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Aim:We examined the incidence and the reversibility of sarcopenia and their associated factors over a 4-year period using the European Working Group on Sarcopenia in Older People (EWGSOP) criteria. Methods:A total of 4000 community-dwelling older adults aged ≥65 years were evaluated for which detailed information regarding demographics, socioeconomic, medical history, lifestyle, and clinical factors were documented at baseline, 2 years, and 4 years later. Sarcopenia was defined according to the EWGSOP algorithm. Incident sarcopenia and its reversibility were documented at each follow-up year, and related to possible factors. Results:At baseline, of the 4000 participants, 361 (9.0%) had sarcopenia. Between baseline and 2-year follow-up, 6.0% of the participants without sarcopenia at baseline had developed sarcopenia, and 18.8% of the initially sarcopenic participants had reverted to normal. Between baseline and 4-year follow-up, the corresponding figures were 6.3% and 14.1%, respectively. The average annual incidence over 4 years was 3.1%. After multivariate adjustments, older age, female sex, presence of chronic obstructive pulmonary disease, presence of stroke, higher physical activity levels, presence of instrumental activities of daily living impairments, and lower body mass index were associated with incident sarcopenia, whereas younger age, female sex, higher body mass index and absence of instrumental activities of daily living impairments, but not physical activity, were associated with its reversibility. Protein and vitamin D intake were not significantly associated with sarcopenia incidence or its reversibility. Conclusion:Sarcopenia incidence increases with age, but is potentially reversible in a Chinese elderly population. High body mass index is protective against sarcopenia incidence and its reversibility. Increasing physical activity and maintaining a healthy weight could be beneficial in the prevention of sarcopenia. Geriatr Gerontol Int 2014; 14 (Suppl. 1): 15-28.

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Summary Body mass index (BMI) and mortality in old adults from the general population have been related in a U‐shaped or J‐shaped curve. However, limited information is available for elderly nursing home populations, particularly about specific cause of death. A systematic PubMed/EMBASE/CINAHL/SCOPUS search until 31 May 2014 without language restrictions was conducted. As no published study reported mortality in standard BMI groups (<18.5, 18.5–24.9, 25–29.9, ≥30 kg/m2), the most adjusted hazard ratios (HRs) according to a pre‐defined list of covariates were obtained from authors and pooled by random‐effect model across each BMI category. Out of 342 hits, 20 studies including 19,538 older nursing home residents with 5,223 deaths during a median of 2 years of follow‐up were meta‐analysed. Compared with normal weight, all‐cause mortality HRs were 1.41 (95% CI = 1.26–1.58) for underweight, 0.85 (95% CI = 0.73–0.99) for overweight and 0.74 (95% CI = 0.57–0.96) for obesity. Underweight was a risk factor for higher mortality caused by infections (HR = 1.65 [95% CI = 1.13–2.40]). RR results corroborated primary HR results, with additionally lower infection‐related mortality in overweight and obese than in normal‐weight individuals. Like in the general population, underweight is a risk factor for mortality in old nursing home residents. However, uniquely, not only overweight but also obesity is protective, which has relevant nutritional goal implications in this population/setting.

This study aimed to investigate the factors associated with viral breakthrough among liver transplant recipients who receive lamivudine monoprophylaxis. Consecutive patients receiving liver transplantation for HBV-related liver disease from June 1999 to October 2000 were studied. All patients received lamivudine 100 mg daily pre- and post-transplant. Serum samples were collected before lamivudine treatment, before liver transplantation, and then every 3-6 months after liver transplantation. Lamivudine-resistant mutations at the YMDD motif of HBV P gene were detected by direct sequencing and HBV DNA was quantified by real-time polymerase chain reaction (PCR). Ten patients, 7 males and 3 females, aged 50.5 +/- 7.9 years, were studied. Three patients had fulminant hepatitis and 7 patients had end-stage cirrhosis before liver transplantation. Lamivudine was started at 4.5 (range 0-40) weeks before liver transplantation. The median post-transplant follow-up was 16 (range 12-23) months. Four patients developed YMDD mutations 10.5 (0-16) months after transplantation with relapse of viraemia (median 1,294, range 51-3,135 MEq/ml). All patients who developed YMDD mutants had end-stage liver cirrhosis, and HBV DNA were detectable on the day of liver transplantation (median 0.62, range 0.086-1.63 MEq/ml). On the contrary, all 3 patients transplanted for fulminant hepatitis did not have YMDD mutation. Among the 3 end-stage cirrhotic patients who had negative HBV DNA before liver transplantation, none developed YMDD mutation. In conclusion, patients transplanted for fulminant hepatitis B and cirrhotic patients in whom HBV DNA could be rendered PCR negative before liver transplantation are unlikely to develop YMDD mutation on lamivudine monoprophylaxis.