Autophagy in non–immune‐mediated rhabdomyolysis: Assessment of p62 immunohistochemistry. Issue 1 (4th November 2022)

• Record Type: Journal Article
• Authors: Acosta, Ignacio Javier; Stenzel, Werner; Hofer, Monika; Brady, Stefen
• Is Part Of: Muscle & nerve. Volume 67:Issue 1(2023)
• Page Start: 73
• Page End: 77
• Publication Date: 2022-11-04
• Subjects: anti‐HMGCR myopathy -- autophagy -- muscle biopsy -- necrotizing autoimmune myopathy -- rhabdomyolysis; Neuromuscular diseases -- Periodicals; Muscles -- Periodicals; Nerves -- Periodicals; 616.74
• DOI: 10.1002/mus.27739
• Languages: English
• ISSNs: 0148-639X

Abstract

Abstract: Introduction/Aims: p62 immunochemistry (IHC) has been shown to aid diagnosis with distinct patterns of muscle fiber staining observed in some inflammatory, hereditary, and degenerative myopathies, such as immune‐mediated necrotizing myopathy (IMNM). The pattern of p62 staining may help narrow the pathological differential diagnosis of rhabdomyolysis. However, there is a lack of information on the pattern of p62 IHC in non–immune‐mediated rhabdomyolysis. In this study we aim to describe histopathological findings in non–immune‐mediated rhabdomyolysis, with particular emphasis on the pattern of p62 IHC. Methods: We retrospectively reviewed the histopathological features of patients with a confirmed diagnoses of non–immune‐mediated rhabdomyolysis referred to our center. Results: Five patients were identified. Rhabdomyolysis was determined to be due to statin‐associated toxicity in three patients, alcohol overuse in one patient, and intensive exercise in one patient. All patients showed increased numbers of necrotic and regenerating muscle fibers. Diffuse and finely granular sarcoplasmic positive p62 staining was present in scattered non‐necrotic muscle fibers in all patients. Discussion: Disturbance of autophagy appears to be a common mechanism in non–immune‐mediated rhabdomyolysis. Our results show p62 IHC is sensitive but lacks specificity. Therefore, the pattern of p62 staining does not distinguish non–immune‐mediated rhabdomyolysis from histopathologically similar IMNM.