porphyria cutanea tarda

PCT is typically characterised by fragile skin and sore blisters in areas of skin that receive higher levels of exposure to sunlight, such as the face and backs of the hands. These blisters burst easily resulting in erosions, crusts, and superficial ulcers. There is often associated darkened skin color and extra facial hair growth. Healing is typically slow, leading to scarring and milia, while changes such as hair loss, and alterations in nails may also occur. A slightly purplish tint may be seen around the eyes. Scleroderma-like thick skin may develop over fingers, scalp, behind the ears, at the back of the neck, or in the front of the chest. The urine may appear dark with a hint of reddishness.

In addition to the skin lesions, chronic liver disease is very common in patients with sporadic PCT. This involves hepatic fibrosis (scarring of the liver), and inflammation. However, liver problems are less common in patients with the inherited form of the disease.{{Cite journal |last=Di Padova |first=C. |last2=Marchesi |first2=L. |last3=Cainelli |first3=T. |last4=Gori |first4=G. |last5=Podenzani |first5=S.A. |last6=Rovagnati |first6=P. |last7=Rizzardini |first7=M. |last8=Cantoni |first8=L. |year=1983 |title=Effects of Phlebotomy on Urinary Porphyrin Pattern and Liver Histology in Patients with Porphyria Cutanea Tarda |journal=The American Journal of the Medical Sciences |volume=285 |issue=1 |pages=2–12 |doi=10.1097/00000441-198301000-00001 |pmid=6824014 |s2cid=23741767}} Additionally, patients will often void a wine-red color urine with an increased concentration of uroporphyrin I due to their enzymatic deficiency.Goljan, E. F. (2011). Pathology (3rd ed., rev. reprint.). Philadelphia, PA: Mosby/Elsevier.{{page needed|date=December 2016}}

Certain vitamin and minerals deficiencies are common in people with porphyria cutanea tarda. The most common deficiencies are beta-Carotene,{{Cite journal |last=Rocchi |first=E. |last2=Stella |first2=A. M. |last3=Cassanelli |first3=M. |last4=Borghi |first4=A. |last5=Nardella |first5=N. |last6=Seium |first6=Y. |last7=Casalgrandi |first7=G. |date=1 July 1995 |title=Liposoluble vitamins and naturally occurring carotenoids in porphyria cutanea tarda |journal=European Journal of Clinical Investigation |volume=25 |issue=7 |pages=510–514 |doi=10.1111/j.1365-2362.1995.tb01737.x |pmid=7556369 |s2cid=44998779}} retinol,{{Cite journal |last=Rocchi |first=E. |last2=Casalgrandi |first2=G. |last3=Masini |first3=A. |last4=Giovannini |first4=F. |last5=Ceccarelli |first5=D. |last6=Ferrali |first6=M. |last7=Marchini |first7=S. |last8=Ventura |first8=E. |date=1 December 1999 |title=Circulating pro- and antioxidant factors in iron and porphyrin metabolism disorders |journal=Italian Journal of Gastroenterology and Hepatology |volume=31 |issue=9 |pages=861–867 |pmid=10669994}} vitamin A{{Cite journal |last=Benoldi |first=D. |last2=Manfredi |first2=G. |last3=Pezzarossa |first3=E. |last4=Allegra |first4=F. |date=1 December 1981 |title=Retinol binding protein in normal human skin and in cutaneous disorders |journal=The British Journal of Dermatology |volume=105 |issue=6 |pages=659–665 |doi=10.1111/j.1365-2133.1981.tb00976.x |pmid=7032574 |s2cid=23170672}} and vitamin C. Beta-Carotene is required to synthesize vitamin A and vitamin A is needed to synthesize retinol. A lack of retinol-binding protein is due to a lack of retinol which is required to trigger its production.

