Royal Brisbane Hospital, Brisbane, Queensland, Australia

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Publications (5)38.95 Total impact

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    ABSTRACT: Abstract In order to test the hypothesis that serum levels of the amino terminal propeptide of type III procollagen (PPCP III) reflect hepatic fibrosis, we have studied PPCP III levels in 30 patients with genetic haemochromatosis (GH), a disease which is characterized by progressive fibrosis without significant inflammation or necrosis. Patients with alcoholic liver disease and chronic hepatitis were included as comparative diseases in which fibrosis occurs concurrently with inflammation and necrosis. Of 13 GH cases with cirrhosis, four (30%) had normal serum PPCP III levels, while of 17 GH cases without cirrhosis, two (12%) had elevated levels. The mean serum concentrations of the cirrhotic and non-cirrhotic GH groups were not significantly different when patients with excessive alcohol consumption (> 80 g/day) were excluded from the GH groups. In 29 subjects with alcoholic liver disease, serum PPCP III correlated significantly with both fibrosis (P < 0.01) and necrosis (P < 0.02) but not with inflammation. In 23 subjects with chronic hepatitis, PPCP III levels correlated significantly with inflammation when assessed histologically (P < 0.01) or as reflected by serum AST (P < 0.01), but not with fibrosis or necrosis. Furthermore, the correlation between PPCP III and inflammation was not strengthened when the three features (inflammation, necrosis and fibrosis) were combined into a single variable. We conclude that elevated PPCP III levels in chronic liver disease do not reflect solely the extent of fibrosis but are also influenced by inflammation and necrosis and are thus of limited clinical value in predicting hepatic histopathology.
    No preview · Article · Mar 2008 · Journal of Gastroenterology and Hepatology
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    ABSTRACT: 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.
    No preview · Article · Mar 2008 · Journal of Gastroenterology and Hepatology
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    ABSTRACT: The pathogenesis of hepatic fibrosis and cirrhosis in genetic hemochromatosis may involve a direct effect of excess iron on collagen synthesis in the liver. To investigate this theory, we measured procollagen messenger RNA levels (types I, III and IV) in the livers of rats in which we produced chronic parenchymal iron overload by feeding them dietary carbonyl iron (2.5%, wt/wt) for up to 18 mo. This feeding resulted in predominantly parenchymal iron deposition in a periportal distribution similar to that seen in genetic hemochromatosis. Increased amounts of collagen fibrils were observed in iron-loaded livers on electron microscopy; all iron-loaded livers showed some periportal fibrosis. Although very high hepatic iron concentrations (range = 340 to 1,100 mumol/gm dry wt) were achieved in the carbonyl iron-loaded rats, we saw no consistent difference between steady-state messenger RNA levels for procollagens types I, III and IV in control and iron-loaded livers examined at five different time points up to 18 mo. Messenger RNA levels of the cytokine transforming growth factor-beta 1, which has been implicated as having a role in the production of extracellular matrix proteins, were also measured. No significant differences were observed between iron-loaded and control livers. These results suggest that excess parenchymal iron does not have a direct effect on the expression of the procollagens or transforming growth factor-beta 1 genes in iron-loaded livers and that factors other than, or in addition to, iron are necessary for fibrosis to occur.
    No preview · Article · Oct 1993 · Hepatology
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    ABSTRACT: A comparison of the antioxidant protective system and presence of lipid peroxidation was made between rats iron-loaded by two different mechanisms. Superoxide dismutase activity, glutathione peroxidase activity, and reduced glutathione concentrations, together with malondialdehyde production, were measured in the livers of rats chronically iron-overloaded by (a) parenteral iron (primarily Kupffer cell iron deposition) and (b) dietary carbonyl iron (mainly parenchymal iron deposition). In carbonyl iron-treated rats, hepatic superoxide dismutase activity was significantly decreased, whereas hepatocyte lipid peroxidation, as measured by malondialdehyde levels, was significantly increased when compared with control rats at or above iron concentrations of 100 and 185 mumol/g dry wt, respectively. However, no significant decrease in superoxide dismutase activity or significant increase in malondialdehyde levels was observed in iron dextran-treated rats. Glutathione peroxidase activities and reduced glutathione concentrations in rats, iron-loaded by either method, were not significantly different from those of control animals. These results suggest that the deposition of iron in the reticuloendothelial cells of the liver does not lead to lipid peroxidation; however, iron deposited in the parenchymal cells of the liver may lead to an altered free radical antioxidant protective system, resulting in lipid peroxidation in these cells at a similar level of iron loading. We conclude that the cellular site of iron deposition as well as the hepatic iron concentration is important in determining iron-induced liver injury.
    No preview · Article · Nov 1989 · Gastroenterology
  • P C Adams · F D Roberts · L W Powell · J W Halliday

    No preview · Article · Jul 1988 · Journal of Chromatography A

Publication Stats

64 Citations
38.95 Total Impact Points


  • 1988-2008
    • Royal Brisbane Hospital
      • Department of Medicine
      Brisbane, Queensland, Australia
  • 1993
    • Queensland Institute of Medical Research
      Brisbane, Queensland, Australia