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Introduction: CTLA-4 gene polymorphism plays an important role in children with type 1 diabetes mellitus (T1DM). However, data on this subject vary among different races and ethnics. Purpose: To analyze CTLA-4 CT-60 A/G and CTLA-4 1822 C/T gene polymorphism among children with T1DM compared to control. Patients and Methods: The CTLA-4 CT-60 A/G and CTLA-4 1822 C/T gene polymorphism in children with T1DM using polymerase chain reaction-restriction fragment length polymorphism in 25 T1DM and 25 controls. The inclusion criteria were patients regularly controlled at the Pediatric Endocrine Outpatient Clinic of Dr. Soetomo Hospital, aged 4-18 years and willing to join this study and the exclusion criteria were T1DM patients hospitalized in the pediatric intensive care unit. In the control group, the inclusion criteria were healthy children, aged 4-18 years and willing to join this study. The exclusion criteria included children with ongoing infection, history of other autoimmune diseases, allergies, or malignancy. Results: The mean age was 12.48 years old, and the mean of T1DM onset was 9.28 years old. The CTLA-4 1822 T allele observed in 62% T1DM and 56% in control (p = 0.388, OR = 0.78, 95% CI = 0.44-1.37) and CTLA-4 CT-60 G allele observed in 52% T1DM and 58% in control (p = 0.393, OR = 1.27, 95% CI = 0.73-2.22). The C/T genotypes was significantly higher in control group (p = 0.045, OR = 3.27, 95% CI = 1.00-10.62). The A/G genotypes was commonly found in control group (p = 0.765, OR = 1.20, 95% CI = 0.37-3.86). The Javanese was the dominant ethnic group in our study. Conclusion: The frequency of CTLA-4 CT-60 A/G polymorphism almost equivalent in T1DM and control group. However, CTLA-4 1822 C/T polymorphism was more prevalent in the control group; thus, this genotype may have a protective effect against T1DM.
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BACKGROUND: Over the past 10 years, infection has remained as the main cause of illness and mortality among children with Acute Lymphoblastic Leukemia on chemotherapy. The high incidence of Hospital-Acquired Pneumonia in children with Acute Lymphoblastic Leukemia on chemotherapy with risk factors should be intervened earlier. METHODS: An observational case control study of children with Acute Lymphoblastic Leukemia on chemotherapy. Patient with Hospital-Acquired Pneumonia considered as case and patient without Hospital-Acquired Pneumonia as control to analyze risk factors that affect the incidence of Hospital-Acquired Pneumonia in children with Acute Lymphoblastic Leukemia on chemotherapy from 2016 to 2018 was performed in the pediatric ward Dr. Soetomo General Academic Hospital with a total sampling technique. Nine risk factors were analyzed: age, gender, nutritional status, length of stay, risk stratification, chemotherapy phase, anemia, neutropenia, and thrombocytopenia. Bivariate and multivariate analysis using chi-square, continuity correction, and logistic regression was used for statistical analysis. RESULTS: 120 children enrolled the study. Analyzed of risk factors showed risk stratification (p = 0.009), chemotherapy phase (p < 0.001), and neutropenia (p < 0.001) was proven to significantly affect the incidence of Hospital-Acquired Pneumonia in children with Acute Lymphoblastic Leukemia on chemotherapy. Age, gender, nutritional status, length of stay, anemia, and thrombocytopenia were not proven to be a risk factor that affects the incidence of Hospital-Acquired Pneumonia in children with Acute Lymphoblastic Leukemia on chemotherapy. CONCLUSION: The incidence of Hospital-Acquired Pneumonia in children with Acute Lymphoblastic Leukemia on chemotherapy is significantly affected by the risk stratification, chemotherapy phase, and neutropenia.
RESUMEN
The human influenza A virus (H3N2) has been the predominant influenza strain since 1992, and one property of this virus is non-agglutination of chicken erythrocytes [Ch(-) virus]. The Ch(-) virus in our study was able to acquire chicken hemagglutination [Ch(+)] by trypsin passage but not by chymotrypsin passage. Moreover, the trypsin-passaged Ch(+) viruses reacquired the Ch(-) property after a further chymotrypsin passage. In particular, genetic analysis showed no evidence of mutations in the hemagglutinin (HA) gene during either trypsin or chymotrypsin passages: the only differences found were in the HA cleavage sites between the trypsin-passaged virus and the chymotrypsin-passaged virus as determined by the N-terminal amino acid sequence. These results suggested that protease-dependent differences at the viral HA cleavage site, rather than genetic mutations, are likely to have a significant effect on the viral ability to produce chicken hemagglutination.
