Vitamin K in hereditary resistance to oral anticoagulant drugs

Ra, O'Reilly

doi:10.1152/ajplegacy.1971.221.5.1327

Cited by 32 publications

(9 citation statements)

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“…In the present study, restriction of dietary intake of vitamin K, to 10 tig of vitamin K, per day produced a decrease in urinary gla excretion in the young subjects as a group but remained unchanged in the elderly as a group. Dietary restriction resulted in a decreased synthesis of gla in the young subjects alone as a group as determined by the decreased excretion of urinary gla in this group during the depletion period (days [5][6][7][8][9][10][11][12][13][14][15][16][17]. The elderly subjects, as a group, failed to display any decreases in the urinary excretion of gla during the depletion period.…”

Section: Discussionmentioning

confidence: 99%

“…Studies that correlate vitamin K, intake with vitamin K status are scant and present limitations for the normal healthy population (5)(6)(7)(8)(9)(10)(11)(12). Indeed, many of the studies published to date have involved sick, hospitalized people who suffered pathological conditions that may have altered their vitamin K requirements (6,12).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, many of the studies published to date have involved sick, hospitalized people who suffered pathological conditions that may have altered their vitamin K requirements (6,12). In other instances the relationship between dietary vitamin K intake and vitamin K status was studied in subjects taking antibiotics (5) or in subjects where metabolic conditions were not adequately controlled (7,8,11). While antibiotics are commonly used in hospital settings, estimates of dietary vitamin K requirements established under these conditions cannot be extrapolated to normal healthy individuals.…”

Section: Introductionmentioning

confidence: 99%

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Dietary induced subclinical vitamin K deficiency in normal human subjects.

Ferland¹,

Sadowski²,

O’Brien³

1993

J. Clin. Invest.

133

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A subclinical vitamin K deficiency was induced in 32 healthy subjects (four groups of eight males and females) aged 20-40 and 60-80 yr residing in the Metabolic Research Unit of the Human Nutrition Research Center on Aging at Tufts University. Volunteers were initially fed (4 d) a baseline-period diet containing the recommended daily allowance for vitamin K which is equivalent to 80 ;tg/d of phylloquinone (vitamin K1).During the baseline period various parameters of vitamin K nutritional status were monitored. The baseline period was followed by a 13-d depletion period during which the subjects were fed a very low vitamin K1 diet (-10 ;ug/d). After depletion, the subjects entered a 16-d repletion period (four stages lasting 4 d each) during which time they were repleted with 5, 15, 25, and 45 ,ug of vitamin K1 per day. Vitamin K1 depletion dramatically and significantly decreased plasma vitamin K1 levels (P < 0.0001) in both elderly and young groups to values 13-18% of day 1 (elderly 0.22 nM, young 0.14 nM). Repleting the subjects with up to 45 ;ig of vitamin K1 per day failed, in the case of the young subjects, to bring plasma vitamin K1 levels back into the normal range. Dietary vitamin K1 restriction induced different responses in the urinary excretion of-y-carboxyglutamic acid between the young and the elderly subjects with values decreasing significantly (P < 0.03) in the young while remaining unchanged in the elderly. The vitamin K1 depletion period had no significant effect on either prothrombin and activated partial thromboplastin times, or Factor VII and protein C (as determined by antigenic and functional assays). By using a monoclonal antibody, descarboxy prothrombin was found to increase slightly but significantly in both groups (P < 0.05) as a consequence of the low vitamin K1 diet. This study clearly shows that a diet low in vitamin K1 can result in a functional subclinical deficiency of vitamin K (decreased urinary y-carboxyglutamic acid excretion) without affecting blood coagulation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dietary induced subclinical vitamin K deficiency in normal human subjects.

Ferland¹,

Sadowski²,

O’Brien³

1993

J. Clin. Invest.

133

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“…In one study (22), neither the antibiotics nor their regimens were stated and, thus, it is impossible to assess the efficacy of the antibiotic regimens in killing intestinal bacteria. In the other study (23), neither neomycin nor tetracycline administration for 4 weeks was able to produce hypoprothrombinemia in four out of five subjects.…”

Section: Discussionmentioning

confidence: 69%

“…Though this view has been held for many years (21), a careful review of the field indicates that there is little solid evidence for this view. Two studies in humans that have been quoted (22,23) as evidence for this point involved a total of only 15 subjects, 12 on antibiotics and 3 not. In one study (22), neither the antibiotics nor their regimens were stated and, thus, it is impossible to assess the efficacy of the antibiotic regimens in killing intestinal bacteria.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of the inhibition of the gamma-carboxylation of glutamic acid by N-methylthiotetrazole-containing antibiotics.

Lipsky¹

1984

Proc. Natl. Acad. Sci. U.S.A.

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Antibiotics that contain a 1-N-methyl-5-thiotetrazole (MTT) side group have been associated with hypoprothrombinemia. In a detergent-treated rat liver microsomal system, MTT inhibited the carboxylation of the y carbon of glutamic acid, a necessary reaction in the synthesis of four of the clotting factors. In the present work, the inhibition by MTT was found to be slow in onset, with a lag time of 15 min before significant inhibition occurred. A preincubation of MTT with the microsomes decreased the lag time and increased the extent of inhibition. Glutathione at 1 mM was found to markedly decrease the ability of MTT to inhibit this reaction. The disulfide dimer of MTT was a more potent inhibitor of the system than was MTT, with inhibition detected as low as 1 jLM dimer. Disulfiram also inhibited the carboxylation system. These results indicate that the sulfhydryl group of MTT is important for the inhibitory effect of MTT and suggest that a slowly formed metabolite of MTT may be directly responsible for the observed inhibition. The inhibitory mechanism of MTT may be analogous to that of disulfiram, which would explain some pharmacologic effects in common with disulfiram. In addition, the in vitro observations presented here and a closer examination of the clinical evidence raise the possibility that MTT-containing antibiotic-induced hypoprothrombinemia may not be a vitamin K reversible phenomenon.

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Recent advances in hepatic vitamin k metabolism and function

Suttie

1987

Hepatology

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Vitamin K in hereditary resistance to oral anticoagulant drugs

Cited by 32 publications

References 0 publications

Dietary induced subclinical vitamin K deficiency in normal human subjects.

Dietary induced subclinical vitamin K deficiency in normal human subjects.

Mechanism of the inhibition of the gamma-carboxylation of glutamic acid by N-methylthiotetrazole-containing antibiotics.

Recent advances in hepatic vitamin k metabolism and function

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