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PubMed1997

Compatibility of commonly used bone marrow transplant drugs during Y-site delivery.

The Y-site compatibility of medications routinely used in bone marrow transplant patients was studied. Two methods were used to evaluate the compatibility of pairs of various i.v. drugs and nutrient fluids. In the first, the drugs were combined in a 1:1 ratio in test tubes, which were visually evaluated immediately and at 1, 4, and 24 hours under normal light and against a white background. The second method involved simulated infusion through a Y-site and a membrane filter. Filter disks were examined under 51 x magnification for precipitates. "Administration" time ranged from one minute to five hours. Most of the combinations were compatible. Exceptions (incompatibilities or inconclusive findings) were amikacin plus a total parenteral nutrient (TPN) admixture; cyclosporine plus dopamine hydrochloride, magnesium sulfate, ondansetron, a parenteral nutrient solution, the TPN admixture, or the TPN admixture with phytonadione; and heparin sodium in either 5% dextrose injection or 0.9% sodium chloride injection plus the TPN admixture or vancomycin. The two study methods were in agreement for all drug combinations except those involving cyclosporine. Cyclosporine in 0.9% sodium chloride injection yielded many fine particles on the filter disk. The combination of cyclosporine with other drugs did not appear to increase the number of particles on the disk, but the results must still be considered inconclusive. Two methods used to determine the compatibility of bone marrow transplant agents when mixed in a Y injection site yielded the same results, except for combinations involving cyclosporine. Most of the combinations were compatible.

Anti-Infective Agents↗

PubMed1988

Comparative effects of cefoxitin and cefotetan on vitamin K metabolism.

The effects of cefoxitin and cefotetan on vitamin K metabolism and clotting parameters in five healthy subjects were investigated. No changes in prothrombin time or in the formation of abnormal prothrombin were seen either during or following the cefoxitin or cefotetan phase. However, when phytonadione (10 mg) (vitamin K1) was administered at the completion of each course of antibiotics, formation of vitamin K 2,3-epoxide was observed only during the cefotetan phase. It is probable, therefore, that cefotetan, a cephamycin antibiotic containing the N-methylthiotetrazole side chain, inhibits hepatic vitamin K 2,3-epoxide reductase. While hypoprothrombinemia and formation of abnormal prothrombin were not seen in healthy subjects, the effect of cefotetan on the coagulation status of vitamin K-depleted patients may be adverse.

Adult↗

PubMedDate not supplied

Antidote use in the critically ill poisoned patient.

The proper use of antidotes in the intensive care setting when combined with appropriate general supportive care may reduce the morbidity and mortality associated with severe poisonings. The more commonly used antidotes that may be encountered in the intensive care unit (N-acetylcysteine, ethanol, fomepizole, physostigmine, naloxone, flumazenil, sodium bicarbonate, octreotide, pyridoxine, cyanide antidote kit, pralidoxime, atropine, digoxin immune Fab, glucagon, calcium gluconate and chloride, deferoxamine, phytonadione, botulism antitoxin, methylene blue, and Crotaline snake antivenom) are reviewed. Proper indications for their use and knowledge of the possible adverse effects accompanying antidotal therapy will allow the physician to appropriately manage the severely poisoned patient.

Antidotes↗

PubMed1995

Oral vitamin K1: an option to reduce warfarin's activity.

OBJECTIVE: To report 6 patients taking oral vitamin K1 (phytonadione) to reduce warfarin's activity. CASE SUMMARY: Six patient cases are summarized in which oral vitamin K1 was used to reduce the international normalized ratio (INR) in patients at risk of bleeding. DISCUSSION: The use of oral vitamin K1 to antagonize warfarin's effects is discussed, as well as the benefits of oral vitamin K1 administration and the disadvantages of parenteral vitamin K1 administration. In addition, an extensive literature review of the discovery and clinical development of warfarin and vitamin K1 is described. CONCLUSIONS: In patients receiving warfarin therapy who have an increased INR and are at risk of bleeding, oral vitamin K1 therapy may be safer, less painful, and more cost-effective than the traditional parenteral route of administration.

Administration, Oral↗

PubMed1999

Potential interaction between azithromycin and warfarin.

