Albendazole (methyl 5-(propylthio)-2-benzimidazolecarbamate) is an oral broad-spectrum anthelmintic antiparasitic agent of the benzimidazole class. Albendazole is similar to mebendazole and thiabendazole, but is better tolerated. The systemic anthelmintic activity is attributed to albendazole sulfoxide, the primary active hepatic metabolite. Albendazole is effective in eradicating infections caused by a variety of nematodes including Echinococcus granulosus (dog tapeworm), Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), Trichinella spiralis (pork worm), Trichuris trichiura (whipworm), Enterobius vermicularis (pinworm), Strongyloides stercoralis (threadworm), Ascaris lumbricoides (roundworm), Ancylostoma duodenale (hookworm), and Necator americanus (hookworm). Albendazole is currently the treatment of choice for treating hydatid cyst disease (larval stage E. granulosus infection), for which it is roughly 70% effective. In sheep-raising areas of Utah, Arizona, and Nevada, E. granulosus is considered to be endemic; however, annual infection rates are low and most human cases in the US occur in immigrants who were exposed in their countries of origin, or in US travelers visiting global endemic areas. Albendazole is also very effective (> 80%) for cysticercosis secondary to T. solium; neurocysticercosis is rare in the US except in immigrants from endemic areas. Albendazole is the only agent used for the treatment of ocular neurocysticercosis. The drug has also shown considerable efficacy in treating microsporidiosis caused by Septata intestinalis. Albendazole was first marketed outside the US in 1982, and common trade names in other countries include Eskazole and Zentel. In the US, albendazole tablets were FDA-approved for treating hydatid cyst disease and neurocysticercosis in June 1996; a chewable tablet formulation was FDA-approved for the same indications in June 2015.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Oral Administration
Oral Solid Formulations
-Administer with food, preferably a high-fat meal, to increase oral bioavailability.
-Albendazole tablets may be chewed or crushed.
Albendazole is generally well tolerated. Gastrointestinal adverse effects reported in patients treated for hydatid disease and neurocysticercosis include nausea (4-6%), vomiting (4-6%), and abdominal pain (6%). The incidence of these effects is positively correlated with dosage, length of treatment, and severity of infection. Fever was less frequently reported (1%). Diarrhea has been noted in post-marketing reports.
Dermatologic and hypersensitivity reactions such as rash (unspecified) and urticaria occur in < 1% of patients given albendazole. Reversible alopecia was reported in <= 2% of patients. Erythema multiforme and Stevens-Johnson syndrome have been noted in post-marketing reports.
Meningeal signs (1%), seizures, and increased intracranial pressure (2%) may occur from the use of albendazole for the treatment of neurocysticercosis; systemic corticosteroid therapy is coprescribed to prevent cerebral hypertensive episodes during the first week of treatment. An increase in CNS symptoms may result as the therapy produces destruction of the cysts within the CNS. Preventative antiepileptic therapy should be employed. Headache (1-11%) and dizziness/vertigo (<= 1%) have also been reported in patients receiving albendazole. Asthenia, blurred vision, and somnolence (drowsiness) have been noted in post-marketing reports.
Albendazole may cause a reduction in total white blood cell counts due to bone marrow suppression; these effects are usually reversible. Leukopenia occurs in < 1% of patients, and results in discontinuation of therapy in 0.7% of patients. Granulocytopenia, pancytopenia, thrombocytopenia, and agranulocytosis have been reported, but are rare in patients receiving albendazole. Aplastic anemia and neutropenia have been noted in post-marketing reports. The risk of bone marrow suppression appears to be higher in patients with liver disease, including hepatic echinococcosis. A CBC with differential should be performed prior to start of therapy and every 2 weeks during treatment.
