Soo Hee Chang

Ulsan University Hospital, Urusan, Ulsan, South Korea

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Publications (4)13.22 Total impact

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    ABSTRACT: There have only been a few studies on the long-term outcomes and prognostic factors after pediatric LDLT. We conducted a retrospective, single-center assessment of the outcomes as well as the demographic and clinical factors that influenced the poor outcomes in 113 children aged <16 (median age 21 months; 6 months-15.5 yr) who underwent 115 LDLTs, predominantly for biliary atresia (60.9%) and FHF (14.8%), between 1994 and 2006 at Asan Medical Center. Left lateral segment or left lobe grafts were implanted into most of these children (86.9%) according to routine procedures. The overall rates of graft survival at one, five, and 10 yr were 89.6%, 83.0%, and 81.5%, respectively, and the overall rates of patient survival were 92.9%, 86.3%, and 84.8%, respectively. Virus-related disease (41.2%) and chronic rejection (29.4%) were the major causes of mortality. On multivariate analysis, UNOS status 1a and 1b and chronic rejection were significant risk factors for both graft and patient loss, whereas the PELD score >25 was a significant risk factor for graft loss. Patient and graft survival may be related not only to post-operative complications, but also to the patient's preoperative clinical condition.
    No preview · Article · Nov 2010 · Pediatric Transplantation
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    ABSTRACT: In order to determine the influence of living donor liver transplantation (LDLT) on long-term growth, we studied the progress of 36 children who had survived more than 5 yr after LDLT from 1994 to 1999. The median age at the transplantation was 1.5 yr (range: 6 months-15 yr) and the median follow-up period was 6.5 yr (range: 5-9 yr). A height standard deviation score (zH) was analyzed for each patient according to medical records. Significant catch-up growth occurred within 2 yr after LDLT with a mean zH changing from -1.2 to 0.0 and was maintained for up to 7 yr post-transplantation (zH-0.1). Younger children (<2 yr) were more growth-retarded at the time of LDLT, but showed higher catch-up growth rates and their final zH was greater than that of older children. Children with liver cirrhosis were more growth-retarded at the time of LDLT, but showed significant catch-up growth and their final height was similar to children with fulminant hepatitis. Growth in children who experienced significant hepatic dysfunction after LDLT was not significantly different from those without graft dysfunction. There was no difference between the types of immunosuppressants used. Our finding suggests that LDLT can result in adequate catchup linear growth, and this effect can persist even after 7 yr post-transplantation.
    Full-text · Article · Nov 2005 · Journal of Korean Medical Science
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    ABSTRACT: Mucolipidosis types II and III are autosomal recessive inherited diseases caused by a deficiency in the lysosomal enzyme N-acetylglucosamine-1 phosphotransferase (GlcNAc-phosphotransferase), which adds phosphate to function as a recognition marker for the uptake and transport of lysosomal enzymes. We investigated mutations in the GNPTA (MGC4170) gene, which codes for the alpha/beta subunits of phosphotransferase, and in the GNPTAG gene, which codes for its gamma subunits in five Korean patients with mucolipidosis type II or IIIA. We identified seven mutations in the GNPTA gene, but none in GNPTAG. The mutations in type II patients included p.Q104X (c.310C>T), p.R1189X (c.3565C>T), p.S1058X (c.3173C>G), p.W894X (c.2681G>A), and p.H1158fsX15 (c.3474_3475delTA), all of which are nonsense or frameshift mutations. However, a splicing site mutation, IVS13+1G>A (c.2715+1G>A) was detected along with a nonsense or a frameshift mutation (p.R1189X or p.E858fsX3 (c.2574_2575delGA)) in two mucolipidosis type IIIA patients. This report shows that mutations in the GNPTA gene coding for the alpha/beta subunits of phosphotransferase, and not mutations in the GNPTAG gene, account for most of the genetic mutations found in Korean patients with mucolipidosis type II or IIIA.
    No preview · Article · Oct 2005 · Human Mutation
  • Sun Yeon Lee · Soo Hee Chang · Kyung Mo Kim

    No preview · Article · Apr 2004 · Gastrointestinal Endoscopy