vitamin-k-semiquinone-radical and Liver-Diseases

The effect of non-vitamin K antagonist oral anticoagulants (NOACs) in patients with atrial fibrillation (AF) and liver disease remains largely unresolved. Therefore, we performed a meta-analysis to compare the efficacy and safety of NOACs with warfarin in this population.. We systematically searched the Cochrane Library, PubMed, and Embase databases for studies reporting the comparisons of NOACs with warfarin in patients with AF and liver disease. A random-effects model was selected to pool the risk ratios (RRs) and 95% confidence intervals (CIs).. A total of six studies with 41,954 participants were included in this meta-analysis. In AF patients with liver disease, compared with warfarin use, the use of NOACs was associated with reduced risks of all-cause death (RR 0.78, 95% CI 0.66-0.93), major bleeding (RR 0.68, 95% CI 0.53-0.88), and intracranial hemorrhage (RR 0.49, 95% CI 0.41-0.59), but had comparable risks of stroke or system embolism (RR 0.80, 95% CI 0.57-1.12) and gastrointestinal bleeding (RR 0.90, 95% CI 0.61-1.34). In AF patients with cirrhosis, NOACs significantly reduced the risks of major bleeding (RR 0.53, 95% CI 0.37-0.76), gastrointestinal bleeding (RR 0.57, 95% CI 0.38-0.84), and intracranial hemorrhage (RR 0.55, 95% CI 0.31-0.97) compared with warfarin.. Based on current publications, the use of NOACs is at least non-inferior to warfarin in patients with AF and liver disease.

Topics: Administration, Oral; Anticoagulants; Atrial Fibrillation; Embolism; Hemorrhage; Humans; Liver Diseases; Stroke; Vitamin K; Warfarin

Several studies have investigated the effectiveness and safety of nonvitamin K antagonist oral anticoagulants (NOACs) vs vitamin K antagonists (VKAs) in patients with atrial fibrillation (AF) and liver disease. Herein, we conducted a meta-analysis to compare the effect of NOACs with VKAs in patients with AF and liver disease. We also conducted a subsidiary analysis to compare the risk of liver injury between NOACs and VKA in AF patients. We systematically searched the PubMed and Embase databases from January 2009 to May 2020 for the relevant studies. Hazard ratios (HRs) with 95% confidence intervals (CIs) were selected and pooled using a random-effects model. A total of six cohorts were included. Compared with VKA use, the use of NOACs was associated with reduced risks of stroke or systemic embolism (HR 0.68, 95% CI 0.49-0.93), all-cause death (HR 0.69, 95% CI 0.63-0.75), and intracranial bleeding (HR 0.49, 95% CI 0.40-0.59), whereas the outcomes of major bleeding (HR 0.72, 95% CI 0.51-1.01) and gastrointestinal bleeding (HR 0.84, 95% CI 0.51-1.36) were not significantly different between groups in AF patients with liver disease. Moreover, compared with VKA use, the use of NOACs was associated with a reduced risk of liver injury (HR 0.72, 95% CI 0.61-0.84) in AF patients. Compared with VKAs, the use of NOACs was associated with reduced risks of stroke or systemic embolism, all-cause death, and intracranial bleeding in AF patients with liver disease, and associated with a reduced risk of liver injury in AF patients.

Topics: Administration, Oral; Anticoagulants; Atrial Fibrillation; Drug Administration Schedule; Humans; Liver Diseases; Stroke; Vitamin K

The purpose of this review article is to summarize the literature on diseases that are documented to have an effect on response to warfarin and other VKAs.. We searched the English literature from 1946 to September 2015 via PubMed, EMBASE, and Scopus for the effect of diseases on response vitamin K antagonists including warfarin, acenocoumarol, phenprocoumon, and fluindione.. Among many factors modifying response to VKAs, several disease states are clinically relevant. Liver disease, hyperthyroidism, and CKD are well documented to increase response to VKAs. Decompensated heart failure, fever, and diarrhea may also elevate response to VKAs, but more study is needed. Hypothyroidism is associated with decreased effect of VKAs, and obese patients will likely require higher initial doses of VKAs.. In order to minimize risks with VKAs while ensuring efficacy, clinicians must be aware of the effect of disease states when prescribing these oral anticoagulants.

Topics: Acenocoumarol; Administration, Oral; Anticoagulants; Cardiovascular Diseases; Diarrhea; Fibrinolytic Agents; Heart Failure; Humans; Hyperthyroidism; Kidney Failure, Chronic; Liver Diseases; Obesity; Phenindione; Phenprocoumon; Vitamin K; Warfarin

The current treatment of thrombotic APS patients includes long-term anticoagulation with oral vitamin K antagonists (VKAs), with warfarin being the one most commonly used. However, the use of VKAs can be challenging, especially in patients with APS. VKAs monitoring in patients with aPL is complicated by the heterogeneous responsiveness to LAs of reagents used in the International Normalized Ratio test, potentially resulting in instability of anticoagulation. For decades, VKAs were the only available oral anticoagulants. However, non-VKA oral anticoagulants, including a direct thrombin inhibitor (dabigatran etexilate) and direct anti-Xa inhibitors (rivaroxaban, apixaban and edoxaban), are currently available. The use of these agents may represent a major step forward since, unlike VKAs, they have few reported drug interactions and they do not interact with food or alcohol intake, thereby resulting in more stable anticoagulant intensity. Most importantly, monitoring their anticoagulant intensity is not routinely required due to their predictable anticoagulant effects. In this review, we discuss the clinical and laboratory aspects of non-VKA oral anticoagulants, focusing on the available evidence regarding their use in patients with APS.

Topics: Administration, Oral; Anticoagulants; Antiphospholipid Syndrome; Antithrombins; Breast Feeding; Factor Xa Inhibitors; Female; Food-Drug Interactions; Hemorrhage; Humans; Kidney Diseases; Liver Diseases; Lupus Coagulation Inhibitor; Pregnancy; Pregnancy Complications; Thrombosis; Vitamin K

Upper gastrointestinal bleeding is one of the most frequent causes of morbidity and mortality in the course of liver cirrhosis. Several treatments are used for upper gastrointestinal bleeding in people with liver diseases. One of them is vitamin K administration, but it is not known whether it benefits or harms people with acute or chronic liver disease and upper gastrointestinal bleeding. This is an update of this Cochrane review.. To assess the beneficial and harmful effects of vitamin K for people with acute or chronic liver disease and upper gastrointestinal bleeding.. We searched The Cochrane Hepato-Biliary Controlled Trials Register (February 2015), the Cochrane Central Register of Controlled Trials (CENTRAL) (Issue 2 of 12, 2015), MEDLINE (Ovid SP) (1946 to February 2015), EMBASE (Ovid SP) (1974 to February 2015), Science Citation Index EXPANDED (1900 to February 2015), and LILACS (1982 to 25 February 2015). We sought additional randomised trials from two registries of clinical trials: the World Health Organization Clinical Trials Search Portal and the metaRegister of Controlled Trials. We looked through the reference lists of the retrieved publications and review articles.. Randomised clinical trials irrespective of blinding, language, or publication status for assessment of benefits and harms. We considered observational studies for assessment of harms only.. \\We aimed to summarise data from randomised clinical trials using Standard Cochrane methodology and assess them according to the GRADE approach.. We found no randomised trials on vitamin K for upper gastrointestinal bleeding in people with liver diseases assessing benefits and harms of the intervention. We identified no quasi-randomised studies, historically controlled studies, or observational studies assessing harms.. This updated review found no randomised clinical trials of vitamin K for upper gastrointestinal bleeding in people with liver diseases. The benefits and harms of vitamin K need to be tested in randomised clinical trials. Until randomised clinical trials are conducted to assess the trade-off between benefits and harms, we cannot recommend or refute the use of vitamin K for upper gastrointestinal bleeding in people with liver diseases.

Topics: Acute Disease; Antifibrinolytic Agents; Chronic Disease; Gastrointestinal Hemorrhage; Humans; Liver Diseases; Vitamin K

The complex nature of haemostasis in patients with liver disease can result in bleeding and/or thrombosis. These opposing outcomes, which have multiple contributing factors, can pose diagnostic and therapeutic dilemmas for physicians. With the high rate of haemorrhagic complications in patients with cirrhosis, we examine the various procoagulants available for use in this population. In this Review, we describe the clinical and current rationale for using each of the currently available procoagulants-vitamin K, fresh frozen plasma (FFP), cryoprecipitate, platelets, recombinant factor VIIa (rFVIIa), antifibrinolytics, prothrombin concentrate complexes (PCC), desmopressin and red blood cells. By examining the evidence and use of these agents in liver disease, we provide a framework for targeted, goal-directed therapy with procoagulants.

Topics: Antifibrinolytic Agents; Coagulants; Deamino Arginine Vasopressin; Erythrocyte Transfusion; Factor VIIa; Factor VIII; Fibrinogen; Hemorrhage; Humans; Liver Diseases; Plasma; Recombinant Proteins; Vitamin K

Adoption of international normalized ratio (INR) to harmonize prothrombin time has greatly improved the safety and effectiveness of vitamin K antagonists (VKA) oral anticoagulant therapy. INR is also a major laboratory variable in calculating the widely used Model for End-Stage Liver Disease (MELD) score for liver transplant organ prioritization. However, since the conventional INR (INRVKA) is calibrated specifically for VKA patients, its interlaboratory variation has a significant impact on the accuracy of MELD score. Though still requiring further clinical validation in large numbers of waitlisted patients, the alternative liver INR calibrated by using plasma from liver disease patients instead of VKA patients may harmonize the differences and thus more suitable for MELD score calculation. The objective of this article is to review the history of INR, MELD score, and liver INR, and discuss the challenges and solutions of liver INR implementation.

Topics: Animals; Anticoagulants; History, 20th Century; History, 21st Century; Humans; International Normalized Ratio; Liver Diseases; Prothrombin Time; Vitamin K; Warfarin

Oral vitamin K antagonists are highly efficacious in the prevention and treatment of thromboembolic disease. Optimal use of these agents in clinical practice is challenged by their narrow therapeutic window. The proportion of time spent in the International Normalized Ratio (INR) range of 2.0-3.0 [time in the therapeutic range (TTR)] has been closely associated with adverse outcomes, i.e., stroke, hemorrhage, mortality. Although TTR is a validated marker, it has several limitations. TTR does not capture short-term risks associated with highly variable periods or periods characterized by extreme deviations in INR. Because TTR measurement is limited to consecutive periods of warfarin exposure, it does not inform the risks associated with gap periods of 56 days or greater as these time intervals are excluded from end-point rate calculations. Because individuals with gaps in monitoring represent a different patient population than those without gaps, e.g., less adherent, more acutely ill, more frequent transitions in health status, TTR analyses are likely most valid and informative for individuals with uninterrupted monitoring of the INR. Duration of warfarin therapy and patient-specific factors have also been shown to influence TTR. Younger age, female sex, lower income, black race, frequent hospitalizations, polypharmacy, active cancer, decompensated heart failure, substance abuse, psychiatric disorders, dementia, and chronic liver disease have all been associated with lower TTR. Targeted strategies to improve TTR are urgently needed.