Albendazole therapy may result in elevated hepatic enzymes. During clinical trials, <= 16% of patients had abnormal liver function tests/elevated hepatic enzymes. Hepatitis and acute hepatic failure have been noted in post-marketing reports. LFTs should be performed prior to start of therapy and every 2 weeks during treatment. Hepatic abnormalities requiring drug discontinuation occur in roughly 3.8% of patients with hydatid cyst disease. In most cases, liver toxicity is reversible upon drug discontinuation.
Acute renal failure (unspecified) and rhabdomyolysis have been noted with albendazole therapy in post-marketing reports.
Albendazole is contraindicated in any person with known hypersensitivity to albendazole, the benzimidazole class of compounds, or any product components.
Use albendazole with caution in patients with hepatic disease or biliary tract disease. Albendazole is extensively metabolized by the liver; hepatic clearance may be impaired if hepatic disease or biliary obstruction are present and may result in increased side effects. Albendazole can cause elevated liver enzymes, which usually resolves after discontinuation of therapy; however, there have been cases of acute liver failure of unknown causality and hepatitis. In addition, patients with increased liver enzymes and those with hepatic echinococcosis are at increased risk for hepatotoxicity and suppression of bone marrow. Monitor liver enzymes (transaminases) and blood counts before the start of each cycle and at least every 2 weeks during treatment. If liver enzymes exceed twice the upper limit of normal, consider discontinuing therapy based on the clinical situation. When liver enzymes return to baseline, consideration may be given to restarting albendazole. If albendazole is restarted, laboratory tests should be monitored frequently.
Central nervous system effects, including dizziness and drowsiness, are common with albendazole therapy. Patients should be advised to avoid activities that require mental alertness, such as driving or operating machinery, until they know how albendazole treatment affects them.
Before initiating albendazole therapy for neurocysticercosis, examine the patient for retinal lesions due to ocular cysticercosis. The benefits of starting albendazole therapy should be weighed against the possibility of retinal damage caused by albendazole-induced changes to existing ocular lesions.
Albendazole may cause bone marrow suppression and should be used cautiously in any patient predisposed to leukopenia or neutropenia or other bone marrow suppression (e.g., recent chemotherapy). A complete blood cell count with differential should be performed at the start of each 28-day treatment cycle and every 2 weeks during each 28-day cycle. Albendazole may be continued if the total white blood cell count and absolute neutrophil count decrease is modest and does not progress. Rare fatalities associated with the use of albendazole have been reported due to granulocytopenia, agranulocytosis, and pancytopenia. Patients with hepatic disease, including hepatic echinococcosis, appear more likely to develop bone marrow suppression leading to pancytopenia, aplastic anemia, agranulocytosis, and leukopenia due to albendazole. Therefore, closer monitoring of blood counts is needed in these patients. Discontinue albendazole if clinically significant decreases in blood cell counts occur.
Patients being treated for neurocystericercosis with albendazole should receive appropriate anticonvulsant and steroid therapy during therapy to prevent neurological symptoms (seizures, increased intracranial pressure, and focal signs) and cerebral hypertensive episodes, especially during the first week of anticysterceral therapy. Inflammatory reactions occur due to parasite death within the brain. For patients treated with albendazole for other indications, pre-existing neurocystericercosis may result in neurological symptoms soon after treatment is initiated; therefore, appropriate steroid and anticonvulsant therapy should started immediately. Experts state that antiparasitic drugs are contraindicated in patients with cerebral edema (cysticercal encephalitis).
Safety and efficacy of albendazole have not been established in neonates and infants, and data are limited in children < 6 years of age. In hydatid disease, infection in infants and young children is uncommon. Neurocysticercosis infections in children are more frequently encountered and the efficacy of albendazole in children appears to be similar to adults.
