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At least 19 recordsLinked to original sources
PubMed1993

Vitamin K deficiency.

Vitamin K (phylloquinone, K1; menaquinone, K2) functions as an essential cofactor for the synthesis of the coagulation protein factors II, VII, IX, X and protein C and S by promoting a unique post-translational modification of specific glutamic acid residues to gamma-carboxylglutamic acid, thus mediating calcium binding to phospholipid surfaces. Vitamin K deficiency results in a depletion of liver stores of phylloquinone, decreased plasma levels of vitamin K1, increased levels of K1 epoxide, appearance of noncarboxylated protein (PIVKA), decreased levels of functioning vitamin K-dependent clotting factors and prolongation of the APTT, PT and thrombotest. When the progression of deficiency leads to abnormal clotting tests a generalized bleeding tendency occurs. Noncarboxylated prothrombin (PIVKA-II) determinations are a sensitive indicator of vitamin K deficiency. Although Vitamin K deficiency can occur at any age (warfarin, fasting, antibiotic therapy, malabsorption syndromes) the major public health problem is related to prevention of early, classic and late hemorrhagic disease of the newborn (HDN). A single dose of oral or parenteral vitamin K prevents classic HDN but the most effective way to prevent early HDN is by giving large doses to the mother prior to delivery (2 weeks). Late HDN in breastfed infant occurs with a prevalence of about 20 per 100,000 live births when no neonatal prophylaxis is given. Parenteral (1 mg) K1 prevents late HDN and single or repeated doses of oral vitamin K reduces the incidence but does not eliminate all late HDN. The optimal (cost, feasibility, effective) mode of neonatal prophylaxis remains to be determined.

Adult↗
PubMed1982

The effect of vitamin E on warfarin-induced vitamin K deficiency.

Vitamin K-deficient animals and humans developed a more severe coagulopathy when treated with vitamin E, which was due to further reduction in the vitamin K-dependent coagulation factors (II, VII, IX, and X). This phenomenon was not seen in normal vitamin K-sufficient animals or human subjects. The mechanism by which vitamin E causes this effect is not known. These coagulation factors are produced by the liver in precursor forms and are converted to functional proteins by a vitamin K-dependent reaction. Analysis of one of these coagulation factors, prothrombin (factor II), in plasma of vitamin K-deficient animals and humans treated with vitamin E was done in this study. The precursor of factor II is antigenically similar to biologically active factor II and can be activated to form thrombin by Echis carinatus venom. The data showed that functional factor II coagulant activity was reduced below base in warfarin-treated humans and animals given vitamin E. Factor II antigen as determined by electroimmunoassay in humans and factor II coagulant activity as measured using Echis venom in animals were unchanged and no different from untreated controls. The data suggest that vitamin E acts at the vitamin K-carboxylase step of carboxylation of precursor prothrombin and not in the synthesis of the precursor protein.

Animals↗
PubMed1988

Vitamin K deficiency from dietary vitamin K restriction in humans.

Vitamin K is required for the maintenance of normal hemostatic function. Ten college-aged male subjects chose diets restricted in vitamin K content for 40 d. Median phylloquinone intakes based on analysis of food composites dropped from 82 micrograms/d during the prestudy period to 40 and 32 micrograms/d at d 9 and 27 of dietary restriction, respectively. Serum phylloquinone concentrations fell from a mean of 0.87 to 0.46 ng/mL during a 21-d period of vitamin K restriction. Supplementation with 50 micrograms phylloquinone/d for 12 d increased serum phylloquinone to 0.56 ng/mL, and supplementation with 500 micrograms phylloquinone/d increased serum phylloquinone to 1.66 ng/mL. Vitamin K restriction resulted in alterations in a functional clotting assay that detects undercarboxylated prothrombin species in plasma and in a decrease in urinary gamma-carboxyglutamic acid. Supplementation with either 50 or 500 micrograms of phylloquinone restored both these indices to near normal values. These data are consistent with a human dietary vitamin K requirement of approximately 1 microgram/kg body wt/d.

