Hystrix-like ichthyosis and deafness (HID) syndrome is a rare ectodermal dysplasia characterized by erythrokeratoderma and hearing impairments. HID syndrome is a nonocular variant of keratitis ichthyosis deafness (KID) syndrome caused by an autosomal dominant mutation in the gap junction protein β 2 (GJB2) gene. The GJB2 gene encodes connexin 26, a transmembrane protein involved in cell–cell attachment in almost all tissues. We report a case of a 25-year-old man with generalized hyperkeratotic plaques, diffuse palmoplantar keratoderma, and nail deformities since birth. The patient also had a history of recurrent bacterial skin infections in the existing hyperkeratotic lesions. Histopathological examination revealed compact hyperkeratosis and irregular acanthosis in the epidermis, along with upper dermal lymphocytic infiltration. Audiometry revealed high-frequency sensorineural hearing loss. Genetic analysis revealed a missense mutation in the GJB2 gene. Based on clinicopathological findings and genetic testing, HID syndrome was diagnosed.

Granuloma annulare is a relatively common inflammatory skin disease. The etiology is unknown; however, drugs have been considered as one of the predisposing conditions, and a few cases of granuloma annulare related to biologics have been recently reported. A 48-year-old man with a 25-year history of psoriasis visited our dermatological clinic. Ustekinumab was administered for the treatment of psoriasis. After 5 years of ustekinumab therapy, erythematous papules with an annular distribution appeared on his trunk and extremities. Skin biopsy supported the diagnosis of generalized granuloma annulare, and the patient continued to receive ustekinumab with oral methotrexate, cyclosporine, and steroids for 9 months. However, as the skin lesions aggravated, oral steroid treatment was continued, and secukinumab was administered instead of ustekinumab. The skin lesions improved and remained stable with the intermittent administration of oral steroids thereafter.