Clinical features and therapeutic challenges of psoriatic arthritis coexisting with antisynthetase syndrome: a case report and literature review

Objective: The coexistence of psoriatic arthritis (PsA) with inflammatory myopathies, including antisynthetase syndrome (ASS), is exceptionally rare and presents significant diagnostic and therapeutic challenges. This study reports a case of PsA overlapping with ASS and reviews the literature to analyze clinical features, immunopathogenesis, and treatment strategies.

Methods: A 52-year-old female with a 10-year history of psoriasis developed PsA and later presented with muscle weakness, mechanic’s hands, and interstitial lung disease (ILD). Serological testing revealed anti-Jo-1 and anti-SSA/Ro52 positivity, confirming ASS. We compare our case with 17 previously reported cases of psoriasis or PsA coexisting with inflammatory myopathies, highlighting similarities and differences in clinical presentation and treatment response.

Results: Psoriasis and inflammatory myopathies share immunopathogenic pathways, including the IL-17/IL-23 axis, type I interferons, and TNF-α. Therapies effective for psoriasis/PsA, such as TNF and IL-17 inhibitors, may exacerbate inflammatory myopathies, while JAK inhibitors and corticosteroids appear more effective in managing overlap cases. Our patient achieved sustained remission with baricitinib and low-dose prednisone after multiple treatment adjustments.

Conclusion: PsA and inflammatory myopathies can coexist, requiring careful differentiation and tailored immunomodulatory therapy. Clinicians should recognize overlapping features and optimize treatment to prevent exacerbations. Further research is needed to establish standardized management strategies for this rare overlap syndrome.

Introduction

Idiopathic inflammatory myopathies (IM) are a group of idiopathic autoimmune disorders characterized by chronic muscle inflammation and weakness. This category includes polymyositis (PM), dermatomyositis (DM), inclusion body myositis, and other subtypes or overlap syndromes. PM and DM are classic IM subtypes – PM involving primarily proximal skeletal muscles, and DM affecting both skin and muscle. These myopathies are relatively rare (for example, DM affects roughly 1–6 per 100,000 adults) (1). Notably, IM can occur in isolation or in association with other autoimmune connective tissue diseases (2). One important overlap subset is anti-synthetase syndrome (ASS), defined by the presence of anti-aminoacyl tRNA synthetase autoantibodies. ASS is characterized by inflammatory myositis accompanied by systemic features such as interstitial lung disease (ILD), non-erosive polyarthritis, Raynaud’s phenomenon, fever, and “mechanic’s hands” (3). Each of these IM subtypes provides a window into autoimmune muscle pathology, and their co-occurrence with other immune-mediated diseases is an area of clinical interest.

Psoriasis, on the other hand, is a common chronic immune-mediated inflammatory disease primarily affecting the skin. It is often accompanied by psoriatic arthritis (PsA) and other systemic comorbidities. Indeed, patients with psoriasis have higher frequencies of concurrent autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus (SLE), systemic sclerosis, Sjögren’s syndrome, and others (4). However, the overlap of psoriasis with idiopathic inflammatory myopathies is exceedingly rare. Co-existence of psoriasis and DM has been documented only in a handful of cases in the literature. A recent review identified roughly 15 reported instances of psoriasis co-occurring with dermatomyositis (including some juvenile and amyopathic DM cases) (5). These observations underscore the rarity of psoriasis–myositis overlap, in contrast to the well-recognized psoriasis–PsA association.

The uncommon overlap between psoriasis and IM subtypes raises intriguing questions about shared pathogenesis and immune crosstalk. Some authors have speculated that common inflammatory pathways might link these conditions. Dermatomyositis, for instance, features a prominent type I interferon signature and involvement of plasmacytoid dendritic cells, immunologic elements also central in psoriasis (4). Furthermore, elevated levels of interleukin-17 (IL-17) have been observed in DM patients, and IL-17–producing T cells infiltrate the lesions of both psoriasis and DM, suggesting a contribution of the IL-23/Th17 axis to both diseases (6). Clinical reports lend support to this mechanistic overlap – notably, therapies targeting the IL-23/IL-17 pathway (e.g. ustekinumab, an IL-12/23 p40 inhibitor used in psoriasis) have shown efficacy in treating refractory “mechanic’s hands” in an antisynthetase syndrome patient (7). Such findings hint at converging immunopathological drivers despite the rarity of co-manifestation.

