Polypharmacy and malnutrition in older people: A narrative review.

Polypharmacy is the simultaneous use of multiple medicines, usually more than five. Polypharmacy is highly prevalent among older individuals and is associated with several adverse health outcomes, including frailty. The role of polypharmacy in nutritional status seems to be crucial: although a clear association between polypharmacy and malnutrition has been widely reported in older people, the magnitude of the effect of increased number of drugs in combination with their type on the risk for malnutrition remains to be largely explored. Therefore, this review aims to discuss the association between polypharmacy and malnutrition in older people and to provide suggestions for its management. Polypharmacy is prevalent among malnourished frail patients, and the relative contribution of comorbidities and polypharmacy to malnutrition is difficult to be determined. Several mechanisms by which commonly used medications have the potential to affect nutritional status have been identified and described. Deprescribing (i.e., a systematic process of identification and discontinuation of drugs or a reduction of drug regimens) could be an essential step for minimizing the effects of polypharmacy on malnutrition. In this regard, the literature suggests that in older patients taking several medications, the best method to solve this problem is the comprehensive geriatric assessment, based on a holistic approach, including drug review, to find potential unnecessary and inappropriate medications. Nutritional and deprescribing interventions must be tailored to patient needs and to the local context to overcome barriers when applied in different settings.

A case of statin-induced liver injury with positive rechallenge with a second statin. Is there a class effect?

OBJECTIVES: Statins have proved to reduce cardiovascular morbidity and mortality in high-risk population and are generally well tolerated, although adverse events can occur. Up to 3% of patients develop aminotransferases elevation, which usually normalizes with continued treatment and hardly is associated with clinical symptoms. Serious statin-related liver injury is exceedingly rare. Furthermore, literature regarding rechallenge with a second statin is extremely poor. Some authors caution that re-exposure to these drugs is associated with a more serious liver injury but safe switching to a second statin after drug-induced liver injury (DILI) is also reported. CASE PRESENTATION: We describe a case of a middle-aged woman who developed hepatocellular liver injury after simvastatin dose escalation; a rechallenge with low dose rosuvastatin caused rapid recurrence of DILI. CONCLUSIONS: In our opinion, clinicians should be very cautious upon rechallenge and closely follow-up patients who experienced statin-induced liver injury when trying re-exposure to another statin.

Statins and nonalcoholic fatty liver disease in the era of precision medicine: More friends than foes.

Nonalcoholic fatty liver disease (NAFLD) describes a spectrum of alcohol-like hepatic histological changes, which occur in the absence of any competing causes of chronic liver disease, notably including significant alcohol consumption. A close and bi-directional relationship links NAFLD with the metabolic syndrome (MetS), and concurrent MetS will hasten the progression to more severe forms of NAFLD, including cirrhosis and hepatocellular carcinoma (HCC). Patients with NAFLD will typically exhibit atherogenic dyslipidemia and increased cardiovascular risk (CVR). Statins are among the most widely prescribed lipid-lowering drugs. Their use has historically been hampered, in individuals with liver disease, owing to the fear of hepatotoxicity. However, studies suggest that statins are not only effective in reducing cardiovascular events, but may also exert multiple beneficial effects on the liver. CVR in those with NAFLD has extensively been covered by our group and others. This updated clinical narrative review will critically examine the effects of statins on the pathogenesis of NAFLD, including the key elementary pathological lesions of NAFLD, i.e. steatosis, inflammation and fibrosis, and its liver-related complications, i.e. cirrhosis, portal hypertension and HCC.