Topics: Age Factors; Anticoagulants; Chronic Disease; Female; Heart Failure; Hemorrhage; Humans; International Normalized Ratio; Liver Diseases; Male; Neoplasms; Sex Factors; Stroke; Substance-Related Disorders; Thromboembolism; Vitamin K; Warfarin

Physicians are occasionally faced with difficult situations in the management of vitamin K antagonists (VKA) due to the lack of sound data available in controlled studies on certain conditions. In this review we would like to address some special but frequent conditions that can be encountered in daily clinical practice. These include the use of VKA in hemodialysis, thromboembolism in patients with liver cirrhosis and the thromboembolic risk in patients who bleed in the course of treatment with VKA. Moreover, two other conditions were examined: what the best way of expressing prothrombin time would be in patients with liver disease and how to behave when a patient treated with VKA shows a subtherapeutic INR. These topics were discussed by a panel of experts during a workshop recently held in Milan by the Italian Federation of Centres for the Diagnosis of Thrombosis and the Surveillance of Antithrombotic Therapies (FCSA). The main aim of the workshop was to provide helpful and practical advice to physicians in the daily management of VKA.

Topics: Anticoagulants; Hemorrhage; Humans; International Normalized Ratio; Italy; Liver Cirrhosis; Liver Diseases; Renal Dialysis; Risk Assessment; Thrombosis; Vitamin K; Vitamins

Upper gastrointestinal bleeding is one of the most frequent causes of morbidity and mortality in the course of liver cirrhosis. Several treatments are used for upper gastrointestinal bleeding in patients with liver diseases. One of them is vitamin K administration, but it is not known whether it benefits or harms patients with acute or chronic liver disease and upper gastrointestinal bleeding.. To assess the beneficial and harmful effects of vitamin K for patients with acute or chronic liver disease and upper gastrointestinal bleeding.. We searched the Cochrane Hepato-Biliary Group Controlled Trials Register (12 June 2012), the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 5 of 12, 2012), MEDLINE (Ovid SP) (1946 to 12 June 2012), EMBASE (Ovid SP) (1974 to 12 June 2012), Science Citation Index EXPANDED (1900 to 12 June 2012), and LILACS (1982 to 19 June 2012). Additional randomised trials were sought from two registries of clinical trials: the Clinical Trials Search Portal of the WHO, and the Metaregister of Controlled Trials. We looked through the reference lists of the retrieved publications and review articles.. Randomised clinical trials irrespective of blinding, language, or publication status for assessment of benefits and harms. Observational studies were considered for assessment of harms only.. Data from randomised clinical trials were to be summarised by standard Cochrane Collaboration methodologies.. We could not find any randomised trials on vitamin K for upper gastrointestinal bleeding in patients with liver diseases in which we could assess benefits and harms. We could not identify quasi-randomised studies, historically controlled or observational studies in which we could assess harms.. This updated review found no randomised clinical trials on the benefits and harms of vitamin K for upper gastrointestinal bleeding in patients with liver diseases. The effects of vitamin K need to be tested in randomised clinical trials. Until randomised clinical trials are conducted to assess the trade off between benefits and harms, we cannot recommend nor refute vitamin K for upper gastrointestinal bleeding in patients with liver diseases.

Topics: Acute Disease; Antifibrinolytic Agents; Chronic Disease; Gastrointestinal Hemorrhage; Humans; Liver Diseases; Vitamin K

Vitamin K (as phylloquinone and menaquinones) is an essential cofactor for the conversion of peptide-bound glutamate to gamma-carboxy glutamic acid (Gla) residues in a number of specialized Gla-containing proteins. The only unequivocal deficiency outcome is a bleeding syndrome caused by an inability to synthesize active coagulation factors II, VII, IX, and X, although there is growing evidence for roles for vitamin K in bone and vascular health. An adult daily intake of about 100 microg of phylloquinone is recommended for the maintenance of hemostasis. Traditional coagulation tests for assessing vitamin K status are nonspecific and insensitive. Better tests include measurements of circulating vitamin K and inactive proteins such as undercarboxylated forms of factor II and osteocalcin to assess tissue and functional status, respectively. Common risk factors for vitamin K deficiency in the hospitalized patient include inadequate dietary intakes, malabsorption syndromes (especially owing to cholestatic liver disease), antibiotic therapy, and renal insufficiency. Pregnant women and their newborns present a special risk category because of poor placental transport and low concentrations of vitamin K in breast milk. Since 2000, the Food and Drug Administration has mandated that adult parenteral preparations should provide a supplemental amount of 150 microg phylloquinone per day in addition to that present naturally, in variable amounts, in the lipid emulsion. Although this supplemental daily amount is probably beneficial in preventing vitamin K deficiency, it may be excessive for patients taking vitamin K antagonists, such as warfarin, and jeopardize their anticoagulant control. Natural forms of vitamin K have no proven toxicity.

Topics: Adult; Anticoagulants; Antifibrinolytic Agents; Bacteria; Blood Coagulation; Bone and Bones; Colon; Diet; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Health; Hospitalization; Humans; Infant, Newborn; Liver Diseases; Nutritional Requirements; Parenteral Nutrition; Practice Guidelines as Topic; Pregnancy; Vitamin K; Vitamin K Deficiency

Upper gastrointestinal bleeding is one of the most frequent causes of morbidity and mortality in the course of liver cirrhosis. Several treatments are used for upper gastrointestinal bleeding in patients with liver diseases. One of them is vitamin K administration, but it is unknown whether it benefits or harms patients with liver disease and upper gastrointestinal bleeding.. To assess the beneficial and harmful effects of vitamin K for patients with liver disease and upper gastrointestinal bleeding.. We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (September 2007), which comprises references identified from comprehensive electronic database searches and handsearching of relevant journals and abstract books of conference proceedings, The Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 3, 2007), MEDLINE (1950 to September 2007), EMBASE (1980 to September 2007), Science Citation Index Expanded (1945 to September 2007), and LILACS (1982 to November 2007). Additional randomised trials were sought from two registries of clinical trials, ClinicalTrials.gov and Sistema de Información Esencial en Terapéutica y Salud, the reference lists of the trials found, and reviews identified by the electronic searches.. Randomised clinical trials.. Data from randomised clinical trials were to be summarised by standard Cochrane Collaboration methodologies.. We could not find any randomised trials on vitamin K for upper gastrointestinal bleeding in patients with liver diseases.. This updated review found no randomised clinical trials on the safety and efficacy of vitamin K for upper gastrointestinal bleeding in patients with liver diseases. The effects of vitamin K need to be tested in randomised clinical trials. Unless randomised clinical trials provide evidence of a treatment effect and the trade off between potential benefits and harms are established, policy-makers, clinicians, and academics should not use vitamin K for upper gastrointestinal bleeding in patients with liver diseases.

Topics: Antifibrinolytic Agents; Gastrointestinal Hemorrhage; Humans; Liver Diseases; Vitamin K

The prothrombin time (PT) test once designed by Dr Quick to investigate patients with obstructive jaundice was later adapted and standardized by means of the international normalized ratio (INR) to monitor patients on treatment with vitamin K antagonists (VKA). After more than 70 years from its introduction it is now time to think about its standardization for those very patients for whom it was intended at the beginning of its history. Two studies carried out independently and published recently in the same issue of a specialized journal do exploit the very same idea on how to accomplish this standardization. Both of them confirm previous anecdotal observations that the INR as devised for patients on VKA (INR(vka)) is not valid to harmonize PT results for patients with chronic liver disease. This fact, that at first sight may appear academic, has important consequences because the PT INR is used to construct the model for end-stage liver disease (MELD) scores, which is widely used to prioritize patients for liver transplantation. The two studies further demonstrate that an alternative calibration model, modified from that recommended by the World Health Organization for patients on VKA, may be feasible also for patients with chronic liver disease. This alternative calibration model, which calls for the substitution of plasmas from patients on VKA with those from patients with chronic liver disease, may be highly beneficial to harmonize the calculation of the MELD score, with important implications for the prioritization of patients for liver transplantation.

Topics: Acylation; Algorithms; Anticoagulants; Blood Coagulation Factors; Calibration; Chronic Disease; Humans; International Normalized Ratio; Liver Diseases; Liver Transplantation; Patient Selection; Protein Processing, Post-Translational; Prothrombin Time; Reproducibility of Results; Severity of Illness Index; Vitamin K

Topics: Blood Component Transfusion; Disseminated Intravascular Coagulation; Hemostasis; Humans; Infant, Newborn; Intracranial Hemorrhages; Liver Diseases; Plasma; Vitamin K

Metabolic bone disease (osteodystrophy) is an important complication of patients with chronic liver disease; its etiology is complex and multifactorial. Osteodystrophy is manifested as osteopenia/osteoporosis. Osteoporosis can predispose patients to bone fractures, increasing morbidity and mortality, especially after liver transplantation. Early evaluation, screening, and treatment of bone disorders in patients with liver disease are essential to minimize fracture risk and to improve clinical outcome and quality of life.

Topics: Ascorbic Acid; Bone and Bones; Bone Diseases, Metabolic; Calcium; Chronic Disease; Humans; Liver Diseases; Nutrition Therapy; Osteoporosis; Vitamin D; Vitamin K

Upper gastrointestinal bleeding is one of the most frequent causes of morbidity and mortality in the course of liver cirrhosis. Several treatments are used for upper gastrointestinal bleeding in patients with liver diseases. However, supplementary interventions are often used as well. One of them is vitamin K administration, but it is unknown whether it benefits or harms patients with liver disease and upper gastrointestinal bleeding.. To assess the beneficial and harmful effects of vitamin K for patients with liver disease and upper gastrointestinal bleeding.. We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (February 2004), which comprises references identified from comprehensive electronic database searches and handsearching of relevant journals and abstract books of conference proceedings, The Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 1, 2004), MEDLINE (1966 to March 2004), EMBASE (1988 to March 2004), and LILACS (1982 to March 2004). Additional randomised trials were sought from the reference lists of the trials found and reviews identified by the electronic searches.. We intended to include randomised clinical trials.. We intended to summarise data by standard Cochrane Collaboration methodologies.. We could not find any randomised trials on vitamin K for upper gastrointestinal bleeding in patients with liver diseases.. We were unable to identify randomised trials on the safety and efficacy of vitamin K for upper gastrointestinal bleeding in patients with liver diseases. The effects of vitamin K need to be tested in randomised clinical trials.