Antisynthetase syndrome itself represents an illustrative example of overlap between an inflammatory myopathy and features that can mimic other rheumatic diseases. Patients with ASS often develop an inflammatory polyarthritis as part of the syndrome, which in a psoriasis patient could be initially mistaken for psoriatic arthritis. Indeed, at least one case report describes a patient with longstanding psoriasis/PsA who subsequently developed dermatomyositis with anti-Jo-1 antibodies (fulfilling ASS), creating a diagnostic challenge of distinguishing PsA from myositis-related arthritis (8). In this paper, we highlight the overlap of psoriasis (and psoriatic arthritis) with an antisynthetase syndrome, situating it within the broader spectrum of psoriatic disease coexisting with inflammatory myopathies. Our aim is to enhance recognition of this uncommon association and discuss its implications for pathogenesis and patient management.

Case presentation

A 52-year-old female teacher was admitted in June 2019 due to a 10-year history of scaly rash and a recent 1-month history of polyarticular swelling and pain. Her initial skin symptoms appeared a decade prior as scaly rash involving her limbs, gradually spreading across her entire body, accompanied by pinpoint bleeding upon scratching. Initially diagnosed as diffuse plaque psoriasis, her skin lesions showed fluctuating severity despite intermittent topical treatment. She had no relevant psoriasis family history.

Approximately six months prior to hospitalization, she began experiencing mild exertional dyspnea and occasional dry cough, untreated at that time. One month before admission, she developed persistent joint pain and swelling involving bilateral metacarpophalangeal joints (MCPJ), proximal interphalangeal joints (PIPJ), knees, and ankles, significantly impairing mobility. Occasional lower back pain was noted, and her lower back pain had inflammatory characteristics. The patient had no Raynaud’s phenomenon, with no dryness of mouth or eyes, recurrent oral ulcers, or alopecia. She had no history of hypertension or diabetes mellitus.

On physical examination, vital signs were stable. Scaly plaques were observed on the dorsal hands and lower extremities (Figure 1A), with scattered dandruff on the scalp. Psoriasis Area and Severity Index (PASI) was 3.9. Bilateral basal lung crackles were audible. Cardiac and abdominal examinations were unremarkable. Both hands displayed mechanic’s hands appearance (Figure 1B), with swelling and tenderness noted at the left PIP2–3 joints and the right knee. The second toe of the left foot and the fourth toe of the right foot exhibited dactylitis, showing a “sausage toe” appearance (Figure 1C). Partial nail thickening and whitening were observed (Figure 1C).

Figure 1

Figure 1. Clinical and Radiological Manifestations of Antisynthetase Syndrome in a Patient with Psoriatic Arthritis. (A) Scaly, erythematous plaques with well-demarcated borders distributed on the lower extremities, characteristic of psoriasis. (B) Hyperkeratosis and fissuring of the thumb, consistent with mechanic’s hands, a hallmark feature of antisynthetase syndrome. (C) Thickened, dystrophic toenails with onychodystrophy and dactylitis, commonly seen in psoriatic arthritis (PsA). (D) High-resolution computed tomography (HRCT) scans showing interstitial lung disease with a nonspecific interstitial pneumonia (NSIP) pattern, which is frequently associated with antisynthetase syndrome (on admission). (E) Interstitial lung disease exacerbated because of inadequate treatment. (F) Computed tomography (CT) scan of the sacroiliac joints showing mild bilateral sacroiliitis, which can occur in psoriatic arthritis.

Routine laboratory investigations were normal, including complete blood count, liver and kidney functions. Autoimmune tests revealed positivity for anti-Jo-1 and anti-SSA-Ro-52 antibodies, with elevated KL-6 levels (983 U/mL; normal 105–435 U/mL). HLA-B27 was negative. Radiographs of hands and knees showed no erosions, whereas chest CT demonstrated interstitial changes consistent with a nonspecific interstitial pneumonia (NSIP) pattern (Figure 1D). Pulmonary function tests revealed restrictive ventilatory impairment with reduced diffusion capacity (DLCO: 60% predicted). Sacroiliac joint CT indicated mild erosion (Figure 1F).

