Vox SanguinisVolume 67, Issue 2 p. 240-240 Third-Generation HIV-1/HIV-2 ELISA Tests Piero Palla, Corresponding Author Piero Palla Department of Transfusion, Santa Chiara Hospital, PisaPz. Toniolo 8 I-56100 Pisa (Italy)Search for more papers by this authorAdolfo Moretti, Adolfo Moretti Department of Transfusion, Santa Chiara Hospital, PisaSearch for more papers by this authorFausto Pecori, Fausto Pecori Department of Transfusion, Santa Chiara Hospital, PisaSearch for more papers by this authorRenato Vanacore, Renato Vanacore Center of Clinical Immunology, University of Pisa, ItalySearch for more papers by this author Piero Palla, Corresponding Author Piero Palla Department of Transfusion, Santa Chiara Hospital, PisaPz. Toniolo 8 I-56100 Pisa (Italy)Search for more papers by this authorAdolfo Moretti, Adolfo Moretti Department of Transfusion, Santa Chiara Hospital, PisaSearch for more papers by this authorFausto Pecori, Fausto Pecori Department of Transfusion, Santa Chiara Hospital, PisaSearch for more papers by this authorRenato Vanacore, Renato Vanacore Center of Clinical Immunology, University of Pisa, ItalySearch for more papers by this author First published: August 1994 https://doi.org/10.1111/j.1423-0410.1994.tb01670.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Jackson Brooks J. Human immunodeficiency virus (HIV): Indeterminate Western blot and latent HIV infection. Transfusion 1992; 32: 497–499. 2 Cavalli P., Pennacchio A., Romanini GI Whole virus lysate or recombinant synthetic ELISA assay of HIV1: Which is better Vox Sang 1992; 63: 234–235. 3 Zaaijer HL, Exel-Oehlers PV, et al. Early detection of antibodies to HIV-1 by third-generation assay. Lancet 1992; 340: 770–772. 4 Palla P., Baicchi U., et al. Test Elisa HIV1 e 2 di 3 gen e sicurezza trasfusionale: valutazione di soggetti W.B. indeterminati, in G. Giorgio, L. Mauro, G. Lotti (eds): Atti del Corso di Aggiornamento: La Moderna Diagnostica in Immunoematologia e delle Malattie Virali Trasmissibili con il Sangue. San Giovanni Rotondo, April 1993, pp. 117–119. 5 Mortimer PP The fallibility of HIV Western blot. Lancet 1991; 337: 286–287. 6 Simon F., Bouchaud O., et al. Reliability of Western blotting for the confirmation of HIV-1 seroconversion. Lancet 1992; 340: 1541–1542. Citing Literature Volume67, Issue2August 1994Pages 240-240 ReferencesRelatedInformation

In this study we faced the problem of etiopathogenesis of EPH Gestosis, focusing our attention on the role of immunitary aspects in determining its onset. We typed HLA-DR in 20 couples with gestosic patient and in 20 control couples. Blood samples were taken into heparin-treated test tubes, from all the couples and HLA typed through standard lymphotoxicity technique in accordance with Terasaky (1). Our results in couples with a gestosic patient, showed homozygosis in 65% of patients and in 70% of partners; in 35% of cases homozygosis was present in both partners, and these were the most severe cases. It is also worth mentioning that in all the couples with gestosic patient, at least one of the partners resulted homozygotic. Homozygosis would therefore represent a predisposing factor in the etiopathogenesis of gestosis, and pre-conception HLA-DR typing of the couple could prove to be a valid alarm signal for gestosis risk.

This study was carried out on 43 patients affected by dilated cardiomyopathy to investigate some of the etiopathological hypotheses on this illness. The Authors investigated: the persistence of virus genoma (coxsackie, HBV) on endomyocardial biopsies; the pattern of the II class major histocompatibility complex (MHC) were in the blood lymphocytes; the microvascular aspect of coronary circulation in the endomyocardial biopsies. Finally, in a separated group of 19 patients, the microvascular circulation was studied on skin biopsies and correlated with diabetic, valvular and normal subject. The results showed a 14% positivity for the presence of the virus genoma and a significant predominate of DR5 in the II class MHC of patients with a worse ventricular function. Capillary vessels of the coronary microcirculation were dilated in the 48% of the patients, especially in more compromised subjects. Viral myocarditis seem to play a role in the etiopathogenesis of dilated cardiomyopathies (DCM) and the pattern of MHC could influence the progression of the illness. The microcirculation is probably a pathophysiological aspect. No etiological hypothesis seems to predominate.

Discontinuous plasma exchange with prostaglandin I2 (5 ng/kg/min) and low dosage heparin (5-6 IU/kg/min) (treatment I), and ACD solution alone (treatment II) was studied. During both treatments the activated partial thromboplastin time remained within the normal range. After treatment I platelet count was not decreased but in vitro platelet aggregation was reduced (p less than 0.001). After treatment II platelet count was reduced and in vitro platelet aggregation unchanged. Prostaglandin I2 at this dosage caused no cardiovascular complications. The physiopathological implications of these differences are discussed.

Blood pressure (BP) decreases significantly in patients with immune complex nephritis and hypertension in the course of therapeutic plasma exchange (TPE). To investigate possible underlying mechanisms of this effect, the variations of supine and upright BP and plasma renin activity (PRA) acutely induced by PE (performed by isovolumetric replacement of plasma with 4% albumin in saline solution) were analyzed in six patients. On the average, both supine and upright BP decreased after TPE; however, statistical significance was obtained only for upright systolic BP. Supine and upright PRA did not change significantly, although a clearly blunted response to posture was observed in three patients. The changes of BP induced by TPE were apparently not due to a functional depression of the renin-angiotensin system, since the more marked decrements in BP were observed in the patients with lower basal PRA.