Topics: Antifibrinolytic Agents; Gastrointestinal Hemorrhage; Humans; Liver Diseases; Vitamin K

To elucidate predisposing factors for enlargement of intracerebral hematoma (ICH) during warfarin therapy, we reviewed 47 patients on warfarin who developed acute ICH and determined relationships among ICH enlargement, INR reversal and clinical data. Among 36 patients treated to counteract the effects of warfarin within 24 h of onset, ICH increased in 10 patients (enlarged group), but remained unchanged in the remaining 26 (unchanged group), while ICH remained unchanged in another 11 patients in whom the effect of warfarin was reversed after 24 h. The international normalized ratio (INR) was counteracted immediately in 11 patients treated with prothrombin complex concentrate (PCC) but gradually in the other 36 treated by reducing the dose of warfarin, or by administering vitamin K or fresh frozen plasma. Multivariate analysis with a logistic regression model showed an INR value <2.0 at admission or for 24 h after immediate INR correction with PCC prevented ICH enlargement (OR 0.069, 95%CI 0.006-0.789, p = 0.031). An INR value of >2.0 within 24 h of ICH seems an important predisposing factor for ICH enlargement.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anticoagulants; Cerebral Hemorrhage; Comorbidity; Diabetes Mellitus; Disease Progression; Female; Humans; Hypercholesterolemia; Hypertension; International Normalized Ratio; Liver Diseases; Male; Middle Aged; Platelet Aggregation Inhibitors; Postoperative Complications; Retrospective Studies; Risk Factors; Tomography, X-Ray Computed; Vitamin K; Warfarin

Topics: Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Humans; Liver Diseases; Liver Transplantation; Vitamin K; Vitamin K Deficiency

Vitamin K is a cofactor for the synthesis of blood coagulation Factors II, VII, IX and X, and inhibitors such as Protein C and S and bone matrix protein. Its active form is a coenzyme in the glutamic acid carboxylation. Vitamin K-dependent factors form enzymatic complexes with calcium and membrane phospholipids. The insufficiency of gamma glutamic carboxylation impairs the hemostatic function. Hereditary deficiencies, antibiotics and oral anticoagulants, decrease the capacity of complex formation giving way to hemorrhage or thrombosis, or bone mass disturbances which are easily treated with administration of Vitamin K. The main causes of Vitamin K deficiency are lack of hepatic storage in newborns, liver insufficiency, malabsorption, dietetic deficiency, therapy with the antibiotics and coumarin administration. For the study of Vitamin K there are methods to measure the Vit K dependent proteins and as well methods to measure specifically the quinonas.

Topics: Adult; Anticoagulants; Blood Coagulation; Blood Coagulation Factors; Coumarins; Enzymes; Humans; Infant, Newborn; Intestinal Absorption; Liver Diseases; Models, Biological; Osteocalcin; Vitamin K; Vitamin K Deficiency

Between 1964 and 1994, at least 52 patients with cutaneous adverse effects of vitamin K have been described in the European and North American literature. A review of the details of these patients is given and 2 new cases reported. Adverse effects are seen not only in patients with liver-function disturbances but also in patients without liver diseases, and occur mostly after intramuscular or subcutaneous administration of vitamin K1, independent of the total dose. Patch and intracutaneous tests often give positive reactions. The mechanism of action is probably in many patients a delayed-type hypersensitivity reaction.

Topics: Adolescent; Adult; Aged; Child; Dermatitis, Allergic Contact; Dermatitis, Contact; Erythema; Europe; Female; Humans; Injections; Intradermal Tests; Liver Diseases; Male; Middle Aged; Patch Tests; United States; Vitamin K; Vitamin K 1

Topics: Blood Coagulation; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Factor VIII; Fibrinogen; Hemostasis; Humans; Liver; Liver Diseases; Prognosis; Risk; Vitamin K

The major clinical importance of plasma protein C is attested to by the strong association between inherited protein C deficiencies of half normal levels and recurrent venous thromboembolic disease. Homozygous protein C deficient individuals do not survive beyond infancy without continuous therapeutic intervention. The spectrum of protein C deficiency is becoming broader and includes patients with both abnormal molecules and half normal levels of functionally active molecules. Rarely, a few young adults with thrombosis have been identified with protein C levels below 25%. Studies of protein C activity have been hampered until the very recent developments of functional assays of plasma protein C. Application of these assays to a wide variety of clinical situations involving thrombotic complications is just beginning and may lead to an explosive proliferation of new data that should prove most fascinating and give much further insight into the contributions of protein C in the regulation of thrombosis.

Topics: Anticoagulants; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Glycoproteins; Half-Life; Humans; Infant, Newborn; Liver Diseases; Male; Necrosis; Protein C; Pulmonary Embolism; Purpura; Skin Diseases; Thromboembolism; Thrombophlebitis; Vitamin K

Topics: Administration, Oral; Anticoagulants; Biological Availability; Coumarins; Humans; Kinetics; Liver Diseases; Malabsorption Syndromes; Pharmaceutical Preparations; Receptors, Drug; Vitamin K

Topics: Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Disseminated Intravascular Coagulation; Fibrinolysis; Hemorrhage; Hemostasis; Humans; Liver Diseases; Thrombosis; Vitamin K

Topics: Animals; Anticoagulants; Barbiturates; Blood Coagulation; Blood Coagulation Factors; Cholestyramine Resin; Clofibrate; Disulfiram; Diuretics; Dogs; Drug Interactions; Heparin; Humans; In Vitro Techniques; Intestinal Absorption; Kinetics; Liver Diseases; Phenylbutazone; Protein Binding; Prothrombin Time; Rats; Receptors, Drug; Salicylates; Serum Albumin; Time Factors; Vitamin K; Vitamin K Deficiency

Topics: Abruptio Placentae; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelet Disorders; Blood Transfusion; Disseminated Intravascular Coagulation; Embolism, Amniotic Fluid; Factor XIII Deficiency; Female; Fetal Death; Fetal Diseases; Fibrin; Fibrinogen; Fibrinolysis; Hemophilia A; Humans; Liver Diseases; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Hematologic; Sepsis; Uterine Hemorrhage; Vitamin K

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Flow Velocity; Blood Platelet Disorders; Blood Transfusion; Cholestasis; Chronic Disease; Diagnosis, Differential; Factor V; Fibrinolysis; Hemorrhage; Hemostasis; Humans; Liver; Liver Diseases; Platelet Adhesiveness; Prognosis; Prothrombin Time; Vitamin K

Topics: Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Transfusion; Hemorrhage; Hemostasis; Heparin; Humans; Liver Diseases; Medical History Taking; Postoperative Complications; Preoperative Care; Surgical Procedures, Operative; Thrombocytopenia; Uremia; Vitamin K

Topics: Anticoagulants; Biopsy; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Drug Resistance; Drug Synergism; Factor IX; Factor VII; Factor X; Fibrinolysis; Humans; Liver; Liver Diseases; Prothrombin; Vitamin K; Vitamin K Deficiency; Warfarin

Topics: Bilirubin; Cholestyramine Resin; Diagnosis, Differential; Eclampsia; Female; Fetus; Hepatitis; Humans; Hyperemesis Gravidarum; Jaundice; Jaundice, Chronic Idiopathic; Liver Diseases; Pregnancy; Pregnancy Complications; Vitamin K

Topics: Administration, Oral; Adrenal Cortex Hormones; Animals; Anti-Bacterial Agents; Anticoagulants; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Clofibrate; Coumarins; Diuresis; Dogs; Heparin; Humans; Hypnotics and Sedatives; Liver Diseases; Metabolic Diseases; Phenylbutazone; Rats; Salicylates; Sulfonamides; Thrombosis; Uremia; Vitamin K

Topics: Anticoagulants; Blood Coagulation; Drug Antagonism; Endocrine System Diseases; Humans; Kidney Diseases; Liver Diseases; Pharmacogenetics; Vitamin K

Paracetamol is one of the most frequent reasons for poisonings across the UK with an estimated 90,000 patients and 150 deaths annually. International normalised ratio (INR) may be elevated due to hepatocellular damage and is frequently used to monitor progress on N-acetyl cysteine. N-acetyl cysteine is associated with reduced activity of vitamin K dependent clotting factors leading to a benign elevation of INR. In asymptomatic children with normal aspartate transaminase/alanine transaminase, isolated borderline elevation of INR following paracetamol overdose should be reviewed for possible N-acetyl cysteine induced elevation of INR. Due to these factors, in those with borderline persistent elevation of INR, N-acetyl cysteine can be safety stopped if INR is falling on two or more consecutive tests and is <3.0.

Topics: Acetaminophen; Acetylcysteine; Child; Humans; International Normalized Ratio; Liver Diseases; Vitamin K

Pesticides can cause serious environmental and human health consequences such as metabolic disruption and even cancers. Preventive molecules such as vitamins can be an effective solution. The present study aimed to investigate the toxic effect of an insecticide mixture formulation of lambda cyhalothrin and chlorantraniliprole (Ampligo® 150 ZC), on the liver of male rabbits (Oryctolagus cuniculus) and the possible ameliorative effect of vitamins A, D3, E, and C mixture. For that, 18 male rabbits were divided into 3 equal groups: Control (distilled water), AP (20 mg/Kg bw of the insecticide mixture every other day, orally for 28 days), AP+ADEC (20 mg/Kg bw of the insecticide mixture + 0,5 ml of vitamin AD3E+ 200 mg/kg bw of vitamin C every other day). The effects were evaluated on body weight, food intake changes, biochemical parameters, liver histology, and immunohistochemical expression of AFP, Bcl2, E-cadherin, Ki67, and P53. Results indicated that AP reduced weight gain (6.71%) and feed intake, increased ALT, ALP, and TC plasma levels, and caused hepatic tissular damages such as dilatation and congestion of the central vein, sinusoidal dilatation, inflammatory cells infiltration, and collagen deposition. Hepatic immunostaining showed an increase in the tissular expression of AFP, Bcl2, Ki67, and P53 and a significant (p < 0,05) decrease in E-cadherin expression. In contrast, supplementation of vitamins A, D3, E, and C mixture improved the previous observed alterations. Our study revealed that a sub-acute exposure to an insecticide mixture of lambda cyhalothrin and chlorantraniliprole induced numerous functional and structural disorders in the rabbit liver and the addition of vitamins ameliorated these damages.

Topics: alpha-Fetoproteins; Animals; Insecticides; Ki-67 Antigen; Liver Diseases; Male; Nitriles; Proto-Oncogene Proteins c-bcl-2; Pyrethrins; Rabbits; Tumor Suppressor Protein p53; Vitamin A; Vitamin K; Vitamins

Balancing the risk of thromboembolism and bleeding in patients with liver disease and atrial fibrillation/flutter is particularly challenging.. To examine the risks of thromboembolism and bleeding with use/non-use of oral anticoagulation (including vitamin K-antagonists and direct oral anticoagulants) in patients with liver disease and AF.. Four hundred and nine of 1,238 patients with liver disease and new atrial fibrillation/flutter initiated anticoagulants. Amongst patients with a CHA2DS2-VASc-score of 1-2 (2-3 for women), five-year thromboembolism incidence rates were low and similar in the anticoagulant (6.5%) versus no anticoagulant (5.5%) groups (average risk ratio 1.19 [95%CI, 0.22-2.16]). In patients with a CHA2DS2-VASc-score>2 (>3 for women), incidence rates were 16% versus 24% (average risk ratio 0.66 [95%CI, 0.45-0.87]). Bleeding risks appeared higher amongst patients with cirrhotic versus non-cirrhotic disease but were not significantly affected by anticoagulant status.. Oral anticoagulant initiation in patients with liver disease, incident new atrial fibrillation/flutter, and a high CHA2DS2-VASc-score was associated with a reduced thromboembolism risk. Bleeding risk was not increased with anticoagulation, irrespective of the type of liver disease.

