α-Klotho (Klotho) is an antiaging hormone with anti-inflammatory and antioxidative properties. Some studies suggest that Klotho increases in response to enhanced oxidative damage and inflammation. Alcoholism is a proinflammatory condition. The aim of this study was to analyze the relationship between Klotho and the serum levels of the inflammatory markers in alcoholic liver disease and to assess its prognostic value. We included 184 alcoholics and 35 age- and sex-matched controls. We determined the serum levels of Klotho, the tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8, and malondialdehyde (MDA), and routine laboratory variables. Patients were followed-up with during 16 ± 18 months; 67 patients died. Klotho levels were higher among cirrhotics (with KW = 37.00 and p < 0.001) and were related to the Child–Pugh score (with KW = 15.96 and p < 0.001) and to the TNF-α (ρ = 0.28; p < 0.001) and MDA (ρ = 0.21; p = 0.006). The child’s groups were associated with mortality, both in the univariate (with the log-rank = 13.56, p = 0.001, Breslow = 12.33, and p = 0.002) and multivariate (with β = 0.43, p = 0.02, and OR = 1.53 (1.07–2.15)) analyses, also introducing Klotho and the TNF-α as dichotomic variables. However, the independent prognostic value of the Child’s groups was displaced by Klotho when only cirrhotics were considered; Klotho, over the median (574.4 pg/mL), was associated with higher mortality (with p = 0.04 and OR = 2.68 (1.06–6.84)). We conclude that Klotho is increased in liver cirrhosis. It is directly related to TNF-α, MDA, and to mortality in cirrhotics.

Background: Sclerostin was initially described as an inhibitor of the Wnt-β catenin bone-forming pathway, but it also exerts important effects on intermediate metabolism and body composition. Osteosarcopenia and altered body fat distribution are common findings in excessive drinkers. The role of sclerostin in these patients is uncertain. We aim to analyze the behavior of sclerostin in excessive drinkers and its relationships with body composition (fat mass, lean mass, bone mass), handgrip strength, body mass index (BMI), liver function and ethanol intake. Methods: 107 male active heavy drinkers and 26 age-matched controls were included. Serum sclerostin was determined by ELISA. Body composition analysis was performed by double X-ray absorptiometry. Handgrip strength was recorded using a dynamometer. Liver function was assessed according to Child’s classification. Results: Sclerostin was higher among Child’s C patients, keeping a relationship with deranged liver function. Obesity, defined according to BMI, and body fat were strongly related to sclerostin, being independent of serum creatinine and of liver function. The relationship of sclerostin with total hip bone mineral density was displaced by BMI. Conclusion: Deranged liver function is associated with higher sclerostin levels in alcoholics. Raised sclerostin levels are related to fat deposition and increased BMI.

Background: The long-term survival of patients hospitalized with COVID-19 and the factors associated with poorer survival months after infection are not well understood. The aims of the present study were to analyze the overall mortality 10 months after admission. Methods: 762 patients with COVID-19 disease were included. Patients underwent a complete clinical evaluation, routine laboratory analysis and chest X-ray. Data collected included demographic and clinical data, such as vascular risk factors, tobacco or alcohol use, comorbidity, and institutionalization. Results: Ten-month mortality was 25.6%: 108 deaths occurred in-hospital, while 87 patients died after discharge. In-hospital mortality was independently related to NT-proBNP values > 503.5 pg/mL [OR = 4.67 (2.38–9.20)], urea > 37 mg/dL [3.21 (1.86–7.31)] and age older than 71 years [OR = 1.93 (1.05–3.54)]. NT-proBNP values > 503.5 pg/mL [OR = 5.00 (3.06–8.19)], urea > 37 mg/dL [3.51 (1.97–6.27)], cognitive impairment [OR = 1.96 (1.30–2.95), cancer [OR = 2.23 (1.36–3.68), and leukocytes > 6330/mm³ [OR = 1.64 (1.08–2.50)], were independently associated with long-term mortality. Conclusions: the risk of death remains high even months after COVID-19 infection. Overall mortality of COVID-19 patients during 10 months after hospital discharge is nearly as high as that observed during hospital admission. Comorbidities such as cancer or cognitive impairment, organ dysfunction and inflammatory reaction are independent prognostic markers of long-term mortality.