Author(s): Dr Anes Yang, Unaccredited Dermatology Registrar, The Skin Hospital, Darlinghurst, Sydney, New South Wales, Australia; Dr Monisha Gupta, Senior Staff Specialist, Department of Dermatology, Liverpool Hospital, Senior Lecturer, University of New South Wales, Sydney, New South Wales, Australia. DermNet NZ Medical Editor: Dr Delwyn Dyall-Smith, Dermatologist, Wagga Wagga, NSW, Australia. DermNet New Zealand Editor in Chief: Adjunct Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. September 2018.

What is chloroquine?

Chloroquine is a synthetic antimalarial medication that was first developed in 1934.

In addition to its antimalarial effects, chloroquine has been used extensively in rheumatology and dermatology since the 1950s.

Despite its early successes, the use of chloroquine has mostly been superseded by hydroxychloroquine, a safer hydroxylated analogue, and its availability is now limited.

Chloroquine has immunomodulatory and anti-inflammatory effects and may also have a photoprotective effect [1].

Who uses chloroquine?

Chloroquine and hydroxychloroquine have the same indications and usage, although the dosage regimens are different. Head-to-head comparisons suggest similar responses with equivalent doses, but greater retinal toxicity with chloroquine [2].

In dermatology, antimalarials such as chloroquine are regarded as appropriate treatments for:

They are sometimes used to treat other inflammatory skin diseases [3].

Skin conditions that may be treated with chloroquine

What are the contraindications with chloroquine?

Children below 6 years of age should not be given chloroquine due to the risk of overdose and acute toxicity.

The chloroquine dose should be reduced in patients with renal disease, as up to 70% of chloroquine is excreted unchanged in the urine. Chloroquine itself can cause reduced kidney function of up to 10% especially in those over 60 years of age. Renal impairment results in higher blood levels and therefore increased toxicity risk.

Chloroquine should be used with caution in patients with known porphyria cutanea tarda (PCT). Chloroquine can be used to treat PCT, but in a very low dose (125 mg twice weekly). 250 mg/d can trigger a porphyria crisis, which can be fatal.

Chloroquine is contraindicated where there is a known hypersensitivity to 4-aminoquinoline compounds.

Chloroquine crosses the placenta and is also found in low levels in breast milk, so pregnancy and lactation are often listed contraindications (see DermNet’s pages on drugs in pregnancy and on lactation and the skin). However, effects on the fetus and baby have been rarely reported and chloroquine has been continued when required for malaria.

Pre-existing retinopathy and other eye problems such as macular degeneration and cataracts make monitoring more difficult, and so can also be relative contraindications.

Although chloroquine can occasionally trigger a flare of psoriasis, this is not an absolute contraindication and the use of the drug should be decided in individual cases.

Tell me more about chloroquine

Chloroquine has similar pharmacokinetics to hydroxychloroquine. After identical doses, the tissue levels of chloroquine are 2.5 times those of hydroxychloroquine. Chloroquine is rapidly and almost completely absorbed from the bowel following oral administration.

Peak plasma concentrations are reached within 4–12 hours but it takes 4–6 weeks for plasma concentrations to stabilise. Therefore, it will take 2–3 months to see a therapeutic effect. Up to 70% is excreted unchanged through the kidneys and up to 40% is metabolised in the liver to an active metabolite.

Chloroquine binds to plasma proteins that are deposited in tissues such as the liver, spleen, kidney and lung. Chloroquine has a particularly high affinity for melanin-containing cells and hence there are very high levels of chloroquine in the skin (mainly epidermis) and retina. Chloroquine has a long half-life, which can vary between 74 hours and 50 days, depending on the cumulative dose.

The drug can remain in the skin for 6–7 months after cessation of therapy.


Chloroquine phosphate is dispensed as a 250 mg tablet, which is equivalent to 155 mg chloroquine base.

Long-term use should aim for < 2.3 mg/kg/d based on actual body weight. Given the tablet size, this usually means it needs to be used intermittently, that is, several times per week instead of daily.

Previously, the maximum daily dose was calculated on ideal body weight, and cumulative dose was recommended to be less than 460 g. These guidelines have been revised.

In PCT, the dose should not exceed 125 mg twice weekly.

Chloroquine can be used together with quinacrine but it should not be used with hydroxychloroquine.

Chloroquine is not marketed in Australia, where it is only available through the Special Access Scheme. It is no longer approved for use in New Zealand but may be available under Section 29. See Medsafe, unapproved medications.

Dosing: hepatic impairment

No dosage adjustment is provided in the manufacturer’s labelling.

Dosing: renal impairment

Creatinine clearance ≥ 10 mL/minute: No dosage adjustment is necessary.

Creatinine clearance < 10 mL/minute: Administer 50% of usual dose.

What are the ocular side effects and risks of chloroquine?

The two main ocular effects of chloroquine are corneal deposits (reversible) and retinal toxicity (irreversible).

Corneal deposits 

Corneal deposits occur rapidly in 90% of patients on chloroquine. They are usually asymptomatic, however patients can experience transient halos and heightened light sensitivity.

Finding corneal deposits on examination does not mean chloroquine should be stopped.

Deposits are dose related, occurring 1–1.5 months after therapy is initiated and resolve after discontinuation of chloroquine.

