Assessing the relationship between topical corticosteroid phobia and susceptibility to misinformation in patients with atopic dermatitis

Abstract

Physical examination revealed a maculopapular erythematous rash on his trunk and extremities (Fig. 1g,h). PBC revealed eosinophilia (1650/µL; 21.0% of WBC 7860/µL). Histopathological examination showed vacuolar dermatitis with spongiotic changes. (Fig. 1i). After discontinuation of apalutamide and administration of daily oral prednisolone (10 mg, 0.15 mg/kg), the skin lesions improved rapidly, and prednisolone was tapered and discontinued within a week.In addition to the three cases presented here, five other cases of apalutamide-induced drug eruption have been reported in the English or Japanese literature (Table 1). 4-7 All of our three cases exhibited maculopapular-type drug eruption accompanied by vacuolar dermatitis. Cutaneous adverse reactions observed in other reports included two cases of toxic epidermal necrolysis (TEN) and lichenoid drug eruption, and one case of urticaria. Both TEN cases died, and the urticaria case could only continue apalutamide treatment with dose reduction. The average time to onset of rash in these eight cases was 9 weeks, which was similar to 68.9 days reported in the PCR1008 study. 1 These intervals are longer than the 4-21 days observed for general drug eruptions, and lichenoid drug eruptions usually develop slowly. 8,9 Therefore, Tohyama assumed that most of the drug eruptions caused by apalutamide were of the lichenoid type. 7 Notably, our Case 1 exhibited lichenoid clinical findings on the extremities, but the histopathological result was not consistent with lichenoid reaction. Apalutamide may cause drug eruptions by a different mechanism than T-cell-mediated drug eruptions. Although rash is considered a common adverse event in clinical trial studies, 1-3 only a few reports describe the characteristics of apalutamide-induced drug eruption. This is the first report of a case series of apalutamide-induced drug eruptions at the same institution. Management of rash caused by apalutamide is important for dermatologists, and further accumulation of data on new cases is desirable.

Topical Corticosteroid Phobia Among Women Affected With Vulvar Lichen Sclerosus: Results From a Cross-sectional Survey

“…27 Furthermore, higher levels of TCP were recorded in subjects considered at a high risk of being misinformed, as determined by the results of a specifically structured questionnaire, namely, the bullshit receptivity score system. 28 In this regard, it should not be overlooked that the mean age of the study patients was relatively high. Online health-seeking behavior and access to online based resources, which seems to fuel corticophobia, 24,27 tend to be less frequent among older subjects.…”

“…On the other hand, previous studies showed that the main sources of misinformation on TCs, in terms of exaggerated risks, are friends/family and the Internet 27 . Furthermore, higher levels of TCP were recorded in subjects considered at a high risk of being misinformed, as determined by the results of a specifically structured questionnaire, namely, the bullshit receptivity score system 28 . In this regard, it should not be overlooked that the mean age of the study patients was relatively high.…”

Corticophobia among Parents of Children with Atopic Dermatitis: Assessing Major and Minor Risk Factors for High TOPICOP Scores

“…This can lead AD patients and their caregivers opting for nonconventional treatment options, to find quick fixes for their cutaneous issues that have great visual and psychosocial impact. Especially at risk of experiencing corticophobia are those who are more susceptible to pseudo-profound information, namely information that is encoded in profound sounding statements, which actually make very little sense [13]. Indeed, AD has a complex multifactorial aetiology, which is at higher risk of formulation of false myths and diffusion of misinformation, as many different systems are involved in the true disease aetiology, including skin-barrier dysfunction, T helper 2 cell-skewed immunity, and dysbiosis [11].…”