The patient was diagnosed with PsA according to CASPAR criteria and ASS based on Connors criteria. Initial treatment for PsA included a weekly subcutaneous injection of etanercept analog (Yisaipu) 50mg and oral cyclosporine 100mg twice daily for ILD. Due to gastrointestinal intolerance of cyclosporine, she was switched to tacrolimus 1mg twice daily and improved skin and joint symptoms but worsened ILD (Figure 1E). Treatment was then adjusted to methylprednisolone and tripterygium glycosides, stabilizing disease. Tapering the glucocorticoid led to worsening skin and joint symptoms. Later, ineffective treatment with adalimumab and subsequent tofacitinib were complicated by pulmonary infection and elevated creatine kinase (CK, 361 U/L). Although secukinumab transiently improved symptoms, CK markedly elevated (2701 U/L) after one year, indicating drug-induced enzyme elevation. Finally, switching to baricitinib (4 mg/day) combined with methylprednisolone (8 mg/day) achieved sustained remission of psoriasis, arthritis, and normalization of CK levels over two years. Figure 2 shows the management flowchart for this patient.

Figure 2

Figure 2. The management flowchart for this patient. EA, etanercept analog, CsA, cyclosporine; ILD, intersitial lung disease; MP, methylprednisolone, TTG, tripterygium glycosides; ADA, adalimumab; Tof, tofacitinib; Sec, secukinumab; CK↑↑, creatine kinase elevated significantly; Bari, baricitinib; ESR, erythrocyte sedimentation rate.

Methods

We systematically searched the PubMed and Embase databases up to May 2025, using the keywords ‘psoriasis’, ‘psoriatic arthritis’, ‘antisynthetase syndrome’, ‘dermatomyositis’, and ‘inflammatory myopathy’. Inclusion criteria were clearly documented cases of psoriasis or PsA overlapping with inflammatory myopathies. Exclusion criteria included incomplete clinical data or unclear diagnoses.

Discussion

To date, a comprehensive search has identified only 17 previously reported cases of psoriasis or psoriatic arthritis coexisting with inflammatory myopathies where clinical details were sufficiently reported, thus our case represents the 18^th documented instance Table 1 summarizes the key clinical characteristics of these cases (2, 5, 8–20). Our patient – to our knowledge is one of the first reported with psoriatic arthritis (PsA) overlapping with anti-Jo1 antisynthetase syndrome (8). This rarity highlights the importance of recognizing the overlap syndrome, as misdiagnosis or delayed diagnosis can lead to suboptimal treatment outcomes. The coexistence of psoriasis and myositis presents unique diagnostic and therapeutic challenges due to overlapping symptomatology and differences in treatment responses. Understanding the shared and distinct immunopathogenic mechanisms between these diseases is critical for optimal patient management.

Table 1

Table 1. Clinical features and treatment of psoriasis with inflammatory myopathies.

Despite being distinct disorders, psoriasis/PsA and inflammatory myopathies share certain inflammatory pathways, which may explain why they rarely coexist. T helper 17 (Th17)/IL-23 axis: Psoriasis is driven largely by IL-23–induced Th17 cells producing IL-17A/F and other cytokines (21, 22). Notably, this same pathway appears active in myositis. Patients with DM/PM have elevated IL-17A levels in serum correlating with disease activity (23), and muscle biopsies show higher IL-17 and IL-23 expression compared to controls (24). An experimental myositis model demonstrated that blocking IL-23 (with anti-IL-23p19 antibodies) suppressed muscle inflammation, highlighting IL-23 as a pathogenic driver in myositis much like in psoriasis (24). Tumor necrosis factor-α: TNF-α is a proinflammatory cytokine central to psoriasis/PsA and also found in inflamed muscle tissue. Muscle from DM/PM patients’ over-expresses TNF-α along with IL-17 and IFN-γ, reflecting broad T-cell activation (25). Anti–TNF therapies (e.g. etanercept, adalimumab) are highly effective for psoriasis, and their use in our case initially helped control skin and joint symptoms. However, TNF inhibition has paradoxically been linked to new-onset or exacerbation of myositis in predisposed patients (25). Indeed, psoriasis patients exposed to TNF blockers in one series had a significantly higher odds of developing myopathy (OR ~4.45) (26), suggesting TNF may also have complex immunoregulatory roles. Type I interferons: DM, especially the cutaneous form, is strongly associated with a type I interferon gene signature. In contrast, psoriasis is classically a Th17/Th1 disease, but type I IFN can act as an upstream trigger – plasmacytoid dendritic cells infiltrating psoriatic skin produce IFN-α that helps initiate psoriatic plaques (27). We specifically highlight the immunopathogenesis of ASS, including anti-aminoacyl-tRNA synthetase antibodies, abnormal activation of autoreactive B cells, and type I interferon-driven immune response, clearly differentiating from dermatomyositis mechanisms. Thus, both conditions exhibit innate and adaptive immune interplay: IFN-α and TNF-α from innate immune cells drive activation of autoreactive T-cells (Th17, Th1), which then release IL-17, IFN-γ, TNF and other mediators. The overlapping cytokine profile (e.g. IL-6, IL-17, TNF, IFN) provides a mechanistic basis for why treating one disease can affect the other. It also suggests a genetic or immunologic predisposition in rare patients who develop both diseases. Notably, no shared HLA risk allele has been identified (psoriasis is tied to HLA-C06:02/B27, whereas antisynthetase/DM have links to HLA-DRB1*03/*08) (28), implying that the overlap arises from convergent inflammatory pathways rather than a common genetic cause. A Retrospective Cohort Study demonstrated that psoriatic patients with PsA or those who had received IL-17i treatment demonstrated a significantly higher risk of developing dermatomyositis (29).