Adult↗
PubMed1983

Warfarin inhibits both procoagulant activity and metastatic capacity of Lewis lung carcinoma cells. Role of vitamin K deficiency.

Chronic vitamin K deficiency, either dietary or pharmacologically induced with warfarin, depressed significantly the growth of lung secondaries in a spontaneously metastasizing murine tumor, the Lewis Lung Carcinoma. This effect was associated with a marked depression of the procoagulant activity of cancer cells, which could contribute to fibrin deposition around the tumor. Cellular anticoagulation may thus be an important mechanism in the antimetastatic effect of warfarin.

Animals↗
PubMed1989

Vitamin K absorption capacity and its association with vitamin K deficiency.

We measured plasma vitamin K concentrations in 194 5-day-old infants three hours after administration of a 4-mg dose of vitamin K (menaquinone-4, Kaytwo syrup, Eisai Co Ltd, Tokyo, Japan). We investigated association with other factors contributing to vitamin K deficiency. These plasma vitamin K concentrations varied greatly among the neonates from values below the limit of detection (2 ng/mL) to more than 1000 ng/mL. The vitamin K concentration was associated with nutritive vitamin K deficiency represented by plasma protein induced by vitamin K absence or antagonist-II (PIVKA-II) values. The wide variation in vitamin K absorption is considered to be one of the major causative factors in infantile vitamin K deficiency.

Administration, Oral↗
PubMed1989

[Activity of enzymes participating in xenobiotic metabolism and the condition of microsomal membranes of rat liver in vitamin K deficiency].

Alimentary deficiency or vitamin K (vitamin K-poor diet) as well as the vitamin deficiency resulting from sinkumar administration are accompanied by a decreased activity of microsomal demethylases, hydroxylase, NADH- and nNADPH-reductases of dichlorophenolindophenol and neotrazolium. The activity of cytosolic enzymes (only glutathione-S-transferases, aryl- and allyl esterases) is diminished in a lesser degree. Vitamin K deficiency does not significantly interfere with the effect of the xenobiotic metabolism enzyme inducer (phenobarbital) or the cytochrome P-450 inhibitor (cobalt chloride). The changes in the enzyme activity result in a decrease of acetanilide biotransformation. A possible reason for the observed changes in the activity of microsomal enzymes is the weakening of hydrophobic and polar interactions in microsomal membranes. This hypothesis was confirmed by experiments with the use of membrane perturbants as well as by solubilization of membrane-bound enzymes.

Acetanilides↗
PubMed1981

Effect of vitamin E on prothrombin levels in warfarin-induced vitamin K deficiency.

Rats rendered lightly vitamin K deficient with warfarin (0.01 mg/100 g, IP) and given the equivalent of 1000 units of vitamin E/kg IM for 7 days, showed a marked reduction in functional factor II activity, but normal factor II levels using Echis venom on coagulation analysis. In 12 humans receiving warfarin, vitamin E was administered in doses of 100 or 400 units/day orally for 4 wk. The results in these patients showed no significant change in the prothrombin time, factor II coagulant activity, or factor II antigen (by electroimmunoassay). However, by using a ratio of factor II coagulant activity to immunoreactive protein, significant reduction was observed when compared to pretreatment ratios. These data suggest that vitamin E acts at the step mediated by vitamin K and not in the synthesis of the factor II precursor. Although the administration of high doses of vitamin E in animals, and possibly humans, with vitamin K deficiency potentiates the vitamin K deficiency, this effect is not clinically obvious with 400 IU/day or less.

Adult↗
PubMed1988

Fracture healing and osteocalcin metabolism in vitamin K deficiency.

