Albendazole

265.33100

265.33

259-414-7

F4216019LN

758644|220008

DTXSID0022563

C47384

Colorless crystals

P - Antiparasitic products, insecticides and repellents

3004909090

92.31000

3.31630

Colourless Crystalline Solid

1.3±0.1 g/cm3

209 °C

1.634

Practically insoluble in water

0-6°C

1.5X10-9 mm Hg at 25 deg C (est)

Henry's Law constant = 7.6X10-14 atm-cu m/mol at 25 °C (est)

pKa = 6.9 (double-bonded nitrogen) (est)

162 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|166.6 Ų [M+H]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]|178.8 Ų [M+Na]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]

Hydroxyl radical reaction rate constant = 2.1X10-10 cu cm/molecule-sec at 25 °C (est)

NONH for all modes of transport

2

R61; R36/37/38

S53; S45; S37/39; S26

FD1100000

T

P281

H361-H373

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl albendazole, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.|Oral dosage form new animal drugs. Albendazole suspension. ... Conditions of use in cattle: Indications for use: Indications for use. For removal and control of the following internal parasites of cattle: Adult liver flukes (Fasciola hepatica); heads and segments of tapeworms (Moniezia benedeni, M. expansa); adult and 4th stage larvae of stomach worms (brown stomach worms including 4th stage inhibited larvae (Ostertagia ostertagi), barberpole worm (Haemonchus contortus, H. placei), small stomach worm (Trichostrongylus axei)); adult and 4th stage larvae of intestinal worms (thread-necked intestinal worm (Nematodirus spathiger, N. helvetianus), small intestinal worm (Cooperia punctata and C. oncophora)); adult stages of intestinal worms (hookworm (Bunostomum phlebotomum), bankrupt worm (Trichostrongylus colubriformis), nodular worm (Oesophagostomum radiatum)); adult and 4th stage larvae of lungworms (Dictyocaulus viviparus). ... Conditions of use in sheep: For removal and control of the following internal parasites of sheep: Adult liver flukes (Fasciola hepatica, Fascioloides magna); heads and segments of common tapeworms (Moniezia expansa) and fringed tapeworm (Thysanosoma actinioides); adult and fourth stage larvae of stomach worms (brown stomach worm (Ostertagia circumcinta and Marshallagia marshalli), barberpole worm (Haemonchus contortus), small stomach worm (Trichostrongylus axei)); adult and fourth stage larvae of intestinal worms (thread-necked intestinal worm (Nematodirus spathiger and N. filicollis), Cooper's worm (Cooperia oncophora), bankrupt worm (Trichostrongylus colubriformis), nodular worm (Oesophagostomum columbianum), and large-mouth bowel worm (Chabertia ovina)); adult and larval stages of lungworms (Dictyocaulus filaria).|Oral dosage form new animal drugs. Albendazole paste. ... Conditions of use in cattle: For removal and control of the following internal parasites of cattle: adult liver flukes (Fasciola hepatica); heads and segments of tapeworms (Moniezia benedeni, M. expansa); adult and 4th stage larvae of stomach worms (brown stomach worms including 4th stage inhibited larvae (Ostertagia ostertagi); barberpole worm (Haemonchus contortus, H. placei); small stomach worm (Trichostrongylus axei)); adult and 4th stages larvae of intestinal worms (thread-necked intestinal worm (Nematodirus spathiger, N. helvetianus); small intestinal worm (Cooperia punctata and C. oncophora)); adult stages of intestinal worms (hookworm (Bunostomum phlebotmum); bankrupt worm (Trichostrongylus colubriformis), nodular worm (Oesophagostomum radiatum)); adult and 4th stage larvae of lungworms (Dictyocaulus viviparus).|Tolerances - (1) Cattle. A tolerance is established for albendazole 2-aminosulfone (marker residue) in liver (target tissue) of 0.2 part per million and in muscle of 0.05 part per million. (2) Sheep. A tolerance is established for albendazole 2-aminosulfone (marker residue) in liver (target tissue) of 0.25 part per million and in muscle of 0.05 part per million.|The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Albendazole is included on this list.

