BackgroundHigh-dose methotrexate (HD-MTX) is widely used as a standard chemotherapeutic agent in pediatric cancers. Most research studies have confirmed the therapeutic efficacy of HD-MTX; however, strategies to prevent side effects vary among institutions, especially in developing countries, with limited monitoring of plasma methotrexate level.ObjectiveTo evaluate the effect of intravenous hydration during HD-MTX administration on plasma methotrexate clearance in pediatric oncology patients.Materials and methodsThis study retrospectively reviewed 165 courses of HD-MTX administered to children with acute lymphoblastic leukemia (ALL), non-Hodgkin’s lymphoma (NHL), or osteosarcoma. Demographic data of patients were collected. Adverse complications related to HD-MTX and 72-hour plasma methotrexate level were analyzed between patients receiving intravenous hydration ≥3,000 mL/m2/day and those receiving hydration <3,000 mL/m2/day.ResultsAmong 56 HD-MTX (1.5 g/m2) courses in ALL, delayed methotrexate clearance was only found in one course administered with hydration <3,000 mL/m2/day. However, no correlation was observed between adverse complications and methotrexate levels. Of 34 HD-MTX (1.5–3 g/m2) courses in NHL, no significant correlation was observed between methotrexate levels and intravenous hydration. However, increased adverse complications were found in the course with delayed methotrexate clearance. Interestingly, among 75 HD-MTX (10–12 g/m2) courses in osteosarcoma, normal methotrexate clearance was successfully achieved in all courses administered with hydration ≥3,000 mL/m2/day compared with those administered with hydration <3,000 mL/m2/day (P=0.007). Furthermore, the courses administered with hydration <3,000 mL/m2/day and had delayed methotrexate clearance were more likely to develop adverse complications.ConclusionIntravenous hydration of ≥3,000 mL/m2/day during HD-MTX administration is essentially required in osteosarcoma and can be considered as optional in ALL with HD-MTX <1.5 g/m2, especially in developing countries with limited monitoring of plasma methotrexate level.
Background Anti-seizure medication (ASM) treatment is one of the significant risk factors associated with abnormal vitamin D status in epilepsy patients. Multiple studies have shown that adult epilepsy patients can exhibit vitamin D deficiency. However, there are few reports investigating pediatric epilepsy patients. In this study, we aimed to identify risk factors related to hypovitaminosis D in pediatric epilepsy patients in Thailand. Methods A cross-sectional retrospective cohort study was conducted in 138 pediatric epilepsy patients who received anticonvulsants from April 2018 to January 2019. Demographic data, seizure types, puberty status, physical activity, duration, and types of anti-seizure medications were analyzed. Patients with abnormal liver function, abnormal renal function, and who received vitamin D supplements or ketogenic diet containing vitamin D were excluded. Levels of serum vitamin D (25(OH)D) were measured. Results All 138 subjects were enrolled, the age ranged from 1.04 – 19.96 years; (mean = 9.65 ± 5.09), the mean serum 25(OH) D level was 26.56 ± 9.67 ng/ml. The prevalence of vitamin D deficiency was 23.2% and insufficiency was 47.8% respectively. Two risk factors—puberty status (OR 5.43, 95% CI 1.879-15.67) and non-enzyme-inhibiting ASMs therapy (OR 3.58, 95% CI 1.117-11.46)—were significantly associated with hypovitaminosis D, as shown by multivariate analyses. Conclusions Our study reports the high prevalence of hypovitaminosis D in pediatric epilepsy patients in Thailand despite being located in the tropical zone. These findings can guide clinicians to measure vitamin D status in pediatric epilepsy patients particularly when they reach puberty and/or are using non-enzyme-inhibiting ASMs therapy. Early detection of vitamin D status and prompt vitamin D supplementation can prevent fractures and osteoporosis later in life. Trial registration TCTR20210215005 (http://www.clinicaltrials.in.th/).
Background:Pantothenate kinase-associated neurodegeneration (PKAN) is a rare neurodegenerative disorder that occurs due to autosomal recessive mutations in the PANK2 gene. Several of these pathogenic mutations have been identified, and ethnic differences seem to play an important role in the clinical outcomes of this disease. Methods and Findings:Herein we present two Thai patients diagnosed with classic PKAN. The patients presented with typical features of progressive dystonia and an "eye-of-the-tiger" signal on their brain MRIs. Molecular analysis of the PANK2 gene was, therefore, performed to study the mechanism underlying this disease state. Clinically, we observed features of generalized dystonia and dysarthria during early childhood in both patients.Brain MRIs showed a central hyperintensity surrounded by a region of hypointensity in the globus pallidus which are hallmarks of this disease. Upon molecular analysis, we identified two missense mutations: c.1475C>T (p.Ala492Val) and c.1103A>G (p.Asp368Gly) and one splice site mutation: c.982-1G>C (IVS2-1G>C) in the PANK2 gene. Interestingly, the c.982-1G>C intronic mutation has previously been reported in only one Thai patient with classic PKAN. Conclusion:Our study demonstrates the clinical and genetic characteristics of classic PKAN in two Thai patients. Generalized dystonia and dysarthria were the main clinical features that differed from classic PKAN in Caucasians. Two unique missense mutations and one recurrent splice-site mutation were identified in Thai patients with classic PKAN.
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