Because psoriasis/PsA and inflammatory myopathies can produce overlapping clinical features, patients with both are at high risk of misdiagnosis. Skin manifestations of dermatomyositis may be mistaken for psoriasis, and vice versa. For example, DM classically causes erythematous scaly papules over extensor joints (Gottron’s papules), which could be confused with psoriatic plaques on the elbows, knees, or knuckles. In one reported case, a 41-year-old woman developed scaly erythematous lesions on her hands, elbows and knees and symmetric polyarthritis; this was initially diagnosed and treated as psoriatic arthritis, only to later be recognized as anti-MDA5 positive dermatomyositis when muscle weakness, rash distribution, and specific antibodies declared themselves (30). Our patient’s presentation also illustrates the potential for diagnostic confusion. She had a ten-year history of psoriasis and nail changes, then developed polyarthritis with dactylitic “sausage” toes and even sacroiliitis on imaging – all classic PsA features. However, concurrently she exhibited mechanic’s hands (hyperkeratotic fissuring of the fingertips) and interstitial lung disease (bibasilar fibrosis on CT with reduced diffusion capacity). Mechanic’s hands and unexplained ILD should raise suspicion for antisynthetase syndrome, but in a patient already known to have psoriatic disease, these findings could easily be attributed to psoriasis (e.g. mistaken as severe hand psoriasis or a drug-induced lung reaction). The key to diagnosis is recognizing features that cannot be explained by psoriasis/PsA alone. In our case, the presence of high-titer anti-Jo-1 antibodies, together with mechanic’s hands and ILD, was a red flag that psoriatic disease alone was not the full story. Indeed, anti-Jo-1 is specific for antisynthetase syndrome and is not associated with psoriasis. Thus, a careful history, thorough physical exam, and autoimmune serologies were crucial to establish the overlap diagnosis.

From a rheumatologic perspective, inflammatory arthritis in antisynthetase syndrome can mimic psoriatic arthritis. Antisynthetase patients often have a symmetric polyarthritis (sometimes erosive) that could be misdiagnosed as rheumatoid or psoriatic arthritis if the other hallmarks of myositis are subtle. Similarly, cutaneous signs like mechanic’s hands can resemble acral psoriasis or chronic hand dermatitis (31). It is noteworthy that antisynthetase syndrome has a range of cutaneous findings (rough, cracked skin on fingers, “dirty” hyperpigmented lesions) that dermatologists caution can look like more common conditions including psoriasis. Muscle symptoms may also be overlooked in the context of psoriatic disease. Patients with PsA frequently report fatigue and diffuse pain, which might mask or delay recognition of true muscle weakness. In our patient, creatine kinase was only mildly elevated at times despite active myositis, making muscle involvement less obvious. Such cases underscore the need for vigilance: clinicians should reassess any psoriatic patient who develops atypical features (unexplained ILD, proximal muscle weakness, distinct rashes) and consider screening with muscle enzymes or autoantibody panels. Conversely, in DM patients with chronic rash, a psoriatic component should be considered if lesions have the classic silver scale or if arthritis and nail dystrophy are present. In summary, diagnosing this overlap requires a high index of suspicion and often a multidisciplinary approach (dermatology, rheumatology, pulmonology) to piece together the two coexisting conditions.