Dayan AD; Preparing to control Schistosomiasis and Soil-transmitted Helminthiasis in the Twenty-First Century; Acta Tropica 86 (2-3): 141-159 (2003)

|Danger|H315 (21.01%): Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P260, P261, P264, P271, P280, P281, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P314, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 144 companies from 15 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Symptoms of overdose include elevated liver enzymes, headaches, hair loss, low levels of white blood cells (neutropenia), fever, and itching.

Albendazole therapy has been associated with transient and asymptomatic elevations in serum aminotransferase levels in up to 50% of patients treated for more than a few weeks. These abnormalities rapidly improve with stopping therapy which is rarely required (~4%). Albendazole has also been associated with rare instances of clinically apparent liver injury. The onset of injury has been within a few days to as long as 2 months of starting therapy or more rapidly with multiple courses of treatment. The injury can also arise 1 to 2 weeks after a short course of albendazole (1 to 3 days). The pattern of serum enzyme elevations is typically hepatocellular or mixed. Allergic features (rash, fever, eosinophilia) may be present but are not prominent. Most cases have been mild and recovery is distinctively rapid once the drug is stopped. Rapid recurrence with rechallenge has been reported but with similar severity. Cases with acute liver failure leading to emergency liver transplantation or death have also occurred.

Regimens in which albendazole with either ivermectin or diethylcarbamazine are given as single annual doses show great promise for controlling lymphatic filariasis occurring either alone or together with other filarial infections. Such combined therapy has the additional benefit of reducing intestinal roundworm infections in school-aged children.|... Plasma levels of /albendazole's/ sulfoxide metabolites can be increased by coadministration of glucocorticoids and possibly praziquantel.

Contraindications are pregnancy and liver cirrhosis.

70% bound to plasma protein

Albendazole's production and use as an anthelmintic drug in humans and animals(1,2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 120(SRC), determined from a log Kow of 1.27(2) and a regression-derived equation(3), indicates that albendazole is expected to have high mobility in soil(SRC). Volatilization of albendazole from moist soil surfaces is not expected to be an important fate process(SRC) based on an estimated Henry's Law constant of the neutral species is 7.6X10-14 atm-cu m/mole(SRC), determined using a fragment constant estimation method(4). Albendazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.5X10-9 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation data were not available(SRC, 2006).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 120(SRC), determined from a log Kow of 1.27(2) and a regression-derived equation(3), indicates that albendazole is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 7.6X10-14 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 5(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Based on an estimated rate constant of 2.6X10-4 L/mole-sec(7), half-lives for the hydrolysis of albendazole at pH 7 and 8 are 840 and 84 years, respectively. Measured half-lives for the direct photolysis of albendazole in sunlit water at pH 5,7, and 9 are 10, 16, and 6 minutes, respectively, under summer conditions and 50, 80, and 20 minutes, respectively, under winter conditions(8,9). Biodegradation data were not available(SRC, 2006).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), albendazole, which has an estimated vapor pressure of 1.5X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase albendazole may be removed from the air by wet or dry deposition(SRC). Albendazole is expected to undergo direct photolysis based on measured half-lives in sunlit waters at pH 5, 7, and 9 of 10, 16, and 6 minutes, respectively, under summer conditions and 50, 80, and 20 minutes, respectively, under winter conditions(3,4).

A base-catalyzed second-order hydrolysis rate constant of 2.6X10-4 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 840 and 84 years at pH values of 7 and 8, respectively(1). Measured half-lives for the direct photolysis of albendazole in sunlit water at pH 5,7, and 9 are 10, 16, and 6 minutes, respectively, under summer conditions and 50, 80, and 20 minutes, respectively, under winter conditions(2,3).

An estimated BCF of 5 was calculated for albendazole(SRC), using an estimated log Kow of 1.27(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of albendazole is estimated as 120(SRC), using a log Kow of 1.27(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that albendazole is expected to have high mobility in soil.

The Henry's Law constant for albendazole is estimated as 7.6X10-14 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that albendazole is expected to be essentially nonvolatile from moist soil and water surfaces(2). Albendazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.5X10-9 mm Hg(SRC), determined from a fragment constant method(3).

