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Objective:To analyze clinical pharmacist interventions in the intensive care units (ICUs) setting of a tertiary care Indian hospital and to assess the pharmacoeconomic impact on drug-related problems (DRPs).Materials and Methods:A postgraduate clinical pharmacist reviewed drug prescriptions over a period of 7 months. Whenever a DRP is identified, it was discussed with a physician and appropriate suggestions were provided, later it was documented on a preprepared form. Clinical significance of each intervention was graded based on the predicted clinical outcome. Acceptance of the interventions is entirely at the discretion of the medical staff. Each intervention was analyzed with respect to potential cost saving and/or additional cost incurred to existing drug therapy. An independent clinical panel was convened, and all the interventions made by the intervening pharmacist were critically reviewed for potential cost savings.Results:The intervening pharmacist made 117 recommendations, of which 94% was accepted by the medical professionals. The most frequent DRP identified was overdose (24%). The total net cost savings made was Rs. 77260.13 (USD 1796.73). This corresponds with Rs. 965.75 per patient and an annualized savings of Rs. 135205.22.Conclusion:Clinical pharmacist interventions had a significant impact on the cost of drug therapy and the patient outcome in intensive care settings of our hospital.

Inhibition of the sEH alleviates diabetes-induced decline in learning and memory.

Background: Myocardial injury due to ischemia-reperfusion (IR) is aggravated in diabetes which is associated with oxidative stress. Alleviating oxidative stress via use of antioxidants has been shown to be effective at minimizing myocardial cell death and improving cardiac function. The aim of the present study was to evaluate the cardioprotective effect of phloroglucinol against myocardial reperfusion injury (MRI) in diabetic rats.Methods: Diabetes was induced in female rats with streptozotocin (50 mg/kg). The diabetic rats were orally treated with phloroglucinol (100 and 200 mg/kg daily for 28 days). After treatment the hearts were isolated and mounted on a Langendorff apparatus. The hearts were subjected to 15 minutes of IR to induce myocardial damage. Cardiac functions including heart rate (HR), resting and developed tension, and rate of change of contraction (+dP/dt max ) were recorded. Cardiac injury biomarkers lactate dehydrogenase (LDH) and creatine kinase (CK-MB) were measured in the heart perfusate. Levels of the antioxidant enzymes reduced glutathione (GSH) and malondialdehyde (MDA) were measured. Hematoxylin and eosin (H&E) staining was also performed. Results:After IR injury, a decrease in HR and +dP/dt max in hearts from diabetic rat was seen compared to healthy rat hearts, which was reversed by phloroglucinol treatment. Myocardial infarct size, measured by H&E staining, was increased in diabetic rats compared to healthy rats and an increase in the activity of LDH and CK-MB in the heart perfusate in diabetic rats was decreased by phloroglucinol treatment.An increase in MDA levels and a decrease in levels of antioxidant enzymes were observed in diabetic rats, which was reversed with phloroglucinol treatment. Conclusion:Phloroglucinol treatment has potential therapeutic promise in the treatment of MRI in diabetes. K E Y W O R D SLangendroff apparatus, myocardial reperfusion injury, phloroglucinol, streptozotocin | 211 PRANAV NAYAK et Al.

Background:Diabetes-induced oxidative stress and hypertension play a major role in the development of nephropathy. Hence, the present study was undertaken to evaluate the protective effects of molsidomine, a nitric oxide donor in streptozotocin (STZ)-induced diabetic nephropathy (DN) in rats.Materials and Methods:Type 1 diabetes was induced through a single dose of STZ (52 mg/kg, i.p.) in male Wistar rats and then treated with molsidomine (5 and 10 mg/kg; p.o.) for 8 weeks. Physical parameters, vital and renal function test including blood glucose, albuminuria, blood urine nitrogen, serum creatinine, and kidney index were determined. Oxidative stress and lipid peroxidation were assessed in the kidney homogenate by means of antioxidant enzymes and malondialdehyde levels.Results:DN rats exhibited a significant renal dysfunction with a reduction in body weight, excessive oxidative stress, and pathological changes. Molsidomine treatment significantly improved vital sign, renal functions, and oxidative stress in DN rats in a dose-dependent manner. The protective effect of molsidomine was also substantiated by pathological changes in the architect of the kidney.Conclusion:Molsidomine shows a significant beneficial effect in Type 1 DN in rats.

Diabetes mellitus (DM) prevalence is increasing at an alarming rate as it was 381 million people globally in 2013 and is estimated to be 463 million people in 2019 rising to 578 million by 2030. It is a disease with high rate of complications such as neuropathy, nephropathy, retinopathy, erectile dysfunction etc. 1,2 Diabetic neuropathy is a family of disorders that damage the different regions of the nervous system, either individually or in combination. It affects pain fibres, motor neurons and autonomic nervous system. 3 It results in large economic costs for its care. [4][5][6] The various kind of neuropathies include peripheral neuropathy, proximal neuropathy, autonomic neuropathy and focal neuropathy. 7 There are a number of reasons for the pathogenesis of diabetic neuropathy and polyol pathway of glucose metabolism is thought as one of the major mechanism. 8 Peripheral neuropathy is a type of nerve damage that usually affects feet and legs and sometimes hands and arms. 9 It is proved that reactive oxygen species (ROS) plays a significant role in the pathophysiology of neuropathic pain in diabetes. 10 Out of all diabetic patients, 50% of patients develop neuropathy and painful neuropathy ranges from 10% to 20% in patients with diabetes. Diabetic patients can experience nerve problems at any time and the problem increases with age, weight and duration. 5 The complications across various countries varies from 10% to 30% and it is higher in developed countries than in developing countries. These complications can lead to painful symptoms and can affect quality of life of the patient. The treatment for the painful diabetic

The results highlight the rationale behind the repositioning of molsidomine therapy for the management of diabetic erectile dysfunction.

Epoxyeicosatrienoic acids (EETs) are epoxide derivatives formed from arachidonic acid and are neuroprotectant. These bioactive lipids are degraded by soluble epoxide hydrolase (sEH). Pharmacological inhibition of sEH enhances the synaptic function in the central nervous system and has a protective role in the age‐related cognitive decline. We have evaluated the hypothesis that the sEH inhibitor TPPU might prevent a diabetes‐induced decline in learning and memory which is associated with alteration in the level of neurotransmitter and oxidative stress. Type 1 diabetes (streptozotocin 52 mg/kg, i.p.) was induced in rats and the animals were treated with TPPU (0.1 and 0.3 mg/kg body weight; p.o.) for 8 weeks. The learning and memory functions were assessed by Barnes maze and step down test. Level of oxidative stress indicators (reduced glutathione and malondialdehyde) and neurotransmitters (γ‐Aminobutyric acid, norepinephrine, and dopamine), and activity of acetylcholinesterase and were measured in the discrete regions of the brain. Our results revealed that treatment with TPPU which penetrates the blood‐brain barrier significantly improved learning and memory performance in diabetic rats with a parallel decrease in the level of blood sugar. Moreover, treatment with TPPU significantly minimized the diabetes‐induced alteration in levels of neurotransmitters and activity of acetylcholinesterase. In addition, TPPU protected anti‐oxidant defense system. Based on our experimental findings, it can be concluded that the inhibition of sEH is a viable strategy for retrieving diabetes‐induced decline in learning and memory.Support or Funding InformationThis study was partially funded by the National Institute of Environmental Health Sciences (NIEHS) [Grant R01 ES002710], NIEHS Superfund Research Program [Grant P42 ES004699], West Coast Central Comprehensive Metabolomics Center [Grant U24 DK097154] to BDH.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.