Topics: Anticoagulants; Atrial Fibrillation; Brain Ischemia; Cohort Studies; Female; Hemorrhage; Humans; Liver Diseases; Male; Risk Assessment; Risk Factors; Stroke; Thromboembolism; Vitamin K

Topics: Anticoagulants; Fibrinolytic Agents; Hemorrhage; Humans; International Normalized Ratio; Liver Diseases; Vitamin K

We characterized the utilization and long-term treatment persistence of direct oral anticoagulants (DOACs) in patients with nonvalvular atrial fibrillation (NVAF) and liver disease.. Using the UK Clinical Practice Research Datalink, we assembled a population-based cohort of NVAF patients with liver disease initiating oral anticoagulants between 2011 and 2020. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) of the association between patient characteristics and initiation of DOACs vs vitamin K antagonists (VKAs). Cox proportional hazards models estimated hazard ratios (HRs) and 95% CIs of the association between patient characteristics and the switch from VKAs to DOACs vs remaining on VKAs. We also assessed the 5-year treatment persistence with DOACs vs VKAs, and whether ischemic stroke or bleeding preceded treatment discontinuation.. Our cohort included 3167 NVAF patients with liver disease initiating DOACs (n = 2247, 71%) or VKAs (n = 920, 29%). Initiators of DOACs were more likely to have prior ischemic stroke (OR 1.44, 95% CI 1.12-1.85) than VKA initiators but less likely to have used antiplatelet agents (OR 0.66, 95% CI 0.53-0.82). Patients switching to DOACs were more likely to have used selective serotonin reuptake inhibitors (HR 1.64, 95% CI 1.13-2.37) than those remaining on VKAs. At 5 years, 31% of DOAC initiators and 9% of VKA initiators remained persistent. Only few patients were diagnosed with ischemic stroke or bleeding prior to treatment discontinuation.. Most NVAF patients with liver disease initiated treatment with DOACs. Long-term persistence with DOACs was higher than with VKAs but remained relatively low.

Topics: Administration, Oral; Anticoagulants; Atrial Fibrillation; Fibrinolytic Agents; Hemorrhage; Humans; Ischemic Stroke; Liver Diseases; Stroke; Vitamin K

While direct oral anticoagulants (DOACs) are increasingly used in patients with liver disease, safety data especially in advanced chronic liver disease (ACLD) are limited.. Liver disease patients receiving DOAC treatment (ACLD: n = 104; vascular liver disease: n = 29) or vitamin K antagonists (VKA)/low-molecular-weight heparin (LMWH; ACLD: n = 45; vascular: n = 13) between January 2010 and September 2020 were retrospectively included. Invasive procedures and bleeding events were recorded. Calibrated anti-Xa peak levels and thrombomodulin-modified thrombin generation assays (TM-TGAs) were measured in a subgroup of 35/28 DOAC patients.. Among patients receiving DOAC, 55 (41.3%) had advanced liver dysfunction (Child-Pugh-stage [CPS] B/C) and 66 (49.6%) had experienced decompensation. Overall, 205 procedures were performed in 60 patients and procedure-related bleedings occurred in 7 (11.7%) patients. Additionally, 38 (28.6%) patients experienced spontaneous (15 minor, 23 major) bleedings during a median follow-up of 10.5 (IQR: 4.0-27.8) months. Spontaneous bleedings in ACLD patients were more common in CPS-B/C (at 12 months: 36.9% vs CPS-A: 15.9%, subdistribution hazard ratio [SHR]: 3.23 [95% CI: 1.59-6.58], P < .001), as were major bleedings (at 12 months: 22.0% vs 5.0%, SHR: 5.82 [95% CI: 2.00-16.90], P < .001). Importantly, CPS (adjusted SHR: 4.12 [91% CI: 1.82-9.37], P < .001), but not the presence of hepatocellular carcinoma or varices, was independently associated with major bleeding during DOAC treatment. Additionally, ACLD patients experiencing bleeding had worse overall survival (at 12 months: 88.9% vs 95.0% without bleeding; P < .001). Edoxaban anti-Xa peak levels were higher in patients with CPS-B/C (345 [95% CI: 169-395] vs CPS-A: 137 [95% CI: 96-248] ng/mL, P = .048) and were associated with lower TM-TGA. Importantly, spontaneous bleeding rates were comparable to VKA/LMWH patients.. Anticoagulants including DOACs should be used with caution in patients with advanced liver disease due to a significant rate of spontaneous bleeding events.

Topics: Administration, Oral; Anticoagulants; Heparin, Low-Molecular-Weight; Humans; Liver Diseases; Retrospective Studies; Vitamin K

Topics: Humans; Liver Diseases; Middle Aged; Thrombin; Vitamin K

Topics: Adolescent; Diabetes Mellitus, Type 1; Diagnosis, Differential; Facies; Female; Hepatomegaly; Humans; Hypoglycemic Agents; Insulin; Liver; Liver Diseases; Puberty, Delayed; Syndrome; Ultrasonography; Vitamin K; Vitamins

Liver disease results in complex alterations of all 3 phases of hemostasis. It is now recognized that hemostasis is rebalanced in chronic liver disease. The fall in clotting factor levels is accompanied by a parallel fall in anticoagulant proteins. High von Willebrand factor levels counteract defects in primary hemostasis. Conventional coagulation tests do not fully reflect the derangement in hemostasis and do not accurately predict the risk of bleeding. Global coagulation assays (thrombin generation, thromboelastography) reflect the interaction between procoagulant factors, anticoagulant factors, platelets, and the fibrinolytic system and show promise for assessing bleeding risk and guiding therapy. These assays are not yet commercially approved or validated. Prevention of bleeding should not be aimed at correcting conventional coagulation tests. Thrombopoietin receptor agonists were shown to increase the platelet count in cirrhotic patients undergoing invasive procedures but may increase the risk of thrombosis. Rebalanced hemostasis in liver disease is precarious and may be tipped toward hemorrhage or thrombosis depending on coexisting circumstantial risk factors. Bacterial infection may impair hemostasis in cirrhosis by triggering the release of endogenous heparinoids. There are no evidence-based guidelines for hemostatic therapy of acute hemorrhage in liver disease. There is currently inadequate evidence to support the use of recombinant FVIIa, prothrombin complex concentrates, or tranexamic acid in acute variceal or other hemorrhage.

Topics: ADAM Proteins; ADAMTS13 Protein; Antifibrinolytic Agents; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Deamino Arginine Vasopressin; Factor VIIa; Fibrinolysis; Hemorrhage; Hemostasis; Humans; International Normalized Ratio; Liver Diseases; Plasma; Prothrombin Time; Receptors, Thrombopoietin; Recombinant Proteins; Risk Factors; Thrombelastography; Thrombin; Vitamin K

Topics: Administration, Oral; Anticoagulants; Blood Coagulation Factors; Clinical Trials as Topic; Contraindications; Humans; Liver Diseases; Practice Guidelines as Topic; Renal Insufficiency; Thromboembolism; Vitamin K

In Japan, γ-carboxylation of blood coagulation factors is the basis for determining adequate intake (AI) for vitamin K in Dietary Reference Intakes (DRIs) issued in 2010. Recently, vitamin K is also known to be essential for preventing fracture. In this study, relative susceptibility of liver and bone to vitamin K deficiency was studied. Thirty-seven elderly institutionalized subjects were evaluated for vitamin K status by measuring serum PIVKA (protein induced by vitamin K absence) -II and ucOC (undercarboxylated osteocalcin) levels, as sensitive markers for hepatic and skeletal vitamin K deficiency, respectively. Serum PIVKA-II and ucOC levels, with their cut-off values in the parentheses, were 20.2±8.9 mAUmL (28 mAU/mL) and 4.7±3.0 ng/mL (4.5 ng/mL), respectively. Median vitamin K intake was approximately 200 μg/day, which is more than 3 times higher than the current Japanese AI. Vitamin K intake was significantly correlated with serum PIVKA-II and ucOC/OC levels, but not with serum ucOC level. Although serum ucOC level is generally a good indicator for vitamin K status, multiple regression analysis revealed that elevated bone turnover marker significantly contributed to serum ucOC level. All subjects had vitamin K intake exceeding AI for vitamin K. Nevertheless, serum PIVKA-II and ucOC concentrations exceeded the cut-off value in 14% and 43% of subjects, respectively. The present findings suggest that vitamin K intake greater than the current AI is required for the skeletal health in the institutionalized elderly.

Topics: Aged; Aged, 80 and over; Biomarkers; Bone and Bones; Diet; Elder Nutritional Physiological Phenomena; Energy Intake; Female; Fractures, Bone; Homes for the Aged; Humans; Liver; Liver Diseases; Male; Nursing Homes; Osteocalcin; Protein Precursors; Prothrombin; Vitamin K; Vitamin K Deficiency

To conduct and report monitoring of vitamin K deficiency bleeding (VKDB) in Great Britain and Ireland following the 1988-90 survey (VKDB-90).. Two 2-year surveys conducted during 1993-4 (VKDB-94) and 2001-02 (VKDB-02).. Data collected from all consultant paediatricians in Great Britain and Ireland.. All infants presenting with bleeding resulting from vitamin K (VK) deficiency.. Incidence of VKDB, related mortality/morbidity and VK prophylaxis recommended/received, noting predisposing features.. Compared with previous studies, VKDB-02 found fewer cases of VKDB (RR: 0.27 (95% CI: 0.12 to 0.59), p<0.001) with no deaths, no long-term morbidity and reduced incidence among those receiving any oral dosing (RR: 0.24 (95% CI: 0.06 to 1.01), p<0.059). Breast-fed infants accounted for the vast majority of cases. The number receiving no prophylaxis fell consecutively over time: 20 of 27 in VKDB-90, 10 of 32 in VKDB-94 and 4 (because of parental refusal) of 7 in VKDB-02. Seven received one oral dose of VK in VKDB-90, 16 in VKDB-94 and none in VKDB-02. Underlying liver disease was found in six cases in VKDB-90, 12 in VKDB-94 and one in VKDB-02.. In the most recent survey, the incidence of VKDB was about one third that in the two earlier studies. Late onset VKDB remains virtually confined to breast-fed infants who have received either no VK or just one oral dose. The effectiveness of oral prophylaxis regimens has improved over the last 15 years, but parental refusal of prophylaxis has become more problematic.

