Mortality and COVID Infection: Predictors of Mortality 10 Months after Discharge.

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.

Klotho Levels and Their Relationship with Inflammation and Survival among Alcoholic Patients.

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 ß = 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.

Sclerostin in Excessive Drinkers: Relationships with Liver Function and Body Composition.

BACKGROUND: Sclerostin was initially described as an inhibitor of the Wnt-ß 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.

Brain-derived neurotrophic factor among patients with alcoholism.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) is involved in neurogenesis and in the protection against oxidative damage and neuronal apoptosis. After exercise, there is an increased expression of this myokine, especially in skeletal muscle and brain. Low BDNF levels have been described in neurodegenerative diseases. Alcoholics show both muscle atrophy and brain atrophy. Thus, this study was performed in order to analyze serum BDNF levels among alcoholics and their associations with brain atrophy and muscle strength. METHODS: Serum BDNF values were determined to 82 male alcoholics and 27 age-matched controls, and compared with handgrip strength, with the presence of brain atrophy, assessed by computed tomography, and with the intensity of alcoholism and liver function derangement. RESULTS: BDNF levels and handgrip strength were significantly lower among patients. Handgrip strength was correlated with BDNF values, both in the whole population and in alcoholics, especially in patients over 59 years of age. BDNF was poorly related to liver dysfunction but showed no relationship with brain atrophy or age. CONCLUSION: Chronic alcoholics show decreased BDNF serum levels that are related to muscle function impairment rather than to age, brain atrophy, liver dysfunction, or the amount of ethanol consumed.

Incidence of cancer and mortality among heavy alcoholics.

BACKGROUND AND AIMS: Cancer risk is increased in alcoholics. Heavy ethanol consumption is also associated with other potentially lethal conditions such as cirrhosis, diabetes, hypertension, dyslipidemia or malnutrition, that increase mortality. The aim of the present study is to analyze the impact on mortality of new cancer development in a cohort of heavy alcoholics. METHODS: Three hundred and thirty nine heavy alcoholics (about 200 g ethanol/daily during more than 15 years), initially admitted for organic problems to our service (reference hospital) were prospectively followed up for a maximum period of 120 months (median = 26, interquartile range = 12-60 months), either as outpatients or during successive admissions. Clinical and laboratory evaluation including incidence of new cancer and drinking habits were recorded at each appointment, as well as mortality. RESULTS: During the study period 57 patients developed cancer and 151 died. Only 75 did not relapse in alcohol drinking. Mortality was related to deranged liver function, relapse of alcohol drinking, and malnutrition, whereas age, the development of new cancer, or the presence of diabetes, dyslipidemia or hypertension did not influence on mortality, especially in cirrhotics and among those who did not quit drinking. Cancer was related to mortality only among non-cirrhotics, together with ethanol abstention and age. CONCLUSIONS: Heavy drinking is associated with high mortality among alcoholic patients admitted to the hospital. If a patient is already cirrhotic or if there is drinking relapse, the development of a new cancer, the concurrent presence of diabetes, hypertension, dyslipidemia, or advanced age have no impact on survival. Mortality is only related to deranged liver function, relapse of alcohol drinking, and malnutrition.

Prognostic Value of Serum Iron, Ferritin, and Transferrin in Chronic Alcoholic Liver Disease.

Ethanol increases iron absorption. Therefore, increased amount of iron reaches the liver, and exerts pro-oxidant effects and stimulates ferritin synthesis and hepatic stellate cell activation, promoting fibrosis and inflammation. These mechanisms would theoretically support a role of ferritin as a marker of the transition to liver cirrhosis, and, consequently, as a prognostic factor, but there is controversy regarding its behavior in alcoholics. We analyzed among 238 severe alcoholics the prognostic value of iron, ferritin, transferrin, transferrin saturation index (TSI) and total iron binding capacity (TIBC), and the relationships of these variables with liver function, proinflammatory markers (C-reactive protein (CRP), interleukin (IL)-6, IL-8, and tumor necrosis factor α), and the presence of cirrhosis. Patients showed higher serum ferritin (Z = 2.50, p = 0.031) but lower transferrin (t(264) = 4.81, p < 0.001), TIBC (t(262) = 4.44, p < 0.001), and iron (Z = 3.19, p = 0.001) values compared with 32 age- and sex-matched controls. Ferritin was related to inflammatory cytokines such as IL-8 (ρ = 0.18, p = 0.012) and to IL-6 (ρ = 0.16, p = 0.016), but not to liver function. On the contrary, cirrhotics showed lower transferrin (t(234) = 4.77, p < 0.001) and TIBC (t(232) = 4.67, p < 0.001), but higher TSI (Z = 3.35, p < 0.001) than non-cirrhotics. Transferrin, TSI, and TIBC were related to liver function impairment (marked differences among the Child's groups regarding transferrin (KW (2) = 22.83, p < 0.001), TSI (KW (2) = 15.81, p < 0.001), and TIBC (KW (2) = 21.38, p < 0.001) but only weakly to inflammation (inverse relationships between IL-6 and total iron (ρ = - 0.16, p = 0.017), TIBC (ρ = - 0.20, p = 0.002), and transferrin (ρ = - 0.20, p = 0.003). In accordance, albumin, IL-6, alcohol quitting, and TSI, in this order, were independently related to mortality, but not ferritin or iron.

Digit ratios among the modern population of the Canary Islands

Sexual differences in the index to ring finger length ratio (2D:4D ratio) have been observed since more than 150 years ago, and they are already present in the foetus. Homeobox genes, which also control the differentiation of testes and ovaries, are involved in finger conformation, which is subjected to the influence of testosterone and estrogen levels. In general, women show larger 2D:4D digit ratios, although differences between sexes are subjected to ethnic variations. This study was performed in order to analyse the absolute values of several digit ratios (2D:4D; 4D:3D; 2D:3D) among 164 young adults of Tenerife (101 women). Finger lengths were directly measured dorsally using a calliper with an accuracy level of 0.01 mm. Dorsal digit lengths were defined as the distance between the fingertip and the dorsal base of the proximal phalanx, in a position in which fingers and palms formed an angle of 90º. We found that 2D:4D of both hands (for instance, women=0.9631 ± 0.02647; men= 0.9535 ± 0.02507 for the left 2D:4D ratios), the left 2D:3D (0.9063 ± 0.02216 in women; 0.8980 ± 0.01931 among men) and the right 4D:3D ratios (0.9377 ± 0.03625 among women vs 0.9471 ± 0.02138 among men) were significantly different among men and women. The magnitude of the difference among sexes is similar to that reported for other populations, and they allow for the elaboration of a discriminant function with an accuracy of 60.4%, that reaches 86% if stature is also included. We applied this discriminant function to a test group composed of 36 randomly selected women and 24 men, obtaining an accuracy of 58.33% and 81.67%, respectively

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