Hepatitis C Support Group
Hepatitis C is a blood-borne viral disease which can cause liver inflammation, fibrosis, cirrhosis and liver cancer. The hepatitis C virus (HCV) is spread by blood-to-blood contact with an infected person's blood. Many people with HCV infection have no symptoms and are unaware of the need to seek treatment. Hepatitis C infects an estimated 150-200 million people worldwide.
PCT is one of the hepatic porphyrias. Large amounts of porphyrins build up in the liver when the disease is becoming active. The disease becomes active when acquired factors, such as iron, alcohol, hepatitis C virus (HCV), HIV,estrogens (used, for example, in oral contraceptives and prostate cancer treatment) and possibly smoking, combine to cause a deficiency of UROD in the liver. Hemochromatosis, an iron overload disorder, also can predispose individuals to PCT.
Symptoms
The symptoms in PCT are confined mostly to the skin. Blisters develop on sun-exposed areas of the skin, such as the hands and face. The skin in these areas may blister or peel after minor trauma. Increased hair growth, as well as darkening and thickening of the skin may also occur. Neurological and abdominal symptoms are not characteristic of PCT.
Liver function abnormalities are common but are usually mild. These sometimes progress to cirrhosis and even liver cancer. PCT is often associated with hepatitis C infection, which also can cause these liver complications. However, liver tests are generally abnormal even in PCT patients without hepatitis C infection.
Diagnosis
The preferred screening test for PCT is a measurement of porphyrins in plasma. This can differentiate PCT from variegate porphyria. The patterns of porphyrins in urine (predominately uroporphyrin and 7-carboxylate porphyrin) and feces (predominately isocoproporphyrin) help to confirm the diagnosis. The presence of an inherited deficiency of UROD can be demonstrated by measuring the enzyme in red blood cells and is present in about 20% of patients with PCT
Treatment and Prognosis
PCT is the most treatable of the porphyrias. Treatment seems to be equally effective in familial and non-familial PCT. Factors that tend to activate the disease should be removed. The most widely recommended treatment is a schedule of repeated phlebotomies (removal of blood), with the aim of reducing iron in the liver. This actually reduces iron stores throughout the body. Usually, removal of only 5 to 6 pints of blood (one pint every one to two weeks) is sufficient, which indicates that iron stores are not excessively increased in most PCT patients. The best guides to response are measurements of serum ferritin and plasma porphyrins. Phlebotomies are stopped when the ferritin falls to -~20ng/ml. Another treatment approach is a regimen of low doses of either chloroquine (125mg twice weekly) or hydroxychloroquine (100mg twice weekly). Usual dosages of these drugs should not be used because they can cause transient but sometimes severe liver damage and worsening of photosensitivity in PCT patients. Recurrences can be treated in the same manner. But PCT usually does not recur after treatment. It is not necessary to continue phlebotomies after a remission has been achieved
Personally no, but there are some that did indeed do some phlebotomy treatments here at DS.