Hämostasestörungen durch Antibiotika

2001 ◽  
Vol 21 (01) ◽  
pp. 12-16
Author(s):  
K. Schrör
Keyword(s):  
Vitamin K ◽  
Parenterale Ernährung ◽  
Vitamin K1 ◽  
Wird Eine

ZusammenfassungHämostasestörungen durch Antibiotika können sowohl die plasmatischen Komponenten des Gerinnungssystems als auch die Thrombozyten betreffen. Ersteres beinhaltet eine verminderte Bildung von Vitamin-K-abhängigen Gerinnungsfaktoren durch Zerstörung der Vitamin-K-bildenden Darmflora (z.B. ß-Laktamantibiotika) und/oder Hemmung der Vitamin-K-Epoxidhydrolase (NMMT-substituierte Zephalosporine) mit nachfolgender Hypoprothrombinämie. Eine Immunthrombozytopenie tritt vor allem nach Trimethoprim/Sulfmethoxazol und anderen Sulfonamidantibiotika auf, ist aber auch für andere Antibiotika gut dokumentiert. Darüber hinaus wird eine direkte Hemmung der Plättchenfunktion durch Interferenz mit der Bindung von Agonisten (ADP, Adrenalin) vorwiegend für Penizilline und einige Zephalosporine beschrieben. Das klinische Bild dieser erworbenen Hämostasestörungen ist zusätzlich durch Risikofaktoren seitens des Patienten bestimmt. Erschwerend wirken schlechter Ernährungsszustand (Hypalbuminämie), parenterale Ernährung (niedriger Vitamin-K-Plasmaspiegel), Niereninsuffizienz (reduzierte Antibiotika-Clearance) und Komedikation zytotoxischer Substanzen (Zytostatika). Therapieoptionen sind neben dem Absetzen der Substanz in Abhängigkeit von Ursache und Schweregrad der Hämostasestörung Vitamin K1, Plättchenkonzentrate oder Frisch-(gefrorenes)Plasma.

Comparison of vitamin K1 and K2 kinetics of vitamin K epoxide reductase C1

2008 ◽  
Vol 28 (S 01) ◽  
pp. S106-S106
Author(s):  
P. Westhofen ◽  
M. Watzka ◽  
M. Hass ◽  
C. Müller-Reible ◽  
D. Lütjohann ◽  
...  
Keyword(s):  
Vitamin K ◽  
Vitamin K1 ◽  
Vitamin K Epoxide Reductase ◽  
Epoxide Reductase ◽  
Kinetics Of

Leitlinien der Europäischen Gesellschaft für Kardiologie

2012 ◽  
Vol 31 (11) ◽  
pp. 821-825
Author(s):  
D. Gulba ◽  
G. Hindricks ◽  
A. Goette ◽  
P. Kirchhof
Keyword(s):  
Vitamin K ◽  
Wird Eine ◽  
Kontrollierte Studien ◽  
Neue Entwicklungen

ZusammenfassungDie Europäische Gesellschaft für Kardiologie (ESC) hat im September 2010 neue Leitlinien für das Management von Vorhofflimmern (VHF) veröffentlicht. Dieses häufige Problem, das etwa ein bis zwei Millionen Menschen in Deutschland betrifft, bedarf einer optimalen Behandlung. Neue Entwicklungen, die sich in den Leitlinien wiederfinden, sind durch weitere Daten unterstützt und ergänzt worden, sodass ein „focussed update“ der ESC-Leitlinien für August 2012 erwartet wird.Für Neurologen scheinen insbesondere die Empfehlungen der adäquaten Detektion von unterkanntem Vorhofflimmern „silent AF“ als Ursache für Schlaganfälle wichtig, zu dessen Diagnose längere EKG-Überwachung erforderlich ist, was etwa bei Patienten mit TIA/Schlaganfall relevant sein könnte. Eine Behandlung mit Antikoagulanzien wird für die Mehrzahl der Patienten mit VHF empfohlen nach Risiko-Scores. Beinahe alle Patienten mit VHF können von einer Therapie mit Vitamin-K-Antagonisten oder möglicherweise mit einem der neuen Anti-koagulanzien profitieren. Da Dabigatran und Rivaroxaben kürzlich zugelassen wurden, steht zu erwarten, dass das focussed update weitere Empfehlungen für den Einsatz dieser Substanzen geben wird. Eine frequenzregulierende Behandlung sollte der erste Schritt zur Behandlung von symptomatischem VHF sein und sollte zum Ziel eine Ruheherzfreuqenz < 100/min haben. Rhythmuserhaltende Behandlung einschließlich der Katheterablation und Antiarrhythmika wird empfohlen, wenn eine frequenzregulierende Behandlung die Symptome von VHF nicht ausreichend unterdrückt. Laufende kontrollierte Studien könnten klären, ob eine rhythmuserhaltende Behandlung, zusätzlich zu Antikoagulation und Frequenzregulierung gegeben, die häufigen Komplikationen von VHF weiter reduzieren kann. Diese Studien werden noch einige Jahre benötigen, bis sie abgeschlossen sind.

