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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.
A daily dose of vitamin K. antagonists (VKAs) may vary and its range depends on various interrelated factors. Low responsiveness to VKA (defined as a failure to achieve a target international normalized ratio [INR]) is associated with polymorphisms of the vitamin K epoxide reductase-oxidase complex gene (VKORC1). A highly prevalent promoter single-nucleotide polymorphism (VKORC1-1639 G>A, rs17878363) impairs VKORC1 expression and determines the interindividual variability of the target INR. We studied 57 patients receiving oral anticoagulation, including 50 subjects treated with acenocoumarol (mean dose: 5.7+2.3 mg/day) and 7 treated with warfarin (mean dose: 9.6±4.2 mg/day). The indications for the use of oral anticoagulant therapy were as follows: deep-vein thrombosis (N = 23); pulmonary embolism (N = 20); arterial thrombosis (N = 5); stroke (N = 4); atrial fibrillation with transient ischemic attacks (N = 2), and history of multiple thromboembolic events (N = 3). Identification of the VKORC1 genomic variation was performed using DNA sequencing methods. The prevalence of the mutated allele (VKORC1-1639A) was 41%. The VKORC1 -1639G allele carriers required a higher daily dose of acenocoumarol (5.9+1.9 mg) than the noncarriers (4.1+3.3 mg; P < 0.001). All of 5 low responded (who failed to achieve a target INR using standard dose requirements of VKAs) were homozygous for the 1639G allele. Low responders did not differ from good responders with respect to age, gender, and body mass index. Our findings suggest the potential benefits from pharmacogenetic testing, and provide evidence that the VKORCl -1639 G>A gene polymorphism may explain at least in part the low responsiveness to acenocoumarol.
Background. Burbot, Lota lota (L.), is a freshwater fish that is related to the marine family Gadidae. Its distribution is widespread in northern Canada. This species is not fished commercially at present. The high content of vitamin A and vitamin D in burbot liver oil was first reported in 1930. Since that time, there have been little or no research studies made on the nutritional components of burbot liver oil. The present study was aimed to assess the key nutritional components present in liver oil isolated from burbot caught in two northern Canadian lakes. Materials and Methods. Liver oil extracted from liver isolated from burbot caught in two northern Canadian lakes was tested for n-3 fatty acids and fat-soluble vitamins. Thermal stability of the liver oil was also evaluated. Burbot tissue was also analyzed for comparison purposes. Results. The contents of n-3 fatty acids, vitamin A and vitamin D of burbot liver oil were found to be comparable to those of the (reference) cod liver oil. Vitamin K content was discovered to be surprisingly high in comparison to known leafy green vegetable food sources. Conclusion. Burbot liver oil could provide a single source of dietary supplement of n-3 fatty acids, vitamin A, vitamin D, and vitamin K to meet the daily recommended nutritional allowances.
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