indication

For the treatment of strongyloidiasis (threadworm), cutaneous larva migrans (creeping eruption), visceral larva migrans, and trichinosis.

pharmacology

Thiabendazole is a fungicide and parasiticide. Thiabendazole is also a chelating agent, which means that it is used medicinally to bind metals in cases of metal poisoning, such as lead poisoning, mercury poisoning or antimony poisoning. Thiabendazole is vermicidal and/or vermifugal against Ascaris lumbricoides ("common roundworm"), Strongyloides stercoralis (threadworm), Necator americanus, Ancylostoma duodenale (hookworm), Trichuris trichiura (whipworm), Ancylostoma braziliense (dog and cat hookworm), Toxocara canis, Toxocara cati (ascarids), and Enterobius vermicularis (pinworm). Thiabendazole also suppresses egg and/or larval production and may inhibit the subsequent development of those eggs or larvae which are passed in the feces.

mechanism of action

The precise mode of action of thiabendazole on the parasite is unknown, but it most likely inhibits the helminth-specific enzyme fumarate reductase.

toxicity

Overdosage may be associated with transient disturbances of vision and psychic alterations. The oral LD 50 is 3.6 g/kg, 3.1 g/kg and 3.8 g/kg in the mouse, rat, and rabbit respectively.

biotransformation

Hepatic. Metabolized almost completely to the 5-hydroxy form which appears in the urine as glucuronide or sulfate conjugates.

absorption

Rapidly absorbed and peak plasma concentration is reached within 1 to 2 hours after the oral administration of a suspension. Some systemic absorption may occur from topical preparations applied to the skin.

half life

The half-life for thiabendazole in both normal and anephric patients is 1.2 hours (range 0.9 to 2 hours). The half-life for the 5-hydroxythiabendazole metabolite in both normal and anephric patients is 1.7 hours (range 1.4 to 2 hours).

route of elimination

It is metabolized almost completely to the 5-hydroxy form which appears in the urine as glucuronide or sulfate conjugates.

drug interactions

Acenocoumarol: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Acenocoumarol by decreasing Acenocoumarol metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Acenocoumarol if Thiabendazole is initiated, discontinued or dose changed.

Alosetron: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Alosetron by decreasing Alosetron metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Alosetron if Thiabendazole is initiated, discontinued or dose changed.

Aminophylline: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Aminophylline by decreasing Aminophylline metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Aminophylline if Thiabendazole is initiated, discontinued or dose changed.

Betaxolol: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Betaxolol by decreasing Betaxolol metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Betaxolol if Thiabendazole is initiated, discontinued or dose changed

Caffeine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Caffeine by decreasing Caffeine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Caffeine if Thiabendazole is initiated, discontinued or dose changed.

Clomipramine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Clomipramine by decreasing Clomipramine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Clomipramine if Thiabendazole is initiated, discontinued or dose changed.

Clozapine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Clozapine by decreasing Clozapine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Clozapine if Thiabendazole is initiated, discontinued or dose changed.

Cyclobenzaprine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Cyclobenzaprine by decreasing Cyclobenzaprine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Cyclobenzaprine if Thiabendazole is initiated, discontinued or dose changed.

Dacarbazine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Dacarbazine by decreasing Dacarbazine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Dacarbazine if Thiabendazole is initiated, discontinued or dose changed.

Doxepin: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Doxepin by decreasing Doxepin metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Doxepin if Thiabendazole is initiated, discontinued or dose changed.

Duloxetine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Duloxetine by decreasing Duloxetine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Duloxetine if Thiabendazole is initiated, discontinued or dose changed.

Flutamide: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Flutamide by decreasing Flutamide metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Flutamide if Thiabendazole is initiated, discontinued or dose changed.

Fluvoxamine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Fluvoxamine by decreasing Fluvoxamine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Fluvoxamine if Thiabendazole is initiated, discontinued or dose changed.

Guanabenz: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Guanabenz by decreasing Guanabenz metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Guanabenz if Thiabendazole is initiated, discontinued or dose changed.

Oxtriphylline: Thiabendazole increases the effect and toxicity of theophylline

Ramelteon: Thiabendazole increases levels/toxicity of ramelteon

Tacrine: The metabolism of Tacrine, a CYP1A2 substrate, may be reduced by strong CYP1A2 inhibitors such as Thiabendazole. Consider modifying therapy to avoid Tacrine toxicity. Monitor the efficacy and toxicity of Tacrine if Thiabendazole is initiated, discontinued or if the dose is changed.

Theophylline: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Theophylline by decreasing Theophylline metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Theophylline if Thiabendazole is initiated, discontinued or dose changed.

Thiothixene: The strong CYP1A2 inhibitor, Thiobendazole, may decrease the metabolism and clearance of Thiothixene, a CYP1A2 substrate. Consider alternate therapy or monitor for changes in Thiothixene therapeutic and adverse effects if Thiobendazole is initiated, discontinued or dose changed.

Tizanidine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Tizanidine by decreasing Tizanidine metabolism and clearance. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Tizanidine if Thiabendazole is initiated, discontinued or dose changed.

Trifluoperazine: The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Trifluoperazine by decreasing Trifluoperazine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Trifluoperazine if Thiabendazole is initiated, discontinued or dose changed.