Managing a patient with both psoriasis/PsA and an inflammatory myopathy is challenging, as therapies must be chosen to control both diseases without provoking the other. There are no established guidelines for this rare overlap, so treatment is largely individualized. Our case vividly demonstrated that a trial-and-error approach may be needed before finding a regimen that balances both conditions. Key therapeutic considerations include the following:

● Tumor Necrosis Factor (TNF) Inhibitors: TNF blockers (etanercept, adalimumab, etc.) are highly effective for moderate-severe psoriasis and PsA, and they were used early in our patient’s course. In the short term, etanercept helped our patient’s skin and joint symptoms. However, TNF inhibition does not treat myositis and may even worsen certain aspects. Our patient’s interstitial lung disease progressed while on etanercept, possibly because her antisynthetase syndrome was insufficiently controlled. There is also evidence that TNF inhibitors can trigger or unmask myositis in predisposed individuals: several reports detail new-onset dermatomyositis occurring after 2–6 months of etanercept or adalimumab therapy for arthritis (32). In one series of psoriasis patients, those exposed to TNF inhibitors had a significantly higher likelihood of developing inflammatory myopathy than those never treated with biologics (26). Although a causal relationship remains controversial, the implication is that TNF has a complex role – its blockade can precipitate autoimmunity (e.g. lupus-like syndromes, vasculitis, and rarely dermatomyositis) (32). We clarify that while TNF inhibitors have been associated with myositis onset or exacerbation, this remains an association rather than definitive causation. Clinicians should remain vigilant when using TNF inhibitors in patients predisposed to inflammatory myopathies.

● IL-17 and IL-23 Inhibitors: Agents targeting the IL-17/IL-23 pathway are highly effective for psoriasis and PsA, but caution is warranted in the setting of myositis. There have been reports of dermatomyositis onset or exacerbation temporally linked to IL-17 blockade. For example, a recent report described a psoriasis patient who experienced severe DM flares associated with secukinumab (IL-17A inhibitor) treatment (19). In our patient, after other therapies failed, we initiated secukinumab to control her psoriatic disease. This achieved partial improvement of skin and joint symptoms, but we observed a significant rise in muscle enzymes (CK climbed to >1200 U/L) despite the patient feeling no immediate weakness. This subclinical CK elevation suggested that IL-17 inhibition was aggravating her myositis. After 1 year on secukinumab, her CK had spiked further (>2700 U/L), prompting us to discontinue the IL-17 inhibitor. IL-23 p19 inhibitors (e.g. guselkumab) have not been reported in this overlap to our knowledge, but IL-12/23 inhibition with ustekinumab has been tried. Notably, one case of juvenile DM with psoriasis was successfully treated with ustekinumab, achieving remission of both skin and muscle inflammation (16). This aligns with mechanistic data that IL-23 is a driver of myositis as well as psoriasis (24). Due to the limited available data, the therapeutic role of newer biologics such as IL-23 inhibitors in PsA-ASS overlap remains unclear. Future studies specifically addressing this gap are warranted to clarify their clinical efficacy and safety.

● JAK Inhibitors: Janus kinase inhibitors (tofacitinib, baricitinib, upadacitinib, etc.) have emerged as an appealing option for overlapping psoriasis and myositis. These oral small molecules broadly modulate cytokine signaling (blocking pathways of IFN, IL-6, IL-12/23, etc.), which means they can potentially treat both Th17-mediated skin disease and interferon-mediated muscle disease simultaneously. Our patient’s most sustained remission was achieved with the JAK1/2 inhibitor baricitinib (4 mg daily) combined with low dose prednisone. Over 12 months, this regimen led to resolution of her arthritis and psoriatic lesions and normalization of CK levels, indicating control of the myositis. JAK inhibitors have shown efficacy in refractory dermatomyositis in recent studies, especially for patients with prominent interferon signatures (e.g. anti-MDA5 DM) – likely by inhibiting type I IFN signaling. In psoriasis and PsA, tofacitinib (a JAK3/1 inhibitor) is an approved therapy that improves both skin and joints. In one reported overlap case, a patient with severe psoriasis who developed DM after adalimumab was switched to the JAK1 inhibitor upadacitinib, with significant improvement in both diseases (5). Our patient similarly experienced improvement when we tried tofacitinib, though an intercurrent infection led us to change course at that time.

