Department of Pediatric Endocrinology, Children's Hospital at SUNY Downstate, Kings County Hospital Center, and Infants and Children's Hospital at Maimonides, 977 48th Street, Brooklyn, NY 11219, USA.
Rev Endocr Metab Disord. 2013 Jun;14(2):119-25. doi: 10.1007/s11154-013-9246-8.
Human immunodeficiency virus (HIV) infection has progressed to a chronic disease and HIV positive individuals are living longer lives. This has lead to an increase in morbidity and mortality due to secondary issues, one being HIV bone disease. HIV infected pediatric and adult populations have a greater incidence in reduction of BMD as compared to the controls. Osteoporosis has been reported to be present in up to 15 % of HIV positive patients. We are starting to understand the mechanism behind the changes in HIV bone disease. Viral proteins interfere with osteoblastic activity either by direct interaction or by the inflammatory process that they induce. Anti-viral management, including highly active antiretroviral therapy (HAART), protease inhibitors, and nucleoside/nucleotide reverse transcriptase inhibitors (NRTI) also are involved in disrupting proper bone metabolism. Vitamin D levels have strong correlation with bone disease in HIV patients, and are dependent not only to chronic disease state, but interaction of pharmacologic management and inflammatory process as well. Work up of the secondary causes of osteopenia and osteoporosis should be undertaken in all patients. DEXA scan is recommended in all post-menopausal women with HIV, all HIV infected men 50 years of age or older and in those with a history of fragility fractures regardless of age or gender. Preventive measures include adequate nutrition, calcium and Vitamin D intake daily, muscle strengthening and balance exercises to increase BMD and reduce fractures. Bisphosphonates are considered to be the first line for the treatment of HIV associated bone disease. This review will describe how the balanced mechanism of bone metabolism is interrupted by the HIV infection itself, the complications that arise from HIV/AIDS, and its treatment options.
人类免疫缺陷病毒(HIV)感染已发展为慢性疾病,HIV 阳性个体的寿命更长。这导致继发性疾病的发病率和死亡率增加,其中之一是 HIV 骨病。与对照组相比,HIV 感染的儿童和成人人群的 BMD 减少发生率更高。据报道,多达 15%的 HIV 阳性患者存在骨质疏松症。我们开始了解 HIV 骨病变化背后的机制。病毒蛋白通过直接相互作用或诱导的炎症过程干扰成骨细胞活性。抗病毒治疗管理,包括高效抗逆转录病毒疗法(HAART)、蛋白酶抑制剂和核苷/核苷酸逆转录酶抑制剂(NRTI),也参与破坏适当的骨代谢。维生素 D 水平与 HIV 患者的骨病密切相关,不仅取决于慢性疾病状态,还取决于药物管理和炎症过程的相互作用。应在所有患者中开展骨质疏松症和骨质疏松症的继发性病因检查。建议对所有 HIV 绝经后妇女、所有 50 岁或以上的 HIV 感染男性以及无论年龄和性别,有脆性骨折史的患者进行 DEXA 扫描。预防措施包括充足的营养、每日摄入钙和维生素 D、肌肉强化和平衡运动,以增加 BMD 并减少骨折。双膦酸盐被认为是治疗 HIV 相关骨病的一线药物。这篇综述将描述 HIV 感染本身如何破坏骨代谢的平衡机制、HIV/AIDS 引起的并发症及其治疗选择。