Topics: Age of Onset; Antifibrinolytic Agents; Birth Weight; Breast Feeding; Health Surveys; Humans; Incidence; Infant; Infant, Newborn; Ireland; Liver Diseases; Male; Prospective Studies; Sex Distribution; United Kingdom; Vitamin K; Vitamin K Deficiency; Vitamin K Deficiency Bleeding

Children with chronic liver disease are at risk for vitamin K deficiency because of fat malabsorption and inadequate dietary intake. The objective of this study was to determine the prevalence of vitamin K deficiency in children with mild to moderate chronic cholestatic and noncholestatic liver disease.. Vitamin K status was examined in 43 children (0.25-15.9 years) with mild to moderate chronic cholestatic liver disease, 29 children (0.9-16.9 years) with chronic mild to moderate noncholestatic liver disease, and in 44 healthy children (1-18 years). Vitamin K status was assessed by the plasma PIVKA-II (protein induced in vitamin K absence) assay (enzyme-linked immunosorbent assay). Plasma PIVKA-II values greater than 3 ng/mL are indicative of vitamin K deficiency.. The mean plasma PIVKA-II (+/-SD) in cholestatic, noncholestatic, and healthy children was 61.9 +/-144, 1.2 +/- 3, and 2.1 +/- ng/mL, respectively (P < 0.002). Fifty-four percent of the children supplemented with vitamin K had plasma PIVKA-II greater than 3 ng/mL. Plasma conjugated bilirubin, total bile acids, and severity of liver disease were positively correlated with plasma PIVKA-II levels (P < 0.05).. Vitamin K deficiency is prevalent in children with mild to moderate chronic cholestatic liver disease, even with vitamin K supplementation. Elevated PIVKA-II levels occurred in children with a normal prothrombin, indicating that more sensitive markers of vitamin K status should be used in children with chronic liver disease. Vitamin K deficiency was related to degree of cholestasis and severity of liver disease in children. Children without cholestasis did not exhibit vitamin K deficiency.

Topics: Adolescent; Case-Control Studies; Child; Child, Preschool; Cholestasis, Intrahepatic; Chronic Disease; Dietary Fats; Enzyme-Linked Immunosorbent Assay; Female; Humans; Infant; Liver Diseases; Malabsorption Syndromes; Male; Nutritional Status; Prevalence; Risk Factors; Severity of Illness Index; Vitamin K; Vitamin K Deficiency

Topics: Child, Preschool; Developmental Disabilities; Diagnosis, Differential; Humans; Hypervitaminosis A; Liver Diseases; Male; Splenomegaly; Vitamin A; Vitamin K

Patients with cystic fibrosis (CF) and pancreatic insufficiency (PI) commonly have vitamin K deficiency, and those with CF-associated liver disease (CFLD) have universal vitamin K deficiency. We evaluated the effectiveness of an oral fat-soluble vitamin combination (ADEKs) to treat patients with vitamin K deficiency.. Patients with PI and CF (mean age, 15 years; range, 0.6 to 46 years) including 6 with advanced CFLD were prospectively enrolled in a study of a fat-soluble vitamin combination taken on a daily basis. None had received vitamin K supplementation for at least 4 months before the study. Fat-soluble vitamin combination supplementation was given for a minimum of 4 months; the mean vitamin K intake was 0.18 mg/d (SD = 0.1, range, 0 to 0.3). The primary outcome was change in plasma PIVKA-II (prothrombin in vitamin K absence).. Before supplementation 58 (81%) of 72 patients had abnormal PIVKA-II levels (>2.9 ng/mL). After supplementation 29 (40%) had abnormal PIVKA-II levels (P =.001). All 6 patients with advanced CFLD had abnormal PIVKA-II levels (median, range of 20.8, 5.5 to 55 ng/mL) before treatment, which corrected to normal in 50% (4.1, 2.1 to 65 ng/mL). Four patients, 2 with CFLD, had a prolonged prothrombin time (>13.5 seconds) at both time periods.. An oral fat-soluble vitamin combination with a modest amount of vitamin K can, as a daily supplement, improve the PIVKA-II levels in patients with PI and CF.

Topics: Adolescent; Adult; Biomarkers; Child; Child, Preschool; Cystic Fibrosis; Female; Humans; Infant; Liver Diseases; Male; Middle Aged; Prospective Studies; Protein Precursors; Prothrombin; Prothrombin Time; Vitamin K; Vitamin K Deficiency; Vitamins

A 17-year-old patient with Shone's disease had to be readmitted to the hospital 3 months after implantation of an artificial aortic valve because of extreme mitral insufficiency with consecutive pulmonary edema and hepatic dysfunction. He had been orally anticoagulated and presented with a high international normalized ratio of 6.7. Emergency replacement of the mitral valve was possible only after administration of prothrombin-complex concentrate, as vitamin K(1) and fresh frozen plasma did not correct the hemostatic defect sufficiently.

Topics: Adolescent; Anticoagulants; Aortic Valve; Aortic Valve Stenosis; Blood Coagulation Factors; Coagulation Protein Disorders; Emergencies; Heart Failure; Heart Valve Prosthesis Implantation; Humans; Liver Diseases; Male; Mitral Valve Insufficiency; Mitral Valve Stenosis; Plasma; Pulmonary Edema; Radiography; Thromboembolism; Ventricular Outflow Obstruction; Vitamin K

Topics: Algorithms; Antithrombin III; Biopsy; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Gastrointestinal Hemorrhage; Humans; Hypersplenism; Hypertension, Portal; Liver; Liver Diseases; Liver Transplantation; Thrombocytopenia; Vitamin K

Topics: Hemorrhage; Humans; Infant, Newborn; Liver Diseases; Vitamin K

Because most emergent surgical operations for patients with spontaneous ruptured hepatocellular carcinoma (HCC) achieved hemostasis only, a conservative approach was chosen for management of initial bleeding in our institute. Elective surgery was performed in selected patients to attempt resection of the HCC after stabilization of the hemorrhage. From 1971, 68 of 87 patients with ruptured HCC received the conservative treatment, and 19 were treated by emergent surgery during the same period. Overall, one week and one month mortality rates were 26.5 per cent, 48.5 per cent in the conservative group, and 31.6 per cent, 47.4 per cent in the emergent operative group, respectively. Two patients in the emergent operative group underwent partial hepatectomy for a resectability of 10.5 per cent. Fifteen patients in the conservative group received elective laparotomy 1-3 weeks after control of the initial bleeding. Six underwent partial hepatectomy with a resectability of 40.0 per cent. In conclusion, conservative management is an effective approach for control of intraperitoneal hemorrhage in patients with ruptured HCC. Elective surgery on selected patients after hemostasis will increase the cancer resection rate in patients who undergo laparotomy and will give a better life expectancy than emergent laparotomy in patients with ruptured HCC.

Topics: Adult; Blood Transfusion; Carcinoma, Hepatocellular; Emergencies; Female; Fluid Therapy; Hemorrhage; Hepatectomy; Hepatic Artery; Humans; Laparotomy; Liver Diseases; Liver Neoplasms; Male; Middle Aged; Narcotics; Neoplasm Staging; Peritoneal Diseases; Recurrence; Rupture, Spontaneous; Survival Rate; Vitamin K

Gammacarboxyglutamic acid (gla) is a non essential amino acid synthesized in presence of vitamin K, predominantly found in coagulation and bone proteins. In 14 cases of deep vein thrombosis and in 11 cases of disseminated intravascular coagulation, compared to 19 normal subjects and 9 patients hospitalized for leg pain, free plasma gla levels were found significantly elevated (respectively 372 +/- 244 and 559 +/- 361 versus 146 +/- 34 and 120 +/- 40 pmol/mL). In six paired plasma and serum, gla levels were similar. These results suggest an involvement of blood coagulation in gla generation with need of a catabolism of the activated factors. A significant decrease was noticed during vitamin K antagonist therapy and liver disease, both instances in which the synthesis of gla containing coagulation factors is affected. During hepatocellular carcinoma with elevated desgamma carboxyprothrombin, gla was found normal, denying an global impairement of the vitamin K metabolism.

Topics: 1-Carboxyglutamic Acid; Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Carcinoma, Hepatocellular; Chronic Disease; Disseminated Intravascular Coagulation; Female; Hemangioma; Humans; Leg; Liver Diseases; Liver Neoplasms; Male; Middle Aged; Pain; Pulmonary Embolism; Skin Neoplasms; Thrombophlebitis; Vitamin K

Topics: Blood Coagulation; Hemostatics; Humans; Liver; Liver Diseases; Liver Neoplasms; Postoperative Period; Vitamin K; Vitamin K 1; Vitamin K 2

The clinical significance of des-gamma-carboxy prothrombin (PIVKA-II) in hepatocellular carcinoma (HCC) was investigated in 112 patients with and without vitamin K administration. The positivity rate of PIVKA-II was significantly decreased in patients receiving vitamin K (28.5%), compared with those without vitamin K administration (54.5%, p less than 0.05). The plasma levels of vitamin K derivatives [phylloquinone (VK1), menaquinone-4 (MK4), and menaquinone-7 (MK7)] measured were not decreased in patients with HCC, but were significantly increased in MK4 and VK1 + MK4 + MK7. The amount of PIVKA-II in plasma did not correlate with the plasma levels of vitamin K derivatives. However, PIVKA-II was decreased by the administration of vitamin K, and all of the six patients with more than 5.0 ng/ml of VK1 + MK4 + MK7 were within normal limits, whereas half of 32 patients with less than that had abnormal levels of PIVKA-II. Thus, it was suggested that PIVKA-II was not elevated due to vitamin K deficiency, but might result from the impaired metabolism or availability of vitamin K in the tumor. Therefore, PIVKA-II should be measured without vitamin K administration.

Topics: alpha-Fetoproteins; Biomarkers; Carcinoma, Hepatocellular; Chi-Square Distribution; Humans; Liver Diseases; Liver Function Tests; Liver Neoplasms; Protein Precursors; Prothrombin; Vitamin K

To determine the incidence of haemorrhagic disease of the newborn in the British Isles, study risk factors, and examine the effect of vitamin K prophylaxis.. Prospective survey of all possible cases of haemorrhagic disease of the newborn as reported by consultant paediatricians using the monthly notification cards of the British Paediatric Surveillance Unit and a follow up questionnaire for each case to validate the diagnosis and accrue further data.. Britain (England, Scotland, and Wales) and Ireland (Northern Ireland and the Irish Republic) during December 1987 to March 1990.. 27 infants classified as having confirmed (n = 25) or probable (n = 2) haemorrhagic disease of the newborn.. 24 of the 27 infants were solely breast fed. 10 suffered intracranial haemorrhage; two of these died and there was clinical concern about the remainder. 20 infants had received no vitamin K prophylaxis, and seven had received oral prophylaxis. Relative risk ratios for these groups compared with babies who had received intramuscular vitamin K were 81:1 and 13:1 respectively. Six infants had hepatitis (alpha 1 antitrypsin deficiency in four), unsuspected until presentation with haemorrhagic disease of the newborn, of whom four had received oral prophylaxis. One other baby had prolonged jaundice. One mother had taken phenytoin during pregnancy.. All newborn infants should receive vitamin K prophylaxis. Intramuscular vitamin K is more effective than oral prophylactic regimens currently used in the British Isles.

