RESUMEN
Studies about the role of self-compassion have focused primarily on psychological well-being, but there is solid evidence to suggest that self-compassion may have larger and more prominent implications in the medical world. Therefore, this systemic review aimed to investigate the effects of self-compassion on psychosocial and clinical outcomes in medically ill patients. A comprehensive search of several databases from their inception to August 10, 2020, was conducted, which included Ovid MEDLINE(R) and Epub Ahead of Print, Ovid Embase, Ovid Cochrane Central Register of Controlled Trials, and Cumulative Index to Nursing and Allied Health Literature (CINAHL). Eligible studies needed to include psychosocial or clinical outcomes of self-compassion in medically ill patients. Nineteen articles (n=2,713 patients; 73.3% females) met our eligibility criteria and were included in this systematic review. There was a negative correlation between self-compassion and psychosocial outcomes such as anxiety, depression, and stress. Moreover, based on self-compassion intervention, there was an improvement in clinical outcomes related to diabetes such as hemoglobin A1c (HbA1c) and blood glucose levels. This systematic review highlights the effect of self-compassion on psychosocial and clinical outcomes. Further studies are needed to evaluate long-term outcomes of a self-compassion-based-intervention to highlight its importance in the role of disease management.
RESUMEN
Introduction Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is the most common enzymopathy in humans, and its distribution has been historically described to be closely associated with that of malaria. North East India provides optimal conditions for transmission of malaria and bears a considerable burden of Plasmodium vivax (P. vivax) malaria. Primaquine, a mainstay in the treatment of vivax malaria, may trigger episodes of acute hemolysis in patients with G6PD deficiency. The present study sought to delineate the frequency and genotypes of G6PD deficiency among patients suffering from vivax malaria infections. Methods Blood specimens from 80 individuals diagnosed with vivax malaria underwent enzyme assay for G6PD deficiency. Samples with deficient phenotype underwent isolation of DNA using a genomic DNA isolation kit (Qiagen India Pvt. Ltd., New Delhi, India). The genomic DNA underwent amplification, serial denaturation, annealing, extension, final extension followed by digestion with restriction endonucleases Nla III and Fok I. The digested products were subjected to horizontal agarose electrophoresis for the separation of digested fragments. Samples without nucleotide 376 adenineâguanine (AâG) mutation were classified as G6PD B. Those with the mutation were further classified into G6PD A(+) and G6PD A(-) based on the presence of Nla III site. Results Twenty-seven out of 80 individuals (33.75%) with P. vivax malaria were found to have G6PD deficiency, of which a majority (n=24) had G6PD B genotype. Three individuals had AsparagineâAspartic Acid mutation at position 376 (AâG), of which G6PD A(+) and G6PD A(-) were present in two and one cases, respectively. Conclusion G6PD deficiency was noted in about a third of patients with vivax malaria. Since primaquine therapy is contraindicated in this group of patients, there is a rationale for looking into screening patients with vivax malaria from the region prior to primaquine therapy. Further large scale studies may substantiate this and help in better genotypic and geographic characterization of G6PD deficiency in the region.