الفهرس 
Bone Marrow Transplant in ChildrenOnly 14 pages are availabe for public view
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Abstract
Iron overload is a common finding in in HSCT recipients and it had many possible etiologies including decreased utilization of iron due to ineffective erythropoeisis, release of iron from injuried tissues, increased intestinal absorption of iron secondary to mucositis and GVHD, hepatic co-morbidities as CHC, this is in addition to blood transfusions.
Hepatic IO is a frequent histopathologic finding among HSCT recipients especially those with CHC. It can mimic or precipitate GVHD, and it can also change the natural course of viral hepatitis.
This study was carried out to estimate the degree of different forms of iron overload (serum & hepatic forms) and its related sequalae in 30 children who underwent successful allogeneic and autologous bone marrow transplantation for hematologic or malignant disorders and who showed persistent abnormal liver functions 6mths after discontinuation of immune suppressive therapy or after local control respectively.
All the studied patients (30/30) were HCV-infected, 3 of them were HBV co-infected. They were all chelation -naïve.
Liver functions were monthly evaluated. Quantitative HCV & HBV PCR were re-assessed for those children whose liver enzymes revealed a striking elevation that could not be attributed to a BMT event as GVHD, disease recurrence or a drug –induced liver dysfunction.
Serum form of iron overload was assessed every three months through evaluation of mean levels of serum ferritin.
U/S guided liver biopsy was set for all children to assess the degree of hemosiderosis, fibrosis, necroinflammation, steatosis, cholestasis, as well as, hepatic GVHD in those with the clinically apparent signs of chronic GVHD.
All liver biopsy events were uncomplicated and no adverse or serious adverse events were reported.
Higher mean levels of serum ferritin were encountered in children who had undergone allogeneic BMT than in the auto-transplanted group of children.
It was also observed that patients with frequent hepatitis flares (>3 times), hepatic GVHD, higher grades of HCV viremia had higher mean levels of serum ferritin (> 1000ng/ml). These findings were confirmed after histologic hepatic evaluation that revealed a strong significant correlation between raised serum ferritin levels, high HCV viremia, clinical GVHD & advanced degrees of hemosiderosis, necroinflammation.
Advanced degrees of hepatic fibrosis were obviously found in BMT recipients with advanced degrees of hemosiderosis and in those with concomitant HBV-HCV infection rather than the group with only HCV infection.
The extent of hepatic necroinflammation was directly affected by higher levels of HCV viremia rather than by the frequency of hepatitis flares.
In conclusion, a significant correlation between serum ferritin & hepatic IO in HSCT recipients can be confirmed which warrants validation of serum ferritin as surrogate marker of hepatic IO in these patients.
It can be also concluded that serum ferritin is strongly and independently associated with advanced liver fibrosis and necroinflammation in HSCT recipients with chronic viral hepatitis.
Consequently, it can be confined that U/S guided liver biopsy can be considered a very valuable diagnostic tool in case of overlapping clinical etiologies of LD with minimal complication rate in the non- thrombocytopenic patient during late post-BMT period.