rifampin and Vitamin-K-Deficiency

An 8-month-old child under tuberculosis treatment presented with multiple ecchymotic lesions. A severe coagulopathy was evidenced compatible with vitamin K deficiency [II (3%), VII (2%), IX (3%) and X (1%)]. It was reversed with vitamin K and plasma administration. Rifampicin-induced vitamin K deficiency is very rare, reported only once before, possibly related to an inhibition of vitamin K cycle.

Topics: Antibiotics, Antitubercular; Blood Coagulation Disorders; Child; Humans; Infant; Male; Plasma; Rifampin; Treatment Outcome; Tuberculosis; Vitamin K; Vitamin K Deficiency

We report a case of probable iatrogenic vitamin K deficiency in the context of antibiotic treatment for endocarditis. The patient was initially admitted with breathlessness and treated for an exacerbation of chronic obstructive pulmonary disease. However, during this period the patient was further diagnosed with endocarditis following repeated temperature spikes. Following initiation of antibiotic treatment for endocarditis the patient was noted to become increasingly anaemic. The patient was noted to have prolonged prothrombin time despite no anticoagulants. Antibiotics have been reported to alter the gut flora causing vitamin K deficiency; thereby, resulting in coagulopathy. We give a brief overview and literature review regarding potential vitamin K deficiency in this clinical context.

Topics: Aged; Anti-Bacterial Agents; Drug Therapy, Combination; Endocarditis, Bacterial; Humans; Male; Rifampin; Vancomycin; Vitamin K Deficiency

We report a male infant with congenital tuberculosis who developed cerebral hemorrhage associated with vitamin K deficiency during treatment with isoniazid and rifampin. Despite an absence of risk factors for vitamin K deficiency, the severe hemorrhagic disorder occurred at 4 months of age. We speculate that vitamin K deficiency in the present case may have resulted from a synergic effect of antituberculosis agents and immaturity of vitamin K metabolism and/or its absorption.

Topics: Cerebral Hemorrhage; Humans; Infant; Infectious Disease Transmission, Vertical; Isoniazid; Male; Rifampin; Streptomycin; Tuberculosis; Vitamin K; Vitamin K Deficiency

Vitamin K deficiency caused by antituberculous agents was examined in clinical patients and in experimental rats. When antituberculous agents given to the patients who had only total elental diet because of small intestinal dysfunction, a marked increase in plasma PIVKA-II and a decrease in thrombo-test value were observed. These changes were quickly normalized by administration of vitamin K, despite of succeeding or stopping of antituberculous agents. In rat experiments, effects of four agents (ethambutol, isoniazid, paraaminosalicylate, and rifampicin) on prothrombin time were studied. Among these agents, only rifampicin prolonged prothrombin time. This prolongation depended on drug doses and duration of administration. In addition to this hypoprothrombinemia, an increase in plasma PIVKA-II was also observed, and these changes were normalized within 24 hours of vitamin K administration. These data suggest that rifampicin inhibits vitamin K epoxide reductase interfering re-use of vitamin K and caused vitamin K deficiency in patients with total elental diet.

Topics: Animals; Antitubercular Agents; Biomarkers; Humans; Male; Middle Aged; Protein Precursors; Prothrombin; Rats; Rats, Sprague-Dawley; Rifampin; Vitamin K Deficiency

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. The coagulation abnormalities were easily corrected by administration of vitamin K. Different mechanisms may be involved, such as a decreased production of menaquinones by intestinal bacteria, a warfarin-like effect by inhibition of the vitamin K epoxide reductase, or an increased oxidative degradation of vitamin K as a result of hepatic microsomal enzyme stimulation. Whatever the mechanism involved, the appearance of this complication in a patient with PBC probably points to the importance of a pre-existing poor vitamin K status. Patients with PBC, treated with rifampicin, should have a regular monitoring of their vitamin K status. Adequate vitamin substitution should be administered, if necessary.

Topics: Female; Humans; Hypoprothrombinemias; Liver Cirrhosis, Biliary; Middle Aged; Prothrombin Time; Rifampin; Vitamin K; Vitamin K Deficiency

Topics: Adult; Aged; Humans; Middle Aged; Prothrombin Time; Rifampin; Vitamin K; Vitamin K Deficiency

Topics: Adult; Drug Synergism; Female; Humans; Hypoprothrombinemias; Isoniazid; Isonicotinic Acids; Rifampin; Streptomycin; Tuberculosis, Pulmonary; Vitamin K Deficiency