Osteocalcin (a vitamin K-dependent, bone-specific protein) is widely accepted as a marker of osteoblastic activity. The present study was conducted to determine if a vitamin K deficiency would affect fracture healing by virtue of an alteration in osteocalcin metabolism. Thirty male Sprague-Dawley rats were divided into two groups. The control group was fed a diet that was lacking in, but offered water replete with vitamin K. The experimental group was fed a vitamin K-deficient diet and was offered water that was lacking in vitamin K. After two weeks, vitamin K deficiency was established in the experimental group as shown by decreased urinary excretion of gamma-carboxyglutamic acid and an elevation of serum prothrombin times to between two to two and one-half times the control values. At this time, a standard, closed femoral fracture was produced. Six weeks later, the animals were killed. The bones were biomechanically tested in torsion. Subsequent to mechanical testing, the calluses were retrieved, and the osteocalcin content and the degree of gamma carboxylation of the osteocalcin in the calluses were measured. The results show that despite significant alterations in the gamma carboxylation of osteocalcin and elevation of prothrombin times to two to two and one-half times the control values, there were no differences in the mechanical properties of the calluses. Furthermore, there were no differences in the content or gamma carboxylation of osteocalcin in these calluses. Apparently, in vitamin K deficiency, fracture callus achieves normal mechanical properties and may have a mechanism for the gamma carboxylation of glutamic acids in osteocalcin despite a substantial depression of this activity in the rest of the body.

1-Carboxyglutamic Acid↗
PubMedDate not supplied

Vitamin K deficiency and osteopenia in disuse-affected limbs of vitamin D-deficient elderly stroke patients.

Bone mineral density is reduced in stroke patients on the hemiplegic and contralateral sides, reflecting a degree of paralysis and vitamin D deficiency. Because the deficiency of vitamin K, a factor essential for site-specific carboxylation of bone Gla protein, is also associated with reduced bone mineral density, an additional contribution of vitamin K to bone changes was assessed in 168 elderly patients with long-standing post-stroke hemiplegia and hypovitaminosis D. Sera were analyzed to relate vitamin K1 concentrations to bone-related biochemical indexes and bone mineral density measured by radiodensitometry of the second metacarpal. Bone mineral density was lower on both sides in patients than in the 56 controls (P < 0.02). Serum vitamin K1 concentrations, which correlated positively with bone Gla protein concentrations (P < 0.0001), were lower in patients (0.48 +/- 0.47 nmol/L) than controls (1.33 +/- 0.49; P < 0.0001). Serum bone Gla protein and 25-hydroxyvitamin D concentrations were lower in patients than controls (P < 0.0001), whereas ionized Ca concentrations were higher in patients (1.277 +/- 0.041 mmol/L) than controls (1.210 +/- 0.049; P < 0.0001), correlating with the Barthel index. Multivariate linear regression identified vitamin K1, bone Gla protein, 25-hydroxyvitamin D, ionized calcium, and the Barthel index as independent bone mineral density determinants on the hemiplegic side and 25-hydroxyvitamin D, calcium, and the Barthel index on the intact side. Immobilization and vitamin K deficiency had stronger osteopenic effects on the hemiplegic side than contralaterally.

Aged↗
PubMed1985

Hypercalciuria during experimental vitamin K deficiency in the rat.

Vitamin K promotes the formation of gamma-carboxylated glutamate (GLA) in several protein species. GLA residues have a high affinity for the Ca ion. In the present study, we tested the hypothesis that experimental vitamin K deficiency in rats could induce changes in Ca metabolism. Vitamin K depletion, which was associated with a reduction in urinary GLA excretion, induced within 7 days a significant increase in cumulative urinary Ca excretion that persisted throughout the 21 days of study. The hypercalciuria of vitamin K-deficient rats was corrected on vitamin K supplementation. No concomitant changes were observed in intestinal Ca absorption determined by a balance technic or of skeletal resorption and apposition rates determined by bone histomorphometry. Plasma Ca, but not total protein concentration, of vitamin k-depleted rats showed a transient decrease at day 15 that disappeared at day 21. plasma sodium, phosphate and 1,25(OH)2 vitamin D concentration, and urinary phosphate, sodium, and creatinine excretion remained unchanged. In conclusion, vitamin k deficiency in the rat induced hypercalciuria that could be of renal origin. Its possible relationship to vitamin K-dependent renal GLA protein remains to be clarified.

