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Biomedical subjects

P Bedossa

Publications and source records attributed to P Bedossa.

At least 145 records · Page 8Linked to original sources
PubMed1991

Efficacy of long term recombinant interferon-alfa in patients with chronic hepatitis C. A clinical, biological, histological and immunohistological study.

A prospective, non randomized trial was conducted in 22 patients with chronic hepatitis C treated for 6 months with interferon-alfa at the dose of 3 million units three times a week followed by decreasing doses for the following 6 months. Transaminase activity measurements were taken at 2, 6, 12, 18, and 24 months and a liver biopsy was performed at zero and 6 months to assess efficacy. Immunohistochemical study of HLA class I and lymphocyte subsets was performed on the biopsy specimen before and after 6 months of treatment. A complete biological response was observed in 82, 82, 60, 64 and 70 percent of patients at 2, 6, 12, 24 and 36 months, respectively. Four patients relapsed including 2 patients who suddenly stopped taking interferon-alfa. An improvement of histological features was observed in 90 percent of patients for necrosis and in 80 percent of patients for inflammation, with an overall improvement in Knodell's score reaching 85 percent. Immunohistochemical studies showed CD8+ cell infiltration already present in the area of necrosis before treatment. These tests also showed that HLA class I expression by the hepatocyte membranes was increased at 6 months and was identical in patients with or without histological improvement.

Adult↗
PubMed1991

Independent risk factors for hepatocellular carcinoma in French drinkers.

The aim of this study was to assess whether markers of hepatitis B virus or hepatitis C virus infection are independent risk factors for hepatocellular carcinoma in drinkers after adjustment for three known risk factors: cirrhosis, age and male sex. Among 2,015 consecutive drinkers admitted, hepatitis C virus antibodies were found by sensitive radioimmunoassay in 1,259. The following five factors have been identified and ranked as risk factors for hepatocellular carcinoma in unidimensional and regression analysis: cirrhosis (p less than 0.001), age (p less than 0.001), male sex (p less than 0.001), presence of HBsAg (p less than 0.001) and presence of hepatitis C virus antibodies (p less than 0.03). Among drinkers with cirrhosis, the patients with hepatocellular carcinoma were older (64 +/- 11 yr vs. 56 +/- 9 yr; p less than 0.001), were more often male (93% vs. 65%; p less than 0.0001) and had higher prevalence of HBsAg (9% vs. 2%; p = 0.02) and hepatitis C virus antibodies (41% vs. 26%; p = 0.02). A simple algorithm permitted us to identify a high-risk population of drinkers: the male cirrhotic patient older than 50 yr. The relative risk of hepatocellular carcinoma in this selected population was 17.7 (95% confidence interval = 9.0 to 37.5; p less than 0.0001). From a pragmatic point of view, the detection of HBsAg or hepatitis C virus antibodies, although independently associated with hepatocellular carcinoma, is not useful in increasing the diagnostic value of this algorithm because of the poor sensitivity of these tests. The weak relationships observed between hepatitis C virus antibodies and hepatocellular carcinoma needs confirmation by more accurate tests.

Age Factors↗
PubMed1991

[Identification and localization on chromosome 1 of a gene controlling the occurrence of periinsulitis in NOD diabetic mice].

Diabetic NOD (Non Obese Diabetic) mice show early pancreatic infiltration of mononuclear cells around Langerhans islets (periinsulitis). Study of (NOD x C57BL/6) F1 and F2 mice reveals that periinsulitis is constantly associated with a similar infiltration of salivary glands (sialitis) and is controlled by a dominant susceptibility locus. Segregation analysis of periinsulitis and microsatellite DNA markers indicates that the gene controlling periinsulitis maps to chromosome 1, close to the Bcl-2 locus.

Animals↗
PubMed1991

[Adenocarcinoma in heterotopic gastric pancreas].

The development of an adenocarcinoma in heterotopic pancreas of the stomach is uncommon and its diagnosis is difficult. We report the case of a 42 year-old man who was admitted for gastric stasis, related to an antral tumour. He had been treated for Hodgkin's disease by radiation therapy. 16 years ago. Gastrectomy was performed. On light microscopy, the gastric wall was infiltrated by pancreatic ectopic tissue, normal in the submucosa, but dedifferentiated with cytological and architectural criteria of malignancy in the muscular and the serous layers. Malignant transformation of an ectopic pancreas is theoretically possible but is very uncommon. In our case, the role of previous radiation therapy as a promoting factor is discussed.

Adenocarcinoma↗
PubMed1990

Deposition and remodelling of elastic fibres in chronic hepatitis.

