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Biomedical subjects

F Caredda

Publications and source records attributed to F Caredda.

At least 37 records · Page 2Linked to original sources
PubMed1986

Detection and further characterization of a newly described microsomal autoantibody associated with chronic delta infection.

Sera from 162 patients with acute or chronic hepatitis and from patients with autoimmune diseases have been investigated for autoantibodies by indirect immunofluorescence on human and animal tissues. A small proportion (14.2%) of young patients with chronic delta hepatitis has been found positive for cytoplasmic staining which was maximal in hepatocytes and renal proximal tubules. This autoantibody has been found to react with microsomal antigenic determinant different from the classic liver-kidney microsomal LKM antigen as demonstrated by fluorescence absorption experiments with purified subcellular organelles and by fluorescence-blocking tests. The microsomal autoantibody displayed also organ and species-specificity different from those shown by the LKM-positive sera. The positive patients showed persistence of the microsomal autoantibody during the follow-up without other serological markers of autoimmunity. There was no evidence of a particular course of chronic delta hepatitis in patients positive for the microsomal autoantibody.

Adolescent↗
PubMed1985

Clinical significance of antibody to the hepatitis delta virus in symptomless HBsAg carriers.

Antibody to the hepatitis delta virus (anti-delta) was detected in 112 out of 2487 (5%) individuals fortuitously found to have the hepatitis B surface antigen (HBsAg) in the blood. Liver function was impaired in 38% (43 of 112) of the anti-delta-positive carriers but in only 9% (215 of 2375) of the anti-delta-negative subjects (p less than 0.001). Liver biopsy specimens were obtained from 31 antibody-positive and 97 antibody-negative subjects with impaired liver function. Important histological changes were observed in 61% of the 31 antibody-positive carriers (7 chronic active hepatitis, 4 active cirrhosis, 8 inactive cirrhosis) but in only 19% of the 97 antibody-negative carriers (p less than 0.001). The presence of anti-delta in serum identifies a subpopulation of apparently healthy HBsAg carriers whose risk of underlying liver disease is four times higher than that in the ordinary carrier. The identification of anti-delta in a symptom-free HBsAg carrier with abnormal liver function is thus an indication for a diagnostic liver biopsy.

Antibodies, Viral↗
PubMed1985

Hepatitis B virus-associated coinfection and superinfection with delta agent: indistinguishable disease with different outcome.

Markers of hepatitis B virus (HBV) and delta agent were prospectively tested in sera of 107 intravenous drug abusers with acute hepatitis positive for hepatitis B surface antigen (HBsAg) associated with delta infection and compared with the findings in addicts with acute classical hepatitis B. On the basis of the presence and titer of IgM antibody to hepatitis B core antigen, 86 of the addicts with delta infection had simultaneously acquired HBV and delta agent, and 21 were chronic carriers of HBsAg experiencing acute delta superinfection. The frequencies of biphasic and severe hepatitis were significantly higher (P less than .05) in delta agent-infected patients than in controls, but the acute clinical and biochemical features of the two varieties of delta disease were not distinguishable. However, in analogy to the clinical outcome of classical hepatitis B, all patients with nonfatal acute HBV/delta coinfection had self-limited illness, whereas 20 of 21 HBsAg carriers superinfected by delta agent developed chronic active hepatitis.

Acute Disease↗
PubMed1985

Attempt to treat acute type B hepatitis with an orally administered thymic extract (thymomodulin): preliminary results.

A double-blind trial with thymomodulin (TM) was performed in a consecutive series of 50 inpatients affected with acute type B hepatitis. Twenty-six randomly selected patients received TM (Leucotrofina, Ellem), 1 ampoule b.i.d. per os for 30 days, and 24 patients received the same amount of placebo for the same period. TM-treated patients showed accelerated AST and ALT decrease and an earlier HBsAg clearance. However, only the difference in ALT decrease was statistically significant in comparison with the controls (p less than 0.02). Before the treatment was started, lymphocyte subsets, as determined by monoclonal antibodies, showed a different pattern in the two groups despite strict randomization. Nevertheless, by the end of the trial, mean T4+/T8+ ratios were increased in the treated group, but remained unchanged in the control group. The trends in the two groups were significantly different (p less than 0.005). Further information is expected from a long-term follow-up.

Acute Disease↗
PubMed1984

The aetiology of acute hepatitis in Zimbabwe.

