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IntroductionImmune thrombocytopenia (ITP) is an immune disorder commonly presents as isolated thrombocytopenia. Generally corticosteroids are the main treatment of ITP. This study was designed to evaluate effectiveness of high dose dexamethasone comparing conventional corticosteroid therapy in the treatment of ITP.Materials and methodsIn a randomized prospective study, sixty adult patients with newly diagnosed primary symptomatic ITP (Platelet count < 20,000) were evaluated. Patients divided into two groups. In group A, thirty patients (mean age of 24.9 years) received Dexamethasone 40 mg/IV/daily for four days (10 mg/q6h); and then Prednisolone 1 mg/kg/day/PO with rapid tapering of prednisolone (10 mg/week). From the other hand, in group B, thirty patients (mean age of 27.2 years) were treated with Prednisolone 1 mg/kg/day/PO for four weeks, then the drug tapered weekly.ResultsAll the patients in group A showed favorable response within the first seven days, 27 cases presented complete response (CR) and three cases revealed response (R). In group B, 11 cases had CR, 13 cases showed R and six cases had No response (NR). After three months, rates of CR were 80% and 23.3% in group A and B; respectively. Responses were 16.7% and 33.3%, NRs were 6.6% and 43.3% in group A and B; respectively (P < 0.0001). After 6 months, CR was 73.3% vs.16.7%, and R was 16.7% vs.36.7% and NR was 10% vs. 46.7% in group A and B; respectively (P < 0.0001). After 12 months, there was no change in response rate in group A, but in group B 53% were non responsive, 40% showed R (chronic ITP) and complete response was observed only in 6.7% (P < 0.0001). Three cases in group A and 12 cases in group B had needed splenectomy (P < 0.00002).ConclusionWe showed that high dose dexamethasone is more effective than conventional steroid therapy in newly diagnosed ITP as initial treatment with less relapses and toxicities.

Intracranial hemorrhage (ICH) is one of the most severe and life-threatening manifestations occurring in the patients with factor XIII (F XIII) deficiency. The aim of this study was to describe the ICH pattern in the patients suffering from F XIII deficiency. In this case series, we investigated 38 patients with severe F XIII deficiency in south of Iran from January to May 2012. ICH pattern, neurologic complications, efficacy of treatment, and incidence of recurrence were reported. The site of ICH was intraparenchymal in 35 patients (92.1 %), subdural in 2 patients (5.2 %), and epidural hemorrhage in 1 patient (2.6 %). Besides, neurologic complications occurred in 21 patients (55.2 %), including locomotor disability in 8, psychological impairment in 7, mental disorders in 5, speech impairment in 4, and visual impairment in 2. Prophylaxis was started with a dose of 10 IU/kg Fibrogammin every 4-6 weeks for all the patients, except for one. All the patients on prophylaxis showed good response without any episodes of recurrence, except for one. The most frequent site of ICH in our patients was intraparenchymal. It seems that long-term prophylactic treatment with a dose of 10 IU/kg Fibrogammin could be effective in the prevention of CNS bleeding in the patients with F XIII deficiency. Moreover, all the patients with severe F XIII deficiency even without severe bleeding symptoms are recommended to undergo prophylactic treatment.

The coronavirus disease-2019 (COVID-19) pandemic has caused an enormous loss of lives. Various clinical trials of vaccines and drugs are being conducted worldwide; nevertheless, as of today, no effective drug exists for COVID-19. The identification of key genes and pathways in this disease may lead to finding potential drug targets and biomarkers. Here, we applied weighted gene co-expression network analysis and LIME as an explainable artificial intelligence algorithm to comprehensively characterize transcriptional changes in bronchial epithelium cells (primary human lung epithelium (NHBE) and transformed lung alveolar (A549) cells) during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Our study detected a network that significantly correlated to the pathogenicity of COVID-19 infection based on identified hub genes in each cell line separately. The novel hub gene signature that was detected in our study, including PGLYRP4 and HEPHEL1, may shed light on the pathogenesis of COVID-19, holding promise for future prognostic and therapeutic approaches. The enrichment analysis of hub genes showed that the most relevant biological process and KEGG pathways were the type I interferon signaling pathway, IL-17 signaling pathway, cytokine-mediated signaling pathway, and defense response to virus categories, all of which play significant roles in restricting viral infection. Moreover, according to the drug–target network, we identified 17 novel FDA-approved candidate drugs, which could potentially be used to treat COVID-19 patients through the regulation of four hub genes of the co-expression network. In conclusion, the aforementioned hub genes might play potential roles in translational medicine and might become promising therapeutic targets. Further in vitro and in vivo experimental studies are needed to evaluate the role of these hub genes in COVID-19.

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