A longitudinal study of elastic fibres was conducted in liver biopsies from 21 patients with chronic viral hepatitis. Biopsies were taken at the start of treatment with alpha-interferon, and after 6 months or 1 year of treatment. No elastic fibres could be detected in portal tracts or fibrous septa when inflammation and necrosis were present, whatever the duration of the disease. Once the liver lesions had healed, elastic fibres were synthesized. Fibres were of two types and patterns: at first, they were thin, long and parallel to each other. Later, they were thicker, shorter and tortuous and were closely wrapped around thick bundles of collagen fibres. These findings suggest that the deposition of elastic fibres acts as a marker of healing in chronic active hepatitis and that their remodelling occurs concomitantly with the deposit of large bundles of collagen fibres.

Biopsy↗
PubMed1990

Expression of histocompatibility antigens and characterization of the lymphocyte infiltrate in hyperplastic polyps of the large bowel.

HLA-DR expression, lymphocyte subsets, and the distribution of proliferating cells were studied in hyperplastic polyps from the colorectum. The density of T-cells (CD5+) (mean of cells/mm2 of tissue +/- SEM) was higher in the lamina propria of hyperplastic polyps (64.2 +/- 4.2) than in normal colonic mucosa (36.7 +/- 2.6, P less than .001). The CD4/CD8 ratio was higher in hyperplastic polyps (6.3 +/- 0.9, P less than .0001) and in colonic adenomas (5.9 +/- 0.9, P less than .001) compared with normal mucosa (2.3 +/- 0.2). Lymphocytes of the lamina propria were never Ki-67 positive either in normal mucosa or in hyperplastic polyps or adenomas. The epithelial layer of hyperplastic polyps and of normal mucosa did not express the HLA-DR antigen, whereas pericryptal fibroblasts and most of the leukocytes of the lamina propria were strongly positive for this antigen. In the epithelial layer proliferating cells were localized exclusively in the lower part of epithelial crypts, as was the case in normal mucosa, whereas in adenomas Ki-67-positive cells were present throughout the entire height of the mucosa. Thus, in hyperplastic polyps lymphocytes are increased in the lamina propria, with a predominance of the CD4 subset in close contact with HLA-DR positive pericryptal fibroblasts.

Adenoma↗
PubMed1990

Lymphocyte subsets and HLA-DR expression in normal pancreas and chronic pancreatitis.

In an attempt to study the mechanisms leading to fibrosis in chronic pancreatitis, an in situ immunohistochemical investigation of lymphocytes and of class II major histocompatibility complex expression (HLA-DR) by epithelial cells has been designed. Samples of normal pancreas (n = 8), chronic calcifying pancreatitis (n = 4), chronic obstructive pancreatitis (n = 6), and diffuse fibrosing pancreatitis (n = 6) have been studied. In normal pancreas, T-lymphocytes were rare and were located in the epithelial layer of pancreatic ducts and in the periductal connective tissue. Duct cells were constantly HLA-DR negative. In chronic calcifying pancreatitis and chronic obstructive pancreatitis, T cells were numerous and were located around ducts and in the spreading areas of fibrous septa. In chronic obstructive pancreatitis, the duct cells strongly expressed the HLA-DR antigen. In diffuse fibrosing pancreatitis, fibrous tissue was devoid of lymphocytes and duct cells never expressed the HLA class II antigen. These results suggest that lymphocytes are involved in the fibrosing process occurring in chronic calcifying pancreatitis and chronic obstructive pancreatitis but not in diffuse fibrosing pancreatitis. The significance of de novo expression of HLA-DR antigen by duct cells is discussed.

Adult↗
PubMed1990

Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis.

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.

Adult↗
PubMed1990

Diagnostic value of serum gamma-glutamyl-transferase activity and mean corpuscular volume in alcoholic patients with or without cirrhosis.

In an attempt to assess the diagnostic values of serum gamma-glutamyltransferase (GGT) and mean corpuscular volume (MCV) variations as markers of liver disease and of abstinence in alcoholic patients, we compared 174 patients with alcoholic cirrhosis, 175 with noncirrhotic alcoholic liver disease and 67 patients with nonalcoholic cirrhosis. GGT and MCV values were checked three times, the day of admission, 7 days later, and on the last sample available during follow-up (1 to 12 months), and were compared according to the liver disease and abstinence. A decrease of GGT activity during the 1st week of hospitalization was noted in alcoholics with (-9 IU/liter) or without (-13 IU/liter) cirrhosis and not in nonalcoholic cirrhosis (+8 IU/liter), without MCV variations. During follow-up, median GGT activity was strikingly different in abstinent patients with (27 IU/liter) or without (21 IU/liter) cirrhosis and in nonabstinent patients (99 IU/liter and 123 IU/liter, respectively) (p less than 0.001). MCV decrease was noted in alcoholics whatever their abstinence or not, contrasting with the absence of decrease in nonalcoholic patients. For the diagnosis of alcoholism in cirrhotic patients, the positive predictive value (PPV) of a GGT or a MCV decrease during the 1st week of hospitalization was 0.82 and 0.78, respectively, and the negative predictive value (NPV) was 0.33 and 0.70, respectively. For abstinence during follow-up, the PPV of a GGT activity less than 50 IU/liter was 0.92 and the NPV was 0.65.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1990

[Acute tuberculous pancreatitis in a patient with acquired immunodeficiency syndrome].

