Inappropriate use of proton pump inhibitors in non-critical indoor patients in a tertiary care teaching hospital in Eastern India

Background: Proton pump inhibitors are one of the most commonly used drugs worldwide. Often they are used for inappropriate indications too, imposing economic burden to patients and governments. Many studies have showed equipotent efficacy of oral and intravenous proton pump inhibitor therapy. Despite that, most of the hospitalized patients receive intravenous proton pump inhibitor without appropriate indications. This study aimed to assess use of proton pump inhibitors in government hospital.Methods: It was an observational cross-sectional study done in the general medicine department of a tertiary care teaching hospital in Eastern India, including 800 noncritical patients. Objective was to assess the use of proton pump inhibitors (indications, route of administration, dosing frequency).Results: 100% patient received intravenous proton pump inhibitor irrespective of diagnosis. 80% of them received it twice daily and 18% received it once daily. Majority of the patients received intravenous proton pump inhibitor despite taking other drugs by oral route.Conclusions: Most of the PPI administration was done without appropriate indication. All patients received Intravenous proton pump inhibitors, which may impose economic burden on a government hospital. Majority of the patients received proton pump inhibitors twice daily. These approaches are not cost effective and need to be rectified.

A rare case report on novel pathogenic mutation of TSC2 gene explained at molecular level

Tuberous sclerosis is a neurocutaneous genetic syndrome inherited as autosomal dominant pattern. This disease is caused by mutations of either of the tumor suppressor genes named TSC1 or TSC2 gene. It encodes for hamartin and tuberinwhich modulates mTOR pathway and regulate cell growth and proliferation. We report a case of a 7 year old child positive for pathogenic variant of TSC2 mutation having multiple seizures, angiofibromas, shagreen patch. Imaging studies are indicative of multiple calcified nodules in sub ependymal region, abnormal subcortical white matter suggestive of tuberous sclerosis. Molecular tests suggested that the mutation occurred results in alteration of splicing mechanism. Due to such alteration, the incomplete TSC2 gene encodes an altered tuberin protein i.e., unable to interact with Ras homologue enriched in brain (Rheb), leading to dysregulation of mammalian target of rapamycin (mTOR) signalling causing tuberous sclerosis disease.