Prolylhydroxylase and procollagen type III in long-term survivors of acute lymphoblastic leukemia (ALL): A biochemical approach to HCV-related liver disease
✍ Scribed by Leonardi, Salvatore ;La Spina, Milena ;La Rosa, Mario ;Schilirò, Gino
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 65 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0098-1532
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✦ Synopsis
Abstract
Background
We examined two proteins, prolylhydroxylase (hPH) and procollagen type III (PIIIP), as possible non‐invasive HCV‐related markers of liver disease. The purpose of this study was to assess whether the measurement of these proteins could serve to monitor HCV related liver damage in acute lymphoblastic leukaemia (ALL) patients.
Procedure
A total of 34 ALL patients, 24 HCV‐seropositive and 10 HCV‐seronegative, who had had increased transaminase values (ALT) for almost 6 months were studied. Serum hPH concentrations were determined by an immuno‐enzymatic assay kit. PIIIP was assayed by the radioimmunoassay method.
Results
Both hPH and PIIIP were increased in ALL patients with chronic hepatitis C. Serum hPH levels were significantly elevated in those with chronic hepatitis C with either normal or high transaminases when compared to those who never were HCV seropositive. The sensitivity and specificity of these protein measurements to evaluate hepatic fibrosis were not supported by histologic confirmation because only 6 out of 12 patients with chronic hepatitis had a liver biopsy.
Conclusions
Our study suggests that PIIIP and hPH values are significantly higher in ALL patients with chronic HCV with either normal or high transaminases. This might suggest that the liver damage is more marked in patients with chronic hepatitis and that the liver damage is related to the HCV rather than chemotherapy. Future studies correlating histologic findings with the serum biochemical markers are required to establish the sensitivity and specificity of hPH and PIIIP in predicting hepatic fibrosis and to confirm this association. Med Pediatr Oncol 2003;41:17–20. © 2003 Wiley‐Liss, Inc.