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Chronic pruritus is a complex and often multifactorial clinical condition that may evolve beyond its initial inflammatory trigger, leading to significant diagnostic and therapeutic challenges. We report the case of a 45-year-old female who developed a persistent and progressively refractory pruritic disorder following arthropod exposure, clinically consistent with bedbug exposure. The condition evolved from an acute inflammatory eruption into a chronic state characterized by severe itch, evolving lesion morphology, and incomplete response to antihistamines and corticosteroids despite stepwise escalation, including leukotriene receptor antagonists and prolonged corticosteroid therapy. The presence of ecchymotic lesions early in the disease course prompted extensive hematologic and autoimmune evaluation, which was unremarkable. Over time, the clinical pattern shifted toward a neurogenic phenotype with strong psychophysiologic modulation, particularly in relation to stress. The patient demonstrated significant improvement following initiation of neuromodulatory therapy with gabapentin and mirtazapine. This case emphasizes the clinical importance of early recognition of a clinically inferred neuroimmune transition to avoid ineffective therapeutic escalation and enable mechanism-based, targeted neuromodulatory management in refractory cases.
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Para et al. (2026) studied this question.
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