A new type of coronavirus named as SARS-CoV-2 pandemic has begun to threaten human health. As with other types of coronaviruses, SARS-CoV-2 affects children less frequently, and it has been observed that the disease is mild. In the pathogenesis of a standard viral infection, the pathogen’s contact with the mucosa is initially followed by an innate immunity response. T cells are the primary decisive element in adaptive immunity capability. For this reason, the adaptive immune response mediated by the thymus is a process that regulates the immune response responsible for preventing invasive damage from a virus. Regulatory T cells (T-reg) are active during the early periods of life and have precise roles in immunomodulation. The thymus is highly active in the intrauterine and neonatal period; it begins to shrink after birth and continues its activity until adolescence. The loss of T-reg function by age results in difficulty with the control of the immune response, increased inflammation as shown in coronavirus disease (COVID-19) as an inflammatory storm. Also, the thymus is typically able to replace the T cells destroyed by apoptosis caused by the virus. Thymus and T cells are the key factors of pathogenesis of SARS-CoV-2 in children. Conclusion: We speculated that thymus activity and T lymphocyte function in children protect them against the virus effects. Stimulating and preventing the inhibition of the thymus can be possible treatment components against COVID-19. What is Known: • The SARS-CoV-2 infection does not often progress with an invasive clinic in children. • Thymus activity and T lymphocyte functions are highly active in children. What is New: • Effective thymus activity and T lymphocyte function in children protect them against the invasive SARS-CoV-2 infection. • Stimulating and preventing the inhibition of the thymus can be possible treatment components against COVID-19.
23 December 2019 in Journal of Paediatrics and Child Health
Objective: The purpose of this experimental study was to evaluate the efficacy of hesperidin (HES) in protecting against methotrexate (MTX)-induced intestinal damage using histopathological and immunohistochemical techniques. Materials and Methods: Seventy-eight male Wistar albino rats were divided into 4 groups that received (a) saline only (control group), n = 19; (b) HES only, n = 19; (c) MTX only, n = 19, and (d) MTX plus HES, n = 21. On the first day of the study, a single dose of MTX (20 mg/kg) was administered intraperitoneally to group 3 and 4 rats. The HES (200 mg/kg) was administered by gavage for 5 days. For the MTX plus HES group, HES (200 mg/kg) was administered by gavage for 5 days after MTX treatment. Rats were sacrificed on the 2nd, 4th and 6th day of the study. Tissue samples from the jejunum were taken for histopathological and immunohistochemical analysis. Results: On the 4th day, crypt injury in the MTX plus HES group (1.00 ± 0.00) was less than that in the MTX group (2.00 ± 0.89; p < 0.05). The small intestinal damage score was lower in the MTX plus HES group (6.33 ± 0.82) as compared to the MTX group (8.00 ± 2.37). Inducible nitric oxide synthase and interleukin-8 levels were lower in the MTX plus HES group (65 and 25%, respectively) as compared to the corresponding values of the MTX group (80 and 52.5%, respectively). On the 6th day, the Ki-67 proliferation index in the MTX group (45%) was lower than that in the MTX plus HES group (76.67%) and the control group (p < 0.05). The small intestinal damage score was high in the HES group on the 4th day due to increased cellular infiltration. On the 6th day, the Ki-67 proliferation index rose in parallel with the decrease in cellular infiltration and therefore histopathological scoring. The proliferation-enhancing effect of HES also appeared in healthy rats. Conclusion: HES seemed to have a protective effect against MTX-induced intestinal injury.
Aim: This study was planned to evaluate bone health in patients with hereditary spherocytosis. Materials and methods: In this prospective study, a total of 30 hereditary spherocytosis patients which followed in the Pediatric Hematology and Oncology Department of KSU Medical Faculty and 30 patients for control group were included. Patient and control group were chosen equal in age and sex. Hemogram and biochemical tests (serum calcium, phosphorus, alkaline phosphatase, parathormone, vitamin D) and osteocalcin were studied from the patient and control groups. Also DXA examination was performed in the patient group. Results: There was a significant difference in hemogram parameters between the two groups due to hemolytic anemia in hereditary spherocytosis patients. In the patient group, osteocalcin was 6.88 ± 4.35 ng/ml, vitamin D was 17.74 ± 7.76 ng/ml and in the control group osteocalcin was 11.93 ± 8.92 ng/ml, vitamin D was 24.04 ± 11.70 ng/ml. There was a statistically significant difference between the vitamin D and osteocalcin levels of the two groups (p = 0.017 and 0.008, respectively). Bone density was assessed in the patient group. In patients DXA results showed lower Z-scores then the normal population according to age and sex. Conclusion: Hereditary spherocytosis patients should be followed closely in terms of development, puberty, bone health as they are in other hemolytic anemias. Nutritional recommendations, vitamin D supplementation, physical activity should be advised to protect bone health.