Disease relevance of Hypoprothrombinemias

• Warfarin-induced hypoprothrombinemia. Potentiation by hyperthyroidism [1].
• Single oral doses of racemic warfarin, 1.5 mg/kg of body weight, were administered with and without 320 mg of trimethoprim and 1600 mg of sulfamethoxazole orally, beginning 7 d before the warfarin and continuing daily throughout the hypoprothrombinemia [2].
• Severe hemorrhage in a patient with circulating anticoagulant, acquired hypoprothrombinemia, and systemic lupus erythematosus [3].
• The occurrence of hypoprothrombinemia in moxalactam patients with peritonitis was not related to dosage, duration of therapy, age, sex, race, or renal or hepatic function [4].
• The only variable associated with bleeding after ES was abnormal labs (thrombocytopenia, elevated creatinine concentration, hypoprothrombinemia) [5].

High impact information on Hypoprothrombinemias

• A highly significant (P less than 0.01) augmentation of the mean warfarin level and hypoprothrombinemia with metronidazole occurred for racemic and S (-)-warfarin; none occurred with R (+)-warfarin [6].
• Cefotetan and hypoprothrombinemia [7].
• Hypoprothrombinemia has occurred frequently with cephalosporins that possess a methylthiotetrazole substitution (cefamandole, moxalactam, and cefoperazone) [8].
• Hypoprothrombinemia and bleeding due to cefoperazone [9].
• Antibiotics that contain a 1-N-methyl-5-thiotetrazole (MTT) side group have been associated with hypoprothrombinemia [10].

Chemical compound and disease context of Hypoprothrombinemias

• Thus, sulfinpyrazone augmented the hypoprothrombinemia of racemic warfarin stereoselectively by reduced metabolic clearance of S-warfarin [11].
• This study illustrated that the incidence of hypoprothrombinemia associated with concurrent cefamandole use is relatively high [12].
• Cimetidine augmented both the hypoprothrombinemia and the blood concentrations of warfarin, but ranitidine did not [13].
• Hypoprothrombinemia in patients with cancer receiving cefoperazone and mezlocillin [14].
• Forty-one patients with cancer who were receiving cefoperazone sodium plus mezlocillin sodium were prospectively followed up for the development of abnormal bleeding or hypoprothrombinemia [14].

Biological context of Hypoprothrombinemias

• The incidence of hypoprothrombinemia (prothrombin time greater than or equal to 2 s above the highest control) associated with concurrent cefamandole nafate usage in our institution was determined [12].
• Although selective delivery of menatetrenone in the liver by the lipid emulsion was due to phagocytosis by non-parenchymal cells, menatetrenone in the whole liver appeared to contribute to recovery from hypoprothrombinemia [15].
• Using normal volunteers, two previous controlled studies of an interaction between warfarin and chlorthalidone, and between warfarin and spironolactone, assert that volume depletion produced by forced diuresis results in the inhibition of warfarin's hypoprothrombinemia [16].
• These observations also raise the possibility that the TPMT genetic polymorphism may represent a risk factor for cefazolin-induced hypoprothrombinemia since subjects who genetically lack TPMT would be unable to catalyze this MTD biotransformation pathway [17].
• In 8 patients treated with Latamoxef we have found a prolongation bleeding time, moderate hypoprothrombinemia, thrombocytopenia and nearly no normalization of APTT and plasma euglobulin fibrinolysis [18].

Gene context of Hypoprothrombinemias

• Cyclooxygenase-2 inhibitor celecoxib: a possible cause of gastropathy and hypoprothrombinemia [19].
• Low serum prealbumin and low serum carotene levels were associated with the development of hypoprothrombinemia [14].
• Sulfinpyrazone increases the hypoprothrombinemia caused by warfarin primarily by inhibition of the cytochrome P-450-mediated oxidation of (S)-warfarin, the biologically more potent enantiomer [20].
• The hypoprothrombinemia mutations were inferred to affect either the cleavage of the propeptide from the Gla domain, the stability of the kringle-1 and -2 domains, or the close association of the A and B chains of the serine protease domain [21].
• A patient with primary biliary cirrhosis (PBC) developed marked hypoprothrombinemia with decreased concentrations of the vitamin K-dependent coagulation factors VII, IX, and X during treatment with rifampicin [22].

References