Placental Transfer of Vitamin K1 and Its Implications in Fetal Hemostasis

1988 ◽  
Vol 60 (01) ◽  
pp. 039-043 ◽  
Author(s):  
L Mandelbrot ◽  
M Guillaumont ◽  
M Leclercq ◽  
J J Lefrère ◽  
D Gozin ◽  
...  
Keyword(s):  
Vitamin K ◽  
High Performance ◽  
Ultrasound Guidance ◽  
Placental Transfer ◽  
Vitamin K1 ◽  
Vitamin K Deficiency ◽  
Prothrombin Activity ◽  
Oral Supplementation ◽  
K Deficiency ◽  
The Mean

SummaryVitamin K status was evaluated using coagulation studies and/ or vitamin IQ assays in a total of 53 normal fetuses and 47 neonates. Second trimester fetal blood samples were obtained for prenatal diagnosis under ultrasound guidance. Endogenous vitamin K1 concentrations (determined by high performance liquid chromatography) were substantially lower than maternal levels. The mean maternal-fetal gradient was 14-fold at mid trimester and 18-fold at birth. Despite low vitamin K levels, descarboxy prothrombin, detected by a staphylocoagulase assay, was elevated in only a single fetus and a single neonate.After maternal oral supplementation with vitamin K1, cord vitamin K1 levels were boosted 30-fold at mid trimester and 60 fold at term, demonstrating placental transfer. However, these levels were substantially lower than corresponding supplemented maternal levels. Despite elevated vitamin K1 concentrations, supplemented fetuses and neonates showed no increase in total or coagulant prothrombin activity. These results suggest that the low prothrombin levels found during intrauterine life are not due to vitamin K deficiency.

Dietary Vitamin and Stability of Oral Anticoagulation: Proposal of a Diet with Constant Vitamin K1 Content

1997 ◽  
Vol 77 (03) ◽  
pp. 504-509 ◽  
Author(s):  
Sarah L Booth ◽  
Jacqueline M Charnley ◽  
James A Sadowski ◽  
Edward Saltzman ◽  
Edwin G Bovill ◽  
...  
Keyword(s):  
Dietary Intake ◽  
Vitamin K ◽  
High Performance ◽  
Case Reports ◽  
Food Composition ◽  
Dietary Guidelines ◽  
Dietary Vitamin ◽  
Vitamin K1 ◽  
The Stability ◽  
The Impact

SummaryCase reports cited in Medline or Biological Abstracts (1966-1996) were reviewed to evaluate the impact of vitamin K1 dietary intake on the stability of anticoagulant control in patients using coumarin derivatives. Reported nutrient-drug interactions cannot always be explained by the vitamin K1 content of the food items. However, metabolic data indicate that a consistent dietary intake of vitamin K is important to attain a daily equilibrium in vitamin K status. We report a diet that provides a stable intake of vitamin K1, equivalent to the current U.S. Recommended Dietary Allowance, using food composition data derived from high-performance liquid chromatography. Inconsistencies in the published literature indicate that prospective clinical studies should be undertaken to clarify the putative dietary vitamin K1-coumarin interaction. The dietary guidelines reported here may be used in such studies.

Vitamin K promotes mineralization, osteoblast-to-osteocyte transition, and an anticatabolic phenotype by γ-carboxylation-dependent and -independent mechanisms

2009 ◽  
Vol 297 (6) ◽  
pp. C1358-C1367 ◽  
Author(s):  
Gerald J. Atkins ◽  
Katie J. Welldon ◽  
Asiri R. Wijenayaka ◽  
Lynda F. Bonewald ◽  
David M. Findlay
Keyword(s):  
Bone Formation ◽  
Vitamin K ◽  
Type I Collagen ◽  
Vitamin K2 ◽  
Type I ◽  
Vitamin K1 ◽  
Vitamin K3 ◽  
Positive Effect