Porphyrins interact with iron, absorbing photons to create reactive oxygen species is the mechanism of action causing the itchy, painful blisters of PCT. The reactive oxygen species consume the skin antioxidants beta-carotene, vitamin E, and vitamin C. Supplementation of these three vitamins reduces the oxidation and potentially diminishes the severity of blister formation.{{Cite journal |last=Böhm |first=F. |last2=Edge |first2=R. |last3=Foley |first3=S. |last4=Lange |first4=L. |last5=Truscott |first5=T. G. |date=31 December 2001 |title=Antioxidant inhibition of porphyrin-induced cellular phototoxicity |journal=Journal of Photochemistry and Photobiology B: Biology |volume=65 |issue=2–3 |pages=177–183 |bibcode=2001JPPB...65..177B |doi=10.1016/s1011-1344(01)00259-7 |pmid=11809377}} No single one of the three vitamins can inhibit the damaging effects of oxidized porphyrins, specifically uroporphyrins and coproporphyrins, but all three working together synergistically are capable of neutralizing their damaging effects.{{citation needed|date=September 2021}}

Image:Uroporphyrinogen-decarboxylase.svg

Image:Autosomal dominant - en.svg pattern.]]

Inherited mutations in the UROD gene cause about 20% of cases (the other 80% of cases do not have mutations in UROD, and are classified as sporadic). UROD makes an enzyme called uroporphyrinogen III decarboxylase, which is critical to the chemical process that leads to heme production. The activity of this enzyme is usually reduced by 50% in all tissues in people with the inherited form of the condition.{{citation needed|date=September 2021}}

Nongenetic factors such as excess iron or partially genetic factors such as alcohol use disorder and others listed above can increase the demand for heme and the enzymes required to make heme. The combination of this increased demand and reduced activity of uroporphyrinogen decarboxylase disrupts heme production and allows byproducts of the process to accumulate in the body, triggering the signs and symptoms of porphyria cutanea tarda.{{citation needed|date=September 2021}}

The HFE gene makes a protein that helps cells regulate the absorption of iron from the digestive tract and into the cells of the body. Certain mutations in the HFE gene cause hemochromatosis (an iron overload disorder). People who have these mutations are also at an increased risk of developing porphyria cutanea tarda.{{citation needed|date=September 2021}}

In the 20% of cases where porphyria cutanea tarda is inherited, it is inherited in an autosomal dominant pattern, which means one copy of the altered gene is sufficient to decrease enzyme activity and cause the signs and symptoms of the disorder.{{citation needed|date=September 2021}}

While inherited deficiencies in uroporphyrinogen decarboxylase often lead to the development of PCT, there are a number of risk factors that can both cause and exacerbate the symptoms of this disease. One of the most common risk factors observed is infection with the Hepatitis C virus.{{Cite journal |last=Azim |first=James |last2=McCurdy |first2=H |last3=Moseley |first3=R. H. |year=2008 |title=Porphyria cutanea tarda as a complication of therapy for chronic hepatitis C |journal=World Journal of Gastroenterology |volume=14 |issue=38 |pages=5913–5 |doi=10.3748/wjg.14.5913 |pmc=2751904 |pmid=18855993 |doi-access=free}} One review of a collection of PCT studies noted Hepatitis C infection in 50% of documented cases of PCT. Additional risk factors include alcohol use disorder, excess iron (from iron supplements as well as cooking on cast iron skillets), and exposure to chlorinated cyclic hydrocarbons and Agent Orange.{{citation needed|date=September 2021}}

It can be a paraneoplastic phenomenon.{{Cite journal |last=Sökmen |first=M |last2=Demirsoy |first2=H |last3=Ersoy |first3=O |last4=Gökdemir |first4=G |last5=Akbayir |first5=N |last6=Karaca |first6=C |last7=Ozdil |first7=K |last8=Kesici |first8=B |last9=Calişkan |first9=C |last10=Yilmaz |first10=B |year=2007 |title=Paraneoplastic porphyria cutanea tarda associated with cholangiocarcinoma: Case report |url=http://www.turkjgastroenterol.org/eng/makale/3551/235/Full-Text |journal=The Turkish Journal of Gastroenterology |volume=18 |issue=3 |pages=200–5 |pmid=17891697}}

• Alcohol
• Estrogen
• Iron{{Cite journal |last=Sampietro |first=M |last2=Fiorelli |first2=G |last3=Fargion |first3=S |year=1999 |title=Iron overload in porphyria cutanea tarda |url=http://www.haematologica.org/cgi/pmidlookup?view=long&pmid=10189391 |journal=Haematologica |volume=84 |issue=3 |pages=248–53 |pmid=10189391}}
• Hepatitis C virus{{Cite web |date=2020-01-12 |title=Porphyria Cutanea Tarda (PCT) |url=https://www.porphyriafoundation.org/for-patients/types-of-porphyria/pct/}}

