11 research outputs found
Anticardiolipin antibodies in chronic hepatitis B and chronic hepatitis D infection, and hepatitis B-related hepatocellular carcinoma. Relationship with portal vein thrombosis
Objective To assess the presence of anticardiolipin antibodies (ACAs) in
patients with chronic hepatitis B virus (HBV) infection, chronic
hepatitis D virus (HDV) infection and HBV-related hepatocellular
carcinoma (HCC) and to associate this with the incidence of portal vein
thrombosis (PVT) in HCC patients.
Patients and methods Sixty-five cirrhotic patients with HBV-related HCC,
28 naive patients with chronic HBV infection and 14 naive patients with
chronic HDV infection were enrolled prospectively in the study.
Thirty-two healthy blood donors were used as controls. The ACAs
(immunoglobulin G and immunoglobulin M) were measured using an
enzyme-linked immunosorbent assay system. Statistical analysis used
non-parametric methodology (chi-squared test Student t-test and Fisher
exact test P value <0.05).
Results Eleven of the 65 patients with HCC (16.9%) showed a positive
ACA titre and 22 of the patients (34%) had PVT. Of these patients,
eight (36%) had a positive ACA titre. In contrast from the 43 patients
without PVT, only three (11%) showed a positive titre. From the 28 HBV
patients, six (21.5%) had a positive ACA titre, and six out of 14
(42.8%) HDV patients also showed a positive ACA titre. Three of the six
ACA positive HBV patients presented an extrahepatic manifestation of the
disease. One out of 32 control patients (3%) had positive ACAs.
Conclusion Both chronic HBV and chronic HDV infections are potent
stimulants for the production of ACAs. The presence of ACAs in a great
proportion of HBV-cirrhosis-related HCC patients with PVT suggests their
possible participation in thrombotic mechanisms and in the
hypercoagulable state that occurs in advanced liver disease and HCC
Cyclosporin A inhibits growth of autocrine tumour cell lines by destabilizing interleukin-3 mRNA
In T cells, cyclosporin A (CsA) exerts its immunosuppressive effect by preventing transcriptional induction of the expression of interleukin(IL)-2. This is achieved by a mechanism that involves binding of a CsA-cyclophilin complex to calcineurin, which in turn inhibits the phosphatase-controlled translocation of transcription factor NFAT to the nucleus. We have previously identified IL-3 as an autocrine oncogenic regulator in tumour cell lines generated by introducing the v-H-ras oncogene into IL-3-dependent mast cells. Here we report that CsA specifically blocks autocrine tumour cell growth. The mechanism involves down-regulation of IL-3 expression by destabilization of the messenger RNA and requires ongoing transcription. Transcripts from exogenous IL-3 genes lacking the (A+U)-rich element (ARE) in the 3' untranslated terminal repeat could not be destabilized, suggesting that at least part of this sequence, which is known to mediate decay of short-lived mRNA, participates in a CsA-sensitive regulatory mechanism