Immune thrombocytopenic purpura (ITP) is an autoimmune condition characterized by low platelet count with mucocutaneous and other bleedings. Clinical manifestations may range from spontaneous formation of purpura and petechiae, especially on the extremities, to epistaxis, bleeding at the gums or menorrhagia, any of which occur usually if the platelet count is below 20,000 per μl. A very low count may result in the spontaneous formation of hematomas in the mouth or on other mucous membranes. Fatal complications, including subarachnoid or intracerebral, lower gastrointestinal or other internal bleeding can arise due to an extremely low count. Vaccines may induce ITP by several mechanisms. Vaccine-associated autoimmunity may stem not only from the antigen-mediated responses but also from other constituents of the vaccine, such as yeast proteins, adjuvants, and preservatives diluents. The most likely is through virally induced molecular mimicry. The binding of pathogenic autoantibodies to platelet and megakaryocytes may cause thrombocytopenia by different mechanisms, such as opsonization, direct activation of complement, or apoptotic pathways. The autoantibodies hypothesis is not sufficient to explain all ITP cases: In the anti-platelet antibody-negative cases, a complementary mechanism based on T cell immune-mediated mechanism has been suggested. In particular, T cell subsets seem dysregulated with an increased production of pro-inflammatory cytokines, as IFN-γ and TNF, and chemokines, as CXCL10. Vaccines are one of the most striking discoveries in human history that changed dramatically life expectancy. Nonetheless, the occurrence of adverse events and autoimmune phenomena has been described following vaccination, and ITP may represent one of this.
SummaryAdministration of intravenous immunoglobulin (IVIg) is a recognized safe and efficient immunomodulation therapy for many autoimmune diseases. Anti-idiotypic antibody binding to pathogenic autoantibodies was proposed as one of the mechanisms attributed to the protective activity of IVIg in autoimmunity. The aim of this study was to fractionate the anti-anticitrullinated protein anti-idiotypic-antibodies (anti-ACPA) from an IVIg preparation and to test it as a treatment for collagen-induced arthritis in mice. IVIg was loaded onto an ACPA column. The eluted fraction was defined as ACPA-specific-IVIg (ACPA-sIVIg). Collagen-induced-arthritis (CIA) was induced in mice. Mice were treated weekly with ACPA-sIVIg, lowdose-IVIg, high-dose-IVIg and phosphate-buffered saline (PBS). Sera-ACPA titres, anti-collagen anitbodies and cytokine levels were analysed by enzymelinked immunosorbent assay (ELISA); antibody-forming-cell activity by enzyme-linked imunospot (ELISPOT) assay; and expansion of regulatory T cell (T reg ) population by fluorescence activated cell sorter (FACS). ACPAsIVIg inhibited ACPA binding to citrullinated-peptides (CCP) in vitro 100 times more efficiently than the IVIg compound. ACPA-sIVIg was significantly more effective than the IVIg-preparation in attenuating the development of collagen-induced arthritis. Splenocytes from CIA mice treated with ACPA-sIVIg reduced the ACPA and anti-collagen-antibody titres, including the number of anti-collagen and ACPA antibody-forming cells. In parallel, splenocytes from ACPA-sIVIg treated mice secreted higher levels of anti-inflammatory cytokines and lower proinflammatory cytokines. The ACPA-sIVIg inhibitory potential was accompanied with expansion of the T reg population. Low-dose IVIg did not affect the humoral and cellular response in the CIA mice in comparison to the PBS-treated mice. Based on our results, IVIg may be considered as a safe compound for treating patients with rheumatoid arthritis by neutralizing pathogenic autoantibodies, reducing proinflammatory cytokines and expanding the T reg population.
Background: Takotsubo cardiomyopathy affects between 1.7% and 2.2% of patients hospitalized with suspected acute coronary syndromes. Characterized by chest pain, electrocardiogram changes, and transient left ventricular apical wall motion abnormality, it is under-recognized and often misdiagnosed. Objectives: In order to better differentiate between St-segment myocardial infarction and Takotsubo cardiomyopathy, we developed a scoring system. Methods: Of the 82 patients enrolled with Takotsubo cardiomyopathy, 67 had ST-segment elevation on electrocardiogram and were compared with 79 ST-elevation myocardial infarction patients. A multi-variant logistic regression model was used to find factors independently associated with Takotsubo cardiomyopathy. The Platelets and Thrombosis in Sheba (PLATIS)-Takotsubo cardiomyopathy is based on a 10-point scoring system: stressful events (3), females (2), no history of diabetes mellitus (2), estimated left ventricular ejection fraction ≤ 40% on admission echo (1), positive troponin on admission (1), and no smoking (1). Patients with Takotsubo cardiomyopathy were older (66 ± 11 vs 60 ± 11 years, p < 0.001), predominantly female (90% vs 15%, p < 0.001), with a lower incidence of diabetes mellitus, dyslipidemia, and smoking. Nevertheless, in-hospital mortality was similar in both groups. Results: In a multivariate logistic regression analysis, the average Platelets and Thrombosis in Sheba-Takotsubo cardiomyopathy scoring was significantly higher in Takotsubo cardiomyopathy compared with ST-elevation myocardial infarction patients (8.35 ± 1.7 vs 3.42 ± 1.6, p < 0.001). With an overall score of ≥7, the receiver-operating characteristic curve was 0.82 with a sensitivity of 75% and a specificity of 89% (positive predictive value = 85% and negative predictive value = 80%). Conclusion: The Takotsubo cardiomyopathy scoring system is a simple, reliable tool that can assist in diagnosing and differentiating between patients with Takotsubo cardiomyopathy and those with ST-elevation myocardial infarction.
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