Advise pregnant women of the potential risk to the fetus with albendazole therapy. Based on findings from animal reproduction studies, albendazole may cause fetal harm when administered to a pregnant woman. However, available human data from a small number of case series and reports on the use of multiple-dose albendazole in the first trimester of pregnancy and several studies on single-dose albendazole use later in pregnancy have not identified any drug-associated risks for major birth defects, miscarriage, or adverse maternal or fetal outcomes. The World Health Organization (WHO) supports the use of albendazole as antihelminthic therapy after the first trimester of pregnancy. Guidelines suggest deferring treatment for neurocysticercosis until after pregnancy unless intracranial pressure is elevated. In animal reproductive studies, oral administration of albendazole during the period of organogenesis caused embryotoxicity and skeletal malformations at doses 0.1 to 0.6 times the maximum recommended human dose (MRHD) based on body surface area and was associated with maternal toxicity at doses 0.6 times the MRHD based on body surface area.
Albendazole and its active metabolite, albendazole sulfoxide, have been reported at low concentrations in human breast milk. There have been no reports of adverse effects on the breast-fed infant and no information on the effects on milk production. A consultative group to the World Health Organization (WHO) suggested that a single oral dose of albendazole may be administered to breast-feeding women; however, there are no recommendations for multiple doses. In single-dose studies (400 mg PO), the mean peak milk concentration of albendazole sulfoxide was 351.9 mcg/L occurring at a mean of 6.9 hours from data of 20 women. The half-life of albendazole sulfoxide in breast milk was 12.4 hours. Based on this information, it was estimated that a fully breast-fed infant would be exposed to less than 0.1 mg/kg of albendazole sulfoxide over 36 hours after a single maternal dose. Consider the developmental and health benefits of breast-feeding along with the mother's clinical need for albendazole and any potential adverse effects on the breast-fed infant from albendazole or the underlying maternal condition.
Albendazole may be associated with reproductive risk. Obtain pregnancy testing before prescribing albendazole to females of reproductive potential. Discuss contraception requirements with the patient. Advise women of reproductive potential to use effective birth control during albendazole treatment and for 3 days after the final dose.
Per the manufacturer, this drug has been shown to be active against most strains of the following microorganisms either in vitro and/or in clinical infections: Echinococcus granulosus, Taenia solium
NOTE: The safety and effectiveness in treating clinical infections due to organisms with in vitro data only have not been established in adequate and well-controlled clinical trials.
This drug may also have activity against the following microorganisms: Ancylostoma duodenale, Ascaris lumbricoides, Capillaria philippinensis, Encephalitozoon intestinalis, Enterobius vermicularis, Microsporum sp., Necator americanus, Strongyloides stercoralis, Taenia saginata, Trichuris trichiura
NOTE: Some organisms may not have been adequately studied during clinical trials; therefore, exclusion from this list does not necessarily negate the drug's activity against the organism.
For the treatment of hydatid cyst disease:
Oral dosage:
Adults >= 60 kg: 400 mg PO twice daily with meals for 28 days followed by a 14-day drug-free period. Repeat for 2 more cycles.
Adults < 60 kg: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 28 days followed by a 14-day drug-free period. Repeat for 2 more cycles.
Children and Adolescents: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 28 days followed by a 14-day drug-free period. Repeat for 2 more cycles. Published data in pediatric patients for this indication are limited, particularly in infants and young children, in whom hydatid disease is uncommon.
For the treatment of cysticercosis*:
Oral dosage:
Adults: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 8 to 30 days; can be repeated as necessary. Surgery is indicated for intraocular cysts; intraocular cysts should be removed before administration of antiparasitic treatment to avoid irreversible eye damage due to the inflammatory response.
Children and Adolescents: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 8 to 30 days; can be repeated as necessary. Surgery is indicated for intraocular cysts; intraocular cysts should be removed before administration of antiparasitic treatment to avoid irreversible eye damage due to the inflammatory response.
For the treatment of neurocysticercosis, including parenchymal and extraparenchymal* cysts:
NOTE: Consider methotrexate as a steroid-sparing agent in patients requiring prolonged courses of anti-inflammatory therapy in subarachnoid disease. Anticonvulsant therapy is recommended in patients with seizures.
