Sections

Workup

Laboratory Studies

Clinical suspicion alone is not enough to make the diagnosis of porphyria cutanea tarda (PCT), and it is confirmed by excess levels of porphyrins in the blood or urine.^[38]

Urinary porphyrin levels are abnormally high in porphyria cutanea tarda patients, with several hundred to several thousand micrograms excreted in a 24-hour period. The excess porphyrin pigment is often grossly evident in visible light and yields a pink fluorescence under Wood lamp (black light) radiation (see image below).

Fluorescence of urine with a Wood light examination. Courtesy of Brooke Army Medical Center Teaching File.

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Chromatographic separation by carboxyl number of increased porphyrins present reveals a predominance of 8- and 7-carboxyl porphyrin fractions, with lesser amounts of 6-, 5-, and 4-carboxyl porphyrins, reflecting a uroporphyrinogen decarboxylase (UROD) defect. A similar array of polycarboxylated porphyrins can be found in serum or plasma specimens. The fecal coproporphyrin fraction is often abnormally high and largely consists of isocoproporphyrin. Erythrocyte porphyrin levels are in the reference range, except in hepatoerythropoietic porphyria, in which zinc protoporphyrin is elevated.

UROD enzyme activity assay in red blood cells is available in multiple laboratories in several countries, including the United States. Enzyme activity data may help determine patterns of inheritance in familial porphyria cutanea tarda and confirm the diagnosis in cases with confusing biochemical data.

Mutation analysis of genes encoding UROD is considered the criterion standard for diagnosis of familial porphyria cutanea tarda. It is most often available at specialized porphyria research centers and is commercially available in the United States. Molecular analysis for hemochromatosis gene (HFE) mutations may be positive.

A thorough evaluation requires determination of hematologic and iron profiles, including serum ferritin, liver function profile, and screening for hepatitis viruses and the human immunodeficiency virus.

Abnormal glucose tolerance and serum antinuclear antibodies are found more frequently among porphyria cutanea tarda populations.^[19]Serum levels of ascorbic acid (vitamin C, a potent antioxidant) are deficient in some patients with porphyria cutanea tarda.^[50]Alpha-fetoprotein presence in serum is useful to screen for hepatocellular carcinoma.

Imaging Studies

Evaluation of the liver for size, iron content, or tumors (most often found in individuals with long-standing active porphyria cutanea tarda) is indicated in selected cases.

Other Tests

Once a diagnosis is established, it is recommended to test for hepatitis C antibodies, HIV antibodies, and the presence of the HFE gene.^[38]Novel noninvasive methods may be useful to assess hepatic fibrosis or cirrhosis.^[51]

Procedures

Skin biopsy findings by light microscopy and direct immunofluorescence techniques may be consistent with a diagnosis of porphyria cutanea tarda but are not unequivocally diagnostic. Similar findings can be observed in other porphyrias and in pseudoporphyrias associated with certain drugs, intensive use of tanning beds or cabinets, or long-term dialysis therapy for renal failure. Direct immunofluorescence examination can help differentiate porphyria cutanea tarda from immunobullous diseases with dermoepidermal junction cleavage (epidermolysis bullosa acquisita, lupus erythematosus) in which the perivascular immunoglobulin deposition found in porphyria cutanea tarda is not observed.

Liver biopsy may be appropriate in selected patients to evaluate iron burden or damage due to ethanol abuse, viral infections, hemochromatosis, or suspected tumors.

Histologic Findings

Skin biopsy specimens of fresh blisters show subepidermal bullae with minimal dermal inflammatory infiltrate and dermal papillae protruding upward into the blister cavity (festooning); thickened upper dermal capillary walls and dermoepidermal basement membrane zones are evident in routinely stained sections and accentuated with the periodic acid-Schiff stain; elastosis, sclerosis of dermal collagen, and hyaline deposits may be seen in the dermis.^[52]Linear, eosinophilic, periodic acid-Schiff–positive globules composed of basement membrane material and degenerating keratinocytes ("caterpillar bodies") may be observed in the blister roof.^[53]Note the image below.

Subepidermal bulla, festooning of rete ridges, hyalinization of blood vessel walls, solar elastosis, and caterpillar bodies. Courtesy of Dirk Elston, MD.

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Ultrastructural examination of dermal vascular walls and the basement membrane zone reveals replication of basal laminae, reflecting multiple episodes of damage and repair.^{[52, 54]}

Direct immunofluorescence examination shows deposition of immunoglobulins and complement in and around the dermal capillaries and at the basement membrane zone.^[52]These deposits do not indicate that porphyria cutanea tarda is an autoimmune disorder; they are believed to be immunoproteins leaked from the damaged vasculature.

Liver biopsy abnormalities range from minimal to severe. Increased iron deposition is frequently present. Other abnormalities may include steatosis, chronic inflammatory infiltrates, fibrosis, cirrhosis, and necrosis. Needlelike intracytoplasmic inclusions believed to be uroporphyrin crystals occur near ferritin iron deposits in hepatocytes.^[55]

Treatment & Management

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Media Gallery

Thickened skin with blisters, scars, and milia. Courtesy of Dirk Elston, MD.
Close-up image of blisters, scarring, and milia. Courtesy of Dirk Elston, MD.
Subepidermal bulla, festooning of rete ridges, hyalinization of blood vessel walls, solar elastosis, and caterpillar bodies. Courtesy of Dirk Elston, MD.
Fluorescence of urine with a Wood light examination. Courtesy of Brooke Army Medical Center Teaching File.

of 4

Author

Anthony W Linfante, Jr, MD Resident Physician, Department of Dermatology, University of Texas Medical Branch School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Meredith M Gavin MD Candidate, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Meredith M Gavin is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Medical Women's Association, Gold Humanism Honor Society, Texas Medical Association

Disclosure: Nothing to disclose.

Brandon Patrick Goodwin, MD Assistant Professor of Dermatology/Dermatopathology, Assistant Lab Director, Dermatopathology Laboratory, University of Texas Medical Branch School of Medicine; Ambulatory Medical Director, UTMB Health Dermatology Clinic

Brandon Patrick Goodwin, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society of Dermatopathology, Houston Dermatological Society, Texas Dermatological Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Julia R Nunley, MD Professor, Department of Dermatology, Virginia Commonwealth University Medical Center

Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, Women's Dermatologic Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Board of Dermatology<br/>Author for: Up-to-date.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Craig A Elmets, MD Professor and Chair, Department of Dermatology, Director, Chemoprevention Program Director, Comprehensive Cancer Center, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, Society for Investigative Dermatology

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: University of Alabama at Birmingham; University of Alabama Health Services Foundation<br/>Serve(d) as a speaker or a member of a speakers bureau for: Ferndale Laboratories<br/>Received research grant from: NIH, Veterans Administration, California Grape Assn<br/>Received consulting fee from Astellas for review panel membership; Received salary from Massachusetts Medical Society for employment; Received salary from UpToDate for employment. for: Astellas.

Maureen B Poh-Fitzpatrick, MD Professor Emerita of Dermatology and Special Lecturer, Columbia University College of Physicians and Surgeons

Maureen B Poh-Fitzpatrick, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, New York Academy of Medicine, New York Dermatological Society

Disclosure: Nothing to disclose.

Porphyria Cutanea Tarda Workup

Laboratory Studies

Imaging Studies

Other Tests

Procedures

Histologic Findings

References

Tables

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