Porphyria cutanea tarda is primarily caused by uroporphyrinogen decarboxylase deficiency (UROD). Uroporphyrinogen decarboxylase occurs in nature as a homodimer of two subunits. It participates in the fifth step in heme synthesis pathway, and is active in the cytosol. This enzymatic conversion results in coproporphyrinogen III as the primary product. This is accomplished by the clockwise removal of the four carboxyl groups present in the cyclic uroporphyrinogen III molecule. Therefore, a deficiency in this enzyme causes the aforementioned buildup of uroporphyrinogen and hepta-carboxylic porphyrinogen, and to a lesser extent hexa-carboxylic porphyrinogen, and penta-carboxylic porphyrinogen in the urine, which can be helpful in the diagnosis of this disorder.{{Cite web |date=7 May 2020 |title=Porphyrin Tests |url=https://labtestsonline.org/understanding/analytes/porphyrins/tab/test/}}{{Cite journal |last=Jackson |first=A. H. |last2=Ferramola |first2=A. M. |last3=Sancovich |first3=H. A. |last4=Evans |first4=N |last5=Matlin |first5=S. A. |last6=Ryder |first6=D. J. |last7=Smith |first7=S. G. |year=1976 |title=Hepta- and hexa-carboxylic porphyrinogen intermediates in haem biosynthesis |journal=Annals of Clinical Research |volume=8 |issue=Suppl 17 |pages=64–9 |pmid=1008499}}

The dermatological symptoms of PCT that include blistering and lesions on sun-exposed areas of the skin are caused by a buildup of porphyrin compounds (specifically uroporphyrinogen) close to the surface of the skin that have been oxidized by free radicals or sunlight.{{Cite journal |last=Miller |first=Dennis M. |last2=Woods |first2=James S. |year=1993 |title=Urinary porphyrins as biological indicators of oxidative stress in the kidney |journal=Biochemical Pharmacology |volume=46 |issue=12 |pages=2235–41 |doi=10.1016/0006-2952(93)90614-3 |pmid=8274157}} The oxidized porphyrins initiate degranulation of dermal mast cells,{{Cite journal |last=Brun |first=Atle |last2=Sandberg |first2=Sverre |year=1991 |title=Mechanisms of photosensitivity in porphyric patients with special emphasis on erythropoietic protoporphyria |journal=Journal of Photochemistry and Photobiology B: Biology |volume=10 |issue=4 |pages=285–302 |bibcode=1991JPPB...10..285B |doi=10.1016/1011-1344(91)80015-A |pmid=1791486}} which release proteases that catabolize the surrounding proteins.{{Cite journal |last=Lim |first=H. W. |year=1989 |title=Mechanisms of phototoxicity in porphyria cutanea tarda and erythropoietic protoporphyria |journal=Immunology Series |volume=46 |pages=671–85 |pmid=2488874}} This begins a cell-mediated positive feedback loop which matches the description of a type 4 delayed hypersensitivity reaction.{{citation needed|date=December 2016}} The resulting blisters, therefore, do not appear immediately but begin to show up 2–3 days after sun exposure. Due to the highly conjugated structure of porphyrins involving alternating single and double carbon bonds, these compounds exhibit a deep purple color, resulting in the discoloration observed in the skin. Excess alcohol intake decreases hepcidin production which leads to increased iron absorption from the gut and an increase in oxidative stress. This oxidative stress then leads to inhibition of uroporphyrinogen decarboxylase, creating an excess of uroporphyrinogen III which is oxidized from the relatively harmless porphyrinogens into their oxidized porphyrins form.{{Cite journal |last=Ryan Caballes |first=F. |last2=Sendi |first2=Hossein |last3=Bonkovsky |first3=Herbert L. |year=2012 |title=Hepatitis C, porphyria cutanea tarda and liver iron: An update |journal=Liver International |volume=32 |issue=6 |pages=880–93 |doi=10.1111/j.1478-3231.2012.02794.x |pmc=3418709 |pmid=22510500}} Concentrated instances of oxidative stress (alcohol, physical trauma, psychological stress, etc.) cause the liver to hemorrhage these porphyrins into the blood stream where they are then susceptible to oxidation.{{citation needed|date=September 2021}}