-for the treatment of neurocysticercosis with 1 to 2 parenchymal cysts:
Oral dosage:
Adults: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 10 to 14 days with corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
Children and Adolescents: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 10 to 14 days with corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
-for the treatment of neurocysticercosis with more than 2 parenchymal cysts:
Oral dosage:
Adults: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 10 to 14 days combined with praziquantel and corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
Children and Adolescents: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 10 to 14 days combined with praziquantel and corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
-for the treatment of neurocysticercosis with a single enhancing lesion:
Oral dosage:
Adults: 15 mg/kg/day (Max: 800 mg/day) PO in 2 divided doses for 7 to 14 days combined with corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
Children and Adolescents: 15 mg/kg/day (Max: 800 mg/day) PO in 2 divided doses for 7 to 14 days combined with corticosteroids. The FDA-approved maximum dosage is 800 mg/day for 8 to 30 days.
-for the treatment of neurocysticercosis with subarachnoid extraparenchymal cysts*:
Oral dosage:
Adults: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses combined with praziquantel and corticosteroids. Continue treatment for 2 to 12 months or until resolution of cystic lesions on neuroimaging studies.
Children and Adolescents: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses combined with praziquantel and corticosteroids. Continue treatment for 2 to 12 months or until resolution of cystic lesions on neuroimaging studies.
-for the treatment of neurocysticercosis with intraventricular extraparenchymal cysts*:
Oral dosage:
Adults: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 14 days. Antiparasitic and corticosteroid therapy is recommended after shunt insertion to decrease subsequent shunt failure when surgical removal of isolated intraventricular cysts is not possible.
Children and Adolescents: 15 mg/kg/day (Max: 1,200 mg/day) PO in 2 divided doses for 14 days. Antiparasitic and corticosteroid therapy is recommended after shunt insertion to decrease subsequent shunt failure when surgical removal of isolated intraventricular cysts is not possible.
For the treatment of ascariasis (roundworm infection)*:
Oral dosage:
Adults: 400 mg PO as a single dose.
Children and Adolescents: 400 mg PO as a single dose.
For the treatment of capillariasis*:
Oral dosage:
Adults: 200 mg PO twice daily for 10 days.
Children 2 years and older and Adolescents: 200 mg PO twice daily for 10 days.
For the secondary treatment of cutaneous larva migrans*:
Oral dosage:
Adults: 400 mg PO once daily for 3 days.
Children: 5 mg/kg/day PO for 3 days.
For the treatment of microsporidiosis* and secondary microsporidiosis prophylaxis* (i.e. long-term suppressive therapy*):
-for the treatment of microsporidiosis* in persons without HIV:
Oral dosage:
Adults: 400 mg PO twice daily for 14 to 28 days.
Infants, Children, and Adolescents: 7.5 mg/kg/dose (Max: 400 mg/dose) PO twice daily for 7 days.
-for the treatment or secondary prophylaxis of disseminated (non-ocular) and gastrointestinal infections associated with microsporidiosis* (not including Enterocytozoon bieneusi or Vittaforma corneae) in persons living with HIV:
Oral dosage:
Adults: 400 mg PO twice daily until CD4 count is more than 200 cells/mm3 for at least 6 months after starting antiretroviral therapy.
Adolescents: 400 mg PO twice daily until CD4 count is more than 200 cells/mm3 for at least 6 months after starting antiretroviral therapy.
Infants and Children: 7.5 mg/kg/dose (Max: 400 mg/dose) PO twice daily until immune reconstitution after starting antiretroviral therapy.
-for the treatment or secondary prophylaxis of disseminated (non-ocular) infections associated with microsporidiosis* and due to Trachipleistophora or Anncaliia in persons living with HIV:
Oral dosage:
Adults: 400 mg PO twice daily in combination with itraconazole until CD4 count is more than 200 cells/mm3 for at least 6 months after starting antiretroviral therapy.