● Corticosteroids and Conventional Immunosuppressants: Systemic corticosteroids remain the first-line therapy for idiopathic inflammatory myopathies and were indispensable in our patient’s regimen. High-dose prednisone or intravenous methylprednisolone often yields rapid improvement in muscle strength and lung function in myositis (15). In our case, prednisone 40 mg daily stabilized the ILD and muscle disease when other drugs were withdrawn. The dilemma is that long-term steroids can worsen psoriasis and PsA (and steroid tapering may trigger psoriasis rebound or pustular flares). We managed this by maintaining a moderate steroid dose until other steroid-sparing agents took effect, and fortunately our patient did not experience a psoriatic flare upon taper. DMARDs: Traditional immunosuppressants like methotrexate (MTX), azathioprine, cyclosporine, and mycophenolate are commonly used as steroid-sparing agents in both psoriasis/PsA and myositis. MTX, for instance, can control PsA and has modest efficacy in myositis, though data are limited. Several reported overlap cases were treated successfully with methotrexate or azathioprine plus prednison (5). In our patient, we attempted cyclosporine and later tacrolimus (calcineurin inhibitors) alongside biologics; however, she did not tolerate cyclosporine and tacrolimus had to be stopped due to ILD progression. Ultimately, unconventional therapies like Tripterygium wilfordii (a Chinese herbal immunosuppressant) were also employed in our case to help control disease activity.

In conclusion, the coexistence of psoriasis/PsA with inflammatory myopathies like DM, PM, or antisynthetase syndrome, while rare, is an important clinical phenomenon that demands careful attention. Recognizing the overlap is clinically significant – it prompts comprehensive evaluation (including for ILD and autoantibodies) and a tailored management strategy. Shared immunopathogenic mechanisms, particularly the IL-17/IL-23 axis and other inflammatory pathways, likely underlie the link between these conditions, and targeting these pathways can be a double-edged sword. Diagnostic vigilance is required to distinguish overlapping features and avoid misdiagnosis. Management must be holistic and often multi-disciplinary, balancing therapies to control both muscle and skin/joint disease. Our case, placed in context with the literature, highlights both the challenges and potential solutions in treating this uncommon overlap syndrome. We acknowledge that conclusions drawn from the present single case and small number of previously reported cases should be interpreted with caution. Individualized treatment strategies remain essential in managing this rare overlap syndrome. As more cases are reported and studied, we will better elucidate the connections between these diseases and optimize care for patients who unfortunately encounter both.

Data availability statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding authors.

Ethics statement

Ethical approval was not required for the study involving humans in accordance with the local legislation and institutional requirements. Written informed consent to participate in this study was not required from the participants or the participants’ legal guardians/next of kin in accordance with the national legislation and the institutional requirements. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author contributions

RY: Writing – original draft. DK: Writing – original draft, Data curation, Conceptualization. YZ: Writing – original draft, Data curation. LL: Writing – original draft, Investigation. YL: Writing – review & editing, Supervision. SL: Visualization, Supervision, Writing – review & editing. XL: Writing – review & editing, Validation.

Funding

The author(s) declare that no financial support was received for the research and/or publication of this article.

Acknowledgments

We thank the patients and all the authors in the study.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declare that no Generative AI was used in the creation of this manuscript.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

1. Furst DE, Amato AA, Iorga ŞR, Gajria K, and Fernandes AW. Epidemiology of adult idiopathic inflammatory myopathies in a U.S. managed care plan. Muscle Nerve May. (2012) 45:676–83. doi: 10.1002/mus.23302

PubMed Abstract | Crossref Full Text | Google Scholar

2. Sofi F, Parrey A, Ahmad M, and Ahmad B. Psoriasis with polymyositis; a rare combination of two autoimmune diseases. Immunopathol Persa. (2018) 4:e01–. doi: 10.15171/ipp.2018.01

Crossref Full Text | Google Scholar

3. Mahler M, Miller FW, and Fritzler MJ. Idiopathic inflammatory myopathies and the anti-synthetase syndrome: a comprehensive review. Autoimmun Rev. (2014) 13:367–71. doi: 10.1016/j.autrev.2014.01.022

PubMed Abstract | Crossref Full Text | Google Scholar

4. Toshiyuki Y. Psoriasis and connective tissue diseases. Int J Mol Sci. (2020) 21(16):5803. doi: 10.3390/ijms21165803

PubMed Abstract | Crossref Full Text | Google Scholar

5. Chu D, Yang W, and Niu J. Concurrence of dermatomyositis and psoriasis: a case report and literature review. Front Immunol. (2024) 15:1345646. doi: 10.3389/fimmu.2024.1345646

PubMed Abstract | Crossref Full Text | Google Scholar

6. Okiyama N, Yamaguchi Y, Kodera M, Hamaguchi Y, Yokozeki H, Ishiguro N, et al. Distinct histopathologic patterns of finger eruptions in dermatomyositis based on myositis-specific autoantibody profiles. JAMA Dermatol. (2019) 155:1080–2. doi: 10.1001/jamadermatol.2019.1668