The strong association of PCT with Hepatitis C virus infection is not entirely understood. Studies have suggested that the cytopathic effect of the virus on hepatocytes can lead to the release of free iron. This iron can disrupt the activity of cytochrome p450, releasing activated oxygen species. These can oxidize the UROD substrate uroporphyrinogen, which can result in the inhibition of UROD and lead to deficient activity of this key enzyme.{{Cite journal |last=Ryan Caballes |first=F. |last2=Sendi |first2=Hossein |last3=Bonkovsky |first3=Herbert L. |date=July 2012 |title=Hepatitis C , porphyria cutanea tarda and liver iron: an update |journal=Liver International |language=en |volume=32 |issue=6 |pages=880–893 |doi=10.1111/j.1478-3231.2012.02794.x |issn=1478-3223 |pmc=3418709 |pmid=22510500}}

Excess alcohol use is frequently associated with both inducing PCT{{EMedicine|article|1103643|Porphyria Cutanea Tarda}} and aggravating a preexisting diagnosis of the disorder. It is thought to do so by causing oxidative damage to liver cells, resulting in oxidized species of uroporphyrinogen that inhibit the activity of hepatic UROD. It is also felt to increase the uptake of iron in liver cells, leading to further oxidation of uroporphyrinogen by the release of activated oxygen species. Additionally, exposure to chlorinated cyclic hydrocarbons can lead to a deficiency in the activity of uroporphyrinogen decarboxylase, causing the buildup of excess uroporphyrinogen. Additionally, alcohol has been shown to increase the activity of the delta-aminolevulinic acid synthetase (ALA synthetase), the rate-limiting enzymatic step in heme synthesis in the mitochondria, in rats.{{Cite journal |last=Held |first=H. |year=2009 |title=Effect of Alcohol on the Heme and Porphyrin Synthesis Interaction with Phenobarbital and Pyrazole |journal=Digestion |volume=15 |issue=2 |pages=136–46 |doi=10.1159/000197995 |pmid=838185}} Therefore, alcohol consumption may increase the production of uroporphyrinogen, exacerbating symptoms in individuals with porphyria cutanea tarda.{{citation needed|date=December 2017}}

While the most common symptom of PCT is the appearance of skin lesions and blistering, their appearance is not conclusive. Laboratory testing commonly reveals high levels of uroporphyrinogen in the urine, clinically referred to as uroporphyrinogenuria. Additionally, testing for common risk factors such as hepatitis C and hemochromatosis is strongly suggested, as their high prevalence in patients with PCT may require additional treatment. If clinical appearance of PCT is present, but laboratories are negative, the diagnosis of pseudoporphyria should be seriously considered.{{citation needed|date=September 2021}}

Some sources divide PCT into two types: sporadic and familial.{{DorlandsDict|seven/000085425|porphyria cutanea tarda}} Other sources include a third type,{{Cite journal |last=Méndez |first=M. |last2=Poblete-Gutiérrez |first2=P. |last3=García-Bravo |first3=M. |last4=Wiederholt |first4=T. |last5=Morán-Jiménez |first5=M.J. |last6=Merk |first6=H.F. |last7=Garrido-Astray |first7=M.C. |last8=Frank |first8=J. |last9=Fontanellas |first9=A. |last10=Enríquez De Salamanca |first10=R. |year=2007 |title=Molecular heterogeneity of familial porphyria cutanea tarda in Spain: Characterization of 10 novel mutations in the UROD gene |journal=British Journal of Dermatology |volume=157 |issue=3 |pages=501–7 |doi=10.1111/j.1365-2133.2007.08064.x |pmid=17627795 |s2cid=43785629 |hdl-access=free |hdl=11268/5436}} but this is less common.

One study used 74% as the cutoff for UROD activity, with those patients under that number being classified as type II, and those above classified as type III if there was a family history, and type I if there was not.{{Cite journal |last=Cruz-Rojo |first=J |last2=Fontanellas |first2=A |last3=Morán-Jiménez |first3=M. J. |last4=Navarro-Ordóñez |first4=S |last5=García-Bravo |first5=M |last6=Méndez |first6=M |last7=Muñoz-Rivero |first7=M. C. |last8=De Salamanca |first8=R. E. |year=2002 |title=Precipitating/aggravating factors of porphyria cutanea tarda in Spanish patients |journal=Cellular and Molecular Biology (Noisy-le-Grand, France) |volume=48 |issue=8 |pages=845–52 |pmid=12699242}}

