Abstract
To the Editor.— Two years ago, I reported inThe 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
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: JAMA: The Journal of the American Medical Association
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
