MATERIALS AND METHODS: Thirty chronic schizophrenia patients were recruited for the study and their demographic data and medication dosage were noted. Symptom severity was scored on the Positive And Negative Syndrome scale for Schizophrenia (PANSS) and blood sampling done. Ten healthy Chinese males were recruited as controls. Phytohaemagglutinin-stimulated production of serum levels of IL-2 were measured by enzyme-linked immunosorbent assay.
RESULTS: IL-2 levels (1327 +/- 596.2) of all 30 patients were significantly lower than that of the Chinese controls (2420 +/- 342.5). This effect was noted throughout the entire duration of the illness. Ethnic and age differences in IL-2 levels were not found. There was, however, a negative correlation with the duration of the illness and a positive correlation with the dosage of medication.
CONCLUSIONS: The results of this study of a population of mostly Chinese patients with schizophrenia replicate an important finding. Data such as this has not been reported previously on Asians of this racial group.
METHODS: Plasma inflammatory cytokines were measured using a cytometric bead array in 87 asymptomatic young adult survivors of childhood ALL (median age, 25 years; age range, 18-35 years) who attended annual follow-up clinic and compared with healthy, age-matched and sex-matched controls. Leukocyte telomere length (LTL) was measured using Southern blot analysis.
RESULTS: Survivors had significant elevation of plasma interleukin-2 (IL-2), IL-10, IL-17a, and high-sensitivity C-reactive protein levels (all P 0.8 mg/dL) was related to increased odds of having metabolic syndrome (odds ratio, 7.256; 95% confidence interval, 1.501-35.074). Survivors also had significantly shorter LTL compared with controls (median, 9866 vs 10,392 base pairs; P = .021). Compared with published data, LTL in survivors was similar to that in healthy individuals aged 20 years older. Survivors who received cranial irradiation had shorter LTL compared with those who had not (P = .013).
CONCLUSIONS: Asymptomatic young adult survivors of childhood ALL demonstrate a biologic profile of chronic inflammation and telomere attrition, consistent with an early onset of cellular processes that drive accelerated aging. These processes may explain the premature development of age-related chronic conditions in childhood cancer survivors. Understanding their molecular basis may facilitate targeted interventions to disrupt the accelerated aging process and its long-term impact on overall health. Cancer 2017;123:4207-4214. © 2017 American Cancer Society.