vitamin-k-semiquinone-radical and Purpura

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: Blood Coagulation Tests; Female; Humans; Infant; Male; Purpura; Vitamin K

Topics: Age Factors; Anemia; Anticoagulants; Antifibrinolytic Agents; Bacterial Infections; Child; Child, Preschool; Disseminated Intravascular Coagulation; Fibrinolysis; Fibrinolytic Agents; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Kidney Diseases; Leukemia; Purpura; Shock; Virus Diseases; Vitamin K; Wounds and Injuries

Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.. Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.. Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.

Topics: Acenocoumarol; Activated Protein C Resistance; Aged; Aged, 80 and over; Anticoagulants; Diabetic Angiopathies; Factor V; Female; Humans; Hyperhomocysteinemia; Leg Ulcer; Male; Necrosis; Phenindione; Polyarteritis Nodosa; Postoperative Complications; Purpura; Thrombophilia; Varicose Ulcer; Vasculitis, Leukocytoclastic, Cutaneous; Vitamin K

Pulsed dye laser treatments usually result in purpura. Any topical application that eliminates or shortens the duration of purpura would be extremely useful.. The purpose of this prospective study was to determine the safety and efficacy of topical vitamin K cream in shortening the duration of laser-induced purpura.. Twenty adult subjects were enrolled. Each subject had five 1.5 cm sites treated with a pulsed dye laser at 585 nm, 450 nsec, 7 mm spot size at each subject's respective threshold fluence. Each subject had a control site where no topical application was used and four other sites where a different formulation was applied to each for 2 weeks before and for 2 weeks after laser irradiation. Five vitamin K formulations with or without retinol were studied: 3% vitamin K in acrylates copolymer cream, 5% vitamin K in acrylates copolymer cream, 1% vitamin K and 0.3% retinol in acrylates copolymer cream, 1% vitamin K and 0.15% retinol in acrylates copolymer cream, 1% free vitamin K cream. Purpuric discoloration at each site was rated on days 0, 1, 3, 7, 10, and 14 after laser treatment on a quartile scale. Each site was assigned 100% discoloration on day 0 after laser irradiation.. Laser-induced purpuric discoloration resolved faster with 1% vitamin K and 0.3% retinol in acrylates copolymer cream than with no topical application. The difference is statistically significant from day 3 onward.. A combination of 1% vitamin K and 0.3% retinol in acrylates copolymer cream hastened the resolution of laser-induced purpura.

Topics: Administration, Topical; Adult; Dermatologic Surgical Procedures; Humans; Laser Therapy; Ointments; Prospective Studies; Purpura; Treatment Outcome; Vitamin A; Vitamin K

Purpura fulminans is a rare syndrome of progressive hemorrhagic necrosis of the skin that may present as a dermatologic emergency. It most commonly affects children during the convalescent phase of a streptococcal infection or a viral exanthem. In adults, it may be associated with sepsis or acquired causes. Its pathogenesis has challenged physicians for decades. It has been discovered that purpura fulminans is almost always associated with disseminated intravascular coagulation and can occur in subjects with inherited or acquired deficiencies of the protein C anticoagulant pathway. Patients with liver compromise may also be potential candidates for coagulopathies secondary to hepatic dysfunction and impaired protein synthesis. It is widely recognized that individuals who consume alcohol on a long-term basis may develop severe hepatotoxicity from ingestion of therapeutic doses of acetaminophen (500 to 1000 mg every 4 to 6 hours). We have observed a patient with chronic alcoholism in whom hepatotoxicity and purpura fulminans developed secondary to the ingestion of acetaminophen.

Topics: Acetaminophen; Adult; Alcoholism; Drug Therapy, Combination; Female; Heparin; Humans; Purpura; Skin; Vitamin K

The vitamin K metabolism of three patients with factitious purpura due to brodifacoum ingestion was studied. These patients, who presented with bleeding disorders due to deficiency of the vitamin K-dependent blood clotting proteins, were refractory to vitamin K1 at standard doses and required fresh frozen plasma to control bleeding until large doses of vitamin K1 were used. Metabolic studies demonstrated a blockade in vitamin K utilization, consistent with the presence of a vitamin K antagonist, but the patients denied use of anticoagulants. Warfarin assays were negative. We show that the factitious purpura in each patient was due to the surreptitious ingestion of brodifacoum, a potent second generation long-acting vitamin K antagonist used as a rodenticide. The coagulopathies responded to long-term therapy with large doses of vitamin K1. The serum elimination half-time for brodifacoum ranged from 16 to 36 days in these patients. The anticoagulant effect is of long duration, requiring chronic vitamin K treatment. With increasing availability of new rodenticides, factitious purpura due to surreptitious ingestion of these potent vitamin K antagonists is emerging as a new problem, previously associated with warfarin, with important implications for diagnosis and treatment.

