Sir,

“She was a famous opera singer; he was a ship magnate both of Greek origin. Although never married they lived as a couple for nine years. She died due to myocardial infarction – a complication of dermatomyositis- from which she had been suffering for years while he had died two years earlier from myasthenia gravis”.

Dermatomyositis is an autoimmune disease affecting mainly females- sometimes associated with underlying malignancy- that +manifests with muscle wakness. An erythematous Vshaped rash on neck, periorbital heliotrope papules on knuckles-Gottron’ s sign. It may be associated with myocarditis and pulmonary interstitial fibrosis [1,2].

Myasthenia gravis is an autoimmune disease caused by the presence of specific antibodies targeting different postsynaptic components of the neuromuscular junction and is clinically characterized by the presence of fatigable muscle weakness.

In the etiopathogenesis plays a central role the thymus and the most frequently detected pathogenic autoantibodies are targeted to the acetylcholine receptor [3,4].

There has been a report of dermatomyositis mimicking myasthenia gravis and a case associating both disorders in the same patient [5,6]. In the case reported here consanguinity was excluded both individuals came from remote areas and no genetic investigation was known to have been performed.

The previous classification of Cell and Coombs has been modified and new scientific information was added According to this TH1 immunity involves M1 macrophages, IFNγ CD4 T cells, iNKT1 cells, CD8 T cells (Tc1, EM4), and IgG3 B cells. It is linked to type 4 delayed-type hypersensitivity, which results in a delayed immune response. In contrast, TH2 immunity is specifically tailored to combat parasites. Notably, TH2 immunity includes two distinct subtypes, TH2a induced in response to endoparasites (helminths) and TH2b induced in response to ectoparasites (insects), emphasizing the nuanced and specialized nature of the immune response against parasitic invaders. TH2a immunity involves inflammatory eosinophils (iEOS), interleukin-4/interleukin-5 CD4 T cells, mast cell tryptase (MCt), iNKT2 cells, and IgG4 B cells. TH2b immunity includes basophils, interleukin-13/interleukin-4 CD4 T cells, mast cells-tryptase/chymase (MCtc), iNKT2 cells, and IgE B cells. The TH2 immunological pathway is intricately associated with type 1 allergic hypersensitivity, representing a specific immune response to allergens. In contrast, TH22 immunity serves as the host’s specialized immune reaction targeting extracellular microorganisms (broadly including extracellular bacteria, protozoa, and fungi). The components of TH22 immunity are diverse and include neutrophils (N1), CD4 T cells that produce interleukin-22, iNKT17 cells, and IgG2 B cells. TH22 immunity is associated with type 3 immune complex-mediated hypersensitivity. THαβ immunity is the host immunological pathway against infectious particles (viruses and prions). Thαβ immunity involves NK cells (NK1), interleukin-10-producing CD4 T cells, iNKT10 cells, CD8 T cells (Tc2,EM1), and IgG1 B cells [7].

DERMATOMYOSITIS IS DOMINATED BY THαβ CELLS

Because the THαβ immune reaction fights against viruses-derived DNA and RNA molecules, dermatomyositis is associated with antiviral THαβ immunity. Virus infections like EBV can also link to the pathophysiology of dermatomyositis [7].

Viral infection can usually exacerbate myasthenia gravis, highlighting the vital role of the THαβ immunological pathway in disease pathogenesis. EBV, parvovirus, and HSV infections have been reported to be associated with the pathogenesis of myasthenia Gravis [7].

These hypotheses are valid in the case described here. A couple shares many identical conditions and environments. The hypothesis that a viral infection might have been responsible for both phenotypes’ dermatomyositis and myasthenia gravis in this case should be taken into account.

This is the first case associating dermatomyositis and myasthenia gravis in a couple and is reported to increase awareness about a common etiologic factor associated with two distinct autoimmunity disorders dermatomyositis and myasthenia gravis.

REFERENCES

1.  Cristofori M, González-Rodríguez JC, Cortés-Marín EE, Sallón A, Sandoval J. Dermatomyositis:A narrative review of skin as a window to muscle and malignancy. Cureus. 2025;17:e88601.

2.  Ali H, On A, Xing E, Shen C, Werth VP. Dermatomyositis:focus on cutaneous features, etiopathogenetic mechanisms and their implications for treatment. Semin Immunopathol. 2025;47:32.

3.  García Estévez DA, Pardo Fernández J. Myasthenia gravis. Update on diagnosis and therapy. Med Clin (Barc). 2023;161:119-27.

4.  Harish Bindignavile S. Myasthenia gravis – an updated review. Int Ophthalmol Clin. 2026;66:55-61.

5.  Jin ZS, Tao XR, Wang ZX. A case report of dermatomyositis mimicking myasthenia gravis. Medicine (Baltimore). 2023;102:e36234.

6.  Sangüesa Gómez C, Flores Robles BJ, Méndez Perles C, Barbadillo C, Godoy H, Andréu JL. Dermatomyositis and myastenia gravis:An uncommon association with therapeutic implications. Reumatol Clin. 2015;11(244-6.

7.  Huang YM, Shih LJ, Hsieh TW, Tsai KW, Lu KC, Liao MT, et al. Type 2 hypersensitivity disorders, including systemic lupus erythematosus, Sjögren’s syndrome, Graves’disease, myasthenia gravis, immune thrombocytopenia, autoimmune hemolytic anemia, dermatomyositis, and graft-versus-host disease, are TH -dominant autoimmune diseases. Virulence. 2024;15:2404225.