While data specific to albendazole were not located(SRC, 2006), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

Occupational exposure to albendazole may occur through dermal contact with this compound at workplaces where albendazole is produced or used. Exposure to albendazole among the general population may be limited to those administered this substance as a drug and to those who administer albendazole to animals. (SRC)

For the treatment of parenchymal neurocysticercosis due to active lesions caused by larval forms of the pork tapeworm, Taenia solium and for the treatment of cystic hydatid disease of the liver, lung, and peritoneum, caused by the larval form of the dog tapeworm, Echinococcus granulosus.

Albendazole is an anthelmintic agent used predominantly in treatment of echinococcosis, a parasitic worm that causes cysts in liver and lung. Albendazole therapy is commonly associated with mild and transient serum enzyme elevations and rarely can lead to clinically apparent acute liver injury.

Anthelmintic Agents

Albendazole has known transformation products that include Albendazole sulfone.

Mesh Headings: anthelmintics, anticestodalagents, antiprotozoal agents|Albendazole is a benzimidazole carbamate, used for the treatment of gastrointestinal infestations with roundworms, lungworms and tapeworms and adult flukes of Fasciola hepatica.|Certain microsporidial species that cause intestinal infections in people with AIDS respond partially (Enterocytozoon bieneusi) or completely (Encephalitozoon intestintalis and related Encephalitozoon species) to albendazole; albendazole's sulfoxide metabolite appears to be especially effective against these parasites in vitro.|MEDICATION: ...Used against nematode infections: Ascaris, Necator, Ancylostoma, Trichuris, Enterobius, and systemic nematodes such as Trichinella spiralis, Gnathostoma spinigerum, and larval Angiostrongylus cantonensis. In addition it is used against the larval stages of the cestodes Echinococcus granulosus and E. multilocularis and for treatment of neurocysticercosis caused by Taenia solium.|For more Therapeutic Uses (Complete) data for ALBENDAZOLE (21 total), please visit the HSDB record page.

Leukopenia has occurred in less than 1% of patients receiving albendazole, and rarely, granulocytopenia, pancytopenia, agranulocytosis, or thrombocytopenia have been reported. Therefore, blood counts should be performed at the start of, and every 2 weeks during, each 28-day treatment cycle. The manufacturer states that if decreases in the total leukocyte count occur, treatment with albendazole may be continued if the decreases are modest and do not progress.|Because albendazole has been associated with mild to moderate increases of hepatic enzymes in about 16% of patients receiving the drug in clinical trials, and may cause hepatotoxicity, liver function tests should be performed prior to each course of albendazole therapy and at least every 2 weeks during treatment with the drug. If clinically important increases in liver function test results occur, albendazole should be discontinued. The drug can be reinstituted when liver enzymes return to pretreatment levels, but laboratory tests should be performed frequently during repeat therapy.|Albendazole may cause harm to the fetus and should be used during pregnancy only if the benefits justify the risk to the fetus and only in clinical circumstances where no alternative management is appropriate. Women of childbearing age should begin treatment only after a negative pregnancy test, and should be cautioned against becoming pregnant while receiving albendazole or within 1 month of completing treatment with the drug.|Teratogenic in animals (rats and rabbits) and is not recommended in pregnancy or in infants younger than 2 years.|For more Drug Warnings (Complete) data for ALBENDAZOLE (9 total), please visit the HSDB record page.

Albendazole is a broad-spectrum anthelmintic. The principal mode of action for albendazole is by its inhibitory effect on tubulin polymerization which results in the loss of cytoplasmic microtubules.

Agents used to treat tapeworm infestations in man or animals. (See all compounds classified as Anticestodal Agents.)|Agents that interact with TUBULIN to inhibit or promote polymerization of MICROTUBULES. (See all compounds classified as Tubulin Modulators.)|Agents that kill parasitic worms. They are used therapeutically in the treatment of HELMINTHIASIS in man and animal. (See all compounds classified as Anthelmintics.)|Substances that are destructive to protozoans. (See all compounds classified as Antiprotozoal Agents.)

