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Biomedical subjects

A Schattner

Publications and source records attributed to A Schattner.

At least 91 records · Page 5Linked to original sources
PubMed1992

Poliovaccines and the course of systemic lupus erythematosus--a retrospective study of 73 patients.

Flare in disease activity occurred in four out of 73 patients (5%) under the age of 45 with systemic lupus erythematosus (SLE) who were immunized against poliomyelitis in a nationwide campaign following the Israeli outbreak of 1988. The flare appeared within 3 months of the immunization, whereas in 37 matched SLE patients who were not immunized, the disease remained stable in the same period. Both oral live-attenuated (OPV) and injected killed poliovaccines (IPV) were implicated in the flares (1/24 and 3/49 patients, respectively). The study was based on detailed questionnaires and confirmed by telephone calls and examination of the patients' hospital medical records. Poliovaccines, including IPV, should not be administered to SLE patients without careful consideration and a further prospective study should be undertaken to determine their safety in SLE.

Adult↗
PubMed1992

Case report: fatal seronegative rickettsial infection diagnosed by the polymerase chain reaction.

A previously healthy man presented with a five day history of high fever and headache, later followed by rash and the appearance of jaundice. On the second hospital day, he suddenly developed seizures, lapsed into a coma, and died. Polymerase chain reaction (PCR) amplification revealed a 434 base pairs DNA fragment common to the genome of typhus and spotted fever group rickettsiae in the patient's blood (estimated at about 1 x 10(2) organisms/ml), and to a lesser degree in the cerebrospinal fluid. However, serological tests for rickettsiae remained negative. PCR techniques may confirm the diagnosis at an early stage, even though the rickettsemia may be minimal and the patient seronegative.

DNA, Bacterial↗
PubMed1992

The quality assurance committee in a general hospital: its use in improvement of the medical record.

A twice-yearly audit of a sample of medical records from each department of a general hospital was initiated by a quality assurance committee and pursued for 8 years. Missing entries that were considered obligatory for good medical performance of each service were identified, and the results (expressed as percent of missing entries of the total) were communicated in graphic form to the specific departments and the senior staff of the hospital. This approach led to an improvement in the medical records (decrease of missing entries), which may reflect a higher quality of medical care. Thus, a sequential audit of medical records by a quality assurance committee may constitute a simple and effective method of monitoring and improving physicians' knowledge and performance.

Hospitals, District↗
PubMed1992

[Cytokines in anorexia nervosa--nutritional or neuroimmunal changes?].

Natural cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor (TNF-alpha) by mononuclear cells in vitro, and PHA-induced interferon (IFN-gamma) production were examined by standard methods in 14 females with anorexia nervosa (AN) and marked weight loss and in 16 normal matched controls. The results were confirmed by neutralization with monoclonal antibodies. In the anorectic patients there was a significant increase in TNF production (16 +/- 5 vs 4 +/- 3 mu/ml), and depressed CMC (4 +/- 2 vs 10 +/- 3 lytic units per 50/10(6) cells) and IFN-gamma production (172.5 +/- 25 vs 367 +/- 34 mu/ml). Following successful refeeding and nutritional rehabilitation, all values returned to normal. Thus there are changes in cytokines and defective natural cytotoxicity in AN, apparently related to undernutrition and not to neuroimmunomodulation. The increased TNF-release may further suppress food intake and enhance tissue catabolism, suggesting that nutritional rehabilitation should be the earliest therapeutic goal in anorexia nervosa.

Anorexia Nervosa↗
PubMed1991

Autoantibodies in male homosexuals and HIV infection.

We have used ELISA to study the frequency of autoantibodies to several antigens in the serum of 17 male homosexuals (MHS) negative for HIV (HIV-), 11 asymptomatic HIV seropositive MHS (HIV+) and patients with ARC (N = 15) or AIDS (N = 13), and compared them to 20 matched healthy heterosexual controls. Serum antibody binding to histones, cardiolipin, ss-A, ss-B and Sm was found to be significantly higher in each of the MHS groups studied as compared to controls (P less than 0.001), and was also increased in the HIV+ patients vs. the HIV- group (P less than 0.05). In contrast, no increase in autoantibodies to ss-DNA, ds-DNA, poly(I), poly(G) or RNP were found in any of the groups tested. These results enlarge the spectrum of autoimmunity previously reported in HIV infection and identify a similar pattern to a lesser degree, already present in HIV- MHS, suggesting a role for HIV or concomitant virus infections in its pathogenesis.

