The interleukin (IL)-17 axis is involved in many inflammatory and autoimmune diseases. Secukinumab, an IL-17 inhibitor, has been approved for psoriasis treatment. There are accumulating cases of lupus erythematosus induced by IL-17 inhibition. Lupus nephritis after IL-17 inhibition has not been reported. We report the case of a 57-year-old man who developed membranous lupus nephritis after secukinumab treatment for psoriasis. Anti-SSA and PM-Scl antibodies were positive. dsDNA, anti-Smith, and anti-histone antibodies were negative, and serum complement was low. Secukinumab was discontinued, while tacrolimus was initiated, subsequently switched to cyclosporin, belimumab, glucocorticosteroid, and hydroxychloroquine with a good response. The relationship between lupus erythematosus and IL-17 inhibition requires further research.

A 50-year-old woman presented with a mandibular second molar and facial pain and was diagnosed with idiopathic trigeminal neuralgia. Carbamazepine (CBZ) was initiated at 300 mg/day, successfully relieving the pain. However, on the 8th day of CBZ treatment, the patient developed symptoms resembling those of systemic lupus erythematosus with malaise, nausea, and facial erythema. CBZ was immediately discontinued. Subsequently, she experienced numbness in both lower limbs and mild fever, which resolved within a few days. Laboratory tests revealed leukopenia (2.8 × 103/μL), elevated C-reactive protein levels (0.46 mg/dL), and the presence of antinuclear antibodies (ANA) and anti-Sjögren\'s syndrome-related antigen A antibodies. The clinical course suggested CBZ-induced drug-induced lupus erythematosus (DILE). This case highlights the possibility of DILE onset even after short-term CBZ treatment, the importance of prompt discontinuation of the causative drug in patients suspected of DILE, and the conduct of ANA testing in diagnosing DILE.

Tumor necrosis factor-alpha (TNF-α) inhibitors are associated with lupus-like disease, known as anti-TNF-α-induced lupus (ATIL). Cytomegalovirus (CMV) was reported to exacerbate lupus in the literature. To date, systemic lupus erythematosus (SLE) triggered by adalimumab in the setting of CMV infection has never been described. We present an unusual case of a 38-year-old female with a past medical history of seronegative rheumatoid arthritis (SnRA) who developed SLE associated with the use of adalimumab and CMV infection. She had severe SLE features including lupus nephritis and cardiomyopathy. The medication was discontinued. She was initiated on pulse steroid therapy and discharged with an aggressive regimen for SLE, including prednisone, mycophenolate mofetil, and hydroxychloroquine. She remained on the medications until a year later upon follow-up. ATIL from adalimumab usually manifests only mild symptoms of SLE such as arthralgia, myalgia, and pleurisy. Nephritis is very rare, and cardiomyopathy is unprecedented. Concomitant CMV infection might contribute to disease severity. Patients with SnRA may have an increased risk of developing SLE later when exposed to such medications and infection.

Although secukinumab has demonstrated high efficacy and favorable safety in moderate-to-severe psoriasis and psoriatic arthritis, patients developing adverse events of special interest (AESI) were reported increasingly in real-world practice. A systematic literature search of the PubMed database was conducted to identify clinical studies or case reports on secukinumab-induced AESI. More than 1077 patients (aged 18-74 years) from 55 studies were reported to have 24 AESI 3 days to 96 weeks after secukinumab treatment. The four most common AESI was inflammatory bowel disease (n > 1000), eczematous drug eruption (n > 30), drug-associated vasculitis (n = 8), and drug-induced lupus erythematosus (n = 4). Most of these AESI were only mild to moderately severe and resolved after secukinumab discontinuation without or with symptomatic treatment. Secukinumab has the potential to develop a number of AESI by probably dysregulating the different expression of polar T-cell axes (Th1, Th2, Th17, Th22, and/or Treg) and driving various cytokines in some patients. Physicians should be aware of these AESI for timely diagnosis and proper treatment.

Drug-induced lupus erythematosus (DILE) is a syndrome that manifests with symptoms similar, but with less severity, to that of systemic lupus erythematosus (SLE). Many medications are reported to be involved in DILE; however, terbinafine (Lamisil) is not a well-known causative agent of this syndrome. In this case report, we present a 22-year-old male patient with no prior medical history presented with worsening fever, rash, joint pain, and weight loss a couple of weeks after starting terbinafine. He underwent an extensive workup which revealed worsening kidney function, proteinuria, and microscopic hematuria, for which he underwent a renal biopsy which revealed class IV lupus nephritis. He was treated with prednisone taper and immunosuppressants with subsequent resolution of his symptoms. Close monitoring for the development of DILE symptoms is recommended after starting terbinafine, especially in patients with a known personal or family history of SLE.

A 74-year-old man developed with left pleural effusion and was suspected of benign asbestos pleural effusion and tuberculous pleurisy. Because of elevation of ADA level in the pleural effusion, diagnostic treatment for tuberculous pleurisy by anti-tuberculosis drugs was performed. However, right pleural effusion, cutaneous/mucosal lesions, leukocytopenia, and fever elevation occurred. The pathology of skin biopsy was consistent with systemic lupus erythematosus (SLE). Since clinical findings did not improve even after discontinuation of all drugs, he received steroid therapy was started and clinical findings improved. He was suspected of late-onset SLE. In conclusion, lupus pleurisy should also be differentiated when pleural effusion is seen in older. Late-onset SLE and drug-induced lupus should be carefully differentiated based on the clinical course.

Cutaneous drug-induced lupus erythematosus (CDILE) is a lupus-like syndrome related to drug exposure which typically resolves after drug discontinuation. It can present as a systemic or a sole cutaneous form and different drugs may be associated with each form. CDILE pharmacoepidemiology is constantly changing. Indeed, older drugs primarily associated with systemic CDILE are no longer prescribed and new drugs associated with either cutaneous or systemic CDILE have emerged. The present study discusses the clinical and laboratory aspects of CDILE and the postulated pathogenesis, and it provides an update on implicated drugs. We performed a literature review to single out the new drugs associated with CDILE in the past decade (January 2010-June 2020). Among 109 drugs reported to induce CDILE in 472 patients, we identified anti-TNFα, proton-pump inhibitors, antineoplastic drugs, and, in particular, checkpoint inhibitors, as emerging drugs in CDILE. Most of the published studies are cases reports or small case series, and further larger studies as well as the development of validated classification criteria are needed to better understand and characterize their implication in CDILE.

暂无摘要。

We report a 38-year-old female patient affected with anti-citrullinated protein antibody (ACPA)-positive rheumatoid arthritis (RA) who developed mild hemolytic anemia (Hb = 10.5 vs. >12 gr/dL), indolent oral ulceration, ANA (1:1280, homogeneous pattern), and anti-dsDNA antibody positivity following 8 months of therapy with an adalimumab biosimilar (GP2017). Rhupus syndrome was diagnosed. Replacing GP2017 with infliximab, anemia, oral ulcer, and anti-dsDNA antibodies quickly disappeared, while low-titers (1:80) ANA are still present after more than a year. The possibility that the patient suffered from rhupus rather than drug-induced lupus erythematosus associated to anti-ACPA positivity RA was discussed. To date, after a 14-month follow-up, no manifestations of LE have reappeared. To the best of our knowledge, this is the first report of adalimumab-induced rhupus.

暂无摘要。