 |
|
Porphyria Cutanea Tarda in Human Immunodeficiency Virus—Infected Patients
Philip R. Cohen, MD;
Sylvia M. Suarez, MD;
Vincent A. DeLeo, MD
JAMA. 1990;264(10):1315-1316.
|
|
| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
|
|
|
The porphyrias are a heterogeneous group of inherited or acquired disorders. Each of the individual porphyrias is a distinct clinical condition resulting from an abnormality of a specific heme synthesis enzyme. Porphyria cutanea tarda (PCT) is biochemically characterized by the reduced activity of uroporphyrinogen decarboxylase. In the familial form of PCT, both erythrocyte and hepatocyte enzyme activity is deficient, whereas in its acquired form, usually only the liver cells have diminished enzyme activity. Patients with PCT typically develop cutaneous lesions secondary to chronic or delayed photosensitivity. Increased skin fragility, bruising, vesicles, bullae, hyperpigmentation, and hypertrichosis are early features, whereas mild to mutilating scarring, milia, and sclerodermoid changes are late manifestations of PCT-associated sensitivity.1
A 48-year-old, homosexual, human immunodeficiency virus (HIV)—seropositive man was evaluated for blisters on his hands and forehead. Prior acquired immunodeficiency syndrome (AIDS)—related infection included oral candidiasis; he was currently receiving zidovudine, trimethoprim and sulfamethoxazole, and nystatin.
. . . [Full Text PDF of this Article]
Author Affiliations
College of Physicians and Surgeons of Columbia University New York, NY
Footnotes
Edited by Roxanne K. Young, Associate Editor.
Reprints not available.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
|