PubMed Abstract | Crossref Full Text | Google Scholar

7. Pinal-Fernandez I, Kroodsma CT, and Mammen AL. Successful treatment of refractory mechanic’s hands with ustekinumab in a patient with the antisynthetase syndrome. Rheumatol (Oxford). (2019) 58:1307–8. doi: 10.1093/rheumatology/kez020

PubMed Abstract | Crossref Full Text | Google Scholar

8. Hanami Y, Kumekawa M, and Yamamoto T. Psoriasis vulgaris in a patient with antisynthetase syndrome. J Dermatol. (2021) 48:e39–40. doi: 10.1111/1346-8138.15636

PubMed Abstract | Crossref Full Text | Google Scholar

9. Pavlovic MD, Zecevic RD, and Zolotarevski L. Psoriasis in a patient with dermatomyositis. Vojnosanit Pregl. (2004) 61:557–9. doi: 10.2298/vsp0405557p

PubMed Abstract | Crossref Full Text | Google Scholar

10. MaChado NP, Camargo CZ, Oliveira AC, Buosi AL, Pucinelli ML, and Souza AW. Association of anti-glomerular basement membrane antibody disease with dermatomyositis and psoriasis: case report. Sao Paulo Med J. (2010) 128:306–8. doi: 10.1590/s1516-31802010000500012

PubMed Abstract | Crossref Full Text | Google Scholar

11. Kim NN, Lio PA, Morgan GA, Jarvis JN, and Pachman LM. Double trouble: therapeutic challenges in patients with both juvenile dermatomyositis and psoriasis. Arch Dermatol. (2011) 147:831–5. doi: 10.1001/archdermatol.2011.49

PubMed Abstract | Crossref Full Text | Google Scholar

12. Dicaro D, Bowen C, and Dalton SR. Dermatomyositis associated with anti-tumor necrosis factor therapy in a patient with psoriasis. J Am Acad Dermatol. (2014) 70:e64–5. doi: 10.1016/j.jaad.2013.11.012

PubMed Abstract | Crossref Full Text | Google Scholar

13. Akiyama M, Ueno T, Kanzaki A, Kuwana M, Nagao M, and Saeki H. Association of psoriasis with Hashimoto’s thyroiditis, Sjogren’s syndrome and dermatomyositis. J Dermatol. (2016) 43:711–2. doi: 10.1111/1346-8138.13265

PubMed Abstract | Crossref Full Text | Google Scholar

14. Kato Y and Yamamoto T. Development of psoriasis with relapse of dermatomyositis-associated interstitial lung disease. Int J Rheum Dis. (2017) 20:660–1. doi: 10.1111/1756-185X.13084

PubMed Abstract | Crossref Full Text | Google Scholar

15. Inkeles MS, No D, and Wu JJ. Clinical improvement of a patient with both amyopathic dermatomyositis and psoriasis following treatment with cyclosporine. Dermatol Online J. (2017) 23(8):13030/qt5qh0n741. doi: 10.5070/D3238036019

PubMed Abstract | Crossref Full Text | Google Scholar

16. Montoya CL, Gonzalez ML, Ospina FE, and Tobon GJ. A rare case of amyopathic juvenile dermatomyositis associated with psoriasis successfully treated with ustekinumab. J Clin Rheumatol. (2017) 23:129–30. doi: 10.1097/RHU.0000000000000430

PubMed Abstract | Crossref Full Text | Google Scholar

17. Xing Y, Xie J, Jiang S, Upasana M, and Song J. Co-existence of Juvenile dermatomyositis and psoriasis vulgaris with fungal infection: A case report and literature review. J Cosmet Dermatol. (2019) 18:1560–3. doi: 10.1111/jocd.12869

PubMed Abstract | Crossref Full Text | Google Scholar

18. Schreiber C, Khamlong M, Raza N, and Huynh BQ. Overlap of psoriatic arthritis and dermatomyositis. J Investig Med High Impact Case Rep. (2021) 9:23247096211057702. doi: 10.1177/23247096211057702

PubMed Abstract | Crossref Full Text | Google Scholar

19. Perna DL, Callen JP, and SChadt CR. Association of treatment with secukinumab with exacerbation of dermatomyositis in a patient with psoriasis. JAMA Dermatol. (2022) 158:454–6. doi: 10.1001/jamadermatol.2021.6011

