Ninety-six patients (mean age 51 years, 61 men and 35 women) were included. All had alcoholic liver disease diagnosed on usual clinical, biochemical, and histological criteria. Two histological scores, one for alcoholic hepatitis and one for fibrosis, were established. Serum N-terminal peptide of type III procollagen and type I collagen were assayed by liquid phase radioimmunoassay. Significant correlations between serum type I collagen and score of fibrosis (r = 0.34, p less than 0.001) and between serum N-terminal peptide of type III procollagen and score of alcoholic hepatitis (r = 0.60, p less than 0.0001) were noted. There was no significant correlation between serum aminotransferases and the score of alcoholic hepatitis. In 25 patients with alcoholic hepatitis reassessed between 3 and 6 months, serum N-terminal peptide of type III procollagen significantly decreased (p less than 0.05) as did the score of alcoholic hepatitis, but serum type I collagen and the score of fibrosis were not modified. These serum markers of collagen metabolism could be useful for the assessment and follow-up in patients with alcoholic liver disease.

Adult↗
PubMed1992

[Severe hepatic steatosis: a cause of sudden death in the alcoholic patient].

The authors report the cases of 4 patients with heavy chronic alcoholic intake who presented with hepatomegaly and jaundice without obvious hepatic failure and who died rapidly. In all 4 cases, histological examination of the liver showed massive microvesicular and macrovesicular steatosis involving approximately 100% of hepatocytes and, in 2 cases, minimal lesions of alcoholic hepatitis. Histochemical study, performed in 3 cases, showed that steatosis was constituted of triglycerides only, and that hepatic glycogen was completely depleted in 2 of 3 cases. No obvious cause of death was found in these 4 patients. Shortly, before their death, the 4 patients had increased their ethanol and decreased their food intake. The authors suggest that death as well as microvesicular steatosis could have be due to acute mitochondrial dysfunction.

Death, Sudden↗