Topics: Age Factors; Breast Feeding; Humans; Incidence; Infant; Infant Food; Infant, Newborn; Ireland; Liver Diseases; Prognosis; Prospective Studies; Risk Factors; Seasons; United Kingdom; Vitamin K; Vitamin K Deficiency Bleeding

Topics: Administration, Oral; Age Factors; Biliary Tract Diseases; Cerebral Hemorrhage; Ecchymosis; Female; Gastrointestinal Hemorrhage; Hemorrhage; Hemothorax; Humans; Infant; Infant, Newborn; Liver Diseases; Male; Sweden; Time Factors; Vitamin K; Vitamin K Deficiency

The alterations of mitochondrial membrane potential during the development of irreversible cell damage were investigated by measuring rhodamine-123 uptake and distribution in primary cultures as well as in suspensions of rat hepatocytes exposed to different toxic agents. Direct and indirect mechanisms of mitochondrial damage have been identified and a role for Ca2+ in the development of this type of injury by selected compounds was assessed by using extracellular as well as intracellular Ca2+ chelators. In addition, mitochondrial uncoupling by carbonylcyanide-m-chloro-phenylhydrazone (CCCP) resulted in a marked depletion of cellular ATP that was followed by an increase in cytosolic Ca2+ concentration, immediately preceding cell death. These results support the existence of a close relationship linking, in a sort of reverberating circuit, the occurrence of mitochondrial dysfunction and the alterations in cellular Ca2+ homeostasis during hepatocyte injury.

Topics: Adenosine Triphosphate; Animals; Calcium; Carbonyl Cyanide m-Chlorophenyl Hydrazone; Cells, Cultured; Chemical and Drug Induced Liver Injury; Fluorescent Dyes; Ionomycin; Kinetics; Liver Diseases; Membrane Potentials; Mitochondria, Liver; Rats; Rats, Inbred Strains; Rhodamine 123; Rhodamines; Vitamin K

Des-gamma-carboxy prothrombin is an abnormal prothrombin which increases in the plasma of patients with hepatocellular carcinoma. To clarify the process of des-gamma-carboxy prothrombin synthesis, immunoreactive prothrombin, des-gamma-carboxy prothrombin, and vitamin K (phylloquinone and menaquinone) concentrations were determined in human liver tissue, including hepatocellular carcinoma. In the patients with elevated plasma des-gamma-carboxy prothrombin levels, both immunoreactive prothrombin and des-gamma-carboxy prothrombin significantly increased in hepatoma tissues compared with non-cancerous liver tissue. On the other hand, no significant difference was observed in the endogenous vitamin K (K1, MK-4, MK7) concentrations between hepatoma and noncancerous portions, in either the cases with or without increase of plasma des-gamma-carboxy prothrombin. These data strongly suggested that in the patients with an increase of plasma des-gamma-carboxy prothrombin, overproduction of prothrombin in hepatoma plays in important role in the synthesis of des-gamma-carboxy prothrombin.

Topics: alpha-Fetoproteins; Analysis of Variance; Biomarkers; Carcinoma, Hepatocellular; Enzyme-Linked Immunosorbent Assay; Humans; Liver Diseases; Liver Neoplasms; Protein Precursors; Prothrombin; Vitamin K

To clarify features of late vitamin K deficiency hemorrhagic disease in Japanese infants, seventeen of 1,687 infants screened by normotests were examined for signs and symptoms suggesting hepatobiliary diseases. Clinical observations disclosed findings suggesting hepatobiliary diseases in 7 of the 17 selected infants with normotest values of less than 40%, and 11 infants had abnormal results in one or more liver function tests. Taken together, 14 of the 17 infants had findings suggesting hepatobiliary diseases. Upon vitamin K supplementation normotest values improved in various degrees in all infants, whether or not they had signs or symptoms of hepatobiliary diseases. Late vitamin K deficiency hemorrhagic disease of infancy may be related to subclinical hepatobiliary diseases.

Topics: Female; Humans; Infant; Infant, Newborn; Liver; Liver Diseases; Liver Function Tests; Male; Mass Screening; Vitamin K; Vitamin K Deficiency Bleeding

We have measured the plasma PIVKA-II levels in 188 cases of various liver disease with HCC and malignant diseases in other organs by an EIA, using a monoclonal antibody (E-1023 kit, Eisai), and also have measured the plasma vitamin K levels in cases of HCC and cholestasis by an HPLC. Plasma PIVKA-II was detected in many cases of HCC (67%, 35 of 52 cases) and cholestasis (60%, 6 of 10 cases). In contrast, the positivities of PIVKA-II in the other diseases including benign liver diseases were very low. Combination assays of PIVKA-II and vitamin K revealed that PIVKA-II correlates with vitamin K in cholestasis but not in HCC, suggesting that PIVKA-II in HCC does not depend on a systemic deficiency of vitamin K. From these results, it was concluded that PIVKA-II is a reliable marker which can reflect the clinical course of HCC.

Topics: Adult; Aged; alpha-Fetoproteins; Antibodies, Monoclonal; Biomarkers; Biomarkers, Tumor; Carcinoma, Hepatocellular; Cholestasis; Embolization, Therapeutic; Female; Humans; Immunoenzyme Techniques; Liver Diseases; Liver Neoplasms; Male; Middle Aged; Predictive Value of Tests; Protein Precursors; Prothrombin; Vitamin K

Activated partial thromboplastin time is one of the most frequently used assay in haemostasis investigation, but sampling of venous blood is often difficult in newborns (as well as some adult patients). We analysed a method described by Zondag et al [9] performed on capillary blood samples. We studied normal adults and newborns, patients with liver diseases, and those receiving therapy with vitamin K antagonists and heparin. Capillary assay was correlated with venous blood in normal subjects, in patients with liver diseases and during therapy by vitamin K antagonists. However results both in newborns and adults during heparin therapy were not accurate.

Topics: Adolescent; Adult; Blood Coagulation Tests; Capillaries; Chronic Disease; Heparin; Humans; Infant, Newborn; Liver Diseases; Methods; Middle Aged; Partial Thromboplastin Time; Vitamin K

Des-gamma-carboxy prothrombin [DCP], a protein induced by vitamin K absence or antagonist-II and also abbreviated PIVKA-II, was evaluated as a serologic marker for hepatocellular carcinoma (HCC). Its plasma levels were measured by enzyme immunoassay (E-1023) using an anti-DCP monoclonal antibody in 514 patients with various diseases. Of 120 patients with HCC, 76 (63%) had abnormal DCP levels greater than 0.1 arbitrary unit (AU)/ml and 58 (48%) showed levels greater than 0.3 AU/ml. When a diagnostic minimum level of 0.3 AU/ml was applied for DCP, false-positive cases of HCC were virtually eliminated. In some patients with HCC, plasma DCP levels normalized after surgical resection of the tumor. However, they rose again later with recurrence of the disease. The sensitivity of DCP in the diagnosis and monitoring of HCC was increased by serial and simultaneous determinations of alpha-fetoprotein (AFP), because high DCP levels were observed more often in low AFP-producing HCC patients. Elevated plasma DCP levels were not related to low vitamin K concentration in the serum. In fact, in many patients vitamin K administration resulted in only a moderate reduction of DCP levels. These results suggested strongly that DCP was synthesized by the hepatoma cells.

Topics: Adenoma, Bile Duct; alpha-Fetoproteins; Antibodies, Monoclonal; Biomarkers; Carcinoma, Hepatocellular; Female; Hepatitis, Chronic; Humans; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Male; Neoplasm Proteins; Neoplasms; Protein Precursors; Prothrombin; Vitamin K

Topics: Humans; Intestinal Absorption; Liver; Liver Diseases; Methods; Protein Biosynthesis; Vitamin K

Topics: Adult; Clonidine; Humans; Hypertension; Liver Diseases; Male; Nifedipine; Porphyrias; Vitamin K

A fast functional assay for protein C was evaluated and compared with a traditional functional and an enzyme linked immunosorbent assay in parallel for the same plasma samples derived from 43 healthy subjects, 12 patients with severe hepatic dysfunction, and 23 patients under stable oral anticoagulation. By all three test systems significantly lower levels of protein C were obtained in both groups of patients compared with normal subjects (p less than 0.0001). No significant between - assay differences were found in normal subjects and in patients with hepatic dysfunction; by correlation analysis coefficients higher than 0.8 were calculated between the measurements of the three tests. In patients under stable oral anticoagulation, however, the immunologic test yielded higher values than the traditional (p less than 0.05) and, more pronounced, the fast functional assay (p less than 0.0001); no or only borderline significant correlations between the results were found. In these patients protein C levels measured with the traditional functional assay were in the same range as the activity levels of factors II, VII, IX, and X, whereas the fast functional test yielded significantly lower levels. The presented results indicate that very similar protein C levels were obtained with both functional and the immunologic assay except in patients under oral anticoagulation.

Topics: Adult; Anticoagulants; Blood Chemical Analysis; Blood Coagulation Factors; Female; Humans; Immunologic Techniques; Liver Diseases; Male; Middle Aged; Protein C; Reference Values; Time Factors; Vitamin K

The des-gamma-carboxyprothrombin (DCP) level was found to be increased in the majority of hepatocellular carcinomas (HCC). This increase has to be distinguished from an increased DCP level linked to a vitamin K deficiency. We studied the evolution of increased DCP level in 6 patients with histologically proven HCC and in 10 without HCC after slow injection of 20 mg of vitamin K1. The DCP assays performed subsequent to the vitamin K1 injection showed: first, a durable normalisation of the DCP level in the patients without HCC, suggesting that the increased DCP was linked, in them, to an underlying vitamin K deficiency; second, a transitory decrease followed by a return to the abnormal level in the patients with HCC. We can conclude that an increased DCP level which persists following vitamin K1 injection is specific for HCC. The minimal delay for the DCP assay after vitamin K1 injection seems to be 15 days.

Topics: Biomarkers; Carcinoma, Hepatocellular; Humans; Liver Diseases; Liver Neoplasms; Protein Precursors; Prothrombin; Vitamin K

The clinical usefulness of plasma abnormal prothrombin, defined as a protein induced by vitamin K absence or antagonist-II: PIVKA-II, as a tumor marker for hepatocellular carcinoma (HCC), was evaluated. Plasma PIVKA-II concentration was determined by an enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody specific for PIVKA-II. Forty-one (65%) out of 63 patients with HCC had an abnormal PIVKA-II level above 0.13 arbitrary units (AU)/ml; the level was above 0.3 AU/ml in 33 patients (52%) and above 0.5 AU/ml in 27 patients (43%). On the other hand, most of the 282 patients with various liver diseases other than HCC had normal or slightly elevated levels of PIVKA-II. Their values were all below 0.5 AU/ml, with the exception of 2 patients with decompensated liver cirrhosis. The patients with PIVKA-II values above 0.5 AU/ml were strongly suspected of having HCC. Plasma PIVKA-II levels were not related to serum alpha-fetoprotein (AFP) levels, but were above 0.5 AU/ml in 14 (44%) out of the 32 patients whose serum AFP levels were below 400 ng/ml. In some patients with HCC, PIVKA-II was increased throughout the course of the disease, and in others it normalized after surgical resection of the tumor. We conclude that the plasma PIVKA-II assay by the ELISA method using a monoclonal antibody is a useful diagnostic tool for monitoring HCC, particularly in HCC patients with low AFP levels.

