ASCORBIC-ACID DEFICIENCY IN PORPHYRIA-CUTANEA-TARDA

Citation
Pr. Sinclair et al., ASCORBIC-ACID DEFICIENCY IN PORPHYRIA-CUTANEA-TARDA, The Journal of laboratory and clinical medicine, 130(2), 1997, pp. 197-201
Citations number
17
Categorie Soggetti
Medical Laboratory Technology
ISSN journal
00222143
Volume
130
Issue
2
Year of publication
1997
Pages
197 - 201
Database
ISI
SICI code
0022-2143(1997)130:2<197:ADIP>2.0.ZU;2-S
Abstract
Porphyria cutanea tarda (POT), the most common form of porphyria, is m anifested as skin photosensitivity caused by excess hepatic production of uroporphyrin and heptacarboxylporphyrin. In experimental animal mo dels, ascorbic acid modulates chemically induced uroporphyrin accumula tion, The purpose of this study was to determine whether ascorbic acid is decreased in the plasma of patients with PCT. Plasma was obtained after an overnight fast from 21 PCT patients, 16 of whom were infected with hepatitis C virus (HCV), and from a separate group of 9 patients with HCV infection but not PCT, Thirteen PCT patients were studied wh en they had active disease and 8 after treatment-induced remission. Pl asma ascorbic acid was low (< 23 mu mol/L) in 11 (85%) of the 13 untre ated PCT patients and deficient (< 11 mu mol/L) in 8 (62%), Two patien ts with normal ascorbic acid levels (45 and 62 mu mmol/L) had consumed multivitamins. In 2 patients with deficient ascorbic acid, plasma lev els returned to normal after phlebotomy treatment, Of the 8 patients s tudied during remission, 4 had normal ascorbic acid values and 4 were deficient (5 to 8 mu mol/L). Plasma ascorbic acid values were normal f or all patients who had HCV but no PCT, These data suggest that plasma ascorbic acid concentrations are commonly low in POT, but this decrea se is unrelated to HCV infection, Ascorbic acid deficiency may be one of the factors that contributes to the pathogenesis of PCT.