The aim of this study was to investigate the level of serum cytokines in different periods of pregnancy associated with anemia. 85 pregnant patients with anemia were examined. 46 of them were in their first pregnancy (1st group), and 39 (2nd group) patients were in their second or further pregnancy period. The comparison group consisted of 19 pregnant women without anemia. The level of hemoglobin and serum iron were determined by using colorimetric method, as well as the level of cytokines IL-2, IL-6, IL-8 and IL-10 were determined using an enzyme-linked immunosorbent assay method. The results showed a significant decrease in hemoglobin and serum iron level in the blood of pregnant women with anemia, significant increase in proinflammatory ytokines, such as IL-2 and IL-8, and a significant decrease in IL-10 compared with pregnant women without anemia were also detected. The most pronounced changes in the cytokine profile were observed in the third trimester and during second or futher pregnancy, which is caused by the progression of anemia.
FCGR2C gene was investigated at first time in Hashimoto disease. The aim of this study is to show with genotype-phenotype correlation analysis of the clinical phenotypic role in autoimmune disease of Hashimoto's thyroiditis of nucleotide polymorphisms or variations in the nature of mutations in FcGR2C gene, responsible for the production of proteins which have an extremely active role in immune system. The study group comprised by 48 patients admitted to Department of Endokrinology of Ege Univercity Faculty of Medicine, Department of Internal Medicine and corresponding to Hoshimoto disease criteries. Also, 25 healthy individuals not diagnosed with Hashimoto thyroid and family history of this disease aggred to participate in the study was included in this study. Looking to the results of this study after analysis of the entire coding region of FCGR2C there was found 12 new mutations. This is 7 mises mutations, 5 sininim aminoacit and also in intron 6 pieces nucleotide was seen. Looking to regions where was found mutations and polymorphisms in this study: Pro83Gln, Pro83Pro, Gln57Gln, Gln63Gln FCGR2C proteins are correspond to the first domain. Mutations and polymorphisms are correspending to second domaine of FCGR2C are Ile183Met, Ser189Thr, Tyr205Phe, Gln57Gln, Gln63Gln, Leu150Leu, Thr203Thr ve Leu204Leu. Furthermore, the frequency of mutant alleles of FCGR2C gene were; %90 in patients group and %70 in healthy control group. After applied for the statistical analysis FCGR2C gene mutations increased significantly (χ2: 10.559 - p: 0.001) in Hashimoto disease patients.
Regular blood transfusion and iron chelation is the primary treatment of thalassemia patientsto maintain their life. Iron chelatormay alter serum total calcium and magnesium level in TDT patients. To evaluateany alteration of serum total calcium and magnesium level in transfusion dependent thalassemia patients treated with iron chelator. The present cross sectional study was carried out in the department of Physiology, BSMMU, Dhaka between September 2017 to February 2019. Thirty cases of TDT, aged 5-40 year were included in the study group. Age and sex matched 30 healthy subjects were also studied as control. All the TDT patients were selected from the outpatient Department of Hematology and Transfusion Medicine, BSMMU, Dhaka. Serum total calcium, magnesium and ferritin levels were measured by colorimetric method. For statistical analysis independent sample t test and Chi-Square test and Pearson correlation coefficient test were used. The mean serum total calcium and magnesium levels were significantly (p<0.05) lower and serum ferritin level was significantly (p<0.001) higher in study group compared to that of control. Again, in this study group 6.7 % TDT patients had hypocalcemia and 13.3% TDT patients had hypomagnecemia. This study may conclude that low serum total calcium and magnesium level may be associated with TDT patients treated by combined deferoxamine (DFO) & deferiprone (DFP) iron chelator.
Autoimmune diseases (AiDs) are characterized by the destruction of host tissues by the host immune system. The etiology of AiDs is complex, with the implication of multiple genetic defects and various environmental factors (pathogens, antibiotic use, pollutants, stress, and diet). The interaction between these two compartments results in the rupture of tolerance against self-antigens and the unwanted activation of the immune system. Thanks to animal models, the immunopathology of many AiDs is well described, with the implication of both the innate and adaptive immune systems. This progress toward the understanding of AiDs led to several therapies tested in patients. However, the results from these clinical trials have not been satisfactory, from reversing the course of AiDs to preventing them. The need for a cure has prompted many investigators to explore alternative aspects in the immunopathology of these diseases. Among these new aspects, the role of antimicrobial host defense peptides (AMPs) is growing. Indeed, beyond their antimicrobial activity, AMPs are potent immunomodulatory molecules and consequently are implicated in the development of numerous AiDs. Importantly, according to the disease considered, AMPs appear to play a dual role in autoimmunity with either anti- or pro-inflammatory abilities. Here, we aimed to summarize the current knowledge about the role of AMPs in the development of AiDs and attempt to provide some hypotheses explaining their dual role. Definitely, a complete understanding of this aspect is mandatory before the design of AMP-based therapies against AiDs.
Childhood nephrotic syndrome is a challenging and often persistent renal disorder, and its incidence varies between different ethnicities and regions. Corticosteroids have been the main treatment for decades and are effective in most children with idiopathic NS, although 10–15% of these children become steroid resistant. Furthermore, some initially steroid sensitive children follow a steroid dependent or frequently relapsing course and are therefore at increased risk for developing steroid toxicity. In such children, alternative immunosuppressive medications are used to induce and/or maintain remission of NS. One such drug, rituximab, is a monoclonal antibody directed against the B lymphocyte CD20 marker which induces depletion of B cells, and has shown promising results in the management of NS in children. In this review, we summarize recent studies on the efficacy and safety of rituximab in the different types of childhood nephrotic syndrome, the known and potential mechanisms of action of rituximab, its possible complications and side effects, and the available and potential biomarkers of rituximab activity.