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Biomedical subjects

J Slusarczyk

Publications and source records attributed to J Slusarczyk.

At least 73 records · Page 4Linked to original sources
PubMed1990

Short-term corticosteroid therapy for chronic active hepatitis B.

Seventeen patients with chronic active type B hepatitis were treated with prednisone for 4 weeks. All were initially hepatitis B e antigen (HBeAg)-positive and 14 were DNA-polymerase-positive as well. In the follow-up period of 1 year, 10 patients became persistently negative for DNA polymerase and 11 cleared HBeAg from serum, while among 17 matched untreated controls only one lost DNA polymerase and HBeAg. However, 1 patient who was initially DNA-polymerase-negative and who lost HBeAg after treatment reactivated to HBeAg after 4 months and DNA polymerase appeared in his serum. He suffered prolonged exacerbation of liver disease after treatment and died of liver failure. Short-term corticosteroid therapy may be of value in patients with chronic active type B hepatitis, however, in some cases such treatment may be disastrous.

Adult↗
PubMed1990

Cytomegalovirus infection presenting as hepatitis.

Among 530 consecutive patients hospitalized for acute hepatitis in the years 1986-1988 cytomegalovirus infection was diagnosed in 5 (0.9%). All 5 patients had symptomatic hepatitis with jaundice, 3 had pruritus. Hematological changes were relatively mild and liver function tests were not essentially different from those found in patients with hepatitis A, B, or non-A, non-B. All biochemical abnormalities returned to normal within 3-5 weeks.

Adolescent↗
PubMed1989

[Delta infection in various forms of hepatitis B].

Blood serum of 126 patients infected by HBV was studied for the presence of anti-delta antibodies. They were found in 8 patients (6.3%): in 5 out of 99 cases of chronic hepatitis in non-drug-addicts and in 3 out of 4 drug-addicts. No delta antibodies were found in 20 HBV carriers or 3 cases of supra-acute hepatitis. The disease in delta virus infected patients had a more severe course, often accompanied by the lack of active replication of HBV. The results of the examinations show to the presence of delta virus infections in Poland.

Acute Disease↗
PubMed1986

Treatment of hepatitis B surface antigen (HBsAg)-positive chronic hepatitis with recombinant leucocyte alpha-A interferon.

A total of 32 individuals with HBsAg-positive and anti-delta-negative chronic hepatitis were treated with recombinant alpha-A interferon in phase I and phase II studies. In 5/32 patients HBsAg could be eliminated and in 19/32 individuals HBeAg became negative including all those who also eliminated HBsAg. Side-effects were tolerable in most patients and were readily reversible upon discontinuation of interferon therapy. In conclusion, treatment of HBsAg-positive chronic hepatitis with interferon seems to be a promising therapeutic approach. Future studies will have to establish the optimal dose, duration of treatment and factors predicting a favourable outcome of the treatment.

Drug Evaluation↗
PubMed1986

Hepatitis B virus and delta infection in male homosexuals.

Six hundred and sixty-six homosexuals were analysed in respect of hepatitis B virus and delta infections. Evidence of ongoing or recent hepatitis B virus infection was found in 450/666 (67.6%) homosexuals; 44 were HBsAg positive. Anti-delta was found in two HBsAg-positive homosexuals. Both individuals had a non-replicative form of HBV infection and biochemical evidence of liver disease. The study confirms that HBV infection is frequent in homosexuals and indicates that delta-infection is rare in male homosexuals.

Berlin↗
PubMed1986

Lack of hepatitis B virus DNA sequences in sera from patients with acute and chronic liver diseases diagnosed as non-A, non-B-hepatitis.

The sera of 15 individuals with transfusion-associated acute or chronic non A, non B hepatitis, which lacked hepatitis B virus markers, were tested for hepatitis B virus DNA by dot blot hybridization test. Three sera of two patients positive in this test, however, also gave positive results when the labeled plasmid was used as probe instead of labeled HBV-DNA, indicating false positive results in the initial test. In conclusion, the data indicated that sera of patients with confirmed non A, non B hepatitis do not contain DNA-sequences in the serum hybridizing with HBV-DNA.

