In the current study we investigated 213 randomly selected Hungarian patients diagnosed with primary Sjögren's syndrome (SS). All patients were monitored for hepatitis C virus (HCV) infection and 13 were positive. We compared HCV-negative and -positive patients and made observations on how HCV infection alters the clinical and laboratory features of Sjögren's syndrome. On the basis of these findings, we conclude that HCV infection is more frequent in Hungarian SS patients than in the normal population and that the presence of this virus has a disease-modifying effect on SS.
Routine screening of Hungarian blood donors for anti-HCV commenced in the second half of 1992. Before this, five available anti-HCV ELISA kits were compared in pilot studies. In the first series, 831 random donor samples were tested by one of the tests and the 12 (1.4%) reactives found were retested by the other four. Six of the reactives were positive in all ELISA. In the second series, 325 samples from donors with elevated transaminase levels were tested by all five kits. Forty-four were found to be reactive by one or more of the tests and 32 (10%) were positive in all five assays. Samples concordantly reactive in the ELISA were positive in second or third generation recombinant immunoblot assay (RIBA 2 or RIBA 3); those that gave discordant results were indeterminate or negative. Eleven concordantly reactive samples from the second series were HCV RNA positive by polymerase chain reaction (PCR). In the first period of screening with Abbott ELISA 2 a repeat-reactivity rate of 0.98% was observed in 171,106 samples tested. Reactives were retested for supplementary testing by Wellcozyme anti-HCV. Donors reactive in both tests and strongly reactive (ELISA ratio (ER) = optical density/cut off > or = 2.5) in either of them were permanently deferred. Those negative in the supplementary ELISA or weakly reactive (1.0 < or = ER < 2.5) in both tests were subjected to RIBA 2. On the basis of RIBA, positive donors were permanently deferred, indeterminates were excluded for 1 year and negatives were readmitted. In 1992, 1,347 supplementary tests were completed; 824 (61%) of the respective donors were permanently deferred, 218 (16%) were deferred for 1 year and 305 (23%) were readmitted.
As a method of increasing supplies of varicella-zoster immunoglobulin, semi-automated screening of blood donors for high titre complement-fixing antibody was initiated. This was compared with the previously used method of donor selection based on a history of varicella or zoster in the past 6 months. About one-third of the "history" donors had titres of greater than or equal to 1 in 64 and generally these levels declined rapidly. In contrast, although only 1.1% of donors in random screening had antibody titres greater than or equal to 1 in 64, these levels usually remained high during repeated donation, enabling the production of pools entirely composed of high titre plasma packs.
As a method of increasing supplies of varicella-zoster immunoglobulin, semiautomated
screening of blood donors for high titre complement-fixing antibody was initiated.
This was compared with the previously used method of donor selection based on a history
of varicella or zoster in the past 6 months. About one-third of the ‘history’ donors had titres
of≥1 in 64 and generally these levels declined rapidly. In contrast, although only 1.1% of
donors in random screening had antibody titres ≥1 in 64, these levels usually remained high
during repeated donations, enabling the production of pools entirely composed of high titre
plasma packs.
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