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Biomedical subjects

R de Franchis

Publications and source records attributed to R de Franchis.

101 records · Page 6Linked to original sources
PubMed1985

In situ identification of immune competent cells in gastrointestinal mucosa: an evaluation by immunoelectronmicroscopy.

The in situ identification of lymphocyte subpopulations by means of immunopathological techniques using specific monoclonal antibodies provides a tool for the study of the gastrointestinal-associated lymphoid tissue (GALT) in health and disease. In this field, monoclonal antibodies have been applied previously using light microscopy and either immunofluorescence or immunoperoxidase; however, these techniques are not sensitive enough to allow precise evaluation of localization of labelling. We describe an immunoelectronmicroscopic method, which defines labelling specificity, since it allows the identification of cells by immunophenotype labelling and ultrastructural markers simultaneously. This in turn allows a better evaluation of the labelled cells and of the relationship between labelled and unlabelled cells. The main features of the method are the use of fresh tissue samples, fixing in paraformaldehyde CaCl2, and the coupling of the immune reaction to an amplification system (avidin-biotin-peroxidase complex). The technique yields a good preservation of cellular ultrastructure, together with a strong and specific immunolabelling. Our results confirm the high specificity of monoclonal antibodies when applied to immunopathology techniques. We confirm the pattern of distribution of various lymphocyte subsets in the jejunal mucosa described by other authors by light microscopy.

Antibodies, Monoclonal↗
PubMed1982

Persistence of circulating HBsAg/IgM complexes in acute viral hepatitis, type B: an early marker of chronic evolution.

Serial serum samples from 110 patients with acute viral hepatitis type B were tested for HBsAg/IgM complexes by a newly developed solid-phase radioimmunoassay. In 102 patients the infection resolved and they recovered from the disease. In these patients, HBsAg/IgM complexes were either absent from the outset of disappeared from serum within four weeks of admission, long before HBsAg had cleared or serum alanine aminotransferase had returned to normal, 8 patients progressed to chronic HBsAg carrier state and chronic liver disease. In these patients, HBsAg/IgM complexes were detectable in the serum on admission, and never disappeared. These results indicate that persistence of circulating complexes containing HBsAg and IgM after the early phase of acute viral hepatitis type B is a predictor of disease chronicity. As early as the fifth week of illness those in whom chronic liver disease developed could be distinguished from those who recovered.

Adolescent↗
PubMedDate not supplied

Intrafamilial spread of hepatitis B virus infection. (Role of chronic hepatitis and of the hepatitis B e antigen).

Two hundred and forty household contacts of 85 chronic HBsAg carriers were studied to assess the relationship between liver histology and 'e' antigen or antibody positivity in the index carrier, and evidence of HBV infection within the family. Liver biopsy results were available in 54 index carriers. The prevalence of HBsAg and anti-HBs in the families of 29 carriers with chronic hepatitis and 25 carriers with either a normal liver or minimal inflammatory changes was not significantly different. Serum from 72 index carriers was available for HBeAg and anti-HBe testing. The prevalence of HBsAg and anti-HBs in the families of 5 HBeAg positive carriers, 59 anti-HBs positive subjects, and 8 carriers negative for both HBeAg and anti-HBe was again not significantly different. Infectivity of a carrier thus does not appear to correlate either with histological evidence of liver damage or with the 'e' antigen or antibody positivity of the carrier.

Adult↗
PubMedDate not supplied

Case-control study of hepatitis B virus infection in chronic liver disease and hepatocellular carcinoma.

The prevalence of serum hepatitis B virus markers was studied in three groups of age- and sex-matched patients: a. 31 patients with liver cirrhosis and hepatocellular carcinoma (c-HCC); b. 31 patients with chronic liver disease (CLD) and c. 62 hospitalized control subjects. The overall exposure rate to the hepatitis B virus was 90% in c-HCC, 80% in CLD and 58% in control subjects. The prevalence of hepatitis B surface antigen (HBsAg) was 29%, 13% and 1.6% in the three groups, respectively. The prevalence of hepatitis B surface antibody was significantly lower in c-HCC (9.6%) than CLD (42%) and control subjects (40%). The serological evidence of continuous viral replication (HBsAg positivity or isolated high titre hepatitis B core antibody positivity) was more common in c-HCC (39%) than CLD (12%) and control subjects (1.6%). The prevalence and patterns of aggregation of serum hepatitis B virus markers were similar in the 31 patients with c-HCC and in 11 patients with HCC without concomitant liver cirrhosis (n-HCC). In conclusion, the overall exposure rate to the hepatitis B virus is similar in c-HCC and CLD. However, serological evidence of continuous viral replication is more common in the former group. A defective clearance of the hepatitis B virus in hepatocellular carcinoma is a possible explanation of the phenomenon. The strength of the association between hepatitis B virus infection and hepatocellular carcinoma appears to be similar in c-HCC and n-HCC.

