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Abstract. Vitamin K belongs to the family of fat-soluble vitamins and plays an important role in hemostasis, bone metabolism and may affect cerebral sphingolipid synthesis. It is a cofactor necessary for posttranslational γ-carboxylation of glutamyl residues in selected proteins such as the osteocalcin, and procoagulation factors II, VII, IX, X. Vitamin K deficient individuals appear to have more undercarboxylated proteins, which are functionally defective. The witamin K deficiency has been frequently documented in patients with cystic fibrosis. The main possible causes of this deficiency include: fat malabsorption due to pancreatic exocrine insufficiency, cholestatic or noncholestatic liver disease, reduced production of vitamin K by colonic flora related to chronic antibiotic treatments, bowel resections and increased mucous accumulation in the bowel. CF patients are more prone to osteopenia, caused by chronic vitamin K shortage, than to coagulopathy. Despite available evidence, which strongly suggests that all CF patients are at risk for developing vitamin K deficiency, its supplementation doses have not been established. Recent recom- mendations from Europe and the UK have suggested varied doses ranging from 0.3 mg/day to 10 mg/week. Further studies, both cross sectional and longitudinal interventional, are still required to determine routine and therapeutic supplementation doses.
Abnormal vitamin K status was documented in patients with chronic kidney diseases (CKD), especially those undergoing hemodialysis. The data related to patients undergoing peritoneal dialysis (PD) are contradictory. Therefore, in the present study we aimed to evaluate vitamin K status in patients with CKD who are treated with continuous ambulatory PD. Twenty-eight patients entered into the study. Dialysis vintage ranged from 3 to 89 months. Vitamin K status was assessed in all subjects using undercarboxylated prothrombin measurement (PIVKA-II). In addition, total protein and albumin levels, total cholesterol, LDL cholesterol, triglyceride, calcium, urea and creatinine concentrations were determined. PIVKA-II concentrations were abnormal in 13 (46.4 %) subjects. BMI values, both total and LDL cholesterol concentrations were significantly higher in patients with than those without vitamin K deficiency. Moreover, PIVKA II levels correlated with BMI values (r = 0.441, p < 0.019), LDL cholesterol (r = 0.434, p < 0.021) and creatinine (r = 0.406, p < 0.032) concentrations. However, through the use of logistic regression analysis and multiple regression analysis, no clinical factor was documented to be the independent risk factor of vitamin K deficiency. In conclusion, vitamin K deficiency is a frequent condition in peritoneally dialyzed patients. Assessment of vitamin K status should become a standard procedure in this group of patients.
Introduction. Cystic fibrosis (CF) patients are at risk of developing vitamin K. deficiency. However, there is no clinical data clearly describing vitamin K status in the youngest age group. Therefore, in the present study we aimed to assess body resources of vitamin K in children aged up to 3 years and to correlate vitamin K status with selected clinical factors. Material and methods. The study comprised 52 CF patients receiving and not receiving vitamin K supplementation. In all subjects, the concentration of the undercarboxylated prothrombin (PIVKA-II), as a marker of vitamin K deficiency, was determined. Results. PIVKA-II concentrations were pathological in 24 (46.2%) CF children, in re- maining 28 (53.8%) patients vitamin K status was found to be normal. No statistical differences in clinical parameters (Z-score for body height and weight, number of hospitalizations and sweat chloride concentrations) neither in distribution of Pseudomonas aeruginosa colonization nor in pancreatic status between selected subgroups with normal and abnormal PIVKA-II concentrations were documented. Normal vitamin K status was more frequent in patients receiving proper vitamin K supplementation (p < 0.0078). However, vitamin K deficiency appeared in 5 out of 21 patients receiving at least 2.5 mg vitamin K/week. In logistic regression model, no clinical parameter was proven to be a risk factor for vitamin K deficiency. 'Conclusion. Vitamin K deficiency is frequent in CF infants and toddlers, and may also appear in those receiving recommended supplementation. There is no strong relationship between clinical expression of the disease and vitamin K status.
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