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Chloroquine/Hydroxychloroquine(US: Aralen): Organs and Systems


Electrocardiographic changes, comprising altered T waves and prolongation of the QT interval, are not uncommon during high-dose treatment with chloroquine. The clinical significance of this is uncertain. With chronic intoxication, a varying degree of atrioventricular block can be seen; first-degree right bundle branch block and total atrioventricular block have been described. Symptoms depend on the severity of the effects: syncope, Stokes-Adams attacks, and signs of cardiac failure can occur. Acute intoxication can cause cardiovascular collapse and/or respiratory failure. Cardiac complications can prove fatal in both chronic and acute intoxication.

Third-degree atrioventricular conduction defects have been reported in two patients with rheumatoid arthritis after prolonged administration of chloroquine.

Intravenous administration can result in dysrhythmias and cardiac arrest; the speed of administration is relevant, but also the concentration reached: deaths have been recorded with blood concentrations of 1 µg/ml; concentrations after a 300 mg dose are usually 50-100 µg/ml.

Long-term chloroquine can cause cardiac complications, such as conduction disorders and cardiomyopathy (restrictive or hypertrophic), by structural alteration of the interventricular septum. Thirteen cases of cardiac toxicity associated with long-term chloroquine and hydroxychloroquine have been reported in patients with systemic autoimmune diseases. The cumulative doses were 600-2281 g for chloroquine and 292-4380 g for hydroxychloroquine.

A 64-year-old woman with systemic lupus erythematosus took chloroquine for 7 years (cumulative dose 1000 g). She developed syncope, and the electrocardiogram showed complete heart block; a permanent pacemaker was inserted. The next year she presented with biventricular cardiac failure, skin hyperpigmentation, proximal muscle weakness, and chloroquine retinopathy. Coronary angiography was normal. An echocar-diogram showed a restrictive cardiomyopathy. A skeletal muscle biopsy was characteristic of chloroquine myopathy. Chloroquine was withdrawn and she improved rapidly with diuretic therapy.

Chloroquine cardiomyopathy occurred during long-term (7 years) treatment for rheumatoid polyarthritis in a 42-year-old woman, who had an isolated acute severe conduction defect, confirmed by histological study with electron microscopy.

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

More than one mechanism may underlie the cardiac adverse effects of chloroquine. Severe hypokalemia after a single large dose of chloroquine has been documented, and some studies show a correlation between plasma potassium concentrations and the severity of the cardiac effects.

Light and electron microscopic abnormalities were found on endomyocardial biopsy in two patients with cardiac failure. The first had taken hydroxychloroquine 200 mg/day for 10 years, then 400 mg/day for a further 6 years; the second had taken hydroxychloroquine 400 mg/day for 2 years. A similar case was reported after the use of 250 mg/day for 25 years.


Respiratory collapse can occur with acute overdosage.

Acute pneumonitis probably due to chloroquine has been described.

A 41-year-old man with chronic discoid lupus erythe-matosus was given chloroquine 150 mg bd for 10 days followed by 150 mg/day. After 2 weeks he developed fever, a diffuse papular rash, dyspnea, and sputum. A chest X-ray showed peripheral pulmonary infiltrates. He improved on withdrawal of chloroquine and treatment with cefpiramide and roxithromycin. No organism was isolated. A subsequent oral challenge with chloroquine provoked a similar reaction.

Nervous system

The incidence of serious nervous system events among patients taking chloroquine for less than a year has been estimated as one in 13 600.

Chloroquine, especially in higher doses, can cause a marked neuromyopathy, characterized by slowly progressive weakness of insidious onset. In many cases this weakness first affects the proximal muscles of the legs. Reduction in nerve conduction time and electromyographic abnormalities typical of both neuropathic and myopathic changes can be found. Histologically there is a vacuolar myopathy. Neuromyopathy is a rare adverse effect and is usually limited to patients taking 250-750 mg/day for prolonged periods. The symptoms can be accompanied by other manifestations of chloroquine toxicity. An 80-year-old woman developed symptoms after taking chloroquine 300 mg/day for 6 months, once more demonstrating that a standard dosage can be too much for elderly people.

A spastic pyramidal tract syndrome of the legs has been reported. In young children the features of an extrapyramidal syndrome include abnormal eye movements, tris-mus, torticollis, and torsion dystonia.

Chloroquine can cause seizures in patients with epilepsy. The mechanism is uncertain, but it may include reductions in inhibitory neurotransmitters and pharmacokinetic interactions that alter anticonvulsant concentrations. Tonic-clonic convulsions were reported in four patients in whom chloroquine was part of a prophylactic regimen. Antiepileptic treatment was required to control the seizures. None had further seizures after withdrawal of the antimalarial drugs.

Chloroquine and desethylchloroquine concentrations have been studied in 109 Kenyan children during the first 24 hours of admission to hospital with cerebral malaria. Of the 109 children 100 had received chloroquine before admission. Blood chloroquine and desethylchloroquine concentrations were no higher in children who had seizures than in those who did not, suggesting that chloroquine does not play an important role in the development of seizures in malaria.

A 59-year-old woman had a generalized convulsion 24 hours after returning from a trip to Vietnam. She had a history of partial complex seizures (controlled with carbamazepine) due to a previous ruptured cerebral aneurysm. For the preceding 3 weeks she had been taking chloroquine 100 mg/day and proguanil 200 mg/day. A blood film was negative for malaria. A CT scan of the brain showed changes compatible with the previous hemorrhage. She was successfully treated with clobazam (dose not stated) until withdrawal of chemoprophylaxis.

The interaction between chloroquine and carbamazepine was not examined. Chloroquine should not be given to adults with a history of epilepsy.