Adolescents: 400 mg PO twice daily in combination with itraconazole until CD4 count is more than 200 cells/mm3 for at least 6 months after starting antiretroviral therapy.
-for treatment or secondary prophylaxis of ocular infections due to microsporidiosis* (not including Enterocytozoon bieneusi or Vittaforma corneae) in persons living with HIV:
Oral dosage:
Adults: 400 mg PO twice daily in combination with topical fumagillin bicylohexylammonium eye drops. Consider treatment discontinuation if signs and symptoms of the ocular infection resolve and the CD4 count is more than 200 cells/mm3.
Adolescents: 400 mg PO twice daily in combination with topical fumagillin bicylohexylammonium eye drops. Consider treatment discontinuation if signs and symptoms of the ocular infection resolve and the CD4 count is more than 200 cells/mm3.
Infants and Children: 7.5 mg/kg/dose (Max: 400 mg/dose) PO twice daily in combination with topical fumagillin until immune reconstitution after starting antiretroviral therapy.
For the treatment of strongyloidiasis*:
Oral dosage:
Adults: 400 mg PO twice daily for 7 days.
Children and Adolescents: 400 mg PO twice daily for 7 days.
For the treatment of trichinosis* (trichinellosis*):
Oral dosage:
Adults: 400 mg PO twice daily for 8 to 14 days.
Children and Adolescents: 400 mg PO twice daily for 8 to 14 days.
For the treatment of trichostrongyliasis*:
Oral dosage:
Adults: 400 mg PO as a single dose.
For the treatment of enterobiasis (pinworm infection)*:
Oral dosage:
Adults: 400 mg PO as a single dose; repeat dose in 2 weeks.
Children and Adolescents 2 to 17 years: 400 mg PO as a single dose; repeat dose in 2 weeks.
Children 1 year: 200 to 400 mg PO as a single dose; repeat dose in 2 weeks.
For the treatment of hookworm infection*:
Oral dosage:
Adults: 400 mg PO as a single dose.
Children and Adolescents: 400 mg PO as a single dose.
For the treatment of trichuriasis (whipworm infection)*:
Oral dosage:
Adults: 400 mg PO once daily for 3 days.
Children and Adolescents: 400 mg PO once daily for 3 days.
For the treatment of giardiasis*:
Oral dosage:
Adults: 400 mg PO once daily for 5 days.
Infants, Children, and Adolescents: 10 mg/kg/dose (Max: 400 mg/dose) PO once daily for 5 days.
Maximum Dosage Limits:
-Adults
15 mg/kg/day PO or 800 mg/day PO for most indications; up to 3200 mg/day PO in HIV patients with microsporidiosis.
-Geriatric
15 mg/kg/day PO or 800 mg/day PO for most indications.
-Adolescents
15 mg/kg/day PO, not to exceed 800 mg/day PO.
-Children
15 mg/kg/day PO, not to exceed 800 mg/day PO.
Patients with Hepatic Impairment Dosing
Patients with abnormal liver function tests prior to beginning albendazole therapy should be carefully evaluated. In patients with evidence of extrahepatic biliary obstruction, the systemic exposure of albendazole sulfoxide is increased and the elimination is prolonged.
Patients with Renal Impairment Dosing
The pharmacokinetics of albendazole in patients with renal impairment have not been studied; however, renal elimination of albendazole and albendazole sulfoxide is negligible and dosage adjustment in renal impairment is not expected to be necessary.
*non-FDA-approved indication
Carbamazepine: (Minor) Enzyme-inducing antiepileptic drugs, such as carbamazepine, appear to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. Monitor patient clinical response closely during treatment.
Cimetidine: (Moderate) Cimetidine administration with albendazole has been reported to increase albendazole bioavailability. Concentrations of albendazole sulfoxide were increased in bile and cystic fluid about 2 fold in patients with hydatid cyst disease treated with cimetidine 10 mg per kg per day concomitantly with albendazole compared to administration of albendazole alone. More data are needed to elucidate the clinical consequence of this interaction.
