RÉSUMÉ
About one-third of annual hospital budget is spent on buying materials and supplies including medicines. In any health facility, be it small health center or a big teaching institution, drugs forms an essential and indispensable element. Non-availability of drugs particularly in the developing countries is due to lack of proper material management. A poor management in a public pharmaceutical supply can result in wastage or blockade of financial resources, irrational utilization of drugs, shortage or overage of essential drugs, increased holding cost, and reduction in flexibility and decline in quality of health care services. Adaptation of a scientific approach of inventory management in healthcare manages all the issues regarding stocking of pharmaceutical items, ensuring safety, stability, efficacy, availability and maintenance of quality of drugs to provide better healthcare services. This review will focus on inventory management and its importance with special emphasis on always better control-vital, essential, desirable (ABC-VED) analysis technique on essential medicine concept and report of various research studies conducted on ABC-VED analysis in different parts of country.
RÉSUMÉ
Background: Metformin, a first-line agent in Type 2 diabetes mellitus, causes gastrointestinal adverse effects in 20-30% of patients, leading to discontinuation in 5-10% of them. Organic cation transporter 1 (OCT1) encoded by SLC22A1, transports metformin from the enterocytes into the bloodstream. Reduced function OCT1 variants could lead to increased luminal concentration of metformin leading to gastrointestinal adverse effects. Two single nucleotide polymorphisms in the SLC22A1 gene were studied in this cross-sectional study with cases and controls. Objective was to determine the association between genetic polymorphisms rs628031 (1222A>G) and rs622342 (1386C>A) in SLC22A1 gene and gastrointestinal adverse effects to metformin therapy in South Indian type 2 diabetes mellitus patients. Methods: The study was conducted in JIPMER, Puducherry, India in T2DM patients (n=300) of South Indian origin, who were categorized into case (N=100) and control (N=200) groups, based on their gastrointestinal tolerance to metformin. DNA was extracted from the patients using whole blood by phenol-chloroform method and genotyping was done using real-time PCR. Results: Minor allele frequency of rs628031 (A allele) and rs622342 (C allele) were 33.8% and 26.5% respectively. Genotype frequencies did not differ significantly between the case and control groups (rs628031, p=0.45, rs622342, p=0.28). Female gender (AOR 3.77; 95% CI 2.07, 6.85; p<0.001) and proton pump inhibitor usage (AOR 7.66; 95% CI 3.01, 19.47; p<0.001) had higher association with metformin intolerance. Conclusions: No significant association was found between the genotypes of single nucleotide polymorphisms (rs628031 and rs622342) in the SLC22A1 gene and gastrointestinal adverse effects to metformin therapy in South Indian type 2 diabetes mellitus patients.
RÉSUMÉ
Background: Diabetic dyslipidemia is associated with atherosclerosis risk factors and cardiovascular disease. Saroglitazar is a dual PPAR ? and ? agonist approved initially for diabetic dyslipidemia and later for managing non-alcoholic steatohepatitis and hyperglycemia in T2DM. This study was conducted to estimate the association of studied PPAR ? and ? gene polymorphisms among patients with diabetic dyslipidemia at baseline and with triglyceride response to saroglitazar administration. Methods: A total of 54 diabetic dyslipidemia patients who are not controlled i.e., triglycerides (TG)>200 mg/dl with moderate intensity of atorvastatin (?10 mg) were recruited to the study. All the patients were given saroglitazar 4 mg once daily for 12 weeks. PPAR? single nucleotide polymorphisms (SNPs) rs1800206, rs4253778, rs135542 and those of PPAR? gene rs3856806, rs10865710, rs1805192 were genotyped by real-time PCR. Results: 54 patients (67% female) with a mean age of 48.01±6.73 years were given saroglitazar 4 mg once daily for 12 weeks. There was a significant decrease in TG (36.9%) from baseline of 292.33±83.81mg/dl (mean±SD) to 184.46±95.90 mg/dl (<0.001) and in HbA1c (0.66%) from baseline of 8.5% to 7.8% (<0.001). PPAR ? and PPAR ? gene variants did not show any association with TG lowering response. Conclusions: Saroglitazar 4mg once daily effectively decreases the TG, non-HDL-C levels, and HbA1c with no major adverse events, and TG lowering response is not associated with the studied polymorphisms.