Poorly absorbed from the gastrointestinal tract due to its low aqueous solubility. Oral bioavailability appears to be enhanced when coadministered with a fatty meal (estimated fat content 40 g)|Albendazole is rapidly converted in the liver to the primary metabolite, albendazole sulfoxide, which is further metabolized to albendazole sulfone and other primary oxidative metabolites that have been identified in human urine. Urinary excretion of albendazole sulfoxide is a minor elimination pathway with less than 1% of the dose recovered in the urine. Biliary elimination presumably accounts for a portion of the elimination as evidenced by biliary concentrations of albendazole sulfoxide similar to those achieved in plasma.|Albendazole is variably and erractically absorbed after oral admin; absorption is enhanced by the presence of fatty foods and possibly by bile salts as well. After a 400-mg oral dose, albendazole cannot be detected in plasma, because the drug is rapidly metabolized in the liver and possibly in the intestine as well, to albendazole sulfoxide, which has potent anthelmintic activity. Both the (+) and (-) enantiomers of albendazole sulfoxide are formed, but in human beings the (+) enantiomer reaches much higher peak concn in plasma and is cleared much more slowly than the (-) form. Total sulfoxide attains peak plasma concn of about 300 ng/mL, but with wide interindividual variation. Albendazole sulfoxide is about 70% bound to plasma proteins ... It is well distributed into various tissues, including hydatid cysts, where it reaches a concn of about one-fifth that in plasma ... Both sulfoxide derivatives are oxidized further to the nonchiral sulfone metabolite of albendazole, which is pharmacologically inactive; this reaction favors the (-) sulfoxide and probably becomes rate limiting in determining the clearance ... Albendazole metabolites are excreted mainly in the urine.|Oral bioavailability of albendazole appears to be increased when the drug is administered with a fatty meal; when the drug is administered with meals containing about 40 g of fat, plasma concentrations of albendazole sulfoxide are up to 5 times higher than those observed when the drug is administered to fasting patients|Sheep bearing permanent ruminal and abomasal cannulae were given a single oral dose of 10 mg/kg bw albendazole as a 2.5% formulation. Albendazole was absorbed unchanged from the rumen. Once in the body it was rapidly degraded, and sulfone metabolites were detected in plasma, the former achieving the greater level. All 3 compounds were present in the abomasum. Presumably albendazole was passed through the stomachs while the metabolites were secreted or diffused into this organ. Non-detectable levels of all 3 compounds were reached in plasma and rumen at 96 hr and in abomasum at 120 hr.|The parent compound was virtually undetectable in the plasma of Sprague Dawley males and females given a single gavage dose of 10.6 mg/kg bw albendazole in an aqueous suspension. Rapid metabolism let to the appearance of the sulfoxide and subsequently the sulfone derivatives in plasma. Both metabolites decreased to very low levels at 18 hr. Daily dosing at 10.6 mg/kg bw in males for a period of 10 days resulted in lower plasma levels of sulfoxide and higher levels of the sulfone. Albendazole induces certain hepatic drug-metabolising enzymes, which may be responsible for enhancing the degradation of sulfoxide to sulfone following repeated administration.|For more Absorption, Distribution and Excretion (Complete) data for ALBENDAZOLE (9 total), please visit the HSDB record page.