Topics: Adenoma, Bile Duct; alpha-Fetoproteins; Antibodies, Monoclonal; Biomarkers; Carcinoma, Hepatocellular; Enzyme-Linked Immunosorbent Assay; Female; Hepatitis, Chronic; Humans; Liver Diseases; Liver Neoplasms; Male; Protein Precursors; Prothrombin; Vitamin K

The course of haemostasis defects was investigated in dimethylnitrosamine (DMNA) acute liver necrosis. Before 18 hr there was no evidence of disseminated intravascular coagulation (DIC) nor of abnormal fibrinolysis. At 12 hr the level of the vitamin-K-dependent factors (factors II, VII, IX and X) was reduced to 25-63% of control. Factors V and VIII:C levels decreased to about 10 and 20% by 12 hr. Factor V was the only molecule which decreased significantly by 6 hr. The rapid decrease of these proteins might be related to an early parenchymal functional impairment attested by early structural lesions observed in the endoplasmic reticulum and nucleus. The isolated decrease of factor V in the absence of any significant change in serum transaminase (SGOT and SGPT) levels is proposed, at least in the rat, as an early criterion of hepatic failure.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Chemical and Drug Induced Liver Injury; Dimethylnitrosamine; Liver Diseases; Platelet Count; Rats; Time Factors; Vitamin K

The components of the factor VIII complex were estimated by immuno- and bioassays in 85 patients with liver disease. The plasma concentrations of the antigens were elevated in 65% (VIII:CAg) and in 76% (VIIIR:Ag) of patients while the biological activities were elevated in only 14% (VIII:C) and 15% (VIII:RiCof). There was no correlation with C-reactive protein, used as a measure of an acute phase reaction (X2 = 0.7; P = 0.1); or with severity of liver disease as judged by prothrombin ratio (P = 1.0) but highest values were observed in patients with cholestatic liver disease. Following parenteral vitamin K there was a significant fall in both the biological activity of VIIIC (36%) and of VIII:CAg (38%) in 13 vitamin K deficient patients (P less than 0.001) but no change in 23 vitamin K replete patients or in the VIIIR:Ag levels in either group. Factor V levels were lower in patients with parenchymal liver disease (0.54 +/- 0.1 units/ml, mean +/- SEM, n = 12; normal range 0.5-1.5 units/ml) than in patients with extrahepatic cholestasis who were vitamin K deficient (1.2 +/- 0.1 units/ml, P less than 0.0001). The levels of protein C antigen, the vitamin K dependent protease which inactivates factors VIII:C and V, was at the lower end of the range in both groups (0.7 +/- 0.1, mean +/- SEM, n = 18, normal range 0.74-1.4 units/ml). There was no significant change in either protein C antigen or factor V following vitamin K. The discrepancy between the biological activity of factor VIII and the antigen levels could represent accumulation of partially degraded factor VIII or production of a hypoactive form. There is no evidence that the reduction in VIIIC and VIII:CAg following vitamin K was mediated by protein C.

Topics: Adolescent; Adult; Aged; Antigens; Factor V; Factor VIII; Female; Glycoproteins; Humans; Liver Diseases; Male; Middle Aged; Platelet Aggregation; Protein C; Ristocetin; Vitamin K; Vitamin K Deficiency; von Willebrand Factor

Detailed coagulation studies were done prospectively on 43 patients with biliary atresia who had undergone Kasai operation (hepatic portoenterostomy). Patients were divided into three groups based on levels of factor V, factor II, and Echis II and/or response to vitamin K: no coagulopathy (46.5% of patients); coagulopathy of liver disease (30.2% of patients); and coagulopathy of vitamin K deficiency (23.3% of patients). Patients with the coagulopathy of liver disease had significantly lower levels of factors XII, V, and antithrombin III as well as longer thrombin times than patients with no coagulopathy or vitamin K deficiency. Factor V levels were decreased only in patients with more advanced liver disease; normal levels of factor V were not usually helpful in differentiating liver disease and vitamin K deficiency. The prothrombin time, factor VII-X levels, and factor II levels were significantly different for all three groups; the most abnormal values occurred in the vitamin K-deficient group. Comparison of the Echis II level to factor II coagulant activity was helpful in deciding whether a coagulopathy was due to liver disease, vitamin K deficiency, or both. Factor VIII levels were elevated in all groups. Factor VIII coagulant activity was significantly higher by the two-stage (TGT) method than by the one-stage (PTT) method. Hypersplenism causing neutropenia and thrombocytopenia was commonly seen after the age of 5 years. Vitamin E deficiency was more common than vitamin K deficiency; however, all vitamin K-deficient patients were vitamin E deficient. Coagulation status correlated well with hepatobiliary scan data, but not serum bilirubin levels. Recommendations for treatment of patients with vitamin K deficiency and/or liver disease are discussed.

Topics: Bile Duct Diseases; Bile Ducts; Bilirubin; Blood Coagulation Disorders; Child; Child, Preschool; Humans; Infant; Liver Diseases; Platelet Count; Vitamin E; Vitamin K; Vitamin K Deficiency

Plasma levels of prothrombin immunoreactive protein (factor II antigen) (II-Ag) and coagulant activity (II-CA) were determined in eight patients with acute hepatitis and in 29 patients with chronic liver disease (cirrhosis). The II-CA was reduced in 23 (62%), II-Ag in 17 (46%), and both were reduced in 13 (36%) of the cases. A disproportionate reduction was noted in 21 (57%); ie, there was more II-Ag found in comparison to the corresponding level of II-Ca. Ninety-six percent (23) of 24 patients with moderate to severe hepatocellular disease showed reduced II-CA levels; 63% (15) showed reduced II-Ag levels, with a disproportionate reduction in II-CA in 67% (16). These data suggest that reduced synthesis as well as impaired carboxylation of prothrombin precursor protein are factors contributing to the coagulopathy in patients with moderate to severe liver disease and that measurement of circulating levels of II-Ag may provide an excellent indication of hepatic synthetic capacity.

Topics: Adolescent; Adult; Blood Coagulation Disorders; Blood Coagulation Tests; Child; Female; Hepatitis; Humans; Infant; Liver; Liver Cirrhosis; Liver Diseases; Male; Middle Aged; Prothrombin; Vitamin K

Topics: Blood Coagulation Factors; Humans; Liver Diseases; Prothrombin Time; Vitamin K

Topics: Humans; Liver Diseases; Prothrombin; Vitamin K

Topics: Coenzyme A; Drug Therapy, Combination; Flavonoids; Humans; Liver Diseases; Liver Extracts; S-Adenosylmethionine; Silymarin; Vitamin B Complex; Vitamin E; Vitamin K

Factor IX antigen and activity were assayed in a group of patients with liver disease and in a group of patients in coumarin therapy. In patients with liver disease there was a similar decrease in activity and antigen. On the other hand factor IX activity is decreased in coumarin treatment with factor IX antigen remaining normal. Factor IX electrophoretic mobility in liver disease is normal.

Topics: Blood Coagulation Disorders; Coumarins; Factor IX; Hemophilia B; Humans; Immunoassay; Liver Diseases; Vitamin K

Topics: Beriberi; Heart; Hemoptysis; History, 20th Century; Humans; Italy; Liver Diseases; Niacinamide; Nicotinic Acids; Pellagra; Periodicals as Topic; Polyneuropathies; Vitamin B Complex; Vitamin K; Vitamins

Topics: Animals; Bilirubin; Cholestasis; Dogs; Liver; Liver Diseases; Liver Function Tests; Monoamine Oxidase; Vitamin K

Topics: Adult; Blood Transfusion; Exchange Transfusion, Whole Blood; Hemorrhagic Disorders; Heparin; Humans; Liver Diseases; Male; Vitamin K

Vitamin K and its analogues are frequently used in treatment of the hypoprothrombinaemia found in disease of the liver, biliary tract and small intestine. Most cases of cutaneous toxicity to vitamin K have been described in the French literature, but only two cases from Britain. This paper reports six patients with chronic liver disease who developed cutaneous reactions around the site of injection of vitamin K, and the results of investigations to futher understanding of the pathogenesis of the rash.

Topics: Adolescent; Adult; Child; Drug Eruptions; Female; Humans; Hypoprothrombinemias; Liver Diseases; Middle Aged; Skin Tests; Vitamin K

The decreased capacity of the liver to synthesize proteins is the main cause of decreased blood levels of clotting factors II, V, VII, IX, X and of antithrombin III in patients with liver disease. Therefore, determination of the activity or concentration of these coagulation proteins is a useful test of liver function and guide to prognosis, provided that other mechanisms which may influence the blood level are carefully considered. Clotting factor assays have an only limited value for the differential diagnosis in liver disease.

Topics: Acute Disease; Antithrombins; Blood Coagulation Disorders; Blood Coagulation Tests; Carcinoma, Hepatocellular; Chronic Disease; Factor IX; Factor V; Factor VII; Factor VIII; Factor X; Factor XIII; Fibrinogen; Hepatitis; Humans; Jaundice, Chronic Idiopathic; Liver Cirrhosis; Liver Diseases; Liver Function Tests; Liver Neoplasms; Neoplasm Metastasis; Prothrombin; Vitamin K

Disorders of coagulation are part of the clinical syndrome in hepatic failure. The pathophysiology of these disorders is discussed; analysis of coagulation defects in hepatic disorders does not help in differential diagnosis of hepatic diseases in the proper sense, but it is of considerable prognostic value. Therapy of hepatic diseases is discussed taking into account the pathophysiology of hepatic disorders; success of any therapeutic approach however is very limited, because of the bad prognosis of the underlying disease.

Topics: Antifibrinolytic Agents; Blood Coagulation Factors; Blood Platelets; Blood Transfusion; Fibrinolysis; Hemorrhagic Disorders; Heparin; Humans; Liver; Liver Diseases; Prognosis; Splenectomy; Thrombocytopenia; Vitamin K

Topics: Evaluation Studies as Topic; Humans; Indicators and Reagents; Liver Diseases; Liver Function Tests; Vitamin K

This article gives a survey of the physiology of blood coagulation in newborn infants, subdivided into the particularities of the plasmic coagulation system and the fibronolysis. Etiology, diagnosis and therapy of the consumption coagulopathy as well as the coagulopathy of production are dealed with.