Azithromycin is considered unlikely to interact with warfarin. Unlike other macrolide antibiotics, it is not hepatically metabolized and did not produce an interaction with warfarin in a single-dose study. A 71-year-old woman with a prosthetic heart valve, stabilized with warfarin, had international normalized ratios (INRs) maintained between 2.5 and 3.5. Six days after she received a prescription for a 5-day course of azithromycin, her INR was 15.16. Phytonadione 10 mg was administered subcutaneously, and warfarin was held for 3 days until her INR fell to 2.10. She then was restabilized with warfarin. Until more information is known about the safety of warfarin and azithromycin, caution is advised when the agents are given together. Close monitoring of INR is recommended, and warfarin dosage adjustment may be necessary.

Aged↗

PubMed1987

Protection against adriamycin (doxorubicin)-induced toxicity in mice by several clinically used drugs.

Protective effects of clinically used drugs against adriamycin (ADM)-induced toxicity were studied in ICR mice. The control mice, which were administered 15 mg/kg of ADM twice, survived 7.48 +/- 1.99 days (mean +/- S.D.). The survival times of mice treated with the following drugs, expressed as a percent of that of the control group, were 293.6% for coenzyme Q10 (Co Q10, 2 mg/kg), 402.2% for dextran sulfate (MDS, 300 mg/kg), 121.6% for flavin adenine dinucleotide (20 mg/kg), 236.3% for adenosine triphosphate disodium (50 mg/kg), 213.7% for reduced glutathione (100 mg/kg), 121.6% for phytonadione (50 mg/kg), 155.2% for inositol nicotinate (Ino-N, 500 mg/kg), 335.5% for nicomol (1000 mg/kg), 157.5% for nicardipine (10 mg/kg) and 123.3% for dipyridamol (50 mg/kg). Anti-hyperlipemic agents such as MDS, nicomol, Ino-N and Co Q10 strongly protected against the ADM-induced toxicity, and the mice administered these drugs lived significantly longer than the control mice. The mechanism of the protective effect was discussed.

Animals↗

PubMed2005

Vitamin K in the treatment and prevention of osteoporosis and arterial calcification.

PURPOSE: The role of vitamin K in the prevention and treatment of osteoporosis and arterial calcification is examined. SUMMARY: Vitamin K is essential for the activation of vitamin K-dependent proteins, which are involved not only in blood coagulation but in bone metabolism and the inhibition of arterial calcification. In humans, vitamin K is primarily a cofactor in the enzymatic reaction that converts glutamate residues into gamma-carboxyglutamate residues in vitamin K-dependent proteins. Numerous studies have demonstrated the importance of vitamin K in bone health. The results of recent studies have suggested that concurrent use of menaquinone and vitamin D may substantially reduce bone loss. Menaquinone was also found to have a synergistic effect when administered with hormone therapy. Several epidemiologic and intervention studies have found that vitamin K deficiency causes reductions in bone mineral density and increases the risk of fractures. Arterial calcification is an active, cell-controlled process that shares many similarities with bone metabolism. Concurrent arterial calcification and osteoporosis have been called the "calcification paradox" and occur frequently in postmenopausal women. The results of two dose-response studies have indicated that the amount of vitamin K needed for optimal gamma-carboxylation of osteocalcin is significantly higher than what is provided through diet alone and that current dosage recommendations should be increased to optimize bone mineralization. Few adverse effects have been reported from oral vitamin K. CONCLUSION: Phytonadione and menaquinone may be effective for the prevention and treatment of osteoporosis and arterial calcification.

Antifibrinolytic Agents↗

PubMed1991

Anticoagulant-related intracerebral hemorrhage in patients with prosthetic heart valves--report of two cases.

Two cases of intracerebral hemorrhage in patients with prosthetic heart valves receiving anticoagulant therapy without preceding embolic cerebral infarction are reported. Phytonadione and fresh frozen plasma were immediately given, and the intracerebral hematoma evacuated successfully. In one case, intractable bleeding occurred perioperatively until the thrombotest value reached 40% or more. This patient later developed fatal massive multiple intracerebral hemorrhages.