Genetic variants associated with hemochromatosis have been observed in PCT patients,{{Cite journal |last=Frank |first=J |last2=Poblete-Gutiérrez |first2=P |last3=Weiskirchen |first3=R |last4=Gressner |first4=O |last5=Merk |first5=H. F. |last6=Lammert |first6=F |year=2006 |title=Hemochromatosis gene sequence deviations in German patients with porphyria cutanea tarda |url=http://www.biomed.cas.cz/physiolres/pdf/55%20Suppl%202/55_S75.pdf |journal=Physiological Research |volume=55 |issue=Suppl 2 |pages=S75–83 |doi=10.33549/physiolres.930000.55.S2.75 |pmid=17298224 |s2cid=1787139}} which may help explain inherited PCT not associated with UROD.

Since PCT is a chronic condition, a comprehensive management of the disease is the most effective means of treatment. Primarily, it is key that patients diagnosed with PCT avoid alcohol consumption, iron supplements, excess exposure to sunlight (especially in the summer), as well as estrogen and chlorinated cyclic hydrocarbons, all of which can potentially exacerbate the disorder. Additionally, the management of excess iron (due to the commonality of hemochromatosis in PCT patients) can be achieved through phlebotomy, whereby blood is systematically drained from the patient. A borderline iron deficiency has been found to have a protective effect by limiting heme synthesis. In the absence of iron, which is to be incorporated in the porphyrin formed in the last step of the synthesis, the mRNA of erythroid 5-aminolevulinate synthase (ALAS-2) is blocked by attachment of an iron-responsive element (IRE) binding cytosolic protein, and transcription of this key enzyme is inhibited.{{Cite journal |last=Thunell |first=S |year=2000 |title=Porphyrins, porphyrin metabolism and porphyrias. I. Update |journal=Scandinavian Journal of Clinical and Laboratory Investigation |volume=60 |issue=7 |pages=509–40 |doi=10.1080/003655100448310 |pmid=11202048 |s2cid=8470078}}

Low doses of antimalarials can be used.{{Cite journal |last=Singal |first=Ashwani K. |last2=Kormos–Hallberg |first2=Csilla |last3=Lee |first3=Chul |last4=Sadagoparamanujam |first4=Vaithamanithi M. |last5=Grady |first5=James J. |last6=Freeman |first6=Daniel H. |last7=Anderson |first7=Karl E. |year=2012 |title=Low-Dose Hydroxychloroquine is as Effective as Phlebotomy in Treatment of Patients with Porphyria Cutanea Tarda |journal=Clinical Gastroenterology and Hepatology |volume=10 |issue=12 |pages=1402–9 |doi=10.1016/j.cgh.2012.08.038 |pmc=3501544 |pmid=22985607}} Orally ingested chloroquine is completely absorbed in the gut and is preferentially concentrated in the liver, spleen, and kidneys.{{Cite web |title=Enforcement Reports |url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/006002s043lbl.pdf%7B%7Bfull+citation+needed%7Cdate=December+2016%7D%7D |url-status=dead |archive-url=https://web.archive.org/web/20220726225643/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/006002s043lbl.pdf%7B%7Bfull+citation+needed%7Cdate=December+2016%7D%7D |archive-date=2022-07-26 |access-date=2022-07-26 |website=www.accessdata.fda.gov}} They work by removing excess porphyrins from the liver via increasing the excretion rate by forming a coordination complex with the iron center of the porphyrin as well as an intramolecular hydrogen bond between a propionate side chain of the porphyrin and the protonated quinuclidine nitrogen atom of either alkaloid.{{Cite journal |last=De Villiers |first=Katherine A. |last2=Gildenhuys |first2=Johandie |last3=Le Roex |first3=Tanya |year=2012 |title=Iron(III) Protoporphyrin IX Complexes of the Antimalarial Cinchona Alkaloids Quinine and Quinidine |journal=ACS Chemical Biology |volume=7 |issue=4 |pages=666–71 |doi=10.1021/cb200528z |pmid=22276975}} Due to the presence of the chlorine atom, the entire complex is more water-soluble allowing the kidneys to preferentially remove it from the blood stream and expel it through urination.{{Cite journal |last=Asghari-Khiavi |first=Mehdi |last2=Vongsvivut |first2=Jitraporn |last3=Perepichka |first3=Inna |last4=Mechler |first4=Adam |last5=Wood |first5=Bayden R. |last6=McNaughton |first6=Don |last7=Bohle |first7=D. Scott |year=2011 |title=Interaction of quinoline antimalarial drugs with ferriprotoporphyrin IX, a solid state spectroscopy study |journal=Journal of Inorganic Biochemistry |volume=105 |issue=12 |pages=1662–9 |doi=10.1016/j.jinorgbio.2011.08.005 |pmid=22079977}}{{Cite journal |last=Alumasa |first=John N. |last2=Gorka |first2=Alexander P. |last3=Casabianca |first3=Leah B. |last4=Comstock |first4=Erica |last5=De Dios |first5=Angel C. |last6=Roepe |first6=Paul D. |year=2011 |title=The hydroxyl functionality and a rigid proximal N are required for forming a novel non-covalent quinine-heme complex |journal=Journal of Inorganic Biochemistry |volume=105 |issue=3 |pages=467–75 |doi=10.1016/j.jinorgbio.2010.08.011 |pmc=3010338 |pmid=20864177}} Chloroquine treatment can induce porphyria attacks within the first couple of months of treatment due to the mass mobilization of porphyrins from the liver into the blood stream. Complete remission can be seen within 6–12 months as each dose of antimalarial can only remove a finite amount of porphyrins and there are generally decades of accumulation to be cleared. Originally, higher doses were used to treat the condition but are no longer recommended because of liver toxicity.{{Cite journal |last=Sweeney |first=G. D. |last2=Saunders |first2=S. J. |last3=Dowdle |first3=E. B. |last4=Eales |first4=L |year=1965 |title=Effects of Chloroquine on Patients with Cutaneous Porphyria of the "symptomatic" Type |journal=British Medical Journal |volume=1 |issue=5445 |pages=1281–5 |doi=10.1136/bmj.1.5445.1281 |pmc=2166040 |pmid=14278818}}{{Cite journal |last=Scholnick |first=Perry L. |last2=Epstein |first2=John |last3=Marver |first3=Harvey S. |year=1973 |title=The Molecular Basis of the Action of Chloroquine in Porphyria Cutanea Tarda |journal=Journal of Investigative Dermatology |volume=61 |issue=4 |pages=226–32 |doi=10.1111/1523-1747.ep12676478 |pmid=4744026 |doi-access=free}} Finally, due to the strong association between PCT and Hepatitis C, the treatment of Hepatitis C (if present) is vital to the effective treatment of PCT.