PubMed Abstract | Crossref Full Text | Google Scholar

20. Xu Z, Xu B, Zhao B, Gao H, Ye S, and Wu J. Treatment of refractory psoriasis with dermatomyositis using upadacitinib. Clin Exp Rheumatol. (2024) 42:458–9. doi: 10.55563/clinexprheumatol/ki4jbt

PubMed Abstract | Crossref Full Text | Google Scholar

21. Griffiths CEM, Armstrong AW, Gudjonsson JE, and Barker J. Psoriasis. Lancet. (2021) 397:1301–15. doi: 10.1016/S0140-6736(20)32549-6

PubMed Abstract | Crossref Full Text | Google Scholar

22. Johnson-Huang LM, Suárez-Fariñas M, Sullivan-Whalen M, Gilleaudeau P, Krueger JG, and Lowes MA. Effective narrow-band UVB radiation therapy suppresses the IL-23/IL-17 axis in normalized psoriasis plaques. J Invest Dermatol. (2010) 130:2654–63. doi: 10.1038/jid.2010.166

PubMed Abstract | Crossref Full Text | Google Scholar

23. Silva MG, Oba-Shinjo SM, Marie SKN, and Shinjo SK. Serum interleukin-17A level is associated with disease activity of adult patients with dermatomyositis and polymyositis. Clin Exp Rheumatol. (2019) 37:656–62.

PubMed Abstract | Google Scholar

24. Umezawa N, Kawahata K, Mizoguchi F, Kimura N, Yoshihashi-Nakazato Y, Miyasaka N, Kimura N, Yoshihashi-Nakazato Y, Miyasaka N, et al. Interleukin-23 as a therapeutic target for inflammatory myopathy. Sci Rep. (2018) 8:5498. doi: 10.1038/s41598-018-23539-4

PubMed Abstract | Crossref Full Text | Google Scholar

25. Kim GT, Cho ML, Park YE, Yoo WH, Kim JH, Oh HJ, et al. Expression of TLR2, TLR4, and TLR9 in dermatomyositis and polymyositis. Clin Rheumatol. (2010) 29:273–9. doi: 10.1007/s10067-009-1316-7

PubMed Abstract | Crossref Full Text | Google Scholar

26. Liewluck T, Ernste FC, and Tracy JA. Frequency and spectrum of myopathies in patients with psoriasis. Muscle Nerve. (2013) 48:716–21. doi: 10.1002/mus.23812

PubMed Abstract | Crossref Full Text | Google Scholar

27. Nestle FO, Conrad C, Tun-Kyi A, Homey B, Gombert M, Boyman O, et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production. J Exp Med. (2005) 202:135–43. doi: 10.1084/jem.20050500

PubMed Abstract | Crossref Full Text | Google Scholar

28. Rothwell S, Cooper RG, Lundberg IE, Miller FW, Gregersen PK, Bowes J, et al. Dense genotyping of immune-related loci in idiopathic inflammatory myopathies confirms HLA alleles as the strongest genetic risk factor and suggests different genetic background for major clinical subgroups. Ann Rheum Dis. (2016) 75:1558–66. doi: 10.1136/annrheumdis-2015-208119

PubMed Abstract | Crossref Full Text | Google Scholar

29. Chen M, Tian N, Cui R, Zhang H, Wang Q, Tong Q, et al. Increased risk of dermatomyositis in patients with psoriasis: A retrospective cohort study. Immunotargets Ther. (2025) 14:139–49. doi: 10.2147/itt.S500811

PubMed Abstract | Crossref Full Text | Google Scholar

30. Cabezas-Rodríguez I, Morante-Bolado I, Brandy-García A, Queiro-Silva R, Mozo L, and Ballina-García F. Anti-MDA5 dermatomyositis mimicking psoriatic arthritis. Reumatol Clin. (2018) 14:224–6. doi: 10.1016/j.reuma.2016.10.010

PubMed Abstract | Crossref Full Text | Google Scholar

31. Okiyama N and Fujimoto M. Cutaneous manifestations of dermatomyositis characterized by myositis-specific autoantibodies. F1000Research. (2019) 8:F1000 Faculty Rev-1951. doi: 10.12688/f1000research.20646.1

PubMed Abstract | Crossref Full Text | Google Scholar

32. Klein R, Rosenbach M, Kim EJ, Kim B, Werth VP, and Dunham J. Tumor necrosis factor inhibitor-associated dermatomyositis. Arch Dermatol. (2010) 146:780–4. doi: 10.1001/archdermatol.2010.142

PubMed Abstract | Crossref Full Text | Google Scholar