Adolescent↗

PubMed1994

Fasciitis in chronic graft-versus-host disease. A clinicopathologic study of 14 cases.

OBJECTIVE: To describe the clinicopathologic features of fasciitis in patients with chronic graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation from human leukocyte antigen (HLA)-identical donors. DESIGN: A retrospective cohort study. SETTING: Tertiary care center. PATIENTS: Patients who had allogeneic bone marrow transplantation and developed chronic GVHD with clinical and pathologic signs of fasciitis. MAIN OUTCOME MEASURE: Analysis of clinical presentations and of deep cutaneo-muscular biopsy specimens. RESULTS: Between January 1974 and January 1991, 14 of 475 patients who had allogeneic bone marrow transplantation developed chronic GVHD that began with the sicca syndrome and liver or digestive tract involvement, or both, 60 to 170 days after the graft was received. Sudden and painful skin swelling was reported 350 to 3745 days after the graft was received. Follow-up over 2 to 7 years showed failure of the fasciitis to respond to steroid therapy or to any conventional treatment of chronic GVHD. Although 7 patients showed moderate improvement, the others remained functionally disabled because of skin tightness, joint stiffness, contractures, and sores. Patients with fasciitis in chronic GVHD had no specific immunogenetic profile and no history of L-tryptophan intake or phytonadione injections. CONCLUSION: Among alloimmune syndromes, fasciitis is a distinct entity that leads to functional disability. This rare form of chronic GVHD may provide clues to understanding the mechanisms involved in fasciitis from other causes.

Adolescent↗

PubMed1997

Correction of excessive anticoagulation with low-dose oral vitamin K1.

BACKGROUND: Despite earlier acceptance of oral vitamin K1 (phytonadione) for the treatment of excessive anticoagulation, some recent guidelines do not recommend its use. OBJECTIVE: To reevaluate the efficacy of oral vitamin K1 in correcting excessive anticoagulation. DESIGN: Case series. SETTING: Anticoagulation clinics at two university medical centers. PATIENTS: 81 outpatients who had an international normalized ratio (INR) greater than 5.0 but did not have significant bleeding. INTERVENTIONS: Withholding 1 or 2 doses of warfarin, administering 2.5 mg of oral vitamin K1, measuring the INR after 24 to 48 hours, and adjusting the warfarin dose. MEASUREMENTS: INRs were obtained from a portable capillary fingerstick monitor or from an automated photooptical coagulometer. RESULTS: In 68 of 71 patients (96%), oral vitamin K1 lowered the INR from between 5.0 and 10.0 to less than 5.0 without inducing resistance to further anticoagulation. CONCLUSIONS: Withholding 1 or 2 doses of warfarin and administering 2.5 mg of oral vitamin K1 is a reliable, safe, and inexpensive way to rapidly correct excessive anticoagulation (INR > 5.0) in patients who do not have serious bleeding episodes and have an INR of less than 10.0.

Administration, Oral↗

PubMed2000

Cutaneous reactions associated with vitamin K1.

BACKGROUND: Vitamin K1 (phytonadione) is a fat-soluble, naturally occurring vitamin used to treat certain coagulation disorders. A review of the adverse cutaneous reactions to Vitamin K1 is important because this diagnosis can be easily overlooked. This is due to their low incidence and because the presentation and morphology can vary considerably. OBJECTIVE: The objective of this article is to summarize the different morphologies, the natural history, and the treatment of the cutaneous reactions reported to Vitamin K1. METHODS: A case of a patient who developed a localized eczematous plaque at the site of a vitamin K1 injection is outlined. A review of the English medical literature focused on the adverse cutaneous reactions associated with intramuscular or subcutaneous use of vitamin K1. RESULTS: Our patient developed a localized eczematous reaction to subcutaneous vitamin K1. The eruption developed within 7 days of her dose of vitamin K1. The eruption persisted for 18 months despite treatment with topical and intralesional steroids. There are three distinct types of cutaneous reactions to vitamin K1: localized eczematous, localized morphea-form, and, very rarely, diffuse maculopapular eruption. The eczematous type (32 cases) appears at the site of injection, and the median number of days between injection and appearance of the eruption is 13 days. The dose range required to initiate the reaction is broad (10 to 410 mg). Thirteen of 32 cases took more than 2 months to resolve. The morphea-form type (7 cases) is a localized morphea-form patch that appears at the site of injection. The average delay before presentation of morphea-form changes was 8.5 months (range: 5 weeks-1.5 years). The dose range is broad (30-2080 mg), and the prognosis for resolution very poor. CONCLUSION: The diagnosis of an adverse cutaneous reaction to vitamin K can be made if the possibility is considered. Many of these reactions are very slow to clear up and some may persist as a chronic sclerodermoid change. Managing these reactions may be frustrating for both the patient and the clinician.