AIDS-Related Complex↗
PubMed1991

Sequential serological studies of homosexual men with and without HIV infection. Epstein-Barr virus activation preceding and following HIV seroconversion.

Viral cofactors may be important in the pathogenesis of HIV infection and the development of AIDS, but their role is still imperfectly understood. Sequential serological studies were performed in a cohort of 100 homosexual men and 70 matched healthy controls over a mean period of 4 years. Of the patients, 18 were found to be HIV+ on admission to the study and 15 seroconverted to HIV+ during the follow up (seroconversion group). Serum antibodies of both IgG and IgA isotypes against Epstein-Barr virus (EBV) and cytomegalovirus (CMV) were determined. IgG antibodies indicate past infection, while a marked increase in IgG titre or a positive IgA titre were taken to indicate active infection or reactivated latent infection. EBV and CMV infections were about two to four times more prevalent in the homosexual men both HIV- and HIV+, compared with controls. Active infections were increased in the homosexual men and particularly in the HIV+ patients. The seroconversion group revealed activation of both EBV and CMV following HIV infection. When the antibody profile of seroconverting patients at the time preceding seroconversion was compared with a matched group of 39 homosexual men who remained HIV-, no change was found in CMV antibodies, but four out of 15 (26.6%) of the patients had high titres of anti-EBV IgA preceding seroconversion, as compared with only one out of 39 (2.6%) of HIV- homosexual men (P less than 0.05). This suggests a role for EBV reactivation in the pathogenesis of HIV infection in some patients.

Antibodies, Viral↗
PubMed1991

Terminal differentiation of myeloleukemic M1 cells induced by IL-6: role of endogenous interferon.

During terminal differentiation of myeloleukemic M1 cells triggered by IL-6, an induction of IFN-activated genes, such as IRF-1, class I MHC, and (2'-5')-A synthetase, is observed. Antibodies to murine type I IFN, inhibit most (2'-5')-A synthetase induction but do not inhibit IL-6-induced growth-arrest and differentiation. IL-6 induction of (2'-5')-A synthetase subforms, however, differs from that of IFN. IL-6 in fact induces a cell surface form of (2'-5')-A synthetase that is not induced by IFN.

2',5'-Oligoadenylate Synthetase↗
PubMed1991

Tumor necrosis factor in familial Mediterranean fever.

PURPOSE: The pleiotropic inflammatory effects of tumor necrosis factor (TNF) prompted a study of this cytokine in familial Mediterranean fever (FMF), a recurrent polyserositis of unknown etiology. PATIENTS AND METHODS: Thirty-six asymptomatic and 24 patients with acute FMF were studied and compared with 20 matched healthy subjects. TNF levels were measured by bioassay in the plasma and in supernatants of peripheral blood mononuclear cells (PBMC) incubated alone or with an inducer (lipopolysaccharide, phytohemagglutinin [PHA], or Sendai virus). Cytotoxicity could be abolished in all cases by preincubation with monoclonal anti-TNF-alpha antibodies. RESULTS: No TNF was found in plasma and non-induced PBMC supernatants. Induced TNF production was markedly decreased in patients with acute FMF and increased in asymptomatic FMF patients to levels over those of control subjects (p less than 0.05). Thus, PHA-induced TNF levels were 4 U/mL in patients with acute FMF, 25 U/mL in asymptomatic patients, and 14 U/mL in healthy control subjects (median values), and the other inducers gave similar results. Retesting of patients first studied during an acute episode when their disease was quiescent also revealed a fivefold increase in TNF production. These results were independent of the use of colchicine, which also had no effect on TNF levels when taken by volunteers (1 mg/day) or when added to the PBMC cultures (10(-7) M). CONCLUSIONS: Since TNF has a very short half-life in plasma, the capacity of PBMC to respond to TNF inducers may more accurately reflect its synthesis. A marked decrease in this response in acute FMF suggests "exhaustion" of cells that are already highly activated to produce TNF and the possible participation of TNF in the pathogenesis of FMF.

Adult↗