Objective. To evaluate the vitamin D status of our critically ill patients and its relevance to mortality. Patients and Methods. We performed a prospective observational study in the medical intensive care unit of a university hospital between October 2009 and March 2011. Vitamin D levels were measured and insufficiency was defined as <20 ng/mL. Results. Two hundred and one patients were included in the study. The median age was 66 (56–77) and the majority of patients were male (56%). The median serum level of vitamin D was 14,9 ng/mL and 139 (69%) patients were vitamin D insufficient on admission. While we grouped the ICU patients as vitamin D insufficient and sufficient, vitamin D insufficient patients had more severe acute diseases and worse laboratory values on admission. These patients had more morbidities and were exposed to more invasive therapies during stay. The mortality rate was significantly higher in the vitamin D insufficient group compared to the vitamin D sufficient group (43% versus 26%, P = 0,027). However, logistic regression analysis demonstrated that vitamin D insufficiency was not an independent risk factor for mortality. Conclusion. Vitamin D insufficiency is common in our critically ill patients (69%), but it is not an independent risk factor for mortality.

In CHB patients, combination of ELF and APRI has a better diagnostic value in predicting fibrosis of F3 or more.

Background: Interventions that reduce the generation or the effects of reactive oxygen species exert beneficial effects in a variety of models of septic shock. We investigatedthe effect of tempol, a low-molecular-weight membrane-permeable radical scavenger, on mesenteric blood flow and organ injury in a murine cecal ligation and puncture (CLP) model of septic shock. Materials and Methods: Forty-four Swiss albino mice were anesthetized with chloral hydrate (400 mg/kg, i.p.) and subjected to CLP (except for the sham-operated animals). The animals were divided randomly into 4 groups: the 1st group was sham operated (sham-operated group, n = 10); the 2nd group underwent CLP and was injected with saline (CLP + saline group, n = 12); the 3rd group was sham operated and treated with tempol (10 mg/kg, i.p., sham-treated + tempol group, n = 10); the 4th group underwent CLP and was treated with tempol (10 mg/kg, i.p., CLP + tempol group, n = 12). Mesenteric arterial blood flow (MABF) was measured by Doppler ultrasound. Poly(adenosine 5′-diphosphate-ribose) polymerase (PARP) activity was examined in the liver, lung, and kidneys. Results: In the CLP + saline group, the MABF was significantly lower than in the sham-operated group (p < 0.001). After tempol administration, MABF values significantly increased (p < 0.05). We observed significantly stronger PARP-positive staining in the lungs and kidney glomeruli in the CLP + saline group than in those of the sham-operated group (p_lung = 0.0148, p_glomeruli = 0.0025). A marked reduction in PARP activity was found in the lung and kidney glomeruli of the CLP + tempol group (p_lung = 0.0026, p_glomeruli = 0.0085). There was no significant effect of CLP on PARP activity in the liver and kidney tubuli (p_liver > 0.05, p_tubuli > 0.05). Conclusion: Tempol improved MABF in a CLP-induced septic shock model. Although tempol could not prevent the activation of PARP in the liver and kidney tubuli, it did attenuate PARP activation in the lung and kidney glomeruli.

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