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Chloroquine retinopathy is a form of toxic retinopathy (damage of the retina) caused by the drugs chloroquine or hydroxychloroquine, which are sometimes used in the treatment of autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. This eye toxicity limits long-term use of the drugs. [3]
Severe side effects may include allergic reactions, retinopathy, and irregular heart rate. [3] [4] Although all risk cannot be excluded, it remains a treatment for rheumatic disease during pregnancy. [5] Hydroxychloroquine is in the antimalarial and 4-aminoquinoline families of medication. [3]
Drug-induced pigmentation of the skin may occur as a consequence of drug administration, and the mechanism may be postinflammatory hyperpigmentation in some cases, but frequently is related to actual deposition of the offending drug in the skin. [2]: 125–6 The incidence of this change varies, and depends on the type of medication involved.
"Potentiates digitalis activity, increases coronary dilation effects of theophylline, caffeine, papaverine, sodium nitrate, adenosine and epinephrine, increase barbiturate-induced sleeping times" [3] Horse chestnut: conker tree, conker Aesculus hippocastanum: Liver toxicity, allergic reaction, anaphylaxis [3] Kava: awa, kava-kava [4] Piper ...
Hydroxychloroquine is more commonly available than chloroquine in the United States. [13] Hydroxychloroquine is used as a prophylactic in India. [24] [25] Hydroxychloroquine and chloroquine have numerous, potentially serious, side effects, such as retinopathy, hypoglycemia, or life-threatening arrhythmia and cardiomyopathy. [26]
Serious side effects include problems with vision, muscle damage, seizures, and low blood cell levels. [ 1 ] [ 4 ] Chloroquine is a member of the drug class 4-aminoquinoline . [ 1 ] As an antimalarial, it works against the asexual form of the malaria parasite in the stage of its life cycle within the red blood cell . [ 1 ]
Postinflammatory hyperpigmentation develops after the original symptoms of an inflammatory skin condition disappear. Common triggers include acne lesions, cuts, burns, or skin conditions like eczema. [1] Additionally, UV sun exposure and sunburn are involved in the development, darkening, and expansion of hyperpigmented skin lesions. [2]
Certain vitamin and minerals deficiencies are common in people with porphyria cutanea tarda. The most common deficiencies are beta-Carotene, [7] retinol, [8] vitamin A [9] and vitamin C. Beta-Carotene is required to synthesize vitamin A and vitamin A is needed to synthesize retinol.
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