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Serum procollagen‐III‐peptide in chronic hepatitis and schistosomiasis
Author(s) -
ROBERTS F. D.,
HALLIDAY J. W.,
COOKSLEY W. G. E.,
SANDFORD N.,
KARAWI M.,
SHAHED M.,
MOHAMED A.,
POWELL L. W.
Publication year - 1986
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1986.tb00130.x
Subject(s) - fibrosis , medicine , schistosomiasis , hepatic fibrosis , inflammation , gastroenterology , liver disease , hepatitis , immunology , endocrinology , pathology , helminths
Abstract Recent reports have suggested that the serum concentration of procollagen‐III‐peptide (PPCP III) reliably reflects the degree of hepatic fibrosis but the topic remains controversial. Serum PPCP III levels have been measured in 40 patients with chronic hepatitis or schistosomiasis. In five patients both diseases were present. The relationship between serum PPCP III levels, hepatic fibrosis and disease activity have been studied histologically and biochemically. The mean serum concentration of PPCP III in patients with chronic hepatitis and in those with active liver disease was significantly higher than that in patients with inactive liver disease. In patients with chronic hepatitis only, serum PPCP III levels correlated with fibrosis, inflammation, and necrosis and also with the combined histological scores. When patients with schistosomiasis as well as hepatitis were included, significant correlations were still observed. In patients with schistosomiasis only, the serum PPCP III levels varied widely and did not correlate with disease activity or with the degree of inflammation, necrosis and fibrosis, either separately or combined. Serum PPCP III concentrations only correlated with serum aspartate amino transferase levels when the patient groups were combined. Serial measurements in 21 patients showed that PPCP III levels varied widely over a short period of time, and that these fluctuations did not significantly correlate with the respective changes in serum AST levels. In conclusion, serum PPCP III concentrations do not reliably reflect hepatic fibrosis, they are influenced by inflammation and activity of the disease, and they probably reflect the end result of the metabolic state of collagen in the liver, that is the combined effect of synthesis and degradation.

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