Hypereosinophilia in Erythrodermic Psoriasis: Superimposed Scabies

Comment

Erythrodermic psoriasis is a severe form of psoriasis. In the 2010 consensus of the National Psoriasis Foundation medical board, it was reported that cyclosporine and infliximab are the fastest and most effective agents in treating erythrodermic psoriasis.¹

Progressive increases in the number of eosinophils prompted us to screen our patients for causes of hypereosinophilia. Increased eosinophil counts have not been linked to treatment with cyclosporine. In contrast, it has been detected that cyclosporine reduces the number of eosinophils in many eosinophilic dermatoses.²

There is no hematologic finding for scabies; therefore, clinical findings are most important in the diagnosis. Crusted scabies is a special form of scabies seen in immunocompromised patients that is characterized by excessive numbers of scabies mites. Peripheral eosinophilia may be observed in this form of the disease.³ In classic scabies, eosinophilia is uncommon in peripheral blood. In contrast with these data, there are 2 cases in the literature of scabies secondary to disorders of keratinization without immune deficiency with different clinical presentations.⁴ In these patients, the most striking and only finding at the time of diagnosis was substantial eosinophilia. These cases were reported with emphasis on eosinophilia as the first sign of scabies infestation in patients with severe hyperkeratosis.⁴ In our patients, the spread of infection may have been facilitated by the immunosuppressive effects of cyclosporine in addition to the existing disease. Crusted scabies after use of cyclosporine for atopic dermatitis has been reported. It was emphasized that suppression of scratching and immunosuppression due to cyclospor-ine caused the spread of scabies mites in the skin.⁵

Burrows, vesicles, and erythematous papules are typical lesions seen in scabies. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. In our patients, widespread erythema and scaling were noted, and pruritus was thought to be due to psoriasis lesions. Because of excessive scaling in the stratum corneum from psoriasis, the clinical features of scabies were concealed and the classic clinical signs of scabies were not present. The patients’ hypereosinophilia led us to investigate the cause. A lesional biopsy and direct microscopy demonstrated scabies mites.

Conclusion

The relationship between psoriasis and scabies previously has been reported in the literature as scabies with crusts mimicking rupioid psoriasis.⁶ However, our patients developed scabies in the setting of psoriasis. Severe scabies can present as erythroderma.⁷ We believe the diagnosis of scabies in our patients would have been more complicated without the preexisting psoriasis, as biopsies of erythrodermic psoriasis often are nonspecific and may contain eosinophils in the inflammatory infiltrate. Although pruritus may be interpreted as a result of the primary dermatologic disease, the presence of hypereosinophilia may suggest scabies in erythrodermic patients. For this reason, peripheral eosinophilia may suggest scabies in patients with erythematous scaly inflammatory skin diseases who are treated with immunosuppressive agents, and a search for scabies mites in skin scrapings should be undertaken.