Drug-induced Myopathies.
Autor: | Steinmeyer J; Laboratory for Experimental Orthopaedics, Dept. of Orthopaedics, Justus Liebig University Giessen, Giessen, Germany., Flechtenmacher J; Professional Association for Orthopaedic and Trauma Surgery (BVOU), Berlin, Germany.; Ortho-Zentrum, Orthopaedic Group Practice at Ludwigsplatz, Karlsruhe, Germany. |
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Jazyk: | English; German |
Zdroj: | Zeitschrift fur Orthopadie und Unfallchirurgie [Z Orthop Unfall] 2023 Apr; Vol. 161 (2), pp. 175-181. Date of Electronic Publication: 2021 Jul 28. |
DOI: | 10.1055/a-1488-6912 |
Abstrakt: | Differential diagnosis of muscle pain and weakness is extensive, including neurological, vertebral, arthrogenic, vascular, traumatic, immunological, endocrine, genetic and infectious aetiologies, as well as medication or toxin-related causes. Muscles are highly sensitive to a large number of drugs, especially with high doses. Although many drug classes can cause toxic myopathy, a significant number of cases are caused by lipid-lowering drugs, long-term use of corticosteroids, and, most often, alcohol misuse. Some drug interactions, e.g. those that are metabolised via the enzyme CYP3A4, can increase the serum levels of the drugs and drug-induced toxicity. A careful history of patient's drug and alcohol consumption is therefore vital. Clinical symptoms depend on the drug, dosage and patient's sensitivity. They can vary from asymptomatic increase in serum levels of creatine kinase, mild myalgia and cramps to muscle weakness, rhabdomyolysis, kidney failure and even death. The pathogenesis is often only partially known and multifactorial. Toxic myopathy is often reversible once the drug is discontinued, alternative drug therapy is started or a different dosage regimen is chosen. Complications such as acute kidney failure must be avoided, and analgesic therapy may be indicated. Competing Interests: The authors declare that they have no conflict of interest./Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht. (Thieme. All rights reserved.) |
Databáze: | MEDLINE |
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