[Viral hepatitis of the delta type].
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Biomedical subjects
Publications and source records attributed to T Laskus.
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The prevalence of hepatitis delta virus (HDV) infection was studied in 140 unselected intravenous drug addicts whose sera were drawn between 1985 and 1986 and in 100 addicts from whom sera were obtained between 1988 and 1989. It was observed that 1.8% of those positive for hepatitis B virus (HBV) markers from the earlier period and 23.2% of those from the later period had detectable anti-delta antibodies. Among drug addicts referred with acute or chronic HBV infection, the first evidence of HDV infection was found in 1986. We conclude that HDV infection was introduced into the Warsaw drug community in the mid 1980s.
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This study evaluated the epidemiology and impact of hepatitis G virus (HGV) infection in patients with chronic hepatitis B and C. Serum samples were obtained from 128 consecutive untreated patients with chronic hepatitis B (72 cases) or C (56 cases). The presence of HGV RNA was determined by PCR amplification of the 5'untranslated region; the sensitivity of the assays was ten template copy equivalents. The prevalence of HGV RNA in hepatitis B and C was found to be 25% and 34%, respectively. HGV-positive and HGV-negative patients did not differ with respect to risk factors for infection, age, sex, or alanine aminotransferase activity. Similarly, there was no difference in the severity of liver disease, as assessed with HAI score. In conclusion, we found a very high prevalence of HGV infection in chronic hepatitis B and C patients in Poland. Nevertheless, no evidence was found that HGV coinfection has any impact on the severity of the underlying disease.
Prevalence of HIV-Ag in both serum and CSF has been determined in 19 HIV infected patients, including 7 patients without any symptoms or only generalized lymphadenopathy, 5 patients with ARC and 7 patients with AIDS. The results have been correlated with clinically evident neurological disorders. HIV-Ag have been detected in 9 out of 12 patients with ARC (AIDS Related Complex) and AIDS. In 8 of them neurological disorders have been present. Out of the remaining 7 patients in only one HIV-Ag has been detected in CSF (p < 025). No correlation between the presence of HIV antigen in CSF and serum has been noted.
Lymphocytes CD8+ have been assayed prospectively in 245 individuals infected with HIV. Percentage and number of CD8+ have been nearly two-fold higher in asymptomatic patients or patients with lymphadenopathy than those in the control group. The number of CD8+ lymphocytes has been rapidly decreasing parallel to the progression of HIV (ARC and AIDS), while their percentage has increased--however insignificantly. There has been a positive correlation between the number of CD4+ and CD8+ cells and all clinical stages of HIV infection.
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In the years 1980-1988 twenty five drug addicts were identified among 1841 patients hospitalized for acute hepatitis in the Dep. of Hepatology at the Institute of Infectious and Parasitic Diseases in Warsaw. 15 drug addicts had hepatitis B and 10 had hepatitis A. It was found, that the course of acute type B hepatitis was milder in drug addicts, than among control group consisting of non-addicts.
Non-A, non-B hepatitis has been diagnosed in 12 blood donors in a plasmapheresis unit. The course of the disease has been symptomatic, accompanied by jaundice, fatigue, and nausea in 8 cases, and subclinical in the remaining 4 patients. Nine patients were followed-up to 2 years and only 2 patients liver biochemical tests were normalized permanently. The biopsies performed, a year after the acute phase of hepatitis period revealed chronic active disease in patients, chronic persistent hepatitis in 2 patients, acute hepatitis in one, and normal liver in one patient. Repeated liver biopsies, performed one year later, have basically shown similar lesions except one patient in whom chronic active hepatitis progressed to incipient liver cirrhosis. No symptoms of the disease have been usually noted in patients with chronic form of the disease, and liver function tests have occasionally been normal.
Chromosomal analysis has been carried out in 4 patients with the symptoms of hepatic coma. An analysis included lymphocytes cultured from peripheral blood. Chromosomal disorders have been assessed with two techniques: structural chromosomal aberrations test, and sister chromatid exchange (SCE) test. It has been shown that the extend of chromosomal damage in the form of the gaps, breaks, acentric chromosomes as well as the presence of ring and dicentric chromosomes, and micronuclear cells have been higher in the examined patients. Such changes may evidence DNA repair disorders, and the presence of micronuclear forms may seem an unfavourable prognosis.
Blood serum concentration of procollagen type III peptides was assayed in 37 patients with chronic active hepatitis, 14 patients with persisting chronic hepatitis, and 11 normal subjects. Mean concentration of these peptides was significantly higher in patients with chronic active hepatitis than in those with persisting chronic hepatitis (25.6 +/- 11.5 ng/mL vs. 14.0 +/- 4.5 ng/mL; p < 0.001), and in individuals without lesions to the liver (25.6 +/- 11.5 ng/mL vs. 12.5 +/- 2.9 ng/mL; p < 0.001). Blood serum concentration of procollagen type III peptides may be helpful in the differential diagnosis of hepatitis.
A case of a 36-year male patient with chronic active hepatitis B is described. A short-term prednisone therapy resulted in the exacerbation of the disease leading to hepatic failure and patient's death. A short-term corticotherapy in some patients with chronic active hepatitis B may prove fatal.
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