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Introduction: Chronic Pancreatitis (CP) is a progressive inflammatory disorder characterised by recurrent episodes of severe abdominal pain. Experimental studies demonstrated protective effects of statins in pancreatic fibrosis. Aim: To assess impact of simvastatin therapy on the severity of pain in patients with idiopathic CP or recurrent acute pancreatitis. Materials and Methods: This prospective, single centre and open-label study included patients with idiopathic CP and recurrent acute pancreatitis, depending upon inclusion and exclusion criteria. Patients were treated with either simvastatin (40 mg per day) (Group-A; n=25) or standard therapy (protonpump inhibitor and antioxidant therapy) (Group-B; n=25). Severity of the pain was assessed using a Visual Analogue Score (VAS) at the start of treatment and at 12-month of treatment. Results: Between June 2017 and August 2017, a total of 50 patients, age ranging from 18 years to 54 years, were included in the study. The study population predominantly included male patients (n=38). The intensity of pain in patients of Group-A reduced significantly (p=0.0001) from 8 (range 6-10) at baseline to 2 (range 0-9) after 12 months of the treatment. There was significant reduction in the intensity of pain in Group-B also {7 (range 6-10) at baseline vs. 5 (range 0-7); p=0.0001}. However, the reduction of VAS score was significantly higher in Group-A as compared to Group-B at 12-month follow-up {6 (range-1-8) vs. 3 (range 0-6); p=0.032}. Conclusion: Simvastatin treatment improved severity of pain in patients with CP or recurrent acute pancreatitis at 12-month follow-up. However, large randomised trials are needed to replicate these findings.

Introduction: Statin discontinuation has been investigated in a wide range of diseases and injuries, but there is a paucity of data in the older adult population with traumatic brain injury (TBI). The purpose of this study was to re-examine the extent to which early discontinuation of pre-injury statin (PIS) therapy increases the risk of poor patient outcomes in older adult patients suffering a TBI.Methods: This was a retrospective observational cohort study of adult trauma patients with a blunt TBI across three trauma centres over four years. Patients were excluded because of no PIS use, age <55years, or a hospital length of stay (LOS) less than three days. Patients found to be intentionally discontinued from statin therapy within 48h of hospital admission for injury-related reasons were excluded. The primary and secondary outcomes were in-hospital mortality and a hospital LOS ≥1 week. Outcomes were analysed using logistic regression.Results: There were 266 patients in the continuation group, and 131 in the discontinuation group. The statin discontinuation group had a significantly higher proportion of patients with a moderate or severe head injury, intubation in emergency department (ED), and disposition to the intensive care unit or operating room. Overall, 23 (6%) patients died while in the hospital. After adjusting for ED Glasgow coma scale, the odds of dying in the hospital were not significantly larger for patients having been discontinued from PIS, compared to those who were continued (OR=1.75, 95%CI=0.71-4.31, p=0.22). Among patients who received an in-hospital statin, the median (interquartile range) time between hospital admission and first administration of statin medication did not differ between patients who died and those who survived (22.8h [10.96-28.91] vs. 22.9h [11.67-39.80], p=0.94). There were no significant differences between study groups in the proportion of patients with a hospital length of stay >1 week (continuation=29% vs. discontinuation=36%, p=0.19).Conclusion: We did not observe a significantly increased odds of in-hospital mortality following PIS discontinuation, compared to PIS continuation, in an older adult population with TBI. It remains to be seen whether statin discontinuation is a proxy variable for injury severity, or whether it exerts deleterious effects after injury. [ABSTRACT FROM AUTHOR]

