Initial seronegative immune-mediated necrotising myopathy with subsequent anti-HMGCR antibody development and response to rituximab: case report.

Anti-HMGCR Case report Immune-mediated necrotizing myopathy Myalgia

Journal

BMC rheumatology
ISSN: 2520-1026
Titre abrégé: BMC Rheumatol
Pays: England
ID NLM: 101738571

Informations de publication

Date de publication:
2020
Historique:
received: 08 01 2020
accepted: 31 03 2020
entrez: 3 7 2020
pubmed: 3 7 2020
medline: 3 7 2020
Statut: epublish

Résumé

Immune-mediated necrotising myopathy (IMNM) is characterised by severe muscle weakness and necrosis with a paucity of inflammation on muscle biopsy. Around 60% of cases are associated with antibodies to the signal recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR); the remainder are seronegative. IMNM is more treatment resistant than inflammatory myopathies. A 69-year-old woman with previous statin exposure presented aged 63 with muscle weakness and raised creatinine kinase (CK). Anti-SRP and anti-HMGCR antibodies were not detected, but muscle biopsy revealed changes consistent with necrotising myopathy. Statins were discontinued, and she was treated with prednisolone and methotrexate achieving disease remission. Clinical and biochemical parameters were largely stable until 6 years after diagnosis she experienced a rapid deterioration. This was found to be associated with new development of anti-HMGCR antibody. Rituximab was commenced, resulting rapidly in remission. She has remained in remission since, following 2 cycles of rituximab. To our knowledge, this is the first reported case of serologically negative IMNM whose subsequent rapid deterioration was associated with development of anti-HMGCR antibody. The response to rituximab and subsequent sustained remission suggests a role for early use of rituximab in aggressive cases of anti-HMGCR myopathy.

Sections du résumé

BACKGROUND BACKGROUND
Immune-mediated necrotising myopathy (IMNM) is characterised by severe muscle weakness and necrosis with a paucity of inflammation on muscle biopsy. Around 60% of cases are associated with antibodies to the signal recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR); the remainder are seronegative. IMNM is more treatment resistant than inflammatory myopathies.
CASE PRESENTATION METHODS
A 69-year-old woman with previous statin exposure presented aged 63 with muscle weakness and raised creatinine kinase (CK). Anti-SRP and anti-HMGCR antibodies were not detected, but muscle biopsy revealed changes consistent with necrotising myopathy. Statins were discontinued, and she was treated with prednisolone and methotrexate achieving disease remission. Clinical and biochemical parameters were largely stable until 6 years after diagnosis she experienced a rapid deterioration. This was found to be associated with new development of anti-HMGCR antibody. Rituximab was commenced, resulting rapidly in remission. She has remained in remission since, following 2 cycles of rituximab.
CONCLUSIONS CONCLUSIONS
To our knowledge, this is the first reported case of serologically negative IMNM whose subsequent rapid deterioration was associated with development of anti-HMGCR antibody. The response to rituximab and subsequent sustained remission suggests a role for early use of rituximab in aggressive cases of anti-HMGCR myopathy.

Identifiants

pubmed: 32613157
doi: 10.1186/s41927-020-00128-5
pii: 128
pmc: PMC7325302
doi:

Types de publication

Case Reports

Langues

eng

Pagination

29

Subventions

Organisme : Medical Research Council
ID : G0802546
Pays : United Kingdom

Informations de copyright

© The Author(s) 2020.

Déclaration de conflit d'intérêts

Competing interestsThe authors declare that they have no competing interests.

Références

JAMA. 2003 Apr 2;289(13):1681-90
pubmed: 12672737
Rheumatology (Oxford). 2009 May;48(5):594-5
pubmed: 19254917
Joint Bone Spine. 2006 Dec;73(6):646-54
pubmed: 17110150
Neuromuscul Disord. 2018 Jan;28(1):87-99
pubmed: 29221629
Nat Rev Neurol. 2011 Jun 08;7(6):343-54
pubmed: 21654717
J Rheumatol. 2019 Jun;46(6):550-551
pubmed: 31154443
Neuromuscul Disord. 2006 May;16(5):334-6
pubmed: 16616848
Arthritis Rheum. 2004 Jan;50(1):209-15
pubmed: 14730618
Medicine (Baltimore). 2014 May;93(3):150-7
pubmed: 24797170
Ann Rheum Dis. 2019 Jan;78(1):131-139
pubmed: 30309969
J Immunol Res. 2014;2014:405956
pubmed: 24741598
Muscle Nerve. 2017 Dec;56(6):1177-1181
pubmed: 28066895
Joint Bone Spine. 2014 Jan;81(1):79-82
pubmed: 23953224
Arthritis Care Res (Hoboken). 2010 Sep;62(9):1328-34
pubmed: 20506493
Pract Neurol. 2019 Aug;19(4):284-294
pubmed: 30826741

Auteurs

Rhys Thomas (R)

Department of Rheumatology, Whipps Cross Hospital, Whipps Cross University Hospital, Barts Health NHS Trust, London, E11 1NR UK.

Su-Ann Yeoh (SA)

Department of Rheumatology, University College London Hospitals NHS Foundation Trust, London, UK.

Rupert Berkeley (R)

Department of Radiology, Royal London Hospital, Barts Health NHS Trust, London, UK.

Andrew Woods (A)

Department of Immunology, Oxford University Hospitals NHS Foundation Trust, Oxford, Oxfordshire UK.

Mike Stevens (M)

Department of Pathology, Barts Health NHS Trust, London, UK.

Silvia Marino (S)

Department of Pathology, Barts Health NHS Trust, London, UK.
Department of Neuropathology, Barts Health NHS Trust, London, UK.

Aleksandar Radunovic (A)

Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, UK.

Classifications MeSH