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.