Antifibrinolytic Agents↗

PubMed2000

[Interaction between warfarin and oral miconazole gel].

We report a case of a 76 year-old woman who had been taking warfarin for seven years because of relapsing deep venous thrombosis. Her daily maintenance dose was 5 mg. Monthly measurements of international normalised ratio (INR) were stable between 2-3. She developed oral candidiasis and miconazole gel was prescribed. One week later she developed bleeding gums. Eight days later she was admitted to the hospital with haematuria. INR was > 10. Warfarin and the miconazole gel were withdrawn. She was treated with phytonadione. INR normalised after four days and she continued warfarin treatment. Caution should be exercised whenever the combination of warfarin and miconazole gel are prescribed.

Aged↗

PubMed2003

[A 50-year history of new drugs in Japan-the development and trends of hemostatics and antithrombotic drugs].

The developments and trends of hemostatic and antithrombotic drugs in Japan were investigated chronologically for the last 50 years after the 2nd World War. 1. Hemostatic drugs are classified into three groups ; capillary stabilizers, blood coagulants and antifibrinolytics. l) As to capillary stabilizers, flavonoid (rutin, 1949), adrenochrome derivative (carbazochrome, 1954) and conjugated estrogen (Premarin, 1964) were introduced therapeutically. Especially, the soluble types of adrenochrome compounds (Adona 1956, S-Adchnon, 1962) were devised and used widely in Japan. 2) Drugs concerning blood coagulation, thrombin, introduced in 1953, and hemocoagulase, a snake venom introduced in 1966, were used clinically. V.K. groups producing various coagulation factors were introduced as V.K1 (Phytonadione, 1962) and V.K2 (rnenatetrenone,1972), and they were admitted in "The Japanese Pharmacopoeia"editions 8 and 14, respectively). 3) Regarding antifibrinolytic drugs, Japanese researchers have made remarkable contributions. e-Aminocapronic acid (Ipsilon, 1962) and tranexamic acid (Transamin, 1965) were developed and used for various abnormal bleedings or hemorrhage associated with plasmin over-activation. tranexamic acid also proved to suppress inflammations of the throat such as tonsillitis, pharyngitis or laryngitis. 2. Antithrombotic drugs are also divided into three groups; anticoagulants, antiplatelet drugs and fibrinolytics.1) The anticoagulants used therapeutically by injection are heparins (Na-salt, 1951; Ca-salt, 1962) and low-molecular-weight heparins such as dalteparin (1992), parnaparin (1994) and reviparin (1999). The low molecule compounds are superior to the original heparins in reducing the risk of bleeding. As oral anticoagulants, coumarin derivatives, dicumarol (1950), ethylbiscoumacetate (1954), phenylindandione (1956) and warfarin (1962) are known. Warfarin potassium is the main drug for oral therapy of thromboembolism lately. Gabexate mesilate (1989) and nafamostat mesilate (1989) were developed in Japan and used for DIC and acute pancreatitis to inhibit protease enzymes. Argatroban is a unique antithrombin product developed by Japanese researchers in 1990, and is used for vascular or cerebral thrombosis. After noticing in 1968 that aspirin inhibits platelet aggregation and prevents myocardial infraction, projects for developing antiplatelet drugs were initiated worldwide. Ticlopidine, originally developed in France, was introduced in 1981 and prevailed widely in Japan for reducing the risk of thrombotic stroke. Aspirin itself was recognized by the FDA (USA) as an antithrombotic drug in 1988, and was also approved by Japanese authorities in 2000. PGE1 clathrate compounds have also been developed as antiplatelet drugs; alprostadil alfadex for injection (1979), and limaprost alfadex for oral use (1988). The PGI2 product, beraprost sodium, for oral use followed them in 1992. Other antiplatelet drugs with unique mechanisms explored in Japan: Ozagrel (1988), which inhibits TXA2 synthetase, cilostazol (1988), which inhibits cAMP phosphodiesterase, and sarpogrelate (1993), which blocks 5HT in platelets, are the notable drugs in this field. Ethyl icosapentate, from fish oil, is available for antiplatelet therapy. Concerning the fibrinolytic system, plasminogen activators are useful for thromboembolism. The streptokinase from bacterial origin developed in the USA and Europe was not introduced, and urokinase (1965) was the first plasminogen activator developed in Japan. Then tissue plasminogen activators (t-PA) tisokinase (cell culture, 1991), alteplase (genetical recombination, 1991), nateplase (genetical recombination, 1996), monteplase (1998) and pamiteplase (1998) were developed and approved for acute myocardial infarction. Nasaruplase (prourokinase, cell culture,1991) was also approved for the same indication. While the development of the hemostatic drugs ceased in the 1960s, avid project studies for antithrombotic drugs including fibrinolytics began in the 1980s and are progressing now towards new molecular targets. This may be due to the increasing tendency of cardiovascular thromboembolic diathesis in Japan. (The figures in parentheses are the years approved by the Japanese Ministry of Health, Labor and Welfare.)

