Green nail syndrome (GN) is a rare condition often caused by Pseudomonas aeruginosa, typically affecting individuals with damaged nails, psoriasis, or those exposed to moist environments. Deucravacitinib, an oral tyrosine kinase 2 (Tyk2) inhibitor, is a treatment for psoriasis, but its role in GN development has not been explored. This report presents a case of GN in a 72-year-old man who developed the condition after four months of deucravacitinib treatment. Given the absence of prior nail psoriasis or trauma, it is suggested that deucravacitinib may have contributed to the development of GN. The inhibition of interleukin-10 (IL-10) signaling by Tyk2 suppression may have impaired the immune response against P. aeruginosa, leading to the infection. This is the first reported case linking deucravacitinib with GN.
Green nail syndrome (GN), characterized by green discoloration of the nail plate, was first described in 1944 by Goldman and Fox as a result of Pseudomonas aeruginosa infection. The condition is typically marked by a triad of green discoloration, proximal paronychia, and distal onycholysis. While P. aeruginosa is an opportunistic pathogen, it generally infects individuals with predisposing factors such as damaged nails, psoriasis, or frequent exposure to moist environments. Commonly, GN is treated with topical antibacterial agents, with resolution typically occurring within four to six months. In rare cases, P. aeruginosa infections may lead to severe complications, particularly in immunocompromised individuals.
Psoriasis, a chronic autoimmune condition, contributes to a range of systemic comorbidities, including psoriatic arthritis, cardiovascular diseases, and metabolic syndromes. In psoriasis vulgaris, activated T helper (Th)1 and Th17 cells play a central role in the inflammation and keratinocyte hyperproliferation observed in affected skin. Treatment for psoriasis includes both injectable therapies targeting IL-17 and IL-23, and oral treatments such as deucravacitinib, a selective Tyk2 inhibitor. This drug has demonstrated efficacy in treating psoriasis vulgaris, but to date, no cases of GN associated with deucravacitinib have been reported.
A 72-year-old male with a decade-long history of psoriasis presented to our dermatology department after worsening symptoms despite topical corticosteroid and calcipotriol treatment. He also had a history of hypertension but no significant history of immune system disorders. On examination, he exhibited scattered erythematous plaques with scaling on his limbs and trunk. His psoriasis area and severity index (PASI) score was 18.4, but no systemic symptoms such as arthritis or gastrointestinal issues were noted. Given the severity of his condition, the patient was started on deucravacitinib, an oral Tyk2 inhibitor, following normal laboratory and radiological results.
Four months into treatment, the patient’s PASI score improved to 4.2; however, green nail syndrome was noted at the follow-up visit. Notably, the patient had no history of nail trauma or frequent exposure to water. Furthermore, there were no signs of nail psoriasis prior to starting treatment, leading to suspicion that deucravacitinib might have contributed to the development of GN.
Bacterial cultures from the nail were negative, and repeated fungal tests also yielded no results. Suspecting P. aeruginosa as the causative agent, we initiated topical treatment with 1% nadifloxacin, a commonly used antibacterial agent for GN. Two months later, there was significant improvement, and complete resolution was achieved after four months.
Deucravacitinib is a novel oral treatment for psoriasis vulgaris that selectively inhibits Tyk2, a member of the Janus kinase (JAK) family involved in the signaling of key cytokines such as IL-12, IL-23, and type I interferons. These cytokines play crucial roles in psoriasis pathogenesis. While deucravacitinib has shown effectiveness in reducing psoriasis symptoms, common side effects include nasopharyngitis, upper respiratory infections, headache, and gastrointestinal issues, though severe adverse events are rare.
In this case, the development of GN is of particular interest. Interleukin-10 (IL-10) plays a critical role in regulating immune responses to P. aeruginosa. Tyk2 mediates IL-10 signaling, which helps maintain an effective immune response against infections. Deucravacitinib’s inhibition of Tyk2 may impair this immune pathway, weakening the T-cell response to P. aeruginosa and promoting bacterial proliferation, which could explain the onset of GN in this patient.
Interestingly, other JAK inhibitors, such as upadacitinib, which also interfere with IL-10 signaling, could theoretically produce similar outcomes, suggesting that this pathway may be a critical point of concern for patients on Tyk2 inhibitors.
While GN is typically associated with risk factors like nail trauma or psoriasis, this patient developed the condition without any of these predisposing factors, highlighting the potential role of Tyk2 inhibition in increasing susceptibility to P. aeruginosa infection.
This case highlights a previously unreported side effect of deucravacitinib therapy: the development of green nail syndrome, potentially linked to impaired IL-10 signaling and a weakened immune response to P. aeruginosa. Given the risks posed by P. aeruginosa, particularly in immunocompromised patients, early detection and treatment of GN are crucial. Further studies and case reports are needed to assess the broader implications of Tyk2 inhibition in immune function and the potential for unexpected side effects, including infections such as GN. As deucravacitinib is a relatively new drug, ongoing monitoring and research are essential to fully understand its safety profile.
Related topics
