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porphyria cutanea tarda/albumin
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[Zinc and porphyria cutanea tarda].
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In 30 patients affected by Porphyria Cutanea Tarda we determined: plasmatic, erythrocytary and urinary zinc (by atomic absorption spectrophotometry); total porphyrins in plasma and in urines, coproporphyrins and protoporphyrins in erythrocytes (by spectrophotometric methods); haptoglobin, hemopexin,
[Treatment of porphyria cutanea tarda using plasma exchange].
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Results in the treatment of 5 patients with porphyria cutanea tarda by plasma exchange are presented. The procedure was applied every second or third day, 2-4 procedures in total. Saline solution, 5% or 12% albumin were used as plasma substitutes. The treatment lead to rapid fall in urine porphyrin
Correlation between levels of free and protein-bound plasma porphyrin and urinary porphyrins in porphyria cutanea tarda.
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Porphyria cutanea tarda (PCT) is a disorder of porphyrin metabolism that leads to massive overproduction and excretion of uroporphyrin. Most plasma porphyrins are bound to albumin and hemopexin. The aim of this work was to analyze the relationship between the concentrations of serum albumin and
Iron and porphyria cutanea tarda.
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In order to evaluate the pathogenetic role of iron in Porphyria cutanea tarda (PCT), the metabolism of iron was studied in 440 patient with PCT and associated chronic liver disease (CLD) and in 91 nonporphyric CLD patients (used as a control group). The parameters considered were the following:
Depletion of histidine and tryptophan serum levels in porphyria cutanea tarda and congenital erythropoietic porphyria patients after irradiation with visible light.
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We have studied the photosensitized oxidation, via singlet oxygen production, of histidine (His) and tryptophan (Trp) in the serum of porphyria patients and in the serum of healthy volunteers before or after addition of hematoporphyrin. It was observed that free plasma His and Trp are good probes of
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location.
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These studies try to elucidate why isocoproporphyrin appears in hexachlorobenzene-poisoned rats' feces. Chronic exposure of hexachlorobenzene to rats produces an experimental model for human porphyria cutanea tarda. After 8 weeks of treatment, rats showed high porphyrin excreta and 50% inhibition of
Urinary porphyrin excretion in hepatitis C infection.
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A high prevalence of hepatitis C virus infection in porphyria cutanea tarda in some populations suggests a close link between viral hepatitis and alteration of porphyrin metabolism. Moreover, there is evidence of a role of porphyrinopathies in hepatocarcinogenesis. The aim of our study was to obtain
Effect of hepatobiliary disease, chronic hepatitis C and hepatitis B virus infections and interferon-alpha on porphyrin profiles in plasma, urine and faeces.
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BACKGROUND
Documentation of the profiles of porphyrins in hepatobiliary disease is limited. Strong associations of hepatitis B and C virus infections with porphyria cutanea tarda have suggested causal relationships. This study aimed to determine the nature of porphyrin abnormalities in hepatobiliary
Iron and the liver.
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Iron is essential for life, but iron overload is toxic and potentially fatal. The liver is a major site of iron storage and is particularly susceptible to injury from iron overload, especially when (as in primary hemochromatosis) the iron accumulates in hepatocytes. Iron can be taken up by the liver
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