Adolescent↗
PubMed1986

[Detection and significance of HBsAg associated receptors for polymerized human serum albumin in acute hepatitis B virus infection].

Receptors for polymerized human serum albumin (R-pHSA) may play a role in the attachment of hepatitis B virus (HBV) to hepatocytes. Therefore, we evaluated the incidence and prognostic value of R-pHSA in acute hepatitis B virus infection. High titers of R-pHSA were found in 12/12 patients with HBeAg positive acute hepatitis B (log2-Titer: 8.5 +/- 1.5). Titers for R-pHSA and HBsAg correlated closely. Furthermore, R-pHSA occurred (log2-titer: 6.5 +/- 1.5) in 10/10 patients with HBeAg positive chronic active hepatitis B (CAH-B). In the course of HBV infection, R-pHSA were eliminated earlier than HBsAg. 4/20 patients which were asymptomatic HBsAg carriers had high titers of R-pHSA in correlation to the histological findings of CAH-B. Asymptomatic HBsAg carriers which were R-pHSA negative had a normal liver histology. R-pHSA were found to be an early prognostic marker in acute hepatitis B infection.

Carrier State↗
PubMed1985

Etiopathogenetic aspects of hepatitis A. I. Excretion of hepatitis A virus, biochemistry of liver function, and humoral immune response in patients with hepatitis A on admission to hospital.

The excretion of hepatitis A virus (HAV) in stools from 30 patients with clinically overt hepatitis A infection on the day of their admission to the hospital was determined and compared with the dynamics and values of biochemical indices of hepatocyte injury as well as with the immune response to HAV. Virus was found in 16 out of 30 stools (53%) collected within 1 week after the appearance of clinical symptoms. In sera obtained on the day of hospitalization both IgM and IgA anti-HAV were detected in all of the 30 patients, while IgG anti-HAV were found in 20 (67%). There was a correlation between HAV excretion and increasing SGPT upon admission to hospital, while the level of SGPT or bilirubin as well as presence or absence of IgG anti-HAV did not correlate with excretion of HAV. HAV from stools was characterized morphologically and physicochemically. The majority of particles visualized by immune electron microscopy had electrondense appearance, while electron-lucid particles were only occasionally encountered. Isopycnic banding of HAV in CsCl revealed a broad range of densities with HAV activity. Rebanding of pooled fractions containing HAV revealed peak amounts of the virus in fractions with densities 1.32-1.33 gm/cm3.

Adolescent↗
PubMed1985

Association of hepatitis Be antigen (HBeAg) with the core of the hepatitis B virus (HBcAg).

Three substances (pronase E, sodium dodecylsulfate (SDS) and guanidine hydrochloride) with different chemical actions partially convert HBcAg to HBeAg. This process retains the integrity of the HBcAg particle, which was not different between HBcAg subpopulations, and does not generate HBcAg or HBeAg sub-units. DNA polymerase activity was destroyed by SDS and guanidine hydrochloride, but not by pronase E. Serum HBeAg could not be converted into HBcAg, suggesting that this might be an irreversible process. The data are consistent with the assumption that HBcAg and HBeAg are coded for by the same gene (C gene of the HBV-DNA).

DNA-Directed DNA Polymerase↗
PubMed1984

Etiopathogenetic aspects of hepatitis A II. Specific and nonspecific humoral immune response during the course of infection.

The anti-HAV humoral immune response in the IgM, IgA, and IgG classes was analyzed weekly in 35 patients with clinically overt hepatitis A during the time of their hospitalization and 2-3 years afterward. In parallel, the dynamics of total immunoglobulins and complement C3 component (C3) levels were determined. The results suggest that the appearance of class-specific anti-HAV is compatible with the course of primary humoral immune response, with IgM and IgA anti-HAV, providing immunity in the early and intermediate phases of the infection, and IgG anti-HAV, providing immunity in the later phase. The overall appearance of anti-HAV, total immunoglobulins, and C3, do not support the view that liver injury is mediated by the humoral immune mechanisms. Instead, the hepatocyte damage is probably caused by direct viral cytotoxicity. This hypothesis is supported by a case of hepatitis A in a patient under immunosuppressive treatment.

Adolescent↗