7 research outputs found

    Low-Energy Multilevel Vertebral Fracture in a Pediatric Patient during Follow-up for Idiopathic Hypercalciuria: A Case Report

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    WOS: 000409960500010Compared to adult studies, there are a limited number of pediatric studies exploring the effects of hypercalciuria on bone mineral density. The aim of this paper was to report a case of low-energy multilevel vertebral fracture in a pediatric patient during follow-up for idiopathic hypercalciuria (IH); it was also attempted to remind clinicians that IH-induced fractures may also occur in children. A 10-year-old male child presented to our outpatient clinic with back pain after jumping off from a height of approximately 50 cm. History of the patient showed that the patient had been followed-up for idiopathic hypercalciuria for 8 years and his father had renal stones and hypercalciuria. There was no abnormality on physical examination, with an exception for tenderness and limitation of movement in lower thoracic and lumbar vertebrae. Complete blood count and biochemical parameters were normal except for an elevated alkaline phosphatase level. Dorsal and lumbar lateral plain graphs showed compression fractures of T4, T6, T8, and L3 vertebrae, therefore, lumbar and dorsal vertebral magnetic resonance imaging (MRI), bone mineral densitometry (BMD), and vitamin D level measurement were ordered. MRI revealed acute compression fracture and medullary edema in L3; there were also chronic osteoporotic fractures in T4, T6, and T8. BMD showed a lumbar total Z score of -2.9 and the Vitamin D level was 13.7 ng/mL (10-24 ng/mL indicates moderate deficiency). A control renal ultrasonography revealed no kidney stones or calcification. The patient was prescribed polyethylene mold thoracolumbar corset and vitamin D support at a dose not to enhance hypercalciuria and nephrocalcinosis. His pain was alleviated at follow-up. Considering that most of the total bone mass is acquired at childhood, identification of causative factors and taking necessary measures at an early stage may prevent future complications of IH

    Central nervous system thrombosis in pediatric acute lymphoblastic leukemia in Turkey: A multicenter study

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    Background: In patients with acute lymphoblastic leukemia (ALL), the risk of thromboembolism increases due to hemostatic changes secondary to the primary disease and due to treatment-related factors. In this multicenter study, we aimed to research the frequency of central nervous system (CNS) thrombosis occurring during treatment, hereditary and acquired risk factors, clinical and laboratory features of patients with thrombosis, treatment approaches, and thrombosis-related mortality and morbidity rates in pediatric ALL patients. Procedure: Pediatric patients who developed CNS thrombosis during ALL treatment from 2010 to 2021 were analyzed retrospectively in 25 different Pediatric Hematology Oncology centers in Türkiye. The demographic characteristics of the patients, symptoms associated with thrombosis, the stage of the leukemia treatment during thrombosis, the anticoagulant therapy applied for thrombosis, and the final status of the patients recorded through electronic medical records were determined. Results: Data from 70 patients with CNS thrombosis during treatment, out of 3968 pediatric patients with ALL, were reviewed. The incidence of CNS thrombosis was 1.8% (venous: 1.5 %; arterial: 0.03%). Among patients with CNS thrombosis, 47 had the event in the first 2 months. Low molecular weight heparin (LMWH) was the most commonly used treatment with a median of 6 months (min–max: 3–28 months). No treatment-related complications occurred. Chronic thrombosis findings occurred in four patients (6%). In five (7%) patients who developed cerebral vein thrombosis, neurological sequelae (epilepsy and neurological deficit) remained. One patient died related to thrombosis, and the mortality rate was 1.4%. Conclusion: Cerebral venous thrombosis and, less frequently, cerebral arterial thrombosis may develop in patients with ALL. The incidence of CNS thrombosis is higher during induction therapy than during other courses of treatment. Therefore, patients receiving induction therapy should be monitored carefully for clinical findings suggestive of CNS thrombosis
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