Dexamethasone: (Moderate) Monitor for an increase in albendazole-related adverse reactions if concomitant use with dexamethasone is necessary. Concomitant use increased the steady-state trough concentrations of albendazole sulfoxide by about 56%.
Ethotoin: (Minor) Antiepileptic drugs (AEDs) are often administered concomitantly with albendazole for the treatment of neurocysticercosis. Hydantoins appear to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. Monitor patient clinical response closely during treatment.
Food: (Moderate) Albendazole tablets should be administered with a fatty meal to increase bioavailability and ensure therapeutic efficacy.
Fosphenytoin: (Minor) Antiepileptic drugs (AEDs) are often administered concomitantly with albendazole for the treatment of neurocysticercosis. Hydantoins appear to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. Monitor patient clinical response closely during treatment.
Grapefruit juice: (Moderate) Grapefruit juice appears to increase the bioavailability of albendazole via reduction of CYP3A4-mediated metabolism in the intestinal mucosa. The AUC and Cmax of albendazole increased approximately 3-fold and the half-life was shortened by 46 percent when administered with grapefruit juice. The clinical consequence of the interaction is not clear, Patients should be advised to not significantly alter their intake of grapefruit juice during albendazole therapy.
Hydantoins: (Minor) Antiepileptic drugs (AEDs) are often administered concomitantly with albendazole for the treatment of neurocysticercosis. Hydantoins appear to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. Monitor patient clinical response closely during treatment.
Phenobarbital: (Minor) Phenobarbital appears to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. It is not clear if these pharmacokinetic interactions affect the therapeutic efficacy of albendazole in the treatment of neurocysticercosis. Monitor patient clinical response closely during treatment.
Phenobarbital; Hyoscyamine; Atropine; Scopolamine: (Minor) Phenobarbital appears to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. It is not clear if these pharmacokinetic interactions affect the therapeutic efficacy of albendazole in the treatment of neurocysticercosis. Monitor patient clinical response closely during treatment.
Phenytoin: (Minor) Antiepileptic drugs (AEDs) are often administered concomitantly with albendazole for the treatment of neurocysticercosis. Hydantoins appear to induce the oxidative metabolism of albendazole. Notably, a significant reduction in the plasma concentration of the active albendazole sulfoxide metabolite may occur. Monitor patient clinical response closely during treatment.
Praziquantel: (Moderate) Monitor for albendazole-related adverse effects if concomitant use with praziquantel is necessary. Concomitant use has been observed to increase albendazole overall exposure by approximately 50%.
Theophylline, Aminophylline: (Moderate) Albendazole has been shown to induce the hepatic CYP1A microsomal enzymes. It is possible that the prescription of albendazole may result in an increased clearance of theophylline via induction of CYP1A enzymes. Conversely, the discontinuation of albendazole therapy may result in a reduced clearance of theophylline, leading to an increase in serum theophylline concentrations. Theophylline serum concentrations and the patient's clinical status should be monitored carefully when albendazole is prescribed and on discontinuation of albendazole therapy. (Moderate) Albendazole has been shown to induce the hepatic CYP1A microsomal enzymes. It is possible that the prescription of albendazole may result in an increased clearance of aminophylline via induction of CYP1A enzymes. Conversely, the discontinuation of albendazole therapy may result in a reduced clearance of aminophylline, leading to an increase in serum aminophylline concentrations. Aminophylline serum concentrations and the patient's clinical status should be monitored carefully when albendazole is prescribed and on discontinuation of albendazole therapy.
