RESUMO
<p><b>OBJECTIVE</b>To analyze the relationship between the early treatment response and the pregnosis in children with acute lymphoblastic leukemia(ALL).</p><p><b>METHODS</b>Two hundred and Seventy-eight ALL children diagnosed and treated in Hainan general hospital from March 2013 to March 2017 were collected. All ALL children received therapy with CCLg-ALL-2008 regimen. The 3 year event-free survival (EFS) rate of ALL children in different groups was analyzed in terms of 4 indexes including sensitivity response to prednison at day 8 (D8-SRP), bone marrow remission at day 15 (D15-BMR) and at day 33 (D33-BMR), and minimal residual disease at day 33 (D33-BMR), and minimal residual disease at day 33(D33-MRD). These 4 indexes and other indexes possibly affecting the prognosis of ALL children were enrolled in Cox regression model for analysis of independent factors affecting the prognosis of ALL children.</p><p><b>RESULTS</b>The D8-SRP test showed that among 269 ALL children, 240(89.22%) cases displayed prednisone poor response (PPR); the 3-year EFS rate in predrisone good response(PGR) group was significantly higher than that in PPR group(P<0.05). The D15-BMR detection showed that among 262 ALL children, the bone marrow remission(BMR) as M1 was observed in 230 cases (87.79%), M2 in 20 cases (7.63%) and M3 in 9 cases (4.58%); the 3-year EFS rate showed as follows:M1 group >M2 group >M3 group(P<0.05). The D33-BMR detection showed that among 257 ALL children, the BMR as M1 was observed in 227 cases (88.33%), M2 in 21 cses(8.17%) and M3 in 9 caes (3.51%); the 3-year EFS rate in 3 groups showed as follows: M1 group >M2 group >M3 group(P<0.05). The D33-MRD detection showed that among 185 ALL children, MRD<10 was found in 128 cases (69.19%), MRD≥10-10 in 43 cases (23.24%), MRD ≥10 in 14 cases (7.57%); the 3-year EFS rate in 3 groups showed as follows: MRD <10 group > MRD≥ 10-10 group>MRD≥10 group. The Cox regression analysis showed that PPR in D8-SRP test, M2 and M3 in D15 and D33 BMR detection, and MRD≥10 in D33 MRD detection as well as T-ALL typing were independent risk factors affecting the prognosis of ALL children.</p><p><b>CONCLUSION</b>The early treatment response can predict the prognosis of ALL children, which is an independent prognostic factor for ALL children.</p>
Assuntos
Criança , Humanos , Intervalo Livre de Doença , Neoplasia Residual , Leucemia-Linfoma Linfoblástico de Células Precursoras , Prednisona , PrognósticoRESUMO
<p><b>OBJECTIVE</b>To investigate the correlations of serum interleukin-18 (IL-18) level and IL-18 gene promoter polymorphisms to the development of sepsis in children.</p><p><b>METHOD</b>Using enzyme-linked immunosorbent assay (ELISA), the authors tested the serum IL-18 level in 90 patients with sepsis and 123 normal controls, and their single nucleotide polymorphisms of the promoter region of IL-18 gene at position -607C/A and -137G/C were detected using polymerase chain reaction with sequence specific primers method and sequencing technique.</p><p><b>RESULT</b>(1) The serum IL-18 level in sepsis groups was (196.56 +/- 157.32) pg/ml that was significantly higher than (66.16 +/- 41.63) pg/ml in normal controls (P < 0.01), the more severe the degree of sepsis was, the more significantly higher the serum IL-18 level was. The serum IL-18 level in non serious sepsis group was (152.87 +/- 114.96) pg/ml that was significantly higher than (66.16 +/- 41.63) pg/ml in normal controls, the serum IL-18 level in serious sepsis group was (191.98 +/- 169.72) pg/ml that was significantly higher than that in non serious sepsis group, and the serum IL-18 level in extremely serious sepsis patients was (323.89 +/- 159.35) pg/ml, the difference was highly significant (P = 0.000). The difference was significant among the groups with different severity of sepsis (P < 0.01). There was a negative correlation between PCIS (pediatric critical illness score) of sepsis and the serum IL-18 level (P < 0.01). (2) There were polymorphisms in IL-18 gene promoter of matched healthy children and sepsis in children. The GG genotype frequency (61.8%) of IL-18-137G/C in healthy children was the highest, followed by GC genotype (35.8%) and CC genotype (2.4%) in sequence. The G allele frequency (79.7%) was higher in IL-18-137G/C of healthy children than C allele (20.3%). The GG genotype frequency (71.1%) of IL-18-137G/C in septic children was the highest, the next were GC genotype (26.7%) and CC genotype (2.2%). The G allele frequency (84.4%) was higher in IL-18-137G/C of septic children than C allele (15.6%). The CA genotype frequency (61.0%) of IL-18-607C/A in healthy children was the highest, followed by CC genotype (26.8%) and AA genotype (12.2%). The C allele frequency (57.3%) was higher in IL-18-607C/A of healthy children than A allele (42.7%). The CA genotype frequency (76.7%) of IL-18-607C/A in septic children was the highest, followed by CC genotype (21.1%) and AA genotype (2.2%) in sequence. The C allele frequency (59.4%) was higher in IL-18-607C/A of septic children than A allele (40.6%). (3) The genotype frequency of IL-18-607 CA was 76.7% in sepsis groups that was significantly higher than 61.0% in normal controls, and the genotype frequency of -607 AA was 2.2% in sepsis groups that was significantly lower than 12.2% in normal controls, the difference was significant (P < 0.05). (4) In the order of -137CC, -137GC, -137GG, the serum IL-18 level in normal controls were as follows: (45.67 +/- 28.36) pg/ml, (53.27 +/- 37.91) pg/ml, (76.91 +/- 42.44) pg/ml, and with (140.50 +/- 60.10) pg/ml, (184.42 +/- 157.33) pg/ml, (237.02 +/- 161.76) pg/ml respectively in sepsis groups. In the order of -607AA, -607CA, -607CC, the serum IL-18 level in normal controls were: (48.80 +/- 32.11) pg/ml, (68.41 +/- 42.53) pg/ml, (70.17 +/- 43.87) pg/ml; and with (141.50 +/- 64.35) pg/ml, (151.21 +/- 121.19) pg/ml, (211.16 +/- 163.64) pg/ml respectively in sepsis groups. The difference was not significant among different groups (P > 0.05).</p><p><b>CONCLUSION</b>The serum IL-18 level in sepsis groups was significantly higher than that in normal controls, which was related to the severity of sepsis. It was possible that the genotype of -607CA carriers was susceptible to sepsis, which mean that the genotype of -607CA might be susceptible genotype of sepsis. However, the genotype of -607AA might play an oppose role in the risk of sepsis.</p>