Fibrinolytic Agents↗

PubMed1992

New histopathologic findings in drug eruptions.

Several new findings associated with hyperpigmentation have been reported in the past decade, the most notable being amiodarone-induced hyperpigmentation, which was shown to demonstrate both a lymphocytic dermatitis as well as yellowish brown granules that can be found within several cell types. The nature of this material has not been elucidated, although the drug or one of its metabolites composes at least a portion of the granules. The nature of the clofazimine-induced hyperpigmentation was shown to be caused by the accumulation of a ceroid lipofuscin within lipid-laden macrophages. Several chemotherapy-induced clinical and histologic changes have been reported in the past decade because of new chemotherapeutic drugs, better recognition of histologic reaction patterns, and the use of higher dosages by oncologists. A unique dermatitis, cutaneous eruption of lymphocyte recovery--although not directly due to use of chemotherapeutic agents--occurs after the return of immunocompetent lymphocytes in the peripheral circulation and skin, producing a maculopapular eruption that demonstrates a nonspecific superficial perivascular dermatitis on biopsy. Another clinically specific reaction, chemotherapy-induced acral erythema, demonstrates a nonspecific histologic pattern characterized by an interface dermatitis. Specific histologic patterns were reported for reactions following use of etoposide--starburst cells--and of busulfan--large atypical keratinocytes. There have been reports of new reactions due to chemotherapeutic agents involving sweat glands: neutrophilic eccrine hidradenitis, characterized by neutrophils and necrosis; and syringosquamous metaplasia, a histologic reaction of the sweat duct characterized by squamous metaplasia. New inflammatory reaction patterns include drug-induced generalized pustular toxic erythema, which histologically shows subcorneal pustules and occasional eosinophils. Cephalosporins were reported to produce a syndrome that clinically and histologically resembles pemphigus. Naproxen is reported to produce a clinical and histologic reaction similar to porphyria cutanea tarda. Quinine and piroxicam both induce a photosensitive dermatitis that histologically shows a nonspecific spongiotic dermatitis. A histologically unique reaction pattern manifesting as a lichenoid giant cell dermatitis may be produced by use of either methyldopa or chlorothiazide. Both phenytoin and carbamazepine produce a dermatitis that histologically imitates mycosis fungoides. Finally, phytonadione injections may produce a clinical and histologic reaction that resembles morphea.

Amiodarone↗

PubMed1991

Computerized surveillance of adverse drug events in hospital patients.

