Sevelamer, has been shown to have many pleiotropic actions on lipid panel, various inflammatory markers, and blood glucose levels in chronic kidney disease patients.We conducted a systematic review and meta-analysis to compare these pleiotropic effects of sevelamer to other phosphate binders used in chronic kidney disease patients. The relevant randomized controlled trials published from 1 January 2001 to 31 November 2019 on the following databases: Cochrane Central Register of Controlled Trials published in The Cochrane Library, PubMed, Scopus and Google Scholar were identified. All the included studies were independently assessed for eligibility and risk of bias. The modified data extraction form of Cochrane was used. This review included 44 studies for qualitative analysis and 28 reports for quantitative analysis. A meta-analysis of three studies (n = 180) showed that glycated haemoglobin had significantly decreased in sevelamer-treated patients (MD: 0.5%; p = <.001). Compared with calcium-based phosphate binders, sevelamer showed a significant reduction in low-density lipoprotein (MD: À19.43 mg/dL; p = <.001) and total cholesterol (MD: À19.98 mg/dL; p < .001). A significant increase in high-density lipoprotein (MD: 1.29 mg/dL; p = .05) was also prominent in sevelamer treated patients. However, we were not able to observe a significant change in other biochemical parameters such as TG, CRP, hs-CRP, FGF-23, IL-6 and albumin as, no statistically significant difference was observed.

Paradoxical seizure is an unusual reaction of seizure aggravation or change in its pattern due to antiepileptics. Decrease in seizure threshold with phenytoin is bound to occur with an increase in serum levels. We herein report a 51-year-old female, who was brought to the intensive care unit with complaints of episodic seizures and frothing. She is a known case of tonic–clonic epilepsy on oral phenytoin 100 mg for past 6 months. Rapid intravenous infusion of 700 mg phenytoin in 100 mL normal saline over a rate of 15 minutes was initiated on admission. This was followed by a sudden abnormality of her baseline blood parameters and an occurrence of paradoxical seizure. The dose of phenytoin was tapered which reversed her condition. The patient was followed up regularly and monitored for fluctuations in her hematological parameters. The mainstay treatment for phenytoin-induced paradoxical seizure and blood dyscrasias is to monitor the patient and dose titration. Dosing of phenytoin remains a challenge for all clinicians which increase the need for such reports.

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Fenofibrate is a peroxisome-proliferator-activator α agonist and it is a widely used drug for hyperlipidemia since its approval in 2004. So, in this review we are focusing on the effect of fenofibric acid's mechanism to alleviate type 1 diabetic micro vascular complications like diabetic retinopathy, diabetic cardiomyopathy in animal models, since the drug is safe, efficacious and more economical when compared with the currently available treatment strategies for juvenile diabetic complications and also a profound observation is needed due to the rarity of research in these therapeutic areas. Important preclinical animal studies published from January 2001 to June 2020 were recognised from databases like PubMed and Cochrane central register of controlled trials. Reviewers screened the articles based on the selection criteria and risk of bias was determined using Systematic Review Centre for Laboratory animal Experimentation risk of bias tool for animal studies. Our literature search yielded a total of 5 studies and after pooling up the data from the 5 preclinical studies, we found that Fenofibrate have the efficacy to prevent type 1 diabetic complications, chiefly diabetic retinopathy and those mechanisms are dependent on peroxisome-proliferator-activator and fibroblast growth factor-21 pathways. Fenofibrate is a well safe and moreover, cost effective medication in preventing type 1 diabetic micro vascular complications especially diabetic retinopathy and also in maintaining the glucose homeostasis in apart from its anti-dyslipidemic effect.

Introduction: Iron-deficiency anemia (IDA) during pregnancy affects the glial cells of the brain of mother, which results in altered neuronal myelination with dysregulation. Although several factors could lead to antenatal depression, IDA is an emerging etiology. The primary objective of this study is to determine the relationship between IDA and antenatal depression among pregnant women. Materials and Methods: This cross-sectional study was conducted at Government Head Quarters and Hospital, in Udhagamandalam. A total of 210 pregnant women in the second trimester were enrolled and categorized into iron-deficient anemia and noniron-deficient anemia groups based on their hematological results. The risk of depression was assessed using the validated Edinburgh Depression Scale (EDS). A Chi-square test for categorical variables and an independent t-test for continuous variables were used. A Pearson's correlation analysis was performed to check the association of EDS scores with participants' demographic characteristics and hematological parameters. Regression analysis was conducted to predict the outcome variable. Results: The distribution of depression was significantly varied between the groups. EDS score was significantly higher in the IDA group in comparison with the non-IDA group (12.78 ± 3.40 vs. 8.82 ± 3.12; P = 0.005; 95% confidence interval 2.94–4.87). The odds of developing antenatal depression are 12 times higher in the iron-deficient group, P < 0.001. Conclusions: Our findings suggest that IDA acts as an independent factor in influencing antenatal depression. The following core competencies are addressed in this article: Medical knowledge, Patient care, Practice-based learning and improvement.