Neuromuscular function

Severe neuromyopathy has been reported in patients taking chloroquine.

Chloroquine-induced neuromyopathy is a complication of chloroquine treatment of autoimmune disorders or long-term use of chloroquine as a prophylactic antimalarial drug.

Chloroquine and Hydroxychloroquine: Organs and Systems: Sensory Systems

Psychological, psychiatric

Many mental changes attributed to chloroquine have been described, notably agitation, aggressiveness, confusion, personality changes, psychotic symptoms, and depression. Acute mania has also been recognized. The mental changes can develop slowly and insidiously. Subtle symptoms, such as fluctuating impairment of thought, memory, and perception, can be early signs, but may also be the only signs. The symptoms may be connected with the long half-life of chloroquine and its accumulation, leading to high tissue concentrations. Chloroquine also inhibits glutamate dehydrogenase activity and can reduce concentrations of the inhibitory transmitter GAB A.

In some cases with psychosis after the administration of recommended doses, symptoms developed after the patients had taken a total of 1.0-10.5 g of the drug, the time of onset of behavioral changes varying from 2 hours to 40 days. Most cases occurred during the first week and lasted from 2 days to 8 weeks.

Transient global amnesia occurred in a healthy 62-year-old man, 3 hours after he took 300 mg chloroquine. Recovery was spontaneous after some hours.

In one center, toxic psychosis was reported in four children over a period of 18 months. The children presented with acute delirium, marked restlessness, outbursts of increased motor activity, mental inaccessibility, and insomnia. One child seemed to have visual hallucinations. In each case, chloroquine had been administered intramuscularly because of fever. The dosages were not recorded. The children returned to normal within 2 weeks.


Hypoglycemia was reported in a fatal chloroquine intoxication in a 32-year-old black Zambian male. Hypoglycemia has also been seen in patients, especially children, with cerebral malaria. Further studies have shown that the hypoglycemia in these African children was usually present before the antimalarial drugs had been started; in a study in Gambia hypoglycemia occurred after treatment with the drug had been started, although it was not necessarily connected with the treatment. Convulsions were more common in hypoglycemic children. This commonly unrecognized complication contributes to morbidity and mortality in cerebral Plasmodium falciparum malaria. Hypoglycemia is amenable to treatment with intravenous dextrose or glucose, which may help to prevent brain damage.

Although hydroxychloroquine has been used to treat porphyria cutanea tarda, there are reports that it can also worsen porphyria.

Electrolyte balance

Severe hypokalemia after a single large dose of chloroquine has been documented, and some studies show a correlation between plasma potassium concentrations and the severity of the cardiac effects. In a retrospective study of 191 consecutive patients who had taken an overdose of chloroquine (mean blood chloroquine concentration 20 µmol/l; usual target concentration up to 6 µmol/l), the mean plasma potassium concentration was 3.0 mmol/1 (0 and was significantly lower in those who died than in those who survived. Plasma potassium varied directly with the systolic blood pressure and inversely with the QRS and QT intervals. Plasma potassium varied inversely with the blood chloroquine.


Chloroquine inhibits myelopoiesis in vitro at therapeutic concentrations and higher. In a special test procedure, a short-lasting anti-aggregating effect could be seen with chloroquine concentrations of 3.2-32 µg/ml. These effects have clinical consequences. Chloroquine and related aminoquinolines have reportedly caused blood dyscrasias at antimalarial doses. Leukopenia, agranulocytosis, and the occasional case of thrombocytopenia have been reported. There is some evidence that myelosuppression is dose-dependent. This is in line with the hypothesis that 4-aminoquinoline therapy merely accentuates the cytopenia linked to other forms of bone marrow damage.

Some studies have pointed to inhibitory effects of chloroquine on platelet aggregability. In an investigation, this aspect of chloroquine was studied in vitro in a medium containing ADP, collagen, and ristocetin. There was a highly significant effect at chloroquine concentrations of 3.2-32 µg/ml. However, there were no significant differences in platelet responses to ADP or collagen 2 or 6 hours after adding chloroquine, compared with pre-drug values. The investigators believed that these data provided no cause for concern in using chloroquine for malaria prophylaxis in patients with impaired hemostasis.

Mouth and teeth

Pigmentation of the palate can occur as a part of a more generalized pigmentation in patients taking chloroquine. Several patients seen with chloroquine retinopathy in Accra have been observed to present with depigmented patches in the skin of the face. This may be associated with a greyish pigmentation of the mucosa of the hard palate. Two such cases are reported here to illustrate the condition. Stomatitis with buccal ulceration has occasionally been mentioned.


Gastrointestinal discomfort is not unusual in patients receiving chloroquine, and diarrhea can occur. Changes in intestinal motility may be to blame; intramuscular injection of chloroquine caused a shortened orofecal time in the five cases in which this was measured. Overdosage can cause vomiting.

Chloroquine and Hydroxychloroquine: Organs and Systems: Skin


Chloroquine can turn the nail bed blue-brown and the nail itself can develop longitudinal stripes and show a blue-grey fluorescence.


Allergic contact dermatitis, which progressed to generalized dermatitis and conjunctivitis, followed later by severe asthma, occurred in a 60-year-old worker in the pharmaceutical industry after exposure to hydroxychloroquine. Patch-testing showed delayed sensitivity to hydroxychloroquine. Equivalent tests in five healthy volunteers were negative. The patch test reactions were pustular, and a biopsy was interpreted as multiform contact dermatitis. Bronchial exposure to hydroxychloroquine dust produced delayed bronchial obstruction over the next 20 hours, progressing to fever and generalized erythema (hematogenous contact dermatitis).

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