Topics: 4-Hydroxycoumarins; Administration, Oral; Adult; Blood Coagulation; Blood Coagulation Disorders; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Purpura; Rodenticides; Vitamin K; Warfarin

Topics: Female; Humans; Infant; Male; Purpura; Vitamin K; Vitamin K Deficiency

Topics: Blood Coagulation Disorders; Diarrhea, Infantile; Female; Humans; Infant; Malabsorption Syndromes; Purpura; Vitamin K; Vitamin K Deficiency

A total of 240 cases of a bleeding syndrome in infants due to prothrombin complex deficiency of unknown aetiology were reviewed. The majority of patients were breast fed, aged 1-2 months and the syndrome was more prevalent in males. Clinical manifestations consisted of bleeding, pallor and mild hepatomegaly in the majority of cases. Mild fever, diarrhoea, jaundice, and upper respiratory tract infection were associated in a few patients. Acute onset, short course and a high rate of intracranial bleeding (65%), particularly subdural and subarachnoid, were observed. The haemostatic defects appeared to be a marked reduction in factor II, VII, IX, and X. Complete blood counts remained relatively normal, with the exception of some changes (anaemia, leukocytosis), in response to the acute bleeding. Liver chemistry was normal or slightly impaired. No specific pathological changes were noted at autopsy, there were mild changes of liver cells, such as rare focal necrosis of liver cells, the proliferation of Kupffer cells, extramedullary haemopoeisis and mild cholestasis. Clinical improvement and correction of hemostatic defects were noted after vitamin K therapy alone or with fresh blood transfusion. Mortality rates were high in infants with intracranial bleeding (40-55%), while the overall mortality rate was 25%. The pathogenesis and the possibility of prevention of the syndrome were discussed.

Topics: Blood Coagulation; Blood Coagulation Factors; Breast Feeding; Cerebral Hemorrhage; Female; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Hypoprothrombinemias; Infant; Infant, Newborn; Liver; Male; Purpura; Thailand; Vitamin K

Topics: Animals; Antifibrinolytic Agents; Blood Coagulation Disorders; Coagulants; Flavonoids; Hemorrhage; Hemorrhagic Disorders; Hemostatics; Humans; Purpura; Snake Venoms; Venoms; Vitamin K

Topics: Adult; Female; Heparin; Humans; Phenindione; Phlebography; Pregnancy; Puerperal Disorders; Purpura; Streptokinase; Thrombophlebitis; Vitamin K

Topics: Acute Disease; Age Factors; Ascorbic Acid; Calcium; Cerebral Hemorrhage; Cortisone; Diet Therapy; Glomerulonephritis; Gluconates; Humans; Male; Middle Aged; Purpura; Rheumatic Diseases; Rutin; Vitamin K

Topics: Blood Coagulation Tests; Blood Protein Electrophoresis; Enteritis; Humans; Hypoproteinemia; Infant; Male; Purpura; Vitamin K

Topics: Blood Coagulation Tests; Factor IX; Factor VII Deficiency; Female; Humans; Infant; Prothrombin; Purpura; Thromboplastin; Vitamin K

Topics: Aminocaproates; Aminocaproic Acid; Aprotinin; Blood Coagulation; Blood Coagulation Disorders; Blood Platelets; Deoxyribonuclease I; Dicumarol; Enzyme Inhibitors; Fibrinolysin; Fibrinolysis; Hemorrhagic Disorders; Heparin; Humans; Kallikreins; Physiology; Plasminogen; Prothrombin; Purpura; Streptodornase and Streptokinase; Streptokinase; Thrombin; Trypsin; Vitamin K; Waterhouse-Friderichsen Syndrome

Topics: Anemia; Anemia, Hypochromic; Chlorpromazine; Heparin; Humans; IgA Vasculitis; Iron; Methenamine; Nandrolone; Neurosurgery; Nitrofurantoin; Paraplegia; Phenindione; Postoperative Care; Prednisolone; Purpura; Rehabilitation; Subarachnoid Hemorrhage; Thrombophlebitis; Urinary Tract Infections; Venous Thrombosis; Vitamin K

Topics: Antifibrinolytic Agents; Factor VII Deficiency; Humans; Hypoprothrombinemias; Infant; Purpura; Vitamin K

Topics: Animals; Antifibrinolytic Agents; Blood; Blood Coagulation; Hemostatics; IgA Vasculitis; Prothrombin; Purpura; Purpura, Thrombocytopenic; Rats; Vitamin K; Vitamins