The Influence of Prophylactic Antibiotics on the Warfarin Anticoagulation Response in the Postoperative Prosthetic Cardiac Valve Patient

Angaran, David M.; Dias, Virgil C.; Arom, Kit V.; Northrup, William F.; Kersten, Thomas E.; Lindsay, William G.; Nicoloff, Demétre M.

doi:10.1097/00000658-198401000-00019

Cited by 21 publications

(9 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…VOLUME 7, NUMBER 3, 1987 tients in the moxalactam group experienced an elevated PT, and the number with an elevation of 4 seconds or longer was also significantly (p < 0.05) greater than the other treatment group.33 Similar results were observed in a comparison of moxalactam/ tobramycin versus ticarcillinit~bramycin,~~ while a more pronounced effect on PT was noted with moxalactam or ~efamandole.~~. 36 These results suggest an earlier onset and a greater magnitude of effect with moxalactam. In Table 3, data are presented that compare moxalactam or cefoperazone with control 33, 39,40 Hypoprothrombinemia was a frequent event with both moxalactam and cefoperazone in these comparative studies, while the control antibiotics generally demonstrated lower frequency.…”

Section: Comparative Trialsmentioning

confidence: 71%

Determinants of Antibiotic‐associated Hypoprothrombinemia

et al. 1987

View full text Add to dashboard Cite

Hypoprothrombinemia is a relatively uncommon event in the hospitalized patient. When it does occur, it often is associated with surgery, dietary vitamin K deficiency, renal dysfunction, malignancy, and broad-spectrum antibiotic therapy. Several mechanisms have been proposed to account for antibiotic-associated hypoprothrombinemia, including eradication of gastrointestinal bacteria, direct inhibition of vitamin K-dependent coagulation, and indirect inhibition of coagulation. The anecdotal reports and comparative studies of antibiotic-associated hypoprothrombinemia were reviewed; these usually implicated broad-spectrum or the use of several antibiotics. The increased frequency of hypoprothrombinemia associated with moxalactam and cefoperazone also raises questions about the role of their N-methylthiotetrazole (NMTT) side chains. The hypoprothrombinemia associated with NMTT antibiotics does not occur in healthy volunteers and is rare in patients without complicating conditions. Although NMTT inhibits vitamin K-dependent carboxylation in vitro, the parent cephalosporins do not. It is not clear whether NMTT-containing antibiotics liberate sufficient amounts of NMTT in vivo to antagonize clotting in patients. Thus, although moxalactam, and possibly cefoperazone, may in some cases be responsible for increases in prothrombin time, most important question for further study is whether the newer NMTT-containing antibiotics pose a risk of hypoprothrombinemia that is greater than that of antibiotics lacking this side chain.

show abstract

Section: Comparative Trialsmentioning

confidence: 71%

Determinants of Antibiotic‐associated Hypoprothrombinemia

et al. 1987

View full text Add to dashboard Cite

show abstract

“…The advantage of the INR over the PT is that values are independent from any testing laboratory, while PT results of one specimen may vary depending on the standard sample used in each laboratory for comparison. Many antibiotics change intestinal bacterial flora and thus bacterial Vitamin K synthesis [45,46]. Vitamin K can not be synthesised by the human body.…”

Section: Vitamin K Antagonists In Afmentioning

confidence: 99%

New Pharmacologic Approaches to Prevent Thromboembolism in Patients with Atrial Fibrillation

Hammwöhner

D’Alessandro²,

Wolfram³

et al. 2007

CVP

View full text Add to dashboard Cite

Atrial fibrillation (AF) is associated with a 6 fold increased risk for ischemic stroke. Observational studies suggest that one in four to five strokes is due to AF. Depending on the risk profile of an individual patient, the yearly risk for ischemic stroke is between 2% and 14%. AF is accompanied by an increased propensity for atrial clot formation due to a combination of decreased atrial blood flow, increased activity of the platelet/plasmatic coagulation system and prothrombotic changes at the atrial endocardium. This review summarizes the current guidelines for thromboembolic prevention in patients with AF. In many cases, continuous oral anticoagulation therapy (OAT) with vitamin K antagonists (VitKAs) is indicated if AF is accompanied by more than one additional risk factor for thromboembolic complications. However, therapeutic range of VitKAs (Phenprocoumon, Warfarin, and others), the most commonly used oral anticoagulants, is narrow and their use requires regular anticoagulation monitoring. Possibly due to these limitations, about one third of eligible patients are not treated with VitKAs. Furthermore, in many treated patients OAT is not well controlled. Thus, in clinical practice anticoagulation therapy in AF is suboptimal. Therefore, new and more convenient pharmacologic approaches to prevent thromboembolism with i.e. direct thrombin inhibitors (DTI), synthetic polysaccharides (factor Xa Inhibitors), and others are discussed, and their possible future role in the treatment of AF is evaluated.