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Female; Fibrinolysis; Hemorrhagic Disorders; Heparin; Humans; Infant, Newborn; Infant, Newborn, Diseases; Liver Diseases; Microcirculation; Plasma Substitutes; Prednisolone; Pregnancy; Streptokinase; Vitamin K; Vitamin K Deficiency

Topics: Alkaline Phosphatase; Bilirubin; Cholestasis; Cholesterol; Cholestyramine Resin; Female; Humans; Liver Diseases; Pregnancy; Pregnancy Complications; Pruritus; Recurrence; Transaminases; Vitamin K

Topics: Animals; Anticoagulants; Blood Coagulation; Blood Coagulation Factors; Fibrinolysis; Liver; Liver Diseases; Prothrombin Time; Rabbits; Rats; Research Design; Vitamin K

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Escherichia coli Infections; Factor IX; Factor VII; Factor X; Female; Gastroenteritis; Heparin; Humans; Infant; Infant, Newborn; Liver Diseases; Male; Prothrombin; Sepsis; Vitamin K; Vitamin K Deficiency

Topics: Acute Disease; Adolescent; Adult; Aged; Alkaline Phosphatase; Aspartate Aminotransferases; Bilirubin; Blood Coagulation Tests; Chemical and Drug Induced Liver Injury; Child; Cholesterol; Fatty Liver; Female; gamma-Globulins; Halothane; Hepatitis A; Humans; Indicators and Reagents; Liver Cirrhosis; Liver Diseases; Liver Function Tests; Male; Methods; Middle Aged; Serum Albumin; Vitamin K

Topics: Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Factor V Deficiency; Factor VIII; Fibrinogen; Heparin; Humans; Liver Diseases; Prothrombin Time; Thromboplastin; Vitamin K; Vitamin K Deficiency

Topics: Adolescent; Adrenal Cortex Hormones; Adult; Aged; Exchange Transfusion, Whole Blood; Female; Hepatic Encephalopathy; Hepatitis A; Hepatitis B; Humans; Hydrocortisone; Liver Diseases; Male; Middle Aged; Neomycin; Thiamine; Vitamin K

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Child; Child, Preschool; Diagnosis, Differential; Disseminated Intravascular Coagulation; Hemolytic-Uremic Syndrome; Hemostasis; Heparin; Humans; Kidney Diseases; Liver Diseases; Protease Inhibitors; Vitamin K; Vitamin K Deficiency; Vitamin K Deficiency Bleeding

Topics: Aminocaproates; Blood Coagulation Disorders; Blood Transfusion; Duodenal Ulcer; Esophageal and Gastric Varices; Esophagitis; Fibrinogen; Fibrinolysis; Gastritis; Gastrointestinal Hemorrhage; Heparin; Humans; Liver Diseases; Phosphorus Isotopes; Portacaval Shunt, Surgical; Stomach Ulcer; Therapeutic Irrigation; Vasopressins; Vitamin K

Topics: Alanine Transaminase; Anti-Bacterial Agents; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Cortisone; Coumarins; Humans; Kidney Diseases; Liver Diseases; Liver Function Tests; Middle Aged; Vitamin K; Water-Electrolyte Balance

Topics: Age Factors; Aged; Anemia; Anti-Bacterial Agents; Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Tests; Ecchymosis; Female; Hematuria; Humans; Liver Diseases; Malabsorption Syndromes; Male; Middle Aged; Vitamin K; Vitamin K Deficiency

Topics: Aortic Coarctation; Autopsy; Heart Defects, Congenital; Humans; Infant, Newborn; Liver; Liver Diseases; Necrosis; Vitamin K; Vitamin K Deficiency Bleeding

Topics: Bile Acids and Salts; Carbohydrate Metabolism; Carbon Isotopes; Carotenoids; Cholesterol; Humans; Intestinal Absorption; Lipid Metabolism; Liver Diseases; Metabolism; Neomycin; Palmitic Acids; Vitamin K; Water-Electrolyte Balance

Topics: Antitubercular Agents; Drug Combinations; Female; Humans; Liver Diseases; Liver Extracts; Male; Middle Aged; Time Factors; Tuberculosis, Pulmonary; Vitamin B 12; Vitamin E; Vitamin K

Topics: Anemia, Neonatal; Blood Transfusion; Exchange Transfusion, Whole Blood; Factor VII; Factor X; Female; Hematocrit; Humans; Infant, Newborn; Infant, Newborn, Diseases; Liver Diseases; Male; Prothrombin; Vitamin K; Vitamin K Deficiency; Vitamin K Deficiency Bleeding

Topics: Anemia, Neonatal; Exchange Transfusion, Whole Blood; Factor V; Factor VII; Factor X; Female; Humans; Hypoglycemia; Hypoxia; Infant, Newborn; Liver Diseases; Male; Nervous System Diseases; Prothrombin; Vitamin K; Vitamin K Deficiency Bleeding

Topics: Adult; Blood Chemical Analysis; Cholestasis; Cholesterol; Cholestyramine Resin; Female; Humans; Liver Diseases; Liver Function Tests; Pregnancy; Pregnancy Complications; Progesterone; Pruritus; Pruritus Ani; Uterine Hemorrhage; Vitamin K

Topics: Adult; Anticoagulants; Biliary Tract Diseases; Humans; Hypoprothrombinemias; Infant, Newborn; Liver Diseases; Malabsorption Syndromes; Vitamin K; Vitamin K Deficiency Bleeding

Topics: Adolescent; Adult; Atrophy; Blood Coagulation Disorders; Blood Coagulation Tests; Child; Hepatitis A; Humans; Liver Diseases; Liver Extracts; Male; Prednisone; Vitamin K

Topics: Blood Coagulation Disorders; Blood Transfusion; Chemical and Drug Induced Liver Injury; Hemorrhage; Hepatitis; Hepatitis A; Humans; Jaundice; Liver; Liver Diseases; Prothrombin Time; Surgical Procedures, Operative; Transplantation; Vitamin K

Topics: Factor VII; Factor VII Deficiency; Factor X; Humans; Hypoprothrombinemias; Liver Diseases; Prothrombin; Vitamin K

Topics: Arrhythmias, Cardiac; Clinical Laboratory Techniques; Digoxin; Female; Goiter; Graves Disease; Hepatomegaly; Humans; Hyperthyroidism; Hypoprothrombinemias; Infant; Infant, Newborn; Infant, Newborn, Diseases; Iodides; Liver Diseases; Maternal-Fetal Exchange; Prednisolone; Pregnancy; Pregnancy Complications; Reserpine; Splenomegaly; Thrombocytopenia; Toxicology; Vitamin K

Topics: Amino Acids; Amino Acids, Essential; Ammonia; Blood Chemical Analysis; Deficiency Diseases; Erythropoiesis; Humans; Liver Diseases; Postoperative Care; Preoperative Care; Proteins; Vitamin A; Vitamin K; Vitamins; Wound Healing

Topics: Adolescent; Arginine; Dialysis; Enema; Glucose; Hepatic Encephalopathy; Hepatitis; Hepatitis A; Humans; Hydrocortisone; Liver Diseases; Mortality; Neomycin; Pathology; Renal Dialysis; Vitamin K

Topics: Geriatrics; Humans; Lipotropic Agents; Liver Diseases; Liver Extracts; Vitamin A; Vitamin K; Vitamins

Topics: Anatomy; Humans; Liver Diseases; Steroids; Vitamin K; Vitamins

Topics: Biochemical Phenomena; Biochemistry; Blood Coagulation Factors; Blood Coagulation Tests; Dicumarol; Enzyme Precursors; Factor IX; Factor VII; Factor X; Humans; Hypoprothrombinemias; Liver Diseases; Liver Function Tests; Prothrombin; Vitamin K; Vitamin K Deficiency

Topics: Biliary Tract; Biliary Tract Diseases; Cholagogues and Choleretics; Gastrointestinal Diseases; Humans; Liver Diseases; Muscle Relaxants, Central; Niacin; Nicotinic Acids; Parasympatholytics; Thiamine; Vitamin K; Vitamins

Topics: Ascorbic Acid; Carbon Tetrachloride; Chronic Disease; Folic Acid; Humans; Liver Diseases; Niacinamide; Vitamin B 12; Vitamin K; Vitamins

Topics: Antifibrinolytic Agents; Hemorrhagic Disorders; Humans; Liver Diseases; Vascular Diseases; Vitamin K

Topics: Animals; Coccidiosis; Humans; Lipid Metabolism; Liver Diseases; Rabbits; Vitamin A; Vitamin E; Vitamin K; Vitamins

Topics: Antifibrinolytic Agents; Liver Diseases; Naphthoquinones; Retinoids; Vitamin K; Vitamin K 1

Topics: Health Services Needs and Demand; Hemostatics; Humans; Liver Diseases; Nutrition Therapy; Prothrombin; Vitamin K

Topics: Antifibrinolytic Agents; Humans; Liver Diseases; Naphthoquinones; Retinoids; Vitamin K; Vitamin K 1

Topics: Antifibrinolytic Agents; Heparin Antagonists; Humans; Hypoprothrombinemias; Liver Diseases; Prothrombin; Vitamin K; Vitamin K 1

Topics: Humans; Liver Diseases; Vitamin B 12; Vitamin K; Vitamins

Topics: Corrinoids; Liver Diseases; Vitamin A; Vitamin B 12; Vitamin K; Vitamins

Topics: Antifibrinolytic Agents; Child; Humans; Infant; Liver Diseases; Naphthoquinones; Retinoids; Vitamin K; Vitamin K 1

Topics: Hemorrhage; Humans; Jaundice; Liver Diseases; Vitamin K

Topics: Amino Acids; Digestion; Glycine; Glycine Agents; Humans; Liver Diseases; Thioctic Acid; Vitamin A; Vitamin K; Vitamins

Topics: Anticoagulants; Blood Coagulation Factors; Dicumarol; Heparin Antagonists; Humans; Liver Diseases; Prothrombin; Vitamin K

Topics: Anemia; beta-Thalassemia; Child; Humans; Infant; Infant Nutrition Disorders; Liver Diseases; Splenomegaly; Vitamin K; Vitamins

Topics: Glycine; Glycine Agents; Humans; Liver Diseases; Thiamine Pyrophosphate; Thioctic Acid; Vitamin A; Vitamin K; Vitamins

Topics: Coma; Hepatic Encephalopathy; Humans; Liver Diseases; Organic Chemicals; Thioctic Acid; Vitamin A; Vitamin K; Vitamins

Topics: Gastrointestinal Diseases; Liver Diseases; Stupor; Thioctic Acid; Thiopental; Vitamin A; Vitamin K; Vitamins

Topics: Administration, Intravenous; Fats; Humans; Lipid Metabolism; Lipotropic Agents; Liver Diseases; Liver Extracts; Vitamin K; Vitamins

Topics: Liver Diseases; Organic Chemicals; Thioctic Acid; Vitamin A; Vitamin K; Vitamins

Topics: Blood Coagulation; Blood Coagulation Factors; Factor V; Factor VII; Humans; Liver Diseases; Prothrombin; Vitamin K; Vitamin K 1

Topics: Addison Disease; Fatty Liver; Liver Diseases; Steatorrhea; Vitamin A; Vitamin K; Vitamins

Topics: Antifibrinolytic Agents; Dentistry; Humans; Hypoprothrombinemias; Liver Diseases; Naphthoquinones; Prothrombin; Tooth Extraction; Vitamin K

Topics: Folic Acid; Humans; Liver Diseases; Liver Extracts; Vitamin B Complex; Vitamin K; Vitamins

Topics: Blood Coagulation; Coumarins; Factor VII; Hemostatics; Heparin Antagonists; Humans; Infant, Newborn; Liver; Liver Diseases; Pregnancy; Thromboembolism; Vitamin K

Topics: Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Factor V; Factor VII; Humans; Liver Diseases; Liver Function Tests; Prothrombin; Prothrombin Time; Vitamin K; Vitamin K 1

Topics: Alkenes; Antifibrinolytic Agents; Humans; Liver Diseases; Vitamin A; Vitamin K; Vitamins

Topics: Humans; Liver Diseases; Vitamin K; Vitamins

Topics: Humans; Liver Diseases; Prothrombin; Vitamin K

Topics: Humans; Liver Diseases; Liver Function Tests; Prothrombin; Vitamin K; Vitamins