Case report
A 60-year-old male with a four year history of a relapsing and remitting itch presented with exacerbation of the itch for the past seven months to a tertiary care center. The rash had spread from the anterior chest to the abdomen, legs, and groin. The patient was initially treated by his general practitioner with mild and moderate topical steroids and topical clotrimazole, which temporarily subsided the itching and reduced the inflammation of the lesions. However, he reported that the lesions would erupt soon after discontinuing the steroid and antifungal creams, resulting in increased inflammation, pruritus and more widespread distribution. The patient continued to seek medical help from various doctors but experienced little to no improvement in his condition. He tried griseofulvin 150mg and terbinafine 250mg daily for five months without any relief. Griseofulvin and terbinafine were discontinued, and daily oral fluconazole 150mg was initiated, which also provided no relief after a month of use. Despite increased efforts to maintain personal hygiene, including showering two to three times per day and using antibacterial soaps, the patient found no relief. For the past month, the patient had been using first-generation oral antihistamines for symptomatic relief. He now states that he has developed dependence as he cannot experience undisturbed sleep without taking his nightly dose.
The patient appeared extremely distressed due to his symptoms and the financial burdens that accompanied his series of failed treatment trials. On examination, there were multiple coalescing irregularly-shaped, centrally clear lesions with erythematous, raised borders distributed across his body (Figures 1). He presented with no associated symptoms that may signify another annular skin eruption, such as subacute cutaneous lupus erythematosus, granuloma annulare, and erythema annulare centrifugum. Viral serology profile, sedimentation rate, antinuclear antibody test, and immunodeficiency workup were unremarkable. Potassium hydroxide preparation from skin scrapings revealed segmented hyphae. Subsequently, skin scrapings were cultured on two separate occasions, and in both instances, Trichophyton rubrum was recovered. At a three month follow-up, the patient still presented with itch and multiple coalescing irregularly shaped lesions with centrally clear areas and erythematous, raised borders distributed across his body. At this time, molecular identification using PCR was performed, which confirmed Trichophyton rubrum as the causative agent. In vitro susceptibility testing was conducted and the strain exhibited susceptibility to itraconazole. Treatment with itraconazole was initiated. At a two month follow-up, the patient appeared content and exhibited clinical improvement.