Hepatic. Rapidly converted in the liver to the primary metabolite, albendazole sulfoxide, which is further metabolized to albendazole sulfone and other primary oxidative metabolites that have been identified in human urine.|Albendazole is converted first to a sulfoxide and then to a sulfone. All of these reactions are catalyzed by flavin monooxygenases (FMO) and/or cytochrome P450. Both enzymes are efficient catalysts of S-oxygenation ...|Albendazole is metabolized in the liver to an active metabolite, albendazole sulfoxide, which accounts for detectable plasma concentrations of the drug; systemic anthelmintic activity of the drug has been attributed to this metabolite.|Albendazole ... is rapidly metabolized in the liver and possibly in the intestine as well, to albendazole sulfoxide, which has potent anthelmintic activity. Both the (+) and (-) enantiomers of albendazole sulfoxide are formed, but in human beings the (+) enantiomer reaches much higher peak concn in plasma and is cleared much more slowly than the (-) form. Total sulfoxide attains peak plasma concn of about 300 ng/mL, but with wide interindividual variation. Albendazole sulfoxide is about 70% bound to plasma proteins and has a highly variable plasma half-life ranging from about 4 to 15 hr. It is well distributed into various tissues, including hydatid cysts, where it reaches a concn of about one-fifth that in plasma. This probably explains why albendazole is more effective than mebendazole for treating hydatid cyst disease. Formation of albendazole sulfoxide is catalyzed by both microsomal flavin monooxygenase and isoforms of cytochrome P450 in the liver and possibly also in the intestine. Hepatic flavin monooxygenase activity appears associated with (+) albendazole sulfoxide formation, whereas cytochromes P450 preferentially produce the (-) sulfoxide metabolite. Both sulfoxide derivatives are oxidized further to the nonchiral sulfone metabolite of albendazole, which is pharmacologically inactive; this reaction favors the (-) sulfoxide and probably becomes rate limiting in determining the clearance and plasma half-life of the bioactive (+) sulfoxide metabolite. Induction of enzymes involved in sulfone formation from the (+) sulfoxide could account for some of the wide variation noted in plasma half-lives of albendazole sulfoxide. Indeed, in animal models, benzimidazoles can induce their own metabolism. Albendazole metabolites are excreted mainly in the urine.|Sheep bearing permanent ruminal and abomasal cannulae were given a single oral dose of 10 mg/kg bw albendazole as a 2.5% formulation. Albendazole was absorbed unchanged from the rumen. Once in the body it was rapidly degraded, and sulfone metabolites were detected in plasma, the former achieving the greater level. All 3 compounds were present in the abomasum. Presumably albendazole was passed through the stomachs while the metabolites were secreted or diffused into this organ. Non-detectable levels of all 3 compounds were reached in plasma and rumen at 96 hr and in abomasum at 120 hr.|For more Metabolism/Metabolites (Complete) data for ALBENDAZOLE (12 total), please visit the HSDB record page.|Albendazole has known human metabolites that include Albendazole oxide.

Terminal elimination half-life ranges from 8 to 12 hours (single dose, 400mg).|Albendazole ... is rapidly metabolized ... to albendazole sulfoxide, which ... has a highly variable plasma half-life ranging from about 4 to 15 hr ... Both /(+) and (-)/ sulfoxide derivatives are oxidized further to the nonchiral sulfone metabolite ... This reaction favors the (-) sulfoxide and probably becomes rate limiting in determining ... plasma half-life of the bioactive (+) sulfoxide metabolite. Induction of enzymes involved in sulfone formation from the (+) sulfoxide could account for some of the wide variation noted in plasma half-lives of albendazole sulfoxide.

Albendazole causes degenerative alterations in the tegument and intestinal cells of the worm by diminishing its energy production, ultimately leading to immobilization and death of the parasite. It works by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. As cytoplasmic microtubules are critical in promoting glucose uptake in larval and adult stages of the susceptible parasites, the glycogen stores of the parasites are depleted. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth.|Benzimidazoles produce many biochemical changes in susceptible nematodes, eg, inhibition of mitochondrial fumarate reductase, reduced glucose transport, and uncoupling of oxidative phosphorylation ... /but/ the primary action ... /should be/ to inhibit microtubule polymerization by binding to beta-tubulin. The selective toxicity of these agents derives from the fact that specific, high-affinity binding to parasite beta-tubulin occurs at much lower concn than does binding to the mammalian protein ... Benzimidazole-resistant Haemonchus contortus display reduced high-affinity drug binding to beta-tubulin and alterations in beta-tubulin isotype gene expression that correlate with drug resistance ... Two identified mechanisms of drug resistance in nematodes involve both a progressive loss of "susceptible" beta-tubulin gene isotypes together with emergence of a "resistant" isotype with a conserved point mutation that encodes a tyrosine instead of phenylalanine at position 200 of beta-tubulin. While this mutation may not be required for benzimidazole resistance in all parasites, eg, Giardia lamblia, benzimidazole resistance in parasitic nematodes is unlikely to be overcome by novel benzimidazole analogs, because tyrosine also is present at position 200 of human beta-tubulin. /Benzimidazoles/|Although the exact mechanism of action of albendazole has not been fully elucidated, the principal anthelmintic effect of benzimidazoles, including albendazole, appears to be the specific, high-affinity binding of the drug to free beta-tubulin in parasite cells, resulting in selective inhibition of parasite microtubule polymerization, and inhibition of microtubule-dependent uptake of glucose. Benzimidazole drugs bind to the beta-tubulin of parasites at much lower concentrations than to mammalian beta-tubulin protein; the drugs do not inhibit glucose uptake in mammals, and do not appear to have any effect on blood glucose concentrations in humans|The mode of action of albendazole is by binding strongly with the tubulin in the cells of nematodes. The intestinal cells of the nematode are particularly affected, resulting in a loss of absorptive function which causes the nematodes to starve to death.

