We would like to respond to the Archives articles by O'Connor et al1 and Cribier et al.2 O'Connor et al reported on the porphyrin abnormalities found in the acquired immunodeficiency syndrome and suggested that the contribution of the hepatitis C virus (HCV) to abnormal porphyrin excretion patterns were characteristic of porphyria cutanea tarda (PCT).
In 1994, we analyzed the urinary excretion patterns of porphyrin derivatives in patients with HCV-induced liver disease and HCV carriers using high-performance liquid chromatography.3 The levels of urinary porphyrins of 63 HCV-positive patients who had liver diseases (including acute hepatitis, chronic hepatitis, liver cirrhosis, and hepatoma), 37 HCV carriers, and 32 healthy volunteers are summarized in the Table. The levels of uroporphyrin were below the detection limit and a coproporphyrin-predominant excretion pattern was observed in all these groups. Only secondary coproporphyria was observed and no PCT-like excretion pattern was observed.
To clarify the
Gomi H, Hatanaka K, Miura T, Matsuo I. Type of Impaired Porphyrin Metabolism Caused by Hepatitis C Virus Is Not Porphyria Cutanea Tarda but Chronic Hepatic Porphyria. Arch Dermatol. 1997;133(9):1170-1171. doi:10.1001/archderm.1997.03890450122020