The authors report a case of tuberculous pancreatitis in a 29 year old Zairan man. Serum antibodies against HIV were positive. T-lymphocyte analysis revealed 18/mm3 OKT4 with an OKT4/OKT8 ratio of 0.43. The initial examination suggested severe acute pancreatitis. Only the postmortem histopathological analysis revealed tuberculous pancreatitis, showing several miliary lesions with caseous necrosis and acid fast bacili (Ziehl stain). Subsequently, cultures (sputum, bronchoalveolar lavage, pleural effusion, ascitis) of bacili identified Mycobacterium tuberculosis. Tuberculous pancreatitis should be considered in subjects with acute pancreatitis according to the epidemiological context, once the most frequent causes of pancreatitis have been eliminated.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Nodular regenerative hyperplasia and pulmonary arterial hypertension].

Two cases of nodular regenerative hyperplasia of the liver coexisting with pulmonary hypertension are described. Regarding its low frequency, nodular regenerative hyperplasia has been found more often than expected in our series of coexisting porto-pulmonary hypertension (2 out of 14 cases, 14 percent). In our 2 cases, pulmonary symptoms occurred before or simultaneously with hepatic symptoms. The high prevalence of this association and the unusual onset setting of symptoms suggest that this association is unfortuitous. A common pathogenesis for pulmonary and hepatic lesions is discussed.

Adult↗
PubMed1989

Syngeneic T cell transfer of diabetes into NOD newborn mice: in situ studies of the autoimmune steps leading to insulin-producing cell destruction.

To overcome the limitations of in situ studies during the chronic spontaneous autoimmune process leading to insulin cell destruction and diabetes in non-obese diabetic (NOD) mice, we have developed a model of acute transfer of diabetes into healthy syngeneic newborns. The injection of 20 x 10(6) T cells from adult diabetic mice produced synchronous insulitis within 3 weeks and diabetes within 4-5 weeks in young recipients, at a time when non-injected control mice do not even exhibit histological changes in their pancreases. Sequential studies of pancreases from T cell-transferred mice showed that lymphoid infiltration was preceded by a strong tissue expression of Ia antigen which was restricted to the vessel-associated cells limiting the islet of Langerhans, and which might play a role in the recruitment of circulating T cells inside the islets. Acute destruction of most of the insulin-producing cells, leading to diabetes, could take place within a few days after insulitis had begun. A majority of the inflammatory cells were T lymphocytes, approximately 30% of which expressed interleukin 2 receptors. L3T4+ T cells largely predominated at the early phase of islet invasion whereas the proportion of Ly-2+ T cells substantially increased later when beta cell destruction occurred. In contrast, only a minority of B cells and macrophages participated to the inflammatory process. These data are in keeping with previous demonstrations that both T cell subsets contribute to the autoimmune disease. Furthermore, they suggest that beta cell injury is mediated through a cytotoxic process, which requires the sequential involvement of L3T4+ (helper) and Ly-2+ (cytotoxic) T cells.

Animals↗
PubMed1989

A longitudinal study of histologic and immunohistologic changes in an experimental model of sclerosing cholangitis.

A longitudinal study of intra and extrahepatic bile duct injuries was performed in an animal model of secondary sclerosing cholangitis induced by formalin injection into the common bile duct. Lymphocytic infiltration inside and around the bile ducts occurred seven days after injection. The disease later evolved to a fibrous cholangitis of the small bile ducts. Septal intrahepatic and extrahepatic bile duct involvement became evident three months after formalin injection. The ductular proliferation led to a progressive biliary cirrhosis with portal to portal fibrous septa. After formalin injection, bile duct cells expressed the Ia antigen in the cytoplasm and/or on the membrane of bile duct cells. The intensity of staining did not correlate with the duration or severity of the disease. Lymphocytes infiltrating into and around the bile duct were mainly T-cells. This study suggests that a local cell-mediated immune response to the injection of a toxic agent induces pathological features similar to those of sclerosing cholangitis in man.

Animals↗