Adult↗
PubMedDate not supplied

Diagnostic value of serum cholylglycine radioimmunoassay in chronic asymptomatic HBsAg carriers.

The correlation between histological liver abnormalities and fasting serum cholylglycine levels was investigated in 75 chronic asymptomatic HBsAg carriers with normal conventional liver tests, to clarify whether serum CG radioimmunoassay could help in distinguishing the carriers with histological liver damage from those with normal histological findings. Mean (+/- SEM) fasting serum CG levels were 11.6 +/- 1.5 micrograms/dl in 56 carriers with normal liver histology, 14.6 +/- 4.2 micrograms/dl in 16 subjects with CPH and 95.6 +/- 54 micrograms/dl in three carriers with CAH. The incidence of abnormal values (greater than 40 micrograms/dl) among carriers with CAH (66%) was significantly higher than in the other two groups (1.8 and 12.5%, respectively). It is concluded that, among chronic asymptomatic HBsAg carriers with normal conventional liver tests, those who show abnormal serum CG levels are likely to have severe histological damage. This justifies the inclusion of CG radioimmunoassay in the routine follow-up of these subjects. The occurrence of false-positive and false-negative results must be considered if the test is used as an aid in the selection of patients for liver biopsy.

Carrier State↗
PubMedDate not supplied

Prevalence of duodenal and jejunal lesions in dermatitis herpetiformis.

Sixty-eight patients with dermatitis herpetiformis underwent jejunal suction biopsies and/or multiple endoscopic duodenal biopsies to evaluate the incidence of small bowel mucosal atrophy and to compare the diagnostic yield of the two methods. Small bowel function tests were also performed to evaluate the extent of functional impairment. Small bowel lesions were observed in 89.4% of jejunal suction biopsies and in 100% of endoscopic duodenal biopsies. Of the 10 patients who underwent both procedures, one had lesions only in the duodenum, one had more severe lesions in the duodenum than in the jejunum, while the remaining 8 patients showed identical lesions at both sites. The 1-h blood d-xylose test after a dose of 5 g proved more sensitive than xylosuria or serum folic acid assay in detecting subclinical malabsorption. Finally, histological features of gluten-sensitive enteropathy can be found in nearly 100% of patients with dermatitis herpetiformis. Upper gastrointestinal endoscopy with duodenal biopsies is at least as sensitive as jejunal suction biopsy in assessing small bowel involvement in dermatitis herpetiformis.

Adolescent↗
PubMedDate not supplied

Eradication of esophageal varices by endoscopic sclerotherapy: how much is enough?

To clarify if complete eradication of varices from the lower esophagus by endoscopic sclerotherapy is really essential to prevent rebleeding, or if reduction of varices below a certain size can be considered a sufficient result, we compared the fate of 72 patients in whom sclerotherapy was stopped after one of the following endoscopic endpoints was reached: complete eradication (15 patients, group 1), partial eradication with residual small white varices (32 patients, group 2), and partial eradication with residual small blue varices (25 patients, group 3). The incidence of variceal recurrences and recurrent bleeding over a median follow-up of 17 months after stopping sclerotherapy did not differ significantly in the three groups. Analysis of the time course of variceal recurrences showed that the recurrence-free interval was almost identical in group 1 and group 2 patients (13 and 14 months, respectively). Group 3 patients had a shorter recurrence-free interval (8.3 months), but the difference was not statistically significant. We conclude that sclerotherapy can be stopped safely when either complete eradication or reduction of varices to small white columns is obtained.

Actuarial Analysis↗
PubMedDate not supplied

Medical treatment of portal hypertension.

Prevention of the first variceal haemorrhage should start when the patients have developed medium sized to large varices. Non-selective beta-blockers are the first-line treatment; band ligation is roughly equivalent to beta-blockers and is the first choice for patients with contraindications or intolerance to beta-blockers. Treatment of acute bleeding should aim at controlling bleeding and preventing early rebleeding and complications, especially infections. Combined endoscopic and pharmacological treatment with vasoactive drugs can control bleeding in up to 90% of patients. All patients who survive a variceal bleed should be treated with beta-blockers or band ligation to prevent rebleeding. All patients in whom bleeding cannot be controlled or who continue to rebleed can be treated with salvage TIPS or, in selected cases, with surgical shunts. Liver transplantation should be considered for patients with severe liver insufficiency in which first-line treatments fail.

Acute Disease↗