Albendazole
Trade names Albenza
Pregnancy category AU: D
Routes of administration By mouth
Pharmacokinetic data Bioavailability <5% Protein binding 70% Metabolism Liver
Elimination half-life 8–12 hours
Excretion Bile duct
Albendazole is a broad-spectrum antihelmintic and antiprotozoal agent of the benzimidazole type.
Albendazole is used for the treatment of a variety of intestinal parasite infections, including ascariasis, pinworm infection, hookworm infection, trichuriasis, strongyloidiasis, taeniasis, clonorchiasis, opisthorchiasis, cutaneous larva migrans, giardiasis, and gnathostomiasis, among other diseases.
Common side effects include nausea, abdominal pain, and headache.
Rare but potentially serious side effects include bone marrow suppression which usually improves on discontinuing the medication.
Liver inflammation has been reported and those with prior liver problems are at greater risk.
it may cause harm if taken by pregnant women.
Albendazole is an effective treatment for:
Flatworms Clonorchiasis Fasciolosis Opisthorchiasis Cestodes (tapeworms) Cysticercosis Echinococcosis Nematodes Anatrichosomiasis Angiostrongyliasis Anisakiasis Ascariasis Baylisascariasis, caused by the raccoon roundworm. Pinworm infection Filariasis Loa loa Gnathostomiasis Gongylonemiasis Hepatic capillariasis caused by Capillaria hepatica Hookworm infections, including cutaneous larva migrans caused by hookworms of genus Ancylostoma. Intestinal capillariasis, as an alternative to mebendazole Mansonelliasis Oesophagostomumiasis Strongyloidiasis Toxocariasis, also called “visceral larva migrans”, Trichinosis Trichostrongyliasis Trichuriasis (whipworm infection) Giardiasis Microsporidiosi Granulomatous amoebic encephalitis Balamuthia mandrillaris, in combination with miltefosine and fluconazole Arthropods Scabies Intestinal myiasis
It is is only FDA-approved for treating hydatid disease caused by dog tapeworm larvae and neurocysticercosis caused by pork tapeworm larvae.
When co-administered, ivermectin and albendazole act in synergy:
Ivermectin targets the parasite’s nervous and muscular systems, causing paralysis, while albendazole disrupts the parasite’s metabolism and microtubules.
Ivermectin/albendazole is indicated for use in people aged five years of age or older, for the treatment of soil-transmitted helminth infections, caused by different types of intestinal parasitic worms, which are spread through soil contaminated by human feces in areas with poor sanitation.
The worms responsible for these diseases are hookworms (Ancylostoma duodenale, Necator americanus), roundworms (Ascaris lumbricoides), whipworms (Trichuris trichiura) and a roundworm called Strongyloides stercoralis.
Ivermectin/albendazole is also indicated for the treatment of microfilaraemia in people with lymphatic filariasis.
Lymphatic filariasis is a neglected tropical disease commonly known as elephantiasis, which impairs the lymphatic system and can lead to the abnormal enlargement of body parts, causing pain, severe disability and social stigma.
Ivermectin/albendazole is indicated for the treatment of cases of lymphatic filariasis caused by Wuchereria bancrofti, a parasite which is responsible for 90% of cases worldwide.
Side effects
The most common side effects of albendazole are experienced by over 10% of people and include headache and abnormal liver function.
Liver enzymes usually increase to two to four times the normal levels.
Elevation of liver enzymes occurs in 16% of patients receiving treatment specifically for hydatid disease and goes away when treatment ends.
An estimated 1–10% of people experience abdominal pain, nausea or vomiting, dizziness or vertigo, increased intracranial pressure, meningeal signs, temporary hair loss, and fever.
The headache, nausea, and vomiting are thought to be caused by the sudden destruction of cysticerci (tapeworm larvae), which causes acute inflammation.
Fewer than 1% of people get hypersensitivity reactions such as rashes and hives, leukopenias, thrombocytopenia, pancytopenia, hepatitis, acute liver failure, acute kidney injury, irreversible bone marrow suppression, and aplastic anemia.
Side effects differ when treating for hydatid disease versus neurocysticercosis.
Treating hydatid disease can also unmask undiagnosed neurocysticercosis.
People receiving albendazole for the treatment of neurocysticercosis can have neurological side effects such as seizures, increased intracranial pressure, and focal signs caused by the inflammatory reaction that occurs when parasites in the brain are killed.