show abstract

“…Cephamandole may enhance the hypoprothrombinaemic response to warfarin due to interference with vitamin K synthesis in the gastrointestinal tract 13,14 and/ or with synthesis of vitamin K-dependent clotting factors 4 . Related cephalosporines with an N-methylthiotetrazole side chain such as cefmetazole, cefmenoxime, cefoperazone and latamoxef may be expected to behave similarly, although there appear to be no reports of an interaction.…”

Section: Drugs Affecting Availability Of Vitamin Kmentioning

confidence: 99%

Interactions of Warfarin

Rehulková¹

2001

BIOMED PAP

View full text Add to dashboard Cite

In this article, the author reviews and updates the basis of interactions with warfarin, illustrated with appropriate examples. The interactions with drugs, medicinal herbs and foods are summarised. 28Cholestyramine binds vitamin K in the gut, thus preventing its absorption 18 . It also decreases the absorption and may interrupt the enterohepatic recirculation of warfarin, resulting in a reduced anticoagulant effect 19,20 .Colestipol does not affect the absorption of warfarin. When colestipol is administered with warfarin, no depressant effects on blood levels are seen 21 . Drugs affecting receptor sensitivityEstrogens increase the synthesis of various clotting factors and may thus reduce the effect of anticoagulants 22, 23 . Oral contraceptives increase clotting factor concentrations and inhibit warfarin metabolism. The net effect depends on balance between these factors. Oral contraceptives are generally contraindicated in most patients taking warfarin since they are trombogenic 1, 24 .Steroids with anabolic or androgenic properties, such as oxymetholone 25, 26, 27 , stanozolol 28, 29 and danazol 30, 31, 32 , may potentiate the action of warfarin allegedly by reducing clotting factor synthesis. The 17-alpha-alkylated steroids appear to be more likely to induce this reaction than the non-substituted steroids 25, 26, 27, 33 . However, there has been a report of topically applied testosterone, which does not have 17-alpha-alkyl substituent, enhancing warfarin 34 .Diuretics may antagonise the action of warfarin by two pharmacodynamic mechanisms 18 : (a) patients in cardiac failure have impaired clotting factor synthesis due to hepatic congestion -correction of this state leads to increased clotting factor synthesis; (b) diuretics also reduce the plasma volume producing an increased concentration of clotting factors which may alter the anticoagulant effect of warfarin 35 . Chlorthalidone 36 and spironolactone 35 have both been associated with a reduction of warfarin activity probably as a consequence of diuresis concentrating the circulating clotting factors. Bumetanide, furosemide and thiazides appear to have no effect on warfarin 23 .Certain cephalosporines, such as cefotetan, cefamandole, cefoperazone, or moxalactam may cause marked hypoprothrombinemia and/or prolonged bleeding time at concurrent use with warfarin 38, 39, 40, 41 . The main mechanism of interaction consists in decreasing synthesis of vitamin K-dependent clotting factors.Clofibrate may potentiate warfarin action, probably by altering receptor sensitivity 23, 37 . Although clofibrate displaces warfarin from albumin binding sites this does not appear to be a principal mechanism of the interaction 42 .Drugs altering thyroid function may affect anticoagulant control, since rates of synthesis and degradation of clotting factors are dependent on thyroid function 7 . Thyroid compounds do enhance the activity of oral anticoagulants by increased metabolism of clotting factors 12 . Dextrothyroxine increases the anticoagulant effect of warfarin ...

show abstract

The Influence of Prophylactic Antibiotics on the Warfarin Anticoagulation Response in the Postoperative Prosthetic Cardiac Valve Patient

Cited by 21 publications

References 14 publications

Determinants of Antibiotic‐associated Hypoprothrombinemia

Determinants of Antibiotic‐associated Hypoprothrombinemia

New Pharmacologic Approaches to Prevent Thromboembolism in Patients with Atrial Fibrillation

Interactions of Warfarin

Contact Info

Product

Resources

About