Porphyria cutanea tarda

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Porphyria cutanea tarda is the most common porphyria and causes blistering and fragility of skin exposed to sunlight.

People have chronically recurring blisters on the sun-exposed areas of their bodies.
Excess iron can build up in the liver, causing liver damage.
Doctors test urine and stool samples for high levels of porphyrins.
Removing blood (phlebotomy), giving chloroquine (or hydroxychloroquine ), or doing both is helpful.

Porphyria cutanea tarda occurs throughout the world. There are two main types:

Type 1: Acquired or sporadic
Type 2: Hereditary or familial

In about 75 to 80% of people with porphyria cutanea tarda, the disorder does not appear to be hereditary and is called sporadic. In the remaining 20 to 25%, the disorder is hereditary and is called familial.
As far as is known, the sporadic form of this porphyria is the only porphyria that can occur in people who do not have an inherited deficiency of an enzyme involved in heme production.
Porphyria cutanea tarda results from underactivity of the enzyme uroporphyrinogen decarboxylase, which leads to accumulation of porphyrins in the liver. Liver disease is common. About 35% of people develop cirrhosis and 7 to 24% develop liver cancer. Skin damage occurs because excess porphyrins produced in the liver are transported by the blood to the skin.
Porphyria cutanea tarda has several common precipitating factors. These factors include

Excess iron in the liver
Moderate or heavy alcohol use
Smoking
Taking estrogens
Infection with hepatitis C virus

Infection with the human immunodeficiency virus (HIV) is a less common precipitating factor. These factors are thought to interact with iron and oxygen in the liver and thereby inhibit or damage the enzyme uroporphyrinogen decarboxylase.