Steroids and anticonvulsants are often given with albendazole when treating neurocysticercosis to avoid these effects.
Those being treated for retinal neurocysticercosis can face retinal damage.
It is contraindicated in the first trimester of pregnancy, and should be avoided up to one month before conception.
Albendazole has been found to be safe in humans during the second and third trimesters.
It can, however, possibly cause infantile eczema when given during pregnancy.
Albendazole sulfoxide is secreted into breast milk at around 1.5% of the maternal dose, though oral absorption is poor enough that it is unlikely to affect nursing infants.
Because of its low solubility, albendazole often cannot be absorbed in high enough quantities to be toxic.
The oral LD50 of albendazole in rats was found to be 2,500 mg/kg.
Overdose affects the liver, testicles, and gastrointestinal tract (GI tract) the most.
Overdose manifests with lethargy, loss of appetite, vomiting, diarrhea, intestinal cramps, dizziness, convulsions, and sleepiness.
The antiepileptics carbamazepine, phenytoin, and phenobarbital lower the plasma concentration and half-life of albendazole sulfoxide’s R(+) enantiomer.
The antacid cimetidine heightens serum albendazole concentrations, increases the half-life of albendazole, and doubles albendazole sulfoxide levels in bile, by interfering with CYP3A4: the half-life of albendazole sulfoxide thus increases from 7.4 hours to 19 hours.
The antacid cimetidine heightens the potency of albendazole.
Paradoxically, cimetidine also inhibits the absorption of albendazole by reducing gastric acidity.
Corticosteroids increase the steady-state plasma concentration of albendazole sulfoxide; dexamethasone can increase the concentration by 56% by inhibiting the elimination of albendazole sulfoxide.
The anti-parasitic praziquantel increases the maximum plasma concentration of albendazole sulfoxide by 50%.
The anti-parasitic levamisole increases the AUC by 75%.
Grapefruit inhibits the metabolism of albendazole within the intestinal mucosa.
Long-term administration of the antiretroviral ritonavir, which works as a CYP3A4 inhibitor, decreases the maximum concentration of albendazole in the plasma as well as the AUC.
As a vermicide, albendazole causes degeneration in the intestinal cells of the worm by binding to β-tubulin, thus inhibiting its polymerization or assembly into microtubules .
Albendazole leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores.
Albendazole also prevents the formation of spindle fibers needed for cell division.
It blocks egg production and development; existing eggs are prevented from hatching, and cell motility, maintenance of cell shape, and intracellular transport are also disrupted.
At higher concentrations, it disrupts the helminths’ metabolic pathways by inhibiting metabolic enzymes.
Due to diminished ATP production, the parasite is immobilized and eventually dies.
Some parasites have evolved some resistance to albendazole by decreasing the binding affinity of albendazole.
To target intestinal parasites, which is the most common indication for prescription, albendazole is taken on an empty stomach to stay within the gut.
1–5% of the drug is successfully absorbed in humans
The absorption also largely depends on gastric pH.
Food stimulates gastric acid secretion, lowering the pH and making albendazole more soluble and thus more easily absorbed.
Oral absorption is especially increased with a fatty meal.
Albendazole dissolves better in lipids, allowing it to cross the lipid barrier created by the mucus surface of the GI tract.
Absorption is also affected by how much of the albendazole is degraded within the small intestine by metabolic enzymes in the villi.
The pharmacokinetics of albendazole differ slightly between men and women: women have a lower oral clearance and volume of distribution, while men have a lower serum peak concentration.
Albendazole undergoes very fast first-pass metabolism.
Most of it is oxidized into albendazole sulfoxide in the liver by cytochrome P450 oxidases (CYPs) and a flavin-containing monooxygenase (FMO).
For systemic parasites, albendazole acts as a prodrug.
Albendazole sulfoxide is able to cross the blood–brain barrier.
It enters the cerebrospinal fluid at 43% of plasma concentrations; its ability to enter the central nervous system allows it to treat neurocysticercosis.
Metabolites are excreted mostly in bile, with only a small amount being excreted in urine (less than 1%) and feces.
Albendazole has no residual effect, and thus protects poorly against reinfestations.
Maximum residue limits (MRLs) for albendazole in food are 5000, 5000, 100, and 100 micrograms per kilogram of body weight (μg/kg) for kidney, liver, fat, and muscle, respectively, and 100 μg/L for milk.
There is a 27-day cattle withdrawal time for meat.