OBJECTIVE: To develop a new method to improve the detection and characterization of adverse drug events (ADEs) in hospital patients. DESIGN: Prospective study of all patients admitted to our hospital over an 18-month period. SETTING: LDS Hospital, Salt Lake City, Utah, a 520-bed tertiary care center affiliated with the University of Utah School of Medicine, Salt Lake City. PATIENTS: We developed a computerized ADE monitor, and computer programs were written using an integrated hospital information system to allow for multiple source detection of potential ADEs occurring in hospital patients. Signals of potential ADEs, both voluntary and automated, included sudden medication stop orders, antidote ordering, and certain abnormal laboratory values. Each day, a list of all potential ADEs from these sources was generated, and a pharmacist reviewed the medical records of all patients with possible ADEs for accuracy and causality. Verified ADEs were characterized as mild, moderate, or severe and as type A (dose-dependent or predictable) or type B (idiosyncratic or allergic) reactions, and causality was further measured using a standardized scoring method. OUTCOME MEASURE: The number and characterization of ADEs detected. RESULTS: Over 18 months, we monitored 36,653 hospitalized patients. There were 731 verified ADEs identified in 648 patients, 701 ADEs were characterized as moderate or severe, and 664 were classified as type A reactions. During this same period, only nine ADEs were identified using traditional detection methods. Physicians, pharmacists, and nurses voluntarily reported 92 of the 731 ADEs detected using this automated system. The other 631 ADEs were detected from automated signals, the most common of which were diphenhydramine hydrochloride and naloxone hydrochloride use, high serum drug levels, leukopenia, and the use of phytonadione and antidiarrheals. The most common symptoms and signs were pruritus, nausea and/or vomiting, rash, and confusion-lethargy. The most common drug classes involved were analgesics, anti-infectives, and cardiovascular agents. CONCLUSION: We believe that screening for ADEs with a computerized hospital information system offers a potential method for improving the detection and characterization of these events in hospital patients.

Adolescent↗

PubMedDate not supplied

The L6 muscle cell line as a tool to evaluate parenteral products for irritation.

A rat skeletal muscle cell line (L6) was evaluated for its utility in assessing cellular damage caused by parenteral administration of eight commercially available pharmaceuticals. The physical forms of the eight pharmaceuticals were diverse, including aqueous and non-aqueous suspensions and solutions. The L6 cells were exposed to therapeutic as well as diluted concentrations of methocarbamol, lorazepam, dimercaprol, phytonadione, menadiol sodium phosphate, penicillin G procaine, penicillin G benzathine, and iron dextran complex. Irritation assessment was based on the depletion of creatine phosphokinase (CK) from treated cultures versus untreated controls. The results obtained correlate well with reports of irritation and side effects noted in clinical use, and demonstrate the versatility of the model for testing suspensions and non-aqueous parenteral solutions. The L6 model is a useful tool to assist in determining the relative local irritancy of parenteral products.

Animals↗

PubMed1978

Drug therapy reviews: clinical use of hemostatic agents.

Systemic hemostatic agents are reviewed. Among the agents discussed are vitamin K preparations (phytonadione, menadione, menadione sodium bisulfite, menadiol sodium diphosphate); and blood products (whole blood, plasma, cryoprecipitate, factor VIII concentrates, factor IX concentrates and fibrinogen concentrates). Normal and abnormal hemostasis and fibrinolysis are discussed, as is the general management of systemic hemostatic defects. Specific disorders covered are clotting factor deficiencies, hemophilia A, factor VIII inhibitors, von Willebrand disease, hemophilia B (Christmas disease), other congenital coagulation disorders, acquired deficiency of factors II, VII, IX and X, and defibrination syndrome.

Antibodies↗

PubMed1987

Carbamate poisoning: the 'other' insecticide.

A 16-month-old child who ingested rat poison, according to her parents, was noted to have signs of cholinergic poisoning. In the emergency department, the child was intubated and given atropine via the endotracheal tube until venous access was established. Phytonadione (vitamin K) and pralidoxime (2-PAM) were also administered. The child recovered after an uneventful hospital course. The toxic agent was determined to be a carbamate insecticide, for which treatment with pralidoxime is considered controversial. Treatment of cholinergic poisoning due to unknown or mixed agents and poisoning caused by known carbamate insecticides are discussed.

Antidotes↗