ReviewHematology. American Society of Hematology. Education Program2024
Porphyria cutanea tarda: a unique iron-related disorder.
Review in Hematology. American Society of Hematology. Education Program, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Oxidation of Uroporphyrinogens During Heme Synthesis: Role of Iron, Susceptibility and Consequences.Biomolecules · 2026Review
- Article
- Understanding the Clinical Spectrum of the Cutaneous and Acute Hepatic Porphyrias.American journal of clinical dermatology · 2026Review
- Updates to gene-disease classifications and inheritance patterns for porphyrias.Molecular genetics and metabolism · 2026Article
- Biosensors for Detection of Labile Heme in Biological Samples.Biosensors · 2025Review
- Porphyrias: Pathophysiology and clinical management recommendations for hepatologists.Hepatology communications · 2025Review
- Pathogenesis and clinical management of liver damage in porphyrias: Mechanisms and therapeutic approaches.World journal of hepatology · 2025Review
- An image of multiple bullous lesions in a patient on hemodialysis.Jornal brasileiro de nefrologiaArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The porphyrias are a group of disorders of heme biosynthesis, each characterized by an enzymatic defect in the heme biosynthetic pathway. Porphyria cutanea tarda (PCT) arises due to the inhibition of uroporphyrinogen decarboxylase (UROD) in the presence of hepatic iron and oxidative stress. Most patients with PCT have evidence of siderosis on liver biopsy, and the disease resolves with iron depletion. PCT manifests as skin fragility, blistering cutaneous lesions on sun-exposed areas, dark urine, and elevated plasma and urine porphyrins. Factors contributing to the development of PCT include alcohol use, hepatitis C virus infection, human immunodeficiency virus, estrogen use, UROD pathogenic variants, and hereditary hemochromatosis. Treatment includes therapeutic phlebotomy to decrease total body iron levels and low-dose hydroxychloroquine, which reduces hepatic porphyrin content. The following review explores the biology of PCT, the critical role of iron in disease pathogenesis, and our approach to the management of these patients.
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Registered trials
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