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[风湿病学中的药物性骨病]

[Drug-induced osteopathy in rheumatology].

作者信息

Fiehn Christoph, Bauhammer Jutta

机构信息

Rheumatologie Baden-Baden, Tätigkeitsschwerpunkt Klinische Immunologie am Medical Center Baden-Baden, Beethovenstr. 2, 76530, Baden-Baden, Deutschland.

出版信息

Z Rheumatol. 2022 Apr;81(3):189-197. doi: 10.1007/s00393-021-01145-6. Epub 2022 Jan 10.

Abstract

Osteopathy in rheumatology can either be primary a condition as a consequence of inflammatory rheumatic diseases but can also be drug induced. The most severe clinical manifestations are insufficiency fractures and osteonecrosis. The risk of fractures is highest for patients treated with glucocorticoids depending on the daily intake, the cumulative glucocorticoid dosage and the duration of administration. An incidence rate of nearly 13% was reported after administration of glucocorticoids lasting > 1 year. Cases of osteonecrosis under glucocorticoids are, in contrast, less frequent and not associated with glucocorticoid-induced osteoporosis. The antiresorptive substances bisphosphonates and denosumab, as well as romosumab are effective and important in treating osteoporosis; however, they can also cause atypical fractures, particularly of the femur as well as osteonecrosis of the jawbone. According to the most recent guidelines the benefits of bisphosphonate treatment have only been verified for 3-5 years and for denosumab for 3 years. There are clear preventive recommendations to avoid osteonecrosis of the jaw. Ultimately, the disease-modifying antirheumatic drugs (DMARD) methotrexate and leflunomide also affect the metabolism of bones. There is a rare but very characteristic form of osteopathy associated with methotrexate, mainly occurring in cases of long-term treatment. The typical manifestations are insufficiency fractures, particularly of the distal tibia, which persist for many years under continuous methotrexate administration. The treatment is the discontinuation of methotrexate and in most cases the fractures will heal within 3-4 months. Leflunomide has been associated with cases of persisting pseudarthrosis that only disappeared after a wash-out of the active metabolite.

摘要

风湿病中的骨病既可以是炎症性风湿性疾病导致的原发性病症,也可能是药物诱发的。最严重的临床表现是不全骨折和骨坏死。使用糖皮质激素治疗的患者骨折风险最高,这取决于每日摄入量、糖皮质激素累积剂量和给药持续时间。使用糖皮质激素超过1年的患者报告的骨折发生率近13%。相比之下,糖皮质激素导致骨坏死的病例较少见,且与糖皮质激素诱发的骨质疏松症无关。抗吸收物质双膦酸盐、地诺单抗以及罗莫单抗在治疗骨质疏松症方面有效且重要;然而,它们也可能导致非典型骨折,尤其是股骨骨折以及颌骨骨坏死。根据最新指南,双膦酸盐治疗的益处仅在3至5年得到证实,地诺单抗治疗的益处仅在3年得到证实。有明确的预防建议以避免颌骨骨坏死。最终,改善病情抗风湿药(DMARD)甲氨蝶呤和来氟米特也会影响骨骼代谢。有一种与甲氨蝶呤相关的罕见但非常典型的骨病形式,主要发生在长期治疗的病例中。典型表现是不全骨折,尤其是胫骨远端骨折,在持续使用甲氨蝶呤的情况下会持续多年。治疗方法是停用甲氨蝶呤,大多数情况下骨折会在3至4个月内愈合。来氟米特与持续性假关节病例有关,只有在清除活性代谢物后才会消失。

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