The vitamin K family members phylloquinone (vitamin K1) and the menaquinones (vitamin K2) are under study for their roles in bone metabolism and as potential therapeutic agents for skeletal diseases. We have investigated the effects of two naturally occurring homologs, phytonadione (vitamin K1) and menatetrenone (vitamin K2), and those of the synthetic vitamin K, menadione (vitamin K3), on human primary osteoblasts. All homologs promoted in vitro mineralization by these cells. Vitamin K1-induced mineralization was highly sensitive to warfarin, whereas that induced by vitamins K2 and K3 was less sensitive, implying that γ-carboxylation and other mechanisms, possibly genomic actions through activation of the steroid xenobiotic receptor, are involved in the effect. The positive effect on mineralization was associated with decreased matrix synthesis, evidenced by a decrease from control in expression of type I collagen mRNA, implying a maturational effect. Incubation in the presence of vitamin K2 or K3 in a three-dimensional type I collagen gel culture system resulted in increased numbers of cells with elongated cytoplasmic processes resembling osteocytes. This effect was not warfarin sensitive. Addition of calcein to vitamin K-treated cells revealed vitamin K-dependent deposition of mineral associated with cell processes. These effects are consistent with vitamin K promoting the osteoblast-to-osteocyte transition in humans. To test whether vitamin K may also act on mature osteocytes, we tested the effects of vitamin K on MLO-Y4 cells. Vitamin K reduced receptor activator of NF-κB ligand expression relative to osteoprotegerin by MLO-Y4 cells, an effect also seen in human cultures. Together, our findings suggest that vitamin K promotes the osteoblast-to-osteocyte transition, at the same time decreasing the osteoclastogenic potential of these cells. These may be mechanisms by which vitamin K optimizes bone formation and integrity in vivo and may help explain the net positive effect of vitamin K on bone formation.

VITAMIN K SUPPLEMENTATION FOR INFANTS RECEIVING MILK SUBSTITUTE INFANT FORMULAS AND FOR THOSE WITH FAT MALABSORPTION

PEDIATRICS ◽  
1971 ◽  
Vol 48 (3) ◽  
pp. 483-487
Author(s):  
Lloyd J. Filer ◽  
Lewis A. Barness ◽  
Richard B. Goldbloom ◽  
Malcolm A. Holliday ◽  
Robert Miller ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Biliary Atresia ◽  
Vitamin K ◽  
Intramuscular Injection ◽  
Casein Hydrolysate ◽  
Vitamin K1 ◽  
Infant Formulas ◽  
Milk Substitute ◽  
Fat Malabsorption ◽  
Clinical Conditions

Certain milk substitute infant formulas, particularly meat-based and casein hydrolysate based formulas, may be low in vitamin K content in relation to the needs of the infants receiving them. Studies are reviewed of a few infants in which inadequate dietary supply of vitamin K from such sources may have been one factor in the development of hypoprothrombinemia, though this could not be established with certainty. On theoretical grounds it seems reasonable to increase the level of vitamin K1 in milk substitute formulas to 100 µg/l, particularly because these products are often used in treatment of clinical conditions which are associated with diminished absorption of this vitamin. Vitamin K1 (phylloquinone) would seem the most appropriate form to be used for supplementation of formulas. In clinical situations associated with malabsorption of fat, e.g., cystic fibrosis of the pancreas or biliary atresia, and prolonged diarrhea or starvation, vitamin K supplementation of feedings or periodic parenteral administration of vitamin K is recommended. When parenteral vitamin K is necessary, intravenous administration is rarely indicated. Subcutaneous or intramuscular injection is preferred.

Maternal Administration of Vitamin K Does Not Improve the Coagulation Profile of Preterm Infants

PEDIATRICS ◽  
1989 ◽  
Vol 84 (6) ◽  
pp. 1045-1050
Author(s):  
Nadya J. Kazzi ◽  
Nestor B. Ilagan ◽  
Keh-Chyang Liang ◽  
George M. Kazzi ◽  
Ronald L. Poland ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Prothrombin Time ◽  
Vitamin K ◽  
Partial Thromboplastin Time ◽  
Intraventricular Hemorrhage ◽  
Time Factors ◽  
Activated Partial Thromboplastin Time ◽  
Vitamin K1 ◽  
Time Activity ◽  
Maternal Administration

The effect of maternal administration of vitamin K1 on cord blood prothrombin time, activated partial thromboplastin time, activity of factors II, VII, and X, and antigen levels of factors II and X in infants &lt; 35 weeks' gestation was evaluated. Pregnant women in preterm labor were randomly assigned to receive 10 mg of vitamin K1 intramuscularly or no injection. If delivery did not occur in 4 days, the dose of vitamin K1 was repeated. Women who continued their pregnancy 4 days beyond the second dose received 20 mg of vitamin K1 orally daily until the end of the 34th week of gestation. The birth weights of infants ranged from 370 to 2550 g and gestational age ranged from 22 to 34 weeks. The prothrombin time, activated partial thromboplastin time, factors II, VII, and X activity, and factors II and X antigen levels were not statistically different in either group of infants. Intraventricular hemorrhage occurred in 25 of 51 control infants and 25 of 47 vitamin K-treated infants. More control infants had grade III intraventricular hemorrhage on day 1 (P = .032), but on day 3 and 14 of life, the severity of intraventricular hemorrhage was comparable in both groups. Infants in whom an intraventricular hemorrhage developed were significantly smaller, younger, and more critically ill than infants without intraventricular hemorrhage. Administration of vitamin K1 to pregnant women at &lt; 35 weeks' gestation does not improve the hemostatic defects nor does it reduce the incidence or severity of intraventricular hemorrhage in their infants.

