Psoriasiform Eruption in Kawasaki Disease: A Rare Cutaneous Manifestation in an Infant

Background: Kawasaki Disease (KD) is an acute systemic vasculitis primarily affecting children under five years old. It is the leading cause of acquired heart disease in pediatrics due to its risk of coronary artery complications. Classic features include bilateral non-exudative conjunctivitis, oropharyngeal changes, extremity edema, polymorphous rash, and cervical lymphadenopathy. The cutaneous findings often resemble morbilliform, scarlatiniform, or urticarial eruptions. Psoriasiform eruptions, however, are rare. This report describes an infant with KD who developed a psoriasis-like rash, highlighting the need to recognize atypical dermatologic presentations and their implications for diagnosis and management. Case Presentation: A previously healthy 4-month-old male presented with a five-day history of fever, irritability, and a generalized maculopapular rash. On admission, he was febrile (39.2°C), tachycardic, and dehydrated. Examination revealed bilateral non-exudative conjunctivitis, cracked lips, a strawberry tongue, and erythema with edema of the palms and soles, but no cervical lymphadenopathy. Laboratory tests showed leukocytosis, anemia, thrombocytosis, and elevated inflammatory markers. Liver function tests revealed mild transaminitis, and a respiratory viral panel detected rhinovirus, while blood cultures were negative. Initial echocardiography was normal. He was diagnosed as KD with high-risk features and treated with IVIG (2 g/kg), IV methylprednisolone (10 mg/kg/day for three days), oral prednisolone (2 mg/kg/day), and high-dose aspirin (50 mg/kg/day). Fever resolved within 36 hours, with clinical and laboratory improvement. However, on day 5, the patient developed erythematous scaly plaques on the trunk and lower extremities, resembling psoriasiform eruptions along with recurrence of lip erythema. Repeat echocardiography revealed mild coronary artery dilation, prompting a second IVIG dose. The rash was managed with emollients and low-potency corticosteroids. At two weeks, systemic symptoms had resolved, but the psoriasiform rash persisted. A skin biopsy supported a psoriasis-like eruption. By six weeks, inflammatory markers had normalized, coronary dimensions remained stable, and the rash gradually faded. Discussion: Psoriasiform eruptions in KD are rare but increasingly recognized. A literature review suggests heterogeneous presentations, including transient pustular or guttate psoriasis and persistent plaque-type lesions. Most cases occur during the acute phase of KD, while others emerge in the convalescent period. While most patients experience complete resolution following standard KD treatment, some cases persist beyond disease resolution. The pathophysiology of KD-associated psoriasis remains speculative. Cytokine dysregulation is a key theory, as KD and psoriasis share IL-6, IL-17, and TNF-alpha-mediated inflammatory pathways that may trigger psoriasiform eruptions. Similarly, the superantigen hypothesis links bacterial superantigens in KD pathogenesis to guttate psoriasis through a common immune pathway. Additionally, IVIG-induced psoriasis has been documented, with IVIG paradoxically triggering inflammatory skin reactions, including psoriasis-like eruptions, which may have occurred in our case. Conclusion: This case adds to the limited literature on KD-associated psoriasiform eruptions. Given the possible immunological overlap between KD and psoriasis, further research is needed to determine whether these eruptions represent a distinct dermatologic phenotype within KD or an immune-mediated sequela of systemic inflammation. Clinicians should recognize atypical cutaneous findings in KD, as they may influence treatment strategies and long-term dermatologic outcomes.