Retinal toxicity 

Irreversible retinal toxicity causing bilateral bull’s-eye retinopathy from chloroquine has been recognised for many years. This is a late stage finding and should not be seen if regular monitoring is conducted. The high affinity of chloroquine for melanin-containing cells, such as those found in the retinal pigment epithelium, is hypothesised to be the cause.

Patients with antimalarial-induced retinal toxicity may not have any visual symptoms initially and will only develop clinical symptoms in the late stages.

Cessation of the drug when definite signs of early retinopathy are found is important as progression to vision loss is then rare. Chloroquine should only be ceased if there are definite signs of retinal toxicity. Possible toxicity should be reassessed after several months with continued drug use. Continued use of chloroquine after the findings of definite retinopathy results in irreversible visual damage including effects on visual acuity, peripheral vision, and night vision.

The retinopathy does not reverse, even with cessation of the chloroquine, and there is no treatment. The risk of retinal toxicity is highest with chloroquine compared to other antimalarials [4].

In 2016, with new scientific data, the American Academy of Ophthalmology revised the screening recommendations for patients to be commenced on chloroquine for greater than one year [5].

The two most important risk factors are duration of treatment and daily dose based on actual body weight, particularly a daily dose of chloroquine exceeding 2.3 mg/kg actual body weight.

Monitoring is of particular importance in those over 60 and in those with renal impairment.

Screening recommendations

Every patient planning to take chloroquine for at least 12 months should undergo a baseline ophthalmic examination within six months of commencing chloroquine and then annually. Fundal examination alone is not sufficient screening. Examination should involve automated visual fields and spectral domain optical coherence tomography (SD OCT) [6].

Other side effects

Cutaneous side effects

Chloroquine can cause:

Gastrointestinal side effects

Nausea, vomiting and diarrhoea are often transient or resolve with dose reduction. Symptoms can be minimised by taking the medication with food.

Haematological effects

Haemolytic anaemia and reduced blood cell counts are very rare at recommended doses but may occasionally occur in patients with G6PD deficiency.

Neuromuscular effects

Neuromyopathy, myalgia and fatigue have been reported with chloroquine use. Care should therefore be taken in patients with myasthenia gravis and dermatomyositis.

Drug interactions with antimalarial medications 

The following medications should be reviewed when used concomitantly with chloroquine: digoxin, methotrexate, D-penicillamine, ciclosporin, beta blockers, amiodarone, penicillin, cimetidine, ritonavir, cholestyramine, antacids, aminoglycosides, corticosteroids, neostigmine, and physostigmine.


Smoking has been reported to inhibit the P450 enzyme system, decreasing the efficacy of chloroquine [7].

What monitoring is required?

  • Full blood count should be checked prior to treatment and monthly for the first 3 months, then every 4–6 months [8].
  • Renal function should be checked at baseline, then after 1 month, after 3 months, and then every 4–6 months to assess for any changes in risk for adverse ocular effects (more frequent surveillance is needed if laboratory values are abnormal or with high-risk patients) [8].
  • Pregnancy test should be undertaken in women of childbearing age at baseline and the patient should understand the need for reliable use of contraception during therapy.
  • Consider testing for G6PD deficiency, especially in individuals originating from Africa, Asia, Oceania, or from Southern Europe.
  • Every patient should undergo a baseline ophthalmic examination within the first six months of commencing chloroquine if the treatment is anticipated to be long-term. In the absence of specific risk factors, annual screening should then be performed.
New Zealand approved datasheets are the official source of information for this prescription medicine, including approved uses and risk information. Check the individual New Zealand datasheet on the Medsafe website.

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Related information



  1. Rodriguez-Caruncho C, Marsol IB. Antimalarials in dermatology: mechanism of action, indications, and side effects. Actas Dermo-Sifiliográficas (English Edition) 2014; 105: 243–52. PubMed
  2. Mittal L, Zhang L, Feng R, Werth VP. Antimalarial drug toxicities in patients with cutaneous lupus and dermatomyositis: A retrospective cohort study. J Am Acad Dermatol 2018; 78: 100–6. Epub 2017/10/11. doi: 10.1016/j.jaad.2017.09.061. PubMed
  3. Ochsendorf FR. Use of antimalarials in dermatology. JDDG: Journal der Deutschen Dermatologischen Gesellschaft 2010; 8: 829–45. PubMed 
  4. Marmor MF. Modern management of antimalarial usage and retinopathy. Journal of Current Ophthalmology. 2017; 29: 143–4. doi: 10.1016/j.joco.2017.07.001. PubMed
  5. Marmor MF, Kellner U, Lai TY, Melles RB, Mieler WF. Recommendations on screening for chloroquine and hydroxychloroquine retinopathy (2016 revision). Ophthalmology 2016; 123: 1386–94. PubMed
  6. Yusuf IH, Lotery AJ, Ardern-Jones MR. Joint recommendations for retinal screening in long-term users of hydroxychloroquine and chloroquine in the United Kingdom, 2018. Br J Dermatol 2018. doi: 10.1111/bjd.16782. PubMed
  7. Fernandez AP. Updated recommendations on the use of hydroxychloroquine in dermatologic practice. J Am Acad Dermatol. 2017; 76: 1176–82. doi: PubMed
  8. Wolverton SE. Comprehensive dermatologic drug therapy: Elsevier Health Sciences; 2012.

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