Chloroquine, hydroxychloroquine, and venesection are typically employed in the management strategy.{{Cite journal |last=Sarkany |first=R. P. E. |year=2001 |title=The management of porphyria cutanea tarda |journal=Clinical and Experimental Dermatology |volume=26 |issue=3 |pages=225–32 |doi=10.1046/j.1365-2230.2001.00825.x |pmid=11422163 |s2cid=35585037}}

PCT prevalence is estimated at 1 in 10,000.{{Cite book |last=Arceci |first=Robert. |title=Pediatric hematolog |last2=Hann |first2=Ian M. |last3=Smith |first3=Owen P. |publisher=Blackwell |year=2006 |isbn=978-1-4051-3400-2 |location=Malden MA}}{{page needed|date=December 2016}} An estimated 80% of porphyria cutanea tarda cases are sporadic. The exact frequency is not clear because many people with the condition never experience symptoms and those that do are often misdiagnosed with anything ranging from idiopathic photodermatitis and seasonal allergies to hives.{{citation needed|date=September 2021}}

{{Reflist}}

• {{RareDiseases|7433|Porphyria cutanea tarda}}

{{Medical resources

| DiseasesDB = 10376

| ICD10 = {{ICD10|E|80|1|e|70}}

| ICD9 = {{ICD9|277.1}}

| ICDO =

| OMIM = 176100

| MedlinePlus =

| eMedicineSubj = derm

| eMedicineTopic = 344

| MeshID = D017119

| Orphanet = 101330

|ICD11={{ICD11|5C58.10}}|NORD=porphyria-cutanea-tarda|GARDNum=7433|GARDName=porphyria-cutanea-tarda}}

{{Diseases of the skin and appendages by morphology}}

{{Vesiculobullous disease}}

{{Heme metabolism disorders}}

Category:Alcohol and health

Category:Autosomal dominant disorders

Category:Hepatitis C virus-associated diseases

Category:Porphyrias

Category:Skin conditions resulting from errors in metabolism

Category:Rare diseases