Benzimidazole antihelmintic agents inhibit the polymerization of tubulin and the microtubule-dependent uptake of glucose by binding free B-tubulin. Albendazole selectively damages cytoplasmic microtubules in the absorptive and intestinal cells of nematodes but not of the host. This microtubular deterioration is irreversible and leads to disruption of absorptive and secretory functions of the cells, which are essential to the organism's survival. This disruption results in accumulation of secretory substances in the Golgi apparatus, decreased glucose uptake, and depleted endogenous glycogen stores in the helminth. Due to diminished energy production the parasite is immobilized and eventually dies. Albendazole is larvicidal in necatoriasis and ovicidal in ascariasis, ancylostomiasis, and trichuriasis. Resistance to albendazole has been documented in animals and is due to loss of affinity to tubulin binding sites.
In general, the following organisms are susceptible to albendazole: Echinococcus granulosus (dog tapeworm), Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), Trichinella spiralis (pork worm), Trichuris trichiura (whipworm), Enterobius vermicularis (pinworm), Strongyloides stercoralis (threadworm), Ascaris lumbricoides (roundworm), Ancylostoma duodenale (hookworm), and Necator americanus (hookworm).
Albendazole is administered orally. In the treatment of hydatid disease, tissue concentrations of albendazole sulfoxide > 500 ng/mL are required for therapeutic efficacy. Albendazole sulfoxide is 70% protein bound and has a half life of approximately 8-12 hours. Concentrations in plasma are approximately 3-fold to 10-fold and 2-fold to 4-fold higher than those seen in cyst fluid and CSF, respectively. Albendazole is extensively metabolized by the liver to albendazole sulfoxide, the primary active metabolite.The primary elimination route is the bile. Renal elimination is negligible (< 1%).
Affected cytochrome P450 isoenzymes and drug transporters: CYP1A
Albendazole induces cytochrome P450 1A enzymes and may induce its own metabolism. After 4 weeks of treatment with albendazole (200 mg 3 times daily), plasma concentrations were 20% lower than those observed in the first half of the treatment period in 12 patients.
-Route-Specific Pharmacokinetics
Oral Route
The chewable tablets have been shown to be bioequivalent to the oral tablets. After oral administration, albendazole is poorly absorbed from the GI tract. To increase bioavailability, it is recommended to give albendazole with a high-fat meal; the absorption of albendazole increases between 5 to 6.5-fold compared to when given with a non-fatty meal. Grapefruit juice also increases albendazole's oral bioavailability. After oral administration, peak plasma concentrations are reached at approximately 4.5 hours (range, 2-10 hours) when given with a fatty meal compared with 3 hours (range, 1-5 hours) in the fasted state. After administration of albendazole (400 mg) regular tablets with a fatty meal, peak plasma concentrations of albendazole sulfoxide were on average 1310 ng/mL (range, 460-1580 ng/mL) in 6 patients with hydatid disease. Concentrations of albendazole sulfoxide appear to increase in a dose-proportional manner over the therapeutic range after administration with a high-fat meal. Average peak plasma concentrations of albendazole sulfoxide after administration of a 400-mg dose of chewable tablets were 804 ng/mL (range, 202-2244 ng/mL) and 218 ng/mL (range, 54-592 ng/mL) in the fed and fasted states, respectively. In the treatment of hydatid disease, tissue concentrations of albendazole sulfoxide > 500 ng/mL are required for therapeutic efficacy.
-Special Populations
Hepatic Impairment
Albendazole plasma concentrations increase significantly in patients with hepatic disease. In 5 patients with evidence of extrahepatic obstruction, the maximum serum concentration and AUC of albendazole were increased by 2-fold and 7-fold, respectively. The rate of absorption/conversion and elimination half-life appeared to be prolonged with mean Tmax and serum elimination half-life values of 10 and 31.7 hours, respectively.
Renal Impairment
Since renal elimination of albendazole and its primary metabolite is negligible, it is unlikely that renal impairment alters the clearance of these agents.
Pediatrics
The pharmacokinetics of albendazole in children (aged >= 6 years) at doses of 10 mg/kg PO are similar to those of adults.
Geriatric
Limited data suggest similar albendazole pharmacokinetics in the elderly as compared to younger adults.