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Chloroquine dosing

Regular cardiac evaluation should be considered for those who have taken a cumulative chloroquine dose of 1000 g, particularly elderly patients. [Pg.723]

Taken in proper doses, chloroquine is an extraordinarily safe drug however, its safety margin is narrow, and a single dose of 30 mg/kg may be fatal. Acute chloroquine toxicity is encountered most frequently with too rapid administration of parenteral doses. Cardiovascular effects include hypotension, vasodilation, depressed myocardial function, cardiac arrhythmias, and cardiac arrest. Confusion, convulsions, and coma denote central nervous system (CNS) dysfunction. Chloroquine doses of >5 g given parenterally usually are fatal. Prompt treatment with mechanical ventilation, epinephrine, and diazepam may be lifesaving. [Pg.673]

Usual doses of antimalarials are hydroxychloroquine, 200 mg twice a day chloroquine, 250-500 mg/day and quinacrine, 100-200 mg/day. Usually, hydroxychloroquine is started first, and if no improvement is noted in 3 months, quinacrine is added. Alternatively, chloroquine is used as a single agent. Dosing should be adjusted for low-weight individuals so that chloroquine dosing is 2.5 mg/kg/day and hydroxychloroquine is 6.5 mg/kg/day. Antimalarial agents are the treatment of choice for widespread forms of cutaneous lupus that do not respond to topical glucocorticoids and sunscreens. Chnical improvement may be delayed for several months. [Pg.1086]

The success of quinine inspired the search for other antimalarials. The greatest impetus for the development of synthetic dmgs came this century when the two World Wars intermpted the supply of cinchona bark to the combatants. A stmcturally related 4-quinolinemethanol is mefloquine (65, Lariam [51773-92-3]) which now serves as an effective alternative agent for chloroquine-resistant P. falciparum. This is a potent substance that requires less than one-tenth the dose of quinine to effect cures. There are some untoward side effects associated with this dmg such as gastrointestinal upset and dizziness, but they tend to be transient. Mefloquine is not recommended for use by those using beta-blockers, those whose job requires fine coordination and spatial discrimination, or those with a history of epilepsy or psychiatric disorders. A combination of mefloquine with Fansidar (a mixture of pyrimethamine and sulfadoxine) is known as Fansimef but its use is not recommended. Resistance to mefloquine has been reported even though the compound has not been in wide use. [Pg.273]

Quinacrine (49) is an acridine that was used extensively from the mid-1920s to the end of World War 11. It acts much like chloroquine and is reasonably effective. Because it causes the skin to turn yellow and, in high doses, causes yellow vision, the dmg is no longer in use as an antimalarial. Pyronaridine (77), a 1-azaacridine developed in China, appears to be effective against mefloquine-resistant, but not entirely against chloroquine-resistant, strains of P falciparum. [Pg.274]

Chloroquine, dapsone, methylene blue (doses >4 mg/kg), nitrofurantoin, phenazopyridine, primaquine, rasburicase, and sulfonamide antimicrobials... [Pg.120]

Chagas disease is caused by a kinetoplastid trypanosoma parasite and affects millions of people in Latin America. The disease is currently incurable. Chemotherapy is based mainly on nitrofuran and nitroimidazole compounds and sterol biosynthesis inhibitors such as ketoconazole (337). Toxicity and high doses are the major problems for these organic drugs. Urbina et al. (338, 339) have found that com-plexation of antiparasitic organic agents such as chloroquine (78)... [Pg.241]

Increased bilirubin levels are caused due to the intake of large doses of such drugs as chloroquine, vitamin K, sulpha-drugs, tetracyclines, paracetamol, nicotinic acid and monoamine oxidase inhibitors (e.g., iproniazid RP 1.0 nialamide RP 1.8 isocarboxazid RP 3.1 phenelzine RP 18 pheniprazine RP31 and tranylcypromine RP 45), where RP designates the Relative Potency based on the tiyptamine potentiation test. The elevated levels are due to hepatic injury, and... [Pg.57]

Corneal deposits during the long-term treatment of RA are not uncommon but the most prominent concern is the danger of producing irreversible retinal damage. At the usual antirheumatic doses these risks seem to be less for hydroxychloroquine than for chloroquine. [Pg.441]

Non-falciparum malaria (like P. vivax) can still be treated with chloroquine although chloroquine resistant P. vivax has been reported from Irian Jaya and Papua New Guinea. In those areas treatment with mefloquine is recommended. To treat the liverstages an additional 2-3 weeks treatment with primaquine is given. It appears that tafenoquine (dosed once a week), a new 8-aminoquinoline, would be a better replacement for primaquine in preventing relapses in P. vivax malaria. [Pg.542]

Hydroxychloroquine is approved for the treatment of both systemic and cutaneous lupus erythematosus. Both chloroquine and quinacrine (Atabrine) are also effective in this skin disease. Low-dose chloroquine is used for the therapy of porphyria cutanea tarda in patients in whom phlebotomy has failed or is contraindicated. Other skin diseases in which the drugs are useful (after sunscreens and avoidance of sun exposure) include polymorphous light eruption and solar urticaria. [Pg.491]

Primaquine is readily absorbed from the gastrointestinal tract, and in contrast to chloroquine, it is not bound extensively by tissues. It is rapidly metabolized, and the metabolites are reported to be as active as the parent drug itself. Peak plasma levels are reached in 4 to 6 hours after an oral dose, with almost total drug elimination occurring by 24 hours. The half-life is short, and daily administration is usually required for radical cure and prevention of relapses. [Pg.614]

Pyrimethamine is well absorbed after oral administration, with peak plasma levels occurring within 3 to 7 hours. An initial loading dose to saturate nonspecific binding sites is not required, as it is with chloroquine. However, the drug binds to tissues, and therefore, its rate of renal excretion is slow. Pyrimethamine has a half-life of about 4 days. Although the drug does undergo some metabolic alterations, the metabolites formed have not been totally identified. [Pg.614]

Standard therapy for these infections includes chloroquine to eradicate erythrocytic forms and primaquine to eradicate liver hypnozoites and prevent a subsequent relapse. Chloroquine is given acutely, and therapy with primaquine is withheld until the G6PD status of the patient is known. If the G6PD level is normal, a 14-day course of primaquine is given. Prompt evaluation of the G6PD level is helpful, since primaquine appears to be most effective when instituted before completion of dosing with... [Pg.1127]


See other pages where Chloroquine dosing is mentioned: [Pg.142]    [Pg.142]    [Pg.142]    [Pg.142]    [Pg.40]    [Pg.262]    [Pg.273]    [Pg.142]    [Pg.145]    [Pg.146]    [Pg.123]    [Pg.1148]    [Pg.197]    [Pg.199]    [Pg.54]    [Pg.1027]    [Pg.242]    [Pg.294]    [Pg.69]    [Pg.109]    [Pg.122]    [Pg.217]    [Pg.265]    [Pg.295]    [Pg.425]    [Pg.434]    [Pg.614]    [Pg.616]    [Pg.242]    [Pg.807]    [Pg.1123]    [Pg.1128]    [Pg.1129]    [Pg.117]    [Pg.164]    [Pg.69]    [Pg.109]    [Pg.122]   
See also in sourсe #XX -- [ Pg.1588 , Pg.2079 ]




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