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Blood, 1 July 2002, Vol. 100, No. 1, pp. 17-21
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Effects of iron overload and hepatitis C virus positivity in
determining progression of liver fibrosis in thalassemia following bone
marrow transplantation
Emanuele Angelucci,
Pietro Muretto,
Antonio Nicolucci,
Donatella Baronciani,
Buket Erer,
Javid Gaziev,
Marta Ripalti,
Pietro Sodani,
Silvia Tomassoni,
Giuseppe Visani, and
Guido Lucarelli
From the Unità Operativa di Ematologia e Centro
Trapianto di Midollo Osseo di Muraglia and the Unità Operativa di
Anatomia Patologica, Azienda Ospedale di Pesaro; and the Dipartimento
di Farmacologia Clinica ed Epidemiologia Consorzio Mario Negri Sud,
Santa Maria Imbaro, Chieti, Italy.
To identify the role of iron overload in the natural history of
liver fibrosis, we reviewed serial hepatic biopsy specimens taken
annually from patients cured of thalassemia major by bone marrow
transplantation. The patients underwent transplantation between 1983 and 1989 and did not receive any chelation or antiviral therapy. Two
hundred eleven patients (mean age, 8.7 ± 4 years) were evaluated for
a median follow-up of 64 months (interquartile range, 43-98 months) by
a median number of 5 (interquartile range, 3-6) biopsy samples per
patient. Hepatic iron concentration was stratified by tertiles (lower,
0.5-5.6 mg/g; medium, 5.7-12.7 mg/g; upper, 12.8-40.6 mg/g dry weight).
Forty-six (22%) patients showed signs of liver fibrosis progression;
the median time to progression was 51 months (interquartile range,
36-83 months). In a multivariate Cox proportional hazard model, the
risk for fibrosis progression correlated to medium hepatic iron content (hazard rate, 1.9; 95% confidence interval [CI], 0.74-5.0), high hepatic iron content (hazard rate, 8.7; 95% CI, 3.6-21.0) and hepatitis C virus (HCV) infection (hazard rate, 3.1; 95% CI, 1.5-6.5). A striking increase in the risk for progression was found in the presence of both risk factors. None of the HCV-negative patients with
hepatic iron content lower than 16 mg/g dry weight showed fibrosis
progression, whereas all the HCV-positive patients with hepatic iron
concentration greater than 22 mg/g dry weight had fibrosis progression
in a minimum follow-up of 4 years. Thus, iron overload and HCV
infection are independent risk factors for liver fibrosis progression,
and their concomitant presence results in a striking increase in risk.
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