1-Carboxyglutamic Acid↗
PubMed1985

The prevalence of vitamin K deficiency in chronic gastrointestinal disorders.

Vitamin K deficiency results in the appearance of abnormal prothrombin, deficient in gamma-carboxyglutamic acid, in the blood. The presence of abnormal prothrombin can be eliminated or lowered by the administration of vitamin K. Since the abnormal prothrombin antigen assay is approximately 1000-fold more sensitive than the prothrombin time for the diagnosis of vitamin K deficiency, this assay was used to evaluate patients with intestinal abnormalities. Vitamin K deficiency was found in 18 of 58 patients (31%) with chronic gastrointestinal disease and/or resection. All patients with vitamin K deficiency had either Crohn's disease involving the ileum or ulcerative colitis treated with sulfasalazine or antibiotics. Abnormal prothrombin levels returned toward normal in patients treated with vitamin K but not in patients who were not treated with vitamin K. The mean plasma vitamin E level in patients with vitamin K deficiency was significantly lower than in vitamin-K sufficient patients (p less than 0.01). We conclude that certain chronic forms of gastrointestinal disorders are associated with vitamin K deficiency.

Adolescent↗
PubMed1993

Prevention of vitamin K deficiency in infancy by weekly administration of vitamin K.

Vitamin K prophylaxis has been developed to prevent classic haemorrhagic disease of the newborn. Single vitamin K administration after birth has been reported to fail, resulting in late haemorrhagic disease of the newborn. The preventive effect of oral administration of vitamin K1 1 mg, repeated weekly during the first three months of life, was studied in 48 healthy breast-fed infants, by determination of thrombotest, PIVKA-II and vitamin K1 concentrations at the age of 4, 8 and 12 weeks. All infants showed normal thrombotest values and PIVKA-II was not detectable. Vitamin K1 concentrations were negatively correlated with the number of days elapsed since the most recent vitamin K administration. Six to seven days after the latest application, mean levels were 1223, 927 and 748 pg/ml at ages 4, 8 and 12 weeks, respectively. In conclusion, weekly administration of vitamin K1 1 mg offers complete protection against vitamin K deficiency and does not result in an accumulation of vitamin K1 in the blood.

Biomarkers↗
PubMed2003

Vitamin K deficiency in severely disabled children.

Vitamin K status was examined in 21 severely disabled children in our hospital from September 2001 to August 2002, and 9 children were found to have a vitamin K deficiency. The 21 patients were divided into two groups: group A, 9 patients with vitamin K deficiency, and group B, 12 patients without vitamin K deficiency. The laboratory data and background factors in the two groups were compared statistically. In group A, all patients received enteral nutrition and anticonvulsants. The protein induced by vitamin K absence-II values were elevated in eight patients. Seven exhibited a bleeding tendency. Six developed vitamin K deficiency in association with infection and four were treated with antibiotics. All showed a good response to the administration of vitamin K. The patients in group A had factors such as use of antibiotics, infection, and elemental nutrition at significantly higher rates than those in group B. Data indicating nutrition factors such as body weight, caloric intake, total protein level, and hemoglobin level were not significantly different between the two groups. Severely disabled children suffer from deficiencies of various nutritional elements. However, vitamin K deficiency in severely disabled children has not been fully investigated. Infection, use of antibiotics, and elemental nutrition are risk factors for vitamin K deficiency in severely disabled children. In severely disabled children, there might be marginal vitamin K intake via enteral nutrition, so more vitamin K supplementation is necessary, especially with infection and use of antibiotics.

Adolescent↗