Introduction: Chronic Pancreatitis (CP) is a progressive inflammatory disorder characterised by recurrent episodes of severe abdominal pain. Experimental studies demonstrated protective effects of statins in pancreatic fibrosis. Aim: To assess impact of simvastatin therapy on the severity of pain in patients with idiopathic CP or recurrent acute pancreatitis. Materials and Methods: This prospective, single centre and open-label study included patients with idiopathic CP and recurrent acute pancreatitis, depending upon inclusion and exclusion criteria. Patients were treated with either simvastatin (40 mg per day) (Group-A; n=25) or standard therapy (protonpump inhibitor and antioxidant therapy) (Group-B; n=25). Severity of the pain was assessed using a Visual Analogue Score (VAS) at the start of treatment and at 12-month of treatment. Results: Between June 2017 and August 2017, a total of 50 patients, age ranging from 18 years to 54 years, were included in the study. The study population predominantly included male patients (n=38). The intensity of pain in patients of Group-A reduced significantly (p=0.0001) from 8 (range 6-10) at baseline to 2 (range 0-9) after 12 months of the treatment. There was significant reduction in the intensity of pain in Group-B also {7 (range 6-10) at baseline vs. 5 (range 0-7); p=0.0001}. However, the reduction of VAS score was significantly higher in Group-A as compared to Group-B at 12-month follow-up {6 (range-1-8) vs. 3 (range 0-6); p=0.032}. Conclusion: Simvastatin treatment improved severity of pain in patients with CP or recurrent acute pancreatitis at 12-month follow-up. However, large randomised trials are needed to replicate these findings. [ABSTRACT FROM AUTHOR]

Personalized medicine is an emerging field with a goal of applying genomic information as a predictor of disease risk as well as individualization of drug therapy. For optimization of drug therapy, significant progress has been made in the past decade in linking genetic variation in genes associated with drug disposition to prediction of drug response and adverse reactions. For most drugs in clinical use, the interplay of many factors, including genetics, demographics, drug-drug interactions, disease states and the environment, result in the interindividual variability observed during drug therapy. Broadly speaking, such determinants of drug response are mediated through modulation of drug concentrations reflective of pharmacokinetic factors, as well as drug targets, often referred to as pharmacodynamics. It is clear that for personalized medicine to become clinically meaningful, genomic as well as clinical and environmental influences must be considered together. We show, for a number of drugs in clinical use, that genomics-guided treatment options not only are becoming feasible but are also on the cusp of showing superiority in terms of clinical outcomes as well as cost-benefit. One of the most widely studied drugs with regard to genomics-guided dosing options is the oral anticoagulant, warfarin. Genetic polymorphisms in the gene encoding cytochrome P450 2C9 ( CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase ( VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial. We will outline the importance of understanding all of the variables that mediate warfarin response as the prerequisite to successful utilization of genotype-guided warfarin therapy. Similarly, HMG Co-A reductase inhibitors, commonly known as statins, also display wide interindividual variability in plasma concentration, response and toxicity due in part to polymorphisms in transporter genes, including SLCO1B1 and ABCG2. Genetic factors are also important considerations in treatment with other therapeutic agents discussed, including clopidogrel and tamoxifen. Implementation of personalized medicine-based treatment options for these and other drugs, the pharmacokinetics or pharmacodynamics of which are impacted by functional genetic variations, will require overcoming a number of challenges, including cost, turnaround time, and demonstration of clinical benefit, as well as better training of health care professionals about genomics in general, and pharmacogenomics in particular. [ABSTRACT FROM AUTHOR]

In this manuscript, three manifestations of statin intolerance will be covered. The first, myopathy, is mostly subjective with variable complaints of myalgias often worsened by exercise, muscle cramping or weakness, and at times associated with a biomarker, elevations in creatine kinase (CK). A rare but serious manifestation can be rhabdomyolysis. The second, liver toxicity, is associated with reversible biochemical increases in transaminases and rarely other liver function tests. Finally, statin-related central nervous system (CNS) toxicity typically defined as cognitive impairment is quite rare and appears to be idiosyncratic. Statin dose alternatives will then be discussed and highlighted in the setting of the new cholesterol-lowering guidelines. Non-statin lipid-altering therapies as well as other alternative therapies will also be reviewed. [ABSTRACT FROM AUTHOR]

The article focuses on a cohort study published within the issue of the periodical regarding the impact of statin in intensive care unit (ICU) admission. It mentions statins used for their cholesterol lowering properties and led to their evaluation for acute inflammatory conditions like sepsis and statin administration may help mitigate delirium in the critically ill though a reduction in cerebral inflammation, alterations in microglial activation, and diminished blood-brain barrier injury.