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Induction isoniazid

HIV - The initial phase of a 6-month tuberculosis regimen consists of isoniazid, rifabutin, pyrazinamide, and ethambutol for patients receiving therapy with protease inhibitors or nonnucleoside reverse transcriptase inhibitors. These drugs are administered a) daily for at least the first 2 weeks, followed by twice weekly dosing for 6 weeks or b) daily for 8 weeks to complete the 2-month induction phase. The second phase of treatment consists of rifabutin and isoniazid administered twice weekly or daily for 4 months. [Pg.1710]

Enzyme induction properties Rifampin has enzyme induction properties that can enhance the metabolism of endogenous substrates including adrenal hormones, thyroid hormones, and vitamin D. Rifampin and isoniazid have been reported to alter vitamin D metabolism. In some cases, reduced levels of circulating 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D have been accompanied by reduced serum calcium and phosphate, and elevated parathyroid hormone. [Pg.1717]

Neuhauser-Klaus. A. Chauhan, P. S. (1987) Studies on somatic mutation induction in the mouse with isoniazid and hydrazine. Mutat. Res., 191, 111-116... [Pg.1010]

The combination of rifampicin and isoniazid reduces serum concentrations of 25-hydroxy cholecalciferol. Rifampicin acts by induction of an enzyme that promotes conversion of 25-hydroxycholecalciferol to an inactive metabolite, and isoniazid acts by inhibiting 25-hydroxyla-tion and 1-hydroxylation (SEDA-14, 258). Children or pregnant women with tuberculosis have increased calcium requirements independent of rifampicin administration... [Pg.644]

Zand R, Nelson SD, Slattery JT, et al. Inhibition and induction of cytochrome P4502El-catalyzed oxidation by isoniazid in humans. Clin Pharmacol Ther 1993 54 142-149. [Pg.638]

Human CYP2E1 is one of the most efficient P450s to catalyze the oxidation of acetaminophen to NAPQI (157-159). Ethanol and isoniazid cause a time-dependent inhibition and induction of acetaminophen oxidation to NAPQI in humans (160,161) that can decrease risk for hepatotoxicity over the interval of concurrent administration and increase risk for hepatotoxicity a few hours after removal of ethanol or isoniazid. The latter induction phase of CYP2E1 may, in part, be responsible for cases of acetaminophen hepatotoxicity associated with the use of ethanol (162-165) or isoniazid (166-168). However, the induction is modest (2- to 3-fold) therefore, other susceptibility factors, genetic and others such as decreased glutathione stores and nutritional status, are likely to play an important role in some individuals (169-174). [Pg.698]

Rifampicin is an enzyme inducer and can increase the incidence and severity of isoniazid-induced hepatitis. Carbamazepine is an enzyme induction agent and interacts with isoniazid, increasing its hepatotoxicity. Isoniazid toxicity is associated with fast acetylator genotype. Although his phenotype was unknown, the interaction with carbamazepine increases risk of this toxicity. [Pg.353]

Induction by increased enzyme synthesis has been described for induction of CYP2B1/2 by octamethylcyclotetrasiloxane (Sarangapani et al. 2002) and CYP1A1 and CYP1A2 by TCDD via interaction with the Ah-receptor (Andersen 1995 Andersen et al. 1997). Induction by decreased enzyme degradation has been described by Chien et al. (1997) for induction of CYP2E1 by ethanol, acetone, and isoniazid via enzyme stabilization. Exposure to such enzyme inducers and stabilizators would result in increasing the clearance of all other coexposed chemicals that are metabolized by the stabilized enzyme. [Pg.64]

Enhanced hepatotoxicity of conventional antituberculosis regimens has been reported in recipients of orthotopic hver transplants, which is not unexpected, because of bouts of organ rejection (25). The authors recommended ofloxacin for these patients on the basis of favorable outcome in six cases. A conventional antituberculosis induction regimen was used initially until hepatotoxicity developed in all six patients. Thereafter they were treated with a combination of ofloxacin and ethambutol, with apparent cure in all. It should be noted that most of the patients took isoniazid + rifampicin for almost 2 months, which is the usual period when hepatotoxic reactions occur. Perhaps one should evaluate substitution of rifampicin with ofloxacin from the very beginning in order to minimize hepatotoxicity, as well as interference with ciclosporin leading to graft rejection noted in an earlier study (26). [Pg.324]

Rothfield NF, Bierer WF, Garfield JW. Isoniazid induction of antinuclear antibodies. A prospective study. Ann Intern Med 1978 88(5) 650-2. [Pg.1929]

Rifampicin is rarely used as monotherapy. The risk of hepatotoxicity appears to be very low in patients with normal liver function, especially if rifampicin is given continuously. When given with isoniazid, rifampicin can cause a fulminant liver reaction. This may be attributable to enhancement of isoniazid hepatotoxicity as a result of enzyme induction by rifampicin. In some cases, jaundice occurred within 6-10 days after beginning isoniazid plus rifampicin (52). High serum transaminase activities, disturbances of consciousness, and centrilobular necrosis were found. All the patients recovered. [Pg.3043]

Thus, the importance of enzyme induction is that it may alter the toxicity of a foreign compound. This can have important clinical consequences and underlie drug interactions. Thus, the antitubercular drug rifampicin is thought to increase the hepatotoxicity of the drug isoniazid, and alcohol may increase susceptibility to the hepatotoxicity of... [Pg.305]

