Chloroquine Disease Interactions

The use of 4-aminoquinolines is generally considered contraindicated in the presence of retinal or visual field changes, whether attributable to 4-aminoquinoline compounds or to any other etiology. However, in the treatment of acute attacks of malaria caused by susceptible strains of plasmodia, these agents may be considered if potential benefits are anticipated to outweigh the risks. 4-aminoquinolines are oculotoxic and can cause dose-related, irreversible retinal damage and vision loss during and up to several years after long-term or high-dose therapy (e.g., in the treatment of systemic lupus erythematosus or rheumatoid arthritis). Ophthalmologic monitoring, including visual acuity, expert slit-lamp, funduscopic, and visual field tests, is recommended at baseline and every three months during prolonged use. Therapy should be discontinued immediately if abnormalities develop in visual acuity, visual field, or retinal macular areas (e.g., pigmentary changes, loss of foveal reflex), or if the patient experiences visual symptoms such as light flashes and streaks that are not fully explainable by difficulties of accommodation or corneal opacities. Other common symptoms that may indicate retinopathy include nyctalopia, photophobia, blurred distance vision, difficulty reading or seeing (e.g., words or letters disappearing or parts of objects missing; misty vision; fog before the eyes), and missing or blacked out areas in the central or peripheral visual field. Retinal changes and visual disturbances may progress even after cessation of therapy. However, in a number of patients, early retinopathy (macular pigmentation sometimes with central field defects) diminished or regressed completely after therapy was discontinued. Paracentral scotoma to red targets, sometimes termed premaculopathy, is indicative of early retinal dysfunction and is usually reversible with cessation of therapy.

The use of aminoquinolines in patients with porphyria may exacerbate the condition. Aminoquinolines should not be used in these patients unless the potential benefits are anticipated to outweigh the risks.

The use of 4-aminoquinolines such as hydroxychloroquine and chloroquine prolong the QT interval. Ventricular arrhythmias and torsades de pointes have been reported in patients taking these agents. Care should be exercised in patients with a prolonged QT interval at baseline or at increased risk for arrythmia. A baseline electrocardiogram should be obtained to assess for QT interval prolongation and other abnormalities. It is recommended to use appropriate diagnostic tools such as ECG to monitor patients during therapy.

Adverse hematologic effects including neutropenia, agranulocytosis, aplastic anemia, and thrombocytopenia have been rarely associated with 4-aminoquinolines. Therapy with 4-aminoquinolines should be administered cautiously in patients with preexisting bone marrow suppression. A complete blood count should be performed periodically in patients on prolonged therapy. If any severe blood disorder appears which is not attributable to the disease under treatment, discontinuance of the drug should be considered.

The use of 4-aminoquinolines has been associated rarely with ototoxicity. Nerve-type deafness, which is usually irreversible, has occurred during long-term, high-dose therapy. Deafness may not be apparent until several weeks after 4-aminoquinoline therapy. Tinnitus and reduced hearing have been reported in patients with preexisting auditory damage. Therapy with 4-aminoquinolines should be administered cautiously in such patients. If new auditory defects develop or if hearing loss becomes worse, therapy should be immediately discontinued and the patient closely monitored.

4-aminoquinolines may cause epileptic seizures in susceptible individuals. Patients with epilepsy or an otherwise low seizure threshold may be at greater risk. Therapy with 4-aminoquinolines, particularly chloroquine, should be administered cautiously in patients with epilepsy.

Hemolysis and acute renal failure have been reported during use of aminoquinolines in patients with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. Therapy with aminoquinolines should be administered cautiously in these patients. Blood cell counts and hemoglobin determinations should be performed regularly. Aminoquinoline therapy should be discontinued immediately if signs suggestive of hemolytic anemia occur, such as marked darkening of the urine or sudden decrease in hemoglobin concentration or erythrocytic count.

Aminoquinolines may concentrate in the liver. Isolated cases of abnormal liver function and fulminant hepatic failure have been reported. Therapy with aminoquinolines should be administered cautiously in patients with hepatic disease or alcoholism and in patients receiving other hepatotoxic drugs. Periodic evaluation of hepatic function should be performed during prolonged therapy.

Certain aminoquinolines such as chloroquine, and hydroxychloroquine should be used with caution in patients with myasthenia gravis (MG). These agents may exacerbate or trigger new onset of symptoms in patients with previously diagnosed MG. It is recommended to advise patients with MG about this possible side effect.

The use of aminoquinolines in patients with psoriasis may precipitate a severe attack of psoriasis. Aminoquinolines should not be used in these patients unless the potential benefits are anticipated to outweigh the risks.