OBJECTIVE: To assess the clinical significance of the changes of cardiac troponin I (cTnl) in Kawasaki disease (KD) before and after the treatment with intravenous immunoglobulins (IVIG). METHODS: Concentrations of serum cTnl, Creatine kinase (CK), Lactic dehydrogenase (LDH) and Glutamic oxalacetic transaminase (GOT) were measured in the KD group (n=58) before and after the treatment with IVIG and in the control group (n=23). RESULTS: ① There was no significant difference in serum CK, LDH and GOT concentrations between the KD group and the control group (P>0.05). There was significant difference in the serum concentrations of cTnl between the two groups ［(0.62±1.08) μg/L vs (0.06±0.06) μg/L］( P<0.01). ② There was significant difference in cTnl before and after the treatment with IVIG ［(0.62±1.08) μg/L vs (0.08±0.15) μg/L］(P<0.01). But no significant difference was found in CK, LDH and GOT before and after the treatment with IVIG (P>0.05). CONCLUSIONS: The measurement of cTnl may be a useful serologic test for the early diagnosis of myocarditis or myocardial cell injury. Early IVIG therapy can prevent cardiovascular pathology in KD patients and cTnl can be used as an index to evaluate the effect of the treatment with IVIG.
OBJECTIVE: To investigate the value of cardiac troponin I (cTnI) compared with creatine kinase isoenzymes (CK-MB) in the diagnosis and progress of myocarditis in children. METHODS: Serum samples from 38 children with viral myocarditis, 24 children with non myocarditis disease and 22 healthy controls were examined for cTnI by the rapid immunochromatographic test and CK-MB was examined by enzymatic velocity analysis. CVB1-6 IgM was determined using ELISA. RESULTS: The positive rates of cTnI and CK-MB in the myocarditis group were 89.5% and 60.5%, which were significantly higher than those in the nonmyocarditis group (8.3% and 29.2% respectively) and healthy control group (0) (P<0.05). 82.4% of positive cTnI occurred within one week of the onset. There were no differences in the positive rates of cTnI and CK-MB between the CVB1-6 IgM positive group and the negative one. CONCLUSIONS: The sensitivity and specificity of cTnI in the diagnosis of myocardial injury are superior to the CK-MB test and the diagnostic window of cTnI may be wider. cTnI appears to be an excellent new clinical marker for the diagnosis and the evaluation of prognosis of myocarditis.
OBJECTIVE: To study serum insulin like growth factor I (IGF-I) and IGF-I binding protein 3 (IGFBP-3) in children with type I diabetes mellitus (DM) and to explore the relationship between GH IGF-I axis and blood sugar. METHODS: ELISA and immunoradioassay were used respectively for IGF-I and IGFBP-3 determination in 63 children with type I DM and 47 normal children. RESULTS: ①Before puberty, there was no statistical difference in serum levels of IGF-I and IGFBP-3 between the diabetic group and control group; but in puberty, serum levels of IGF-I［(178.2±65.9) ng/ml］ and IGFBP-3［(2 956.0±847.6) ng/ml］ in the diabetic group were significantly lower than those of the control group ［(229.6±54.5) ng/ml, (3 393.2±748.9) ng/ml］(P<0.01 or 0.05). ② Serum levels of IGF-I andIGFBP-3 ［(143.0±67.5) and (2 740.0±449.8) ng/ml］ were elevated in children with recent onset type I DM after insulin therapy compared with the pre treatment group ［(54.8±44.3) and (2 233.8±336.2) ng/ml］(P<0.05). ③ In the diabetic group, HbA IC was negatively correlated to serum levels of IGF-I (r=-0.32, P<0.01) and IGFBP-3 (r=-0.29, P<0.05). ④ In the diabetic group, HbAIC and insulin dose in puberty were higher than those in prepuberty ［(9.0±1.8)% vs (7.8±1.8)%, (0.86±0.30) U/kg vs (0.64±0.38) U/kg］(P<0.05). CONCLUSIONS: Serum levels of IGF-I and IGFBP-3 decrease in children with type I DM, especially during puberty. This suggests that GHIGF-I axis is severely disturbed in these adolescents, probably an important cause of poor blood sugar control.
OBJECTIVE: To observe the effect of gangliosides (GM1) on the apoptosis and expression of Bax and Bcl-2, two genes involved in apoptosis. METHODS: An HIE model was produced in 7day old SpragueDawley (SD) rats by unilateral carotid artery ligation followed by hypoxic insult (8% oxygen) for 2.5 hours. Six of these HIE rats were treated promptly with GM1 (30 mg/kg daily for 3 days) and 6 were not given any treatment as the controls. Apoptosis was examined using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining and the expression of Bax and Bcl-2 was detected by the immunohistochemical streptoavidinbiotinperoxidase complex (SABC) method in all neonatal rats. RESULTS: Apoptosis was noted in the cerebral neurons of the neonatal rats after HI injuries. Apoptosis secondary to HI could be eliminated with prompt treatment with GM1 after the HI insult. The number of apoptotic cells in the cortex and hippocampus decreased from 75.25±4.94 and 47.25±6.6 to 55.75±6.71 and 32.14±4.88 respectively (P<0.01). Bax and Bcl-2 were expressed in all neonatal rats. Bax was expressed to a greater extent and Bcl-2 to a lesser extent in HIE neonatal rats compared with neonatal rats with prompt treatment with GM1(P<0.05). CONCLUSIONS: Prompt treatment with GM1 after HI injuries in neonatal rats results in decreased neuronal apoptosis. GM1 could partly affect the expression of Bax and Bcl-2. The results suggest that neonatal neuronal apoptosis after HI injuries may be related to changes in the expression of these two genes.