Antithrombotische Therapie des chronischen Koronarsyndroms

2020 ◽  
Vol 49 (03) ◽  
pp. 97-101
Author(s):  
Matthias Leschke
Keyword(s):  
Vitamin K ◽  
Antithrombotische Therapie ◽  
Wird Eine ◽  
P2y12 Inhibitor

ZUSAMMENFASSUNGIn den neuen ESC-Leitlinien zum chronischen Koronarsyndrom werden aktuelle, evidenzbasierte antithrombotische Therapiekonzepte angeführt. Auf der Basis der aktuellen Studienlage wird bei Patienten mit Vorhofflimmern und Koronarstenting bevorzugt eine duale antithrombotische Therapie aus einem NOAK und einem P2Y12-Inhibitor empfohlen. In der Phase des chronischen Koronarsyndroms wird bei Patienten mit zuvor erfolgtem Koronarstenting oder nachgewiesener chronischer Koronarer Herzkrankheit eine Monotherapie mit einem NOAK oder einem Vitamin-K-Antagonisten empfohlen. Für Patienten mit einem erhöhten ischämischen Ereignisrisiko, aber geringem Blutungsrisiko wird eine verlängerte intensivierte antithrombotische Therapie mit einer zweiten antithrombotischen Substanz diskutiert. Im direkten Vergleich einer verlängerten dualen Plättchenhemmung bei Post-Myokardinfarkt-Patienten (PEGASUS-Prinzip) erscheint eine antithrombotische Therapie aus niedrigdosiertem Rivaroxaban kombiniert mit ASS aufgrund des Mortalitätsbenefits mit möglicherweise geringerer Blutungsneigung vorteilhafter (COMPASS-Strategie).

scholarly journals Association of dietary vitamin K and risk of coronary heart disease in middle-age adults: the Hordaland Health Study Cohort

BMJ Open ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. e035953
Author(s):  
Teresa R Haugsgjerd ◽  
Grace M Egeland ◽  
Ottar K Nygård ◽  
Kathrine J Vinknes ◽  
Gerhard Sulo ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vitamin K ◽  
Lower Risk ◽  
Saturated Fatty Acids ◽  
Vitamin K2 ◽  
Health Study ◽  
Dietary Vitamin ◽  
Study Cohort ◽  
Vitamin K1

ObjectiveThe role of vitamin K in the regulation of vascular calcification is established. However, the association of dietary vitamins K1 and K2 with risk of coronary heart disease (CHD) is inconclusive.DesignProspective cohort study.SettingWe followed participants in the community-based Hordaland Health Study from 1997 - 1999 through 2009 to evaluate associations between intake of vitamin K and incident (new onset) CHD. Baseline diet was assessed by a past-year food frequency questionnaire. Energy-adjusted residuals of vitamin K1 and vitamin K2 intakes were categorised into quartiles.Participants2987 Norwegian men and women, age 46–49 years.MethodsInformation on incident CHD events was obtained from the nationwide Cardiovascular Disease in Norway (CVDNOR) Project. Multivariable Cox regression estimated HRs and 95% CIs with test for linear trends across quartiles. Analyses were adjusted for age, sex, total energy intake, physical activity, smoking and education. A third model further adjusted K1 intake for energy-adjusted fibre and folate, while K2 intake was adjusted for energy-adjusted saturated fatty acids and calcium.ResultsDuring a median follow-up time of 11 years, we documented 112 incident CHD cases. In the adjusted analyses, there was no association between intake of vitamin K1 and CHD (HRQ4vsQ1 = 0.92 (95% CI 0.54 to 1.57), p for trend 0.64), while there was a lower risk of CHD associated with higher intake of energy-adjusted vitamin K2 (HRQ4vsQ1 = 0.52 (0.29 to 0.94), p for trend 0.03). Further adjustment for potential dietary confounders did not materially change the association for K1, while the association for K2 was slightly attenuated (HRQ4vsQ1 = 0.58 (0.28 to 1.19)).ConclusionsA higher intake of vitamin K2 was associated with lower risk of CHD, while there was no association between intake of vitamin K1 and CHD.Trial registration numberNCT03013725

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