Frailty has emerged as a major health issue among older patients. A consensus on definition and diagnosis is yet to be achieved. Various biochemical abnormalities have been reported in frailty. Activation of sirtuins, a conserved family of NAD-dependent proteins, is one of the many mimics of calorie restriction which improves lifespan and health in experimental animals. In this cross-sectional study, we assessed the circulating sirtuin levels in 119 (59.5%) nonfrail and 81 (40.5%) frail individuals, diagnosed by Fried's criteria. Serum SIRT1, SIRT2, and SIRT3 were estimated by surface plasmon resonance (SPR) and Western blot. Serum sirtuins level in mean+SD; SIRT1 (nonfrail –4.67 ± 0.48 ng/μL; frail – 3.72 ± 0.48 ng/μL; P < 0.0001), SIRT2 (nonfrail – 15.18 ± 2.94 ng/μL; frail – 14.19 ± 2.66 ng/μL; P = 0.016), and SIRT3 (nonfrail-7.72 ± 1.84 ng/μL; frail – 6.12 ± 0.97 ng/μL; P < 0.0001) levels were significantly lower among frail patients compared with the nonfrail. In multivariable regression analysis, lower sirtuins level were significantly associated with frailty after adjusting age, gender, diabetes mellitus, hypertension, cognitive status (Mini Mental State Examination scores) and number of comorbidities. For detecting the optimum diagnostic cutoff value a ROC analysis was carried out. The area under curve for SIRT1 was 0.9037 (cutoff – 4.29 ng/μL; sensitivity – 81.48%; specificity – 79.83%) and SIRT3 was 0.7988 (cutoff – 6.61 ng/μL; sensitivity – 70.37%; specificity – 70.59%). This study shows that lower circulating SIRT1 and SIRT3 levels can be distinctive marker of frailty.
failure is a common health problem among older adults, arising out of multiple etiologic factors that are often irreversible, 1 and reversible causes of myocardial dysfunction are often overlooked. A case of reversible heart failure due to hypocalcaemia resulting from vitamin D deficiency is reported. CASE REPORTAn 87-year-old man was referred from another hospital with progressive and disabling shortness of breath of 1 week duration after he developed an episode of ventricular tachycardia (VT) with spontaneous remission. He had mild fever and productive cough. Before this illness, he was in his usual state of health, with well-controlled hypertension and chronic obstructive pulmonary disease (COPD), and was competent in all basic activities of daily living. He had never smoked but had had pulmonary tuberculosis in his early 30s; simple renal cysts had been detected during earlier investigation for hypertension.Examination revealed a dyspneic man with blood pressure of 134/70 mmHg, regular pulse of 120 beats per minute, respiratory rate of 32 breaths per minute, and oxygen saturation of 86% on room air and 95% with 2 L of oxygen through nasal prongs. Respiratory examination found inspiratory and expiratory wheeze with bilateral basal crackles. Cardiovascular examination revealed tachycardia and cardiomegaly. The rest of the examination was normal.Laboratory evaluation revealed calcium 5.6 mg/dL (normal 8.1-10.4 mg/dL), phosphate 3.5 mg/dL (normal 2.5-4.5 mg/dL), alkaline phosphatase 156 IU (normal 80-240 IU), vitamin D3 11 ng/mL (normal 30-100 ng/mL), parathyroid hormone (PTH) 15.58 pg/mL (normal 15-65 pg/mL), and magnesium 1.6 mg/dL (normal 1.8-2.4 mg/dL). Electrocardiogram showed tachycardia, and echocardiogram revealed dilated cardiomyopathy, mild concentric left ventricular hypertrophy (LVH), and ejection fraction (EF) of 35% to 40%. Twenty-four-hour Holter monitoring revealed frequent supraventricular ectopic heart beats and one run of nonsustained VT. Investigations for reactivated tuberculosis were negative. Contrastenhanced computed tomography of the chest and abdomen showed consolidation in the left upper lobe on a background of fibrocalcific changes in both upper lobes of the lung and bilateral simple renal cortical cysts.He refused any invasive investigation, so coronary angiogram was not performed.A diagnosis of severe vitamin D deficiency with hypocalcemia-induced dilated cardiomyopathy, congestive heart failure, COPD, and pneumonia was made. He was treated using calcium gluconate and magnesium infusion, and hypocalcemia and hypomagnesemia were corrected. Oral calcium and magnesium and vitamin D3 supplementation were started. Heart failure was treated using intravenous diuretics, and COPD was controlled using nebulized bronchodilators. His pneumonia was treated using intravenous amoxicillin with clavulanate and azithromycin initially, followed by oral amoxicillin with clavulanate for 1 week. He was discharged to home in 2 weeks. Detailed followup assessment after 6 months revealed amelioration of mos...
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