The cause of acute viral hepatitis in 141 patients admitted to both Infectious Diseases Hospitals in Harare (Zimbabwe) was hepatitis A in 44, hepatitis B in 86 and hepatitis Non-A Non-B in 11. The wide distribution of hepatitis A and B viruses and early exposure to both in Zimbabwe are shown by the high positivity rate for anti-HAV antibody in patients under 10 years old (87.5%) and for anti-HBs antibody in patients over 20 (60%). Among the 86 hepatitis B cases, e and delta systems were also investigated: 66 patients (76.5%) were HBeAg positive, six (7%) anti-HBe positive and 14 (16.5%) negative for both; only one was anti-delta positive. Two cases of fulminant liver failure (both occurring in HBsAg and anti-HBc IgM positive, but delta-markers negative patients) and five cases of hepatoma (only one of whom was negative for all HBV markers) are described.

Acute Disease↗
PubMed1984

Prolonged course and relapses of acute type A hepatitis.

Sixty-nine consecutive patients with acute type A hepatitis were followed-up to establish the natural history of the disease. Illicit drug abusers were not included in this study. 19% (13/69) of the patients at 6th month, and 6% (4/69) at 12th month showed aminotransferase (ALT) values at least two folds the upper levels. The histological examinations performed in 5 of these cases suggest that persistence of abnormal ALT levels may be related to a misdiagnosed chronic liver disease preexisting the acute type A hepatitis. Three of the 69 patients had a relapsing hepatitis with two peaks of serum ALT 6-8 weeks apart. The illness resolved uneventfully in all these patients. The exclusion of exposure to liver toxins such as alcohol or drugs, as well as other known hepatitis virus infection in these cases, suggests that the two distinct episodes of hepatitis could be the result of the sequential infection of hepatitis A and non-A, non-B viruses.

Acute Disease↗
PubMed1984

Polymorphonuclear leucocyte function during acute viral hepatitis.

Polymorphonuclear (PMN) phagocytosis was tested in three groups of 12 patients (non drug-addicts) hospitalized for acute A, B and non-A, non-B hepatitis. The same test was performed in 12 parenteral drug-addicts (P.D.A.) with non-A, non-B hepatitis, in 12 P.D.A. with type B hepatitis and in 30 P.D.A. without evidence of acute hepatitis. Percent of phagocytosis was evaluated at time of admission to hospital, at discharge and three months after the acute episode. A statistically significant reduction of phagocytosis was present in each of the non-addicts group at time of admission to hospital. At the discharge this reduction was confirmed for type B and non-A, non-B hepatitis, whereas an improvement was noted for type A hepatitis. Control tests carried out 3 months later evidenced that also in patients affected with type B and non-A, non-B hepatitis the percentages of phagocytosis had reached almost normal values. An increased percent of phagocytosis resulted from incubation of patients' PMN with normal human serum. Among drug-addicts the percentages of phagocytosis do not differ from the data recorded in non-addicts patients during the acute stage of the disease. However, three months after the acute episode, a deficit of phagocytic activity was still present in drug-addicts. These data would support the hypothesis that a serum factor impairing the PMN phagocytosis in acute hepatitis is present. Circulating immune complexes were found in the same sera. They might play an important role in inhibitory effect on neutrophils phagocytic activity.

Acute Disease↗
PubMed1984

Acute type B hepatitis in parenteral drug-addicts (PDA): prognostic value of circulating HBsAg/IgM complexes.

Fifty-three parenteral drug-addicts with acute viral hepatitis type B were tested by a solid-phase radioimmunoassay for circulating HBsAg/IgM complexes in the acute phase and in the follow-up. Among the 47 recovered patients HBsAg/IgM complexes were either absent from the onset of the disease, or disappeared from serum within 4 weeks of admission, long before HBsAg had cleared or serum alanine aminotransferase has returned to normal. On the contrary, HBsAg/IgM complexes persisted indefinitely among the 6 patients who developed a chronic HBsAg-positive hepatitis. These results indicate that sequential serum testing for HBsAg/IgM complexes might be of value in predicting the long-term outcome of acute type B hepatitis of parenteral drug-addicts.

Acute Disease↗
PubMed1982

Influence of delta infection on severity of hepatitis B.

The prevalence of serum markers of primary delta infection was determined in 532 patients with acute benign hepatitis B seen in Italy, and in 111 patients with fulminant hepatitis B seen in Italy, France and England. Patients with fulminant hepatitis had significantly higher prevalence of delta markers (43/111, 39%) than did those with benign hepatitis (101/532, 19%). In 25 of the 43 patients with delta-positive fulminant hepatitis, serum markers indicated a primary hepatitis B infection while in the remaining 18, IgM antibody to hepatitis B core antigen was absent, indicating that hepatitis B preceded superinfection with the delta agent. The increased morbidity of HBsAg hepatitis with delta infection may result from the cumulative simultaneous exposure to hepatitis B virus and delta, or from superinfection of HBsAg carriers with delta.

Acute Disease↗