Infections can act as environmental triggers inducing or promoting autoimmune disease in genetically predisposed individuals. Identification of microbial peptides similar to self-tissues may by molecular mimicry, provide the inducing mechanism for an immune response. The aim of this study was to identify autoantibodies (autoAbs) in nonautoimmune individuals during acute bacterial, viral, or parasitic infections. Specific Abs or specific infections with an increased autoAb load may shed insight into the mechanisms of autoimmune disease. Sera from 88 patients with acute infections (41 bacterial, 23 viral, 17 parasitic, and 7 rickettsial) were tested by the ELISA method for antinuclear antibodies (ANA) 8 Pro, and Abs to thyroid peroxidase (TPO), thyroglobulin, phospholipids, annexin-V, laminin, anti-Saccharomyces cervisiae (ASCA), and prothrombin, along with 80 normal controls. Elevated titers of Abs to annexin-V and prothrombin were the most prevalent in viral, parasitic, and rickettsial infections and to laminin in viral and parasitic infections. Elevated titers of ASCA and ANA were found in viral and bacterial infections. Antiphospholipid Abs were found in parasitic and Q-fever infections. Thirty-four individuals harbored elevated titers of at least two Abs. An autoAb burden was detected in individuals with hepatitis A, hepatitis B, toxoplasma or Q-fever infections. In nonautoimmune individuals with various (bacterial, viral, parasitic, and rickettsial) infections, elevated titers of Abs to annexin-V, prothrombin, laminin, ASCA, ANA, and phospholipids were most frequently detected.

Mean platelets volume (MPV) has been shown to correlate with impaired reperfusion and increased mortality in patients with ST-elevation myocardial infarction (STEMI) treated with primary precutaneous coronary intervention (PCI). We aimed to study whether the same association exists in STEMI patients treated with thrombolysis. Included in the study were STEMI patients receiving thrombolysis. Thrombolysis failure was defined as a need for rescue precutaneous coronary intervention (PCI), in-hospital mortality, unplanned PCI during hospitalization or complete occlusion of the culprit coronary artery in a follow-up angiography. MPV levels were compared between patients with failed or successful thrombolysis. Of the 122 patients, 30 had failed thrombolysis while the other 92 fulfilled the criteria for successful treatment. There were no significant differences in demographic or clinical baseline characteristics of the two groups. Mean MPV was significantly higher in patients with failed thrombolysis compared to patients with successful treatment (9.2 +/- 1.1fl and 8.7 +/- 1.0fl respectively, p = 0.019 in multivariate analysis). The prevalence of thrombolysis failure was significantly higher in patients with MPV > 8.6 fl compared to those with MPV

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