Prognostic value of muscle mass assessed by DEXA in elderly hospitalized patients.

OBJECTIVES: To analyze the prognostic value of lean mass measured by DEXA and to compare it with lean muscle mass assessed by anthropometrics, calf circumference, subjective assessment and with physical muscle function tests in elderly hospitalized patients. METHODS: We study 187 hospitalized patients aged ≥65 years. We assessed nutrition by anthropometrics, mid arm muscle area, triceps skinfold and calf circumference, by subjective nutritional assessment and by DEXA, lean and fat mass and bone mineral density (BMD); muscle function by handgrip strength, gait speed, standing balance and stand-up test; disability and activities of daily living and the clinical frailty score; and comorbidity by Charlson index. Outcomes were assessed by mortality at 100 days and long-term follow up. RESULTS: Male sex showed higher comorbidity and mortality although females were older, with decreased muscle mass and function, disabled and frailer. Long term mortality was also related to decreased lean mass evaluated by subjective assessment, midarm anthropometry, calf circumference and DEXA (appendicular lean and fat mass and BMD); muscle function impairment assessed by gait speed, standing balance and stand-up test; frailty; disability and comorbidity. Variables with long term independent predictive value were comorbidity, inability to perform any of the muscle function tests: gait speed, standing balance and stand-up; subjective nutritional score, appendicular lean mass under the 10th percentile and male sex. CONCLUSIONS: Females are older and frailer but with lower comorbidity; they showed a better survival. The best predictive mortality factor was comorbidity, but DEXA appendicular lean mass under the 10th percentile showed an independent and high predictive value on mortality.

Prognostic value of physical function tests and muscle mass in elderly hospitalized patients. A prospective observational study.

AIM: To determine the prognostic value for mortality of physical function tests, muscle mass loss, disability and frailty in elderly hospitalized patients. METHODS: We prospectively included 298 hospitalized patients aged >60 years (152 men and 146 women). We assessed comorbidity using the Charlson Comorbidity Index; nutrition by body mass index, midarm muscle area and subjective nutritional score; physical muscle function by handgrip strength, gait speed, standing balance and stand up test; disability using the Barthel test and activities of daily living; frailty by the clinical frailty scale and Fried frailty index; and cognitive impairment by the Pfeiffer test. We assessed 100-day and long-term mortality. RESULTS: We found a high prevalence of malnutrition, comorbidity, cognitive impairment, physical function impairment, disability and frailty. Mortality at 100 days was 15.1%, with a long-term median survival of 989 days. Mortality was significantly related to age, comorbidity, nutritional status, physical function, disability and frailty. Serum vitamin D3 levels were not related to mortality. Independent prognostic value for long-term mortality was shown by: (i) incapacity to carry out any of the walking, stand up and standing balance tests; (ii) male sex; (iii) aged >80 years; (iv) impaired handgrip strength or gait speed; (v) Charlson Comorbidity Index ≥1; and (6) impaired muscle mass of subjective nutritional score. CONCLUSIONS: In elderly hospitalized patients, there is an important role of muscle regarding prognosis, mainly related to physical function, but also and independently regarding muscle mass. Geriatr Gerontol Int 2018; 18: 57-64.

Cirrosis hepática criptogenética y mutaciones de factores protrombóticos, ¿una mera asociación? / Cryptogenetic liver cirrhosis and prothrombotic mutations - a mere association?

En la cirrosis hepática es frecuente que se produzca activación de la trombina y microtrombosis en las raicillas de la vena porta intrahepática, en parte debido al déficit de proteína C, y en parte a alteración del equilibrio coagulación-anticoagulación-fibrinólisis. Por eso hay una incidencia aumentada de trombosis portal. La trombina no solo puede generar la formación de un trombo, sino que puede activar a las células estrelladas y estimular la fibrogénesis. Además, la isquemia asociada a la trombosis puede promover la síntesis de factores de crecimiento involucrados en la fibrogénesis. La coincidencia en un mismo paciente de mutaciones protrombóticas, como factor V Leiden o polimorfismos del PAI- 1, puede acelerar todo este proceso. Presentamos dos casos de cirrosis criptogenética en los que los únicos factores identificables capaces de causar fibrogénesis acelerada fueron mutaciones del factor V y del PAI-1. Estas observaciones, además de apoyar la hipótesis de que las citadas mutaciones puedan por sí mismas llegar a provocar cirrosis, sugieren que es recomendable determinar si existen polimorfismos del factor V, PAI-1 y protrombina en el estudio de la cirrosis criptogenética (AU)