Perry, W. and Jenkins, M. V. (1986) Hepatic mixed function oxidase induction during rifampicin/isoniazid therapy in Indian vegetarians. Int. J. Clin. Pharmacol. Ther. Toxicol. 24, 344—348. [Pg.267]

Consistent with its blood gas partition coefficient, induction of anesthesia and recovery from enflurane are relatively slow (Table 13-1). Enflurane is metabolized to a modest extent (2-8% of absorbed enflurane) by hepatic CYP2E1. Fluoride ions are a by-product of enflurane metabolisrrr but plasma fluoride levels are low and nontoxic. Patients taking isoniazid exhibit enhanced metabolism of enflurane with a consequent elevation of serum fluoride. [Pg.235]

Drug Interactions Barbiturates combine with other CNS depressants to cause severe depression ethanol is the most frequent offender, and interactions with first-generation antihistamines also are common. Isoniazid, methylphenidate, and monoamine oxidase inhibitors also increase the CNS-depressant effects. Other prominent drag interactions occin as a result of the induction of hepatic drug-metabolizing enzymes by barbiturates see above). [Pg.274]

Anti-infective drugs Ciprofloxacin can greatly increase the risk of seizure induction in patients taking anticonvulsants. Erythromycin produces a rapid 100-200% rise in carbamazepine levels. There is a possibility of reduced plasma levels of the protease inhibitors indinavir and saquinavir with carbamazepine. Isoniazid increases carbamazepine serum levels, and leads to the possible emergence of toxicity (disorientation and aggression). Mefloquine may antagonize the anticonvulsant effect of carbamazepine. Ritonavir, a protease inhibitor, may cause toxicity by raising carbamazepine plasma levels. [Pg.181]

Fig. 1.3 An enzyme induction interaction. Rifampicin (600 mg daily plus isoniazid) increased the metabolism of ciclosporin in this patient thereto reducing the trough serum levels. He subsequently died because his heart transplant rejected (after Tronsp/ont Proc, 16, Van Buren D, Wideman CA, Ried M, Gibbons S, n Buren CT, Jarowenko M, Flechner SM, Frazier OH, Cool DA, Kahan BD. The antagonistic effect of ri mpidn upon cyclosporine bioavailability. 1642—5, Copyright Els ier (1984)). Fig. 1.3 An enzyme induction interaction. Rifampicin (600 mg daily plus isoniazid) increased the metabolism of ciclosporin in this patient thereto reducing the trough serum levels. He subsequently died because his heart transplant rejected (after Tronsp/ont Proc, 16, Van Buren D, Wideman CA, Ried M, Gibbons S, n Buren CT, Jarowenko M, Flechner SM, Frazier OH, Cool DA, Kahan BD. The antagonistic effect of ri mpidn upon cyclosporine bioavailability. 1642—5, Copyright Els ier (1984)).
Chien JY, Peter RM, Nolan CM, Wartell C, Slattery JT, Nelson SD, Carithers RL, Thummel KE. Influence of pol3fmorphic AT-acetyltransferase phenotype cn the inhibition and induction of acetaminophen bioactivation widi long-term isoniazid inPharmacolTher( 99T)6 24-34. [Pg.196]

Pessayre D, Bentata M, Degott C, Nouel O, Miguet J-P, Rueff B, Benhamou J-P. Isoniazid-rifampin fulminant hepatitis, A possible consequence of the enhancement of isoniazid hepatotoxicity by enzyme induction. Gastroenterology (1977) 72,284-9. [Pg.311]

Antituberculous treatment with rifampicin, isoniazid and etham-butol has been shown to increase the non-renal clearance of cimetidine by about 50%. This is probably due to enzyme induction caused by rifampicin. However, the total clearance is unchanged and so this interaction would appear to be of little clinical importance. ... [Pg.963]

With combined therapy, it was suggested that the effects of rifampicin might be more apparent during the initial 7 days, but that by week 4 the effect of isoniazid might predominate, because of its reduced inactivation by rifampicin combined with a reduction in the effect of rifampicin by auto-induction of its own metabolism. High theophylline levels in the isolated ease above may have been due to liver impairment brought about by the eombined use of rifampicin and isoniazid, or alcoholism. ... [Pg.1196]

Isoniazid appears to cause a dual interaction. During administration, it inhibits the activity of cytochrome P450 isoenzyme CYP2E1, the enzyme involved in the metabolism of chlorzoxazone. Shortly after stopping isoniazid, the metabolism of chlorzoxazone is increased, possibly because of induction of CYP2E1, although this effect was only evident in the slow acetylators. ... [Pg.1253]

Campbell DH, Me Casland GE (1944) In vitro anaphylactic response to polyhaptenic and monohaptenic simple antigens. J Immunol 49 315 Cannat A, Seligmann M (1968) Induction by isoniazid and hydralazine of antinuclear factors in mice. Clin Exp Immunol 3 99... [Pg.123]


See other pages where Induction isoniazid is mentioned: [Pg.168]    [Pg.111]    [Pg.173]    [Pg.554]    [Pg.1583]    [Pg.217]    [Pg.614]    [Pg.686]    [Pg.255]    [Pg.524]    [Pg.1925]    [Pg.3040]    [Pg.3042]    [Pg.539]    [Pg.1252]    [Pg.306]    [Pg.77]    [Pg.375]    [Pg.419]    [Pg.786]    [Pg.129]    [Pg.424]    [Pg.10]    [Pg.196]    [Pg.344]   
See also in sourсe #XX -- [ Pg.386 , Pg.418 , Pg.419 , Pg.621 ]




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Isoniazid

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