Effects of Chloroquine on Patients with Cutaneous Porphyria of the “Symptomatic” Type

Abstract

The administration of chloroquine to patients with symptomatic porphyria causes a transient reaction in which pyrexia and malaise are accompanied by a marked increase in urine porphyrin excretion. The excretion of porphyrin precursors, δ-aminolaevulinic acid and porphobilinogen increases only slightly. This reaction is associated with clinical and biochemical evidence of liver damage, in particular, a rise in serum glutamic oxaloacetic transaminase activity. It is thought that the porphyrin excreted in the urine is released from the liver. After the reaction patients are not affected by further administration of chloroquine; it is not known for how long this refractory state persists. The reaction resembles in some ways the primaquine-induced haemolysis of red cells deficient in glucose-6-phosphate dehydrogenase. Patients with symptomatic porphyria have improved clinically after chloroquine therapy, but this is attributed to other factors; evidence of hepatic dysfunction argues against the use of chloroquine in this condition. © 1965, British Medical Journal Publishing Group. All rights reserved.