![]() ![]() The GH resistance in NS children with PTPN11 mutations may contribute to short stature and their relatively poor response to rhGH 25). Several studies have reported the association between PTPN11 mutation and GH resistance by a postreceptor signaling defect 25, 26). During treatment, there were no serious adverse events including the cardiac dysfunction, hypertrophic cardiomyopathy, malignancy, hyperglycemia, or thrombocytopenia with bleeding tendency. The bone age/chronologic age ratio increased from 0.62☐.13 at the start of treatment to 0.68☐.15, 0.79☐.1, and 0.86☐.1, respectively, after 1, 2, and 3 years of treatment and the end of treatment ( P=0.02, P=0.001, and P=0.001, respectively). Serum IGFBP-3 SDS changed from –0.15☐.40 to –0.09☐.34, which was not statistically significant ( P=0.074). GV increased from 4.64☐.80 cm/yr at baseline to 6.79☑.26 and 6.41☑.54 cm/yr at the second and third years ( P=0.001 and P=0.003, respectively). GV during the first year of treatment was highest (8.57☑.49 cm/yr). Height SDS, GV, and serum IGF-1 SDS levels were significantly increased after rhGH therapy ( Table 2). The mean age at the start of treatment was 7.97☑.81 years (range, 5.7 to 11.3 years). ![]()
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