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To the Editor.—
Two years ago, I reported in The Journal (223:515,1973) the correction of the hepatic abnormalities as well as the cutaneous manifestations of porphyria cutanea tarda (PCT) by the oral administration of chloroquine, and suggested that this agent, directly or indirectly, selectively destroyed those cells (or their organelles) that were responsible for abnormal porphyrin synthesis. Although I still believe this to be the case, longer observation of the two patients reported, and of three additional patients with PCT who were similarly treated, has revealed a slight to moderate increase in uroporphyrin excretion six months to three years after initial treatment. This would imply that all porphyrinproducing structures had not been destroyed, or that they were capable of regeneration. The rise after only six months would favor the former explanation; the increase after three years, the latter.Alcohol intake was evidently not causally related to the rise. The patient
Kowertz MJ. Retreatment With Chloroquine in Porphyria Cutanea Tarda. JAMA. 1975;233(1):22. doi:10.1001/jama.1975.03260010024008