Thrombin activation and microthrombosis of intrahepatic portal venules is a common feature in liver cirrhosis, due in part to relative protein C deficiency and altered coagulation-anticoagulation-fibrinolysis balance. Extension of this microthrombotic process to larger portal vessels explains the increased incidence of portal vein thrombosis in liver cirrhosis. Thrombin not only leads to thrombosis, but also activates liver stellate cells and promotes fibrogenesis. Also, ischemia associated with thrombosis up-regulates the expression and secretion of growth factors involved in fibrogenesis. The coincidence in a given patient of prothrombotic mutations, such as factor V Leiden or PAI-1 polymorphisms, can accelerate the fibrogenetic process. We hereby present two cases of liver cirrhosis in which etiologic evaluation was negative except for the finding of a factor V Leiden mutation in one case and the 4G/5G PAI polymorphism in the second case. These observations support the hypothesis that these mutations may be involved in the etiology of some cases of cirrhosis, or, at least, accelerate the evolution of the disease. It is therefore convenient to search for the presence of prothrombotic mutations in patients with cryptogenetic cirrhosis(AU)

Pulmonary thromboembolism in a patient with May-Thurner syndrome: a case report

A 41-year-old woman was admitted to the emergency room with symptoms compatible with deep vein thrombosis affecting the left lower extremity and pulmonary thromboembolism. A CT scan was consistent with pulmonary emboli and thrombosis of the iliac veins extending to the inferior vena cava, which persisted even after correct systemic fibrinolytic therapy. For this reason, a venography was performed and local thrombolysis was administered. Venography revealed a compression of the left common iliac vein caused by the right common iliac artery, so that the patient was diagnosed with May-Thurner syndrome. The clinical features of this anatomical condition and sometimes lethal clinical syndrome are discussed

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Cryptogenetic liver cirrhosis and prothrombotic mutations - A mere association?

Thrombin activation and microthrombosis of intrahepatic portal venules is a common feature in liver cirrhosis, due in part to relative protein C deficiency and altered coagulation-anticoagulation-fibrinolysis balance. Extension of this microthrombotic process to larger portal vessels explains the increased incidence of portal vein thrombosis in liver cirrhosis. Thrombin not only leads to thrombosis, but also activates liver stellate cells and promotes fibrogenesis. Also, ischemia associated with thrombosis up-regulates the expression and secretion of growth factors involved in fibrogenesis. The coincidence in a given patient of prothrombotic mutations, such as factor V Leiden or PAI-1 polymorphisms, can accelerate the fibrogenetic process. We hereby present two cases of liver cirrhosis in which etiologic evaluation was negative except for the finding of a factor V Leiden mutation in one case and the 4G/5G PAI polymorphism in the second case. These observations support the hypothesis that these mutations may be involved in the etiology of some cases of cirrhosis, or, at least, accelerate the evolution of the disease. It is therefore convenient to search for the presence of prothrombotic mutations in patients with cryptogenetic cirrhosis.

Síndrome serotoninérgico por linezolid y metoclopramida / Serotoninergic syndrome due to linezolid and metoclopramide

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Effects of selenium on liver and muscle contents and urinary excretion of zinc, copper, iron and manganese.

Selenium is a main component of glutathione peroxidase (GPX), a key antioxidant enzyme. Other elements, such as zinc, copper, manganese and iron, are also involved in the pathogenesis of oxidative damage as well as in other important metabolic pathways. The effects of selenium supplementation on the metabolism of these elements have yield controversial results .The aim of this study is to analyse the effects of selenium supplementation on liver, muscle and urinary excretion of zinc, copper, iron and manganese in a situation of oxidative stress, such as protein deficiency. The experimental design included four groups of adult male Sprague-Dawley rats, which received the Lieber-DeCarli control diet, an isocaloric 2 % protein-containing diet and another similar two groups to which selenomethionine (6 mg/l liquid diet) was added. After sacrifice (5 weeks later), muscle, liver and serum selenium were determined, as well as muscle, liver and urinary zinc, copper, manganese and iron and liver GPX activity and liver malondialdehyde. Selenium addition led to decreased liver copper, increased muscle copper, increased copper excretion and increased liver iron, whereas zinc and manganese parameters were essentially unaltered. Muscle, liver and serum selenium were all significantly correlated with liver GPX activity.