Osteoporosis and neurological complications are consequences of acute lymphoblastic leukemia (ALL). Collagen type I alpha 1 gene (COL1A1) polymorphism is associated with osteoporosis. This study aimed to detect the COL1A1 polymorphism and the neurological complications in ALL patients and their association with decreased lumbar spine bone mineral density (BMDLS). This study included 100 pediatric ALL patients and 100 controls. All participants were subjected to laboratory assessment and assessment of BMDLS at the start of the study and 3 years later. COLIA1 genotyping was done once for all participants. At the start of the study, there was a significant decrease in osteocalcin (OC), alkaline phosphatase (ALP), and BMDLS levels in the patients. G/T variants and “T” alleles were significantly more detected in the patients (34% and 35% respectively); also, significant differences were detected between patients with polymorphism (G/T and T/T) and those without polymorphism (G/G) regarding OC, ALP, and BMDLS. After 3 years, significant decrement in BMDLS, OC, and ALP was detected in the patients. Twenty-four patients had neurological complications and seven patients had bone fractures. Those patients had significant decrement in BMDLS, OC, and ALP levels. As regards COL1A1 gene polymorphism, the GT and TT variants were significantly detected in fractured patients, while there was no significant difference regarding GT and TT variants in the patients with neurological complications. T allele, neurological complications, high-risk stratification, and age were significantly associated with decreased BMDLS. T allele was the most significant risk factor. COLIA1 gene polymorphism, decreased BMDLS, and neurological complications were significantly detected in pediatric ALL patients. COLIA1 gene polymorphism is a significant risk factor for decreased BMDLS in pediatric ALL patients. There is no significant relation between COLIA1 gene polymorphism and the development of neurologic complications.

中文翻译：

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儿童急性淋巴细胞白血病患者的 COL1A1 多态性和神经系统并发症及其与骨密度改变的关联

骨质疏松症和神经系统并发症是急性淋巴细胞白血病 (ALL) 的后果。I 型胶原蛋白 1 基因 (COL1A1) 多态性与骨质疏松症有关。本研究旨在检测 ALL 患者的 COL1A1 多态性和神经系统并发症，以及它们与腰椎骨矿物质密度 (BMDLS) 降低的关联。该研究包括 100 名儿科 ALL 患者和 100 名对照。在研究开始时和 3 年后，所有参与者都接受了实验室评估和 BMDLS 评估。对所有参与者进行一次 COLIA1 基因分型。在研究开始时，患者的骨钙素 (OC)、碱性磷酸酶 (ALP) 和 BMDLS 水平显着降低。在患者中检测到的 G/T 变异和“T”等位基因明显更多（分别为 34% 和 35%）；此外，在 OC、ALP 和 BMDLS 方面，在具有多态性（G/T 和 T/T）的患者和没有多态性（G/G）的患者之间检测到显着差异。3 年后，在患者中检测到 BMDLS、OC 和 ALP 显着下降。24 名患者出现神经系统并发症，7 名患者出现骨折。这些患者的 BMDLS、OC 和 ALP 水平显着下降。COL1A1基因多态性方面，骨折患者中GT和TT变异显着，神经系统并发症患者GT和TT变异无显着差异。T 等位基因、神经系统并发症、高风险分层和年龄与 BMDLS 降低显着相关。T等位基因是最重要的危险因素。COLIA1 基因多态性，BMDLS 降低，在儿科 ALL 患者中显着检测到神经系统并发症。COLIA1 基因多态性是儿童 ALL 患者 BMDLS 降低的重要危险因素。COLIA1 基因多态性与神经系统并发症的发生之间没有显着关系。