RESUMO
AIM: From an early age, exercise is key to managing type 1 diabetes (T1D). However, hypoglycemia around aerobic exercise is a major barrier to physical activity in children. We explore whether intermittent high-intensity aerobic exercise (IHE), designed to mimic spontaneous childhood physical activity patterns, offers better protection against glycemic drop than continuous moderate-intensity exercise (CME). METHODS: Five boys and 7 girls with T1D (9.8 ± 1.4y) performed ergo cycle-based randomized CME and IHE of identical duration and total mechanical load [50 %PWC170vs. 15sec(150 %PWC170)/30 sec passive recovery; both during two 10-min sets, 5 min in-between]. Capillary glycemia during exercise and interstitial glucose during recovery were compared between exercises and an inactive condition, controlling for baseline glycemia, carbohydrate and insulin. RESULTS: The exercise-induced decrease in capillary glycemia was attenuated by 1.47 mmol·L-1 for IHE vs. CME (P < 0.05). No symptomatic hypoglycemic episodes occurred during exercises. Post-exercise time in hypoglycemia did not differ between conditions. During early recovery, CME reduced time spent > 16.7 mmol·L-1 compared with inactive days (P < 0.05; CME: 0 %; IHE: 16,7 %; INACTIVE: 41,7 %). CONCLUSION: IHE appeared to limit the glycemic drop compared to CME. Performing 20-min CME or IHE was not associated with increased hypoglycemic risk compared to being inactive. CME appeared even transiently protective against serious hyperglycemia.
Assuntos
Diabetes Mellitus Tipo 1 , Hipoglicemia , Masculino , Feminino , Criança , Humanos , Adolescente , Diabetes Mellitus Tipo 1/terapia , Diabetes Mellitus Tipo 1/complicações , Glicemia , Exercício Físico , Hipoglicemia/prevenção & controle , Hipoglicemia/complicações , Hipoglicemiantes/uso terapêutico , InsulinaRESUMO
Hypoparathyroidism in children is most often due to mutations in genes involved in parathyroid development and calcium homeostasis signaling. Some rare cases result from autoimmune attack on the parathyroid glands as a part of the type 1 polyglandular failure syndrome (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy). The majority of cases of pediatric hypoparathyroidism are well controlled under conventional treatment with calcium and vitamin D analogs. However, this treatment may be difficult to manage, especially in two situations: 1) in the context of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy and 2) activating mutations in the calcium-sensing receptor. We successfully treated three patients with hypoparathyroidism with continuous subcutaneous administration of rhPTH(1-34) (recombinant human PTH(1-34)), two of which were refractory to conventional therapy.