Folate deficiency is associated with all except
a. Chloroquine does not produce folate deficiency, while rests of them do. Chloroquine has been found to be active against the asexual erythrocytic forms of all species of malaria parasites; P. vivax, P. ovale, P. malariae and susceptible strains of P. falciparum. It is a rapid acting blood schizontocide with some gametocytocidal activity against P. ovale, P. vivax, P. malariae and immature gametocytes of P. falciparum.
b. Chloroquine may cause blood dyscrasias, including agranulocytosis, aplastic anemia, neutropenia, or thrombocytopeniA. Discontinuance of the drug should be considered, if any severe blood severe blood disorder appears which is not attributable to the disease under treatment. Complete blood cell counts should be made periodically if patients are given prolonged therapy.
c. Chloroquine may cause hemolytic anemia in G6PD deficient patients, although this is unlikely when chloroquine is given in therapeutic doses. The drug should be administered with caution to patients having G6PD deficiency.
d. Because chloroquine may concentrate in the liver, the drug should be used with caution in patients with hepatic function impairment, alcoholism and in patients receiving other hepatotoxic drugs.
e. Chloroquine may cause corneal opacities, keratopathy or retinopathy. Although chloroquine may have a temporary effect on visual accommodation during short-term treatment, irreversible retinal damage may occur with prolonged treatment. Therefore, patients should be advised to discontinue the medication and seek immediate medical advice if they notice any deterioration in their vision, which persists for more than 48 hours.
f. Caution is advised in cases of porphyria, renal disease, severe gastrointestinal and neurological disorders and in patients with myasthenia gravis.
g. Chloroquine has a temporary effect on visual accommodation and patients should be warned that they should not drive or operate machinery if they are affected (BG Katzung’ 10th Edition, pp-848-49).