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ ... Adverse effects include fever, reversible leucopenia, headache, nausea, dizziness, sleeplessness, epigastric pain and diarrhoea.|/CASE REPORTS/ Albendazole is a benzimidazole with wide spectrum coverage as an antiparasitic drug. Reported side effects have been minimal. ... The case of a patient who died with severe prolonged pancytopenia beginning during the third week of therapy for a pulmonary echinococcal cyst /is reported/. This case was a 68-year-old man who presented with a large cystic lung mass. His medical history was significant for Child-Pugh class B cirrhosis. A prolonged course of albendazole was initiated. Two weeks later, the patient presented in septic shock with severe pancytopenia. The patient was initially resuscitated, but died after 10 days with no marrow recovery. Autopsy was consistent with albendazole-induced pancytopenia. This is the third human case of pancytopenia and the first death reported in relation to albendazole-induced pancytopenia. Neutropenia seems to be related more to higher dosage and longer duration of use. Albendazole sulfoxide peak dose and half life are significantly prolonged by liver disease and concomitant administration of certain drugs. The severity and duration of albendazole-induced pancytopenia in this case was likely related to the underlying liver disease. Frequent serial monitoring of blood counts and cessation of medication with any evidence of marrow toxicity in such patients is warranted.|/OTHER TOXICITY INFORMATION/ Albendazole at 10 to 12 mg/kg/day has been given continuously for 3 to 6 mo without producing serious or irreversible toxicity.

Albendazole

Oral: Tablets, film-coated: 200 mg Albenza, Tiltab ( with povidone), (GlaxoSmithKline).|Trade names: Eskadole, Valbazen.

Analyte: albendazole; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: albendazole; matrix: chemical identification; procedure: thin-layer chromatography with comparison to standards|Analyte: albendazole; matrix: chemical purity; procedure: dissolution in glacial acetic acid; addition of oracet blue B indicator; titration with perchloric acid to a violet-colored endpoint|Analyte: albendazole; matrix: pharmaceutical preparation (oral suspension); procedure: ultraviolet absorption spectrophotometry with comparison to standards (chemical identification)|For more Analytic Laboratory Methods (Complete) data for ALBENDAZOLE (10 total), please visit the HSDB record page.

Analyte: albendazole; matrix: blood (serum); procedure: high-performance liquid chromatography with ultraviolet detection at 273 nm; limit of detection: 500 ng/mL|Analyte: albendazole; matrix: blood (plasma), body fluid (abomasal, duodenal, rumen); procedure: high-performance liquid chromatography with ultraviolet detection at 292 nm; limit of detection: 20 ng/mL|Analyte: albendazole; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 254 nm|Analyte: albendazole; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 292 nm|For more Clinical Laboratory Methods (Complete) data for ALBENDAZOLE (11 total), please visit the HSDB record page.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients|Pharmaceuticals|Pharmaceuticals -> Anthelmintics

Veterinary Drug -> ANTHELMINTHIC_AGENT;