{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T17:32:00Z","timestamp":1789061520773,"version":"build-2803163510"},"reference-count":89,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,3,17]],"date-time":"2015-03-17T00:00:00Z","timestamp":1426550400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J of Inher Metab Disea"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Rhabdomyolysis results from the rapid breakdown of skeletal muscle fibers, which leads to leakage of potentially toxic cellular content into the systemic circulation. Acquired causes by direct injury to the sarcolemma are most frequent. The inherited causes are: i) metabolic with failure of energy production, including mitochondrial fatty acid \u00df\u2010oxidation defects,\n                    <jats:italic>LPIN1<\/jats:italic>\n                    mutations, inborn errors of glycogenolysis and glycolysis, more rarely mitochondrial respiratory chain deficiency, purine defects and peroxysomal \u03b1\u2010methyl\u2010acyl\u2010CoA\u2010racemase defect (AMACR), ii) structural causes with muscle dystrophies and myopathies, iii) calcium pump disorder with\n                    <jats:italic>RYR1<\/jats:italic>\n                    gene mutations, iv) inflammatory causes with myositis. Irrespective of the cause of rhabdomyolysis, the pathology follows a common pathway, either by the direct injury to sarcolemma by increased intracellular calcium concentration (acquired causes) or by the failure of energy production (inherited causes), which leads to fiber necrosis. Rhabdomyolysis are frequently precipitated by febrile illness or exercise. These conditions are associated with two events, elevated temperature and high circulating levels of pro\u2010inflammatory mediators such as cytokines and chemokines. To illustrate these points in the context of energy metabolism, protein thermolability and the potential benefits of arginine therapy, we focus on a rare cause of rhabdomyolysis, aldolase A deficiency. In addition, our studies on lipin\u20101 (LPIN1) deficiency raise the possibility that several diseases involved in rhabdomyolysis implicate pro\u2010inflammatory cytokines and may even represent primarily pro\u2010inflammatory diseases. Thus, not only thermolability of mutant proteins critical for muscle function, but also pro\u2010inflammatory cytokines per se, may lead to metabolic decompensation and rhabdomyolysis.\n                  <\/jats:p>","DOI":"10.1007\/s10545-015-9827-7","type":"journal-article","created":{"date-parts":[[2015,3,16]],"date-time":"2015-03-16T07:08:49Z","timestamp":1426489729000},"page":"621-628","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["Acute rhabdomyolysis and inflammation"],"prefix":"10.1002","volume":"38","author":[{"given":"Yamina","family":"Hamel","sequence":"first","affiliation":[{"name":"Institut Imagine, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 1163 Paris 75015 France"},{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris Cit\u00e9, Facult\u00e9 de m\u00e9decine Paris Descartes Paris 75015 France"},{"name":"Centre de R\u00e9f\u00e9rence des Maladies 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