ABSTRACT
The onset of psoriasis is often seen in HIV infection, called HIV-associated psoriasis. Although HIV-associated psoriasis is usually refractory, there are some cases relieved only by antiretroviral therapy. In those cases, the pathogenesis may be formed differently from psoriasis vulgaris. We present the case of a 42-year-old Japanese man with HIV-associated psoriasis. The patient developed a systemic scaly eruption, especially on the soles. Histopathological examination showed typical psoriatic findings and plasma cell infiltration into the dermis. The eruption dramatically remitted with antiretroviral therapy alone, without systemic treatment for psoriasis. In immunohistological findings, few CD4+ cells were seen in the patient's skin. In addition, immunofluorescent staining revealed more BDCA-2 and CD123 double-positive plasmacytoid dendritic cell infiltration into the dermis than that of psoriasis vulgaris. We suggest that the immune response to HIV including plasmacytoid dendritic cell infiltration may involve in the development and remission of HIV-associated psoriasis.
Subject(s)
Anti-Retroviral Agents/therapeutic use , Dendritic Cells/immunology , HIV Infections/drug therapy , Psoriasis/drug therapy , Adult , Dermis/cytology , Dermis/immunology , Dermis/pathology , HIV Infections/complications , HIV Infections/immunology , Humans , Interleukin-3 Receptor alpha Subunit/analysis , Lectins, C-Type/analysis , Male , Membrane Glycoproteins/analysis , Psoriasis/immunology , Psoriasis/pathology , Receptors, Immunologic/analysis , Treatment OutcomeABSTRACT
Rubinstein-Taybi syndrome (RTS) is an autosomaldominant hereditary disease, which contains many skeletal and organ anomalies as well as mental retardation. Although high incidence of keloids in RTS is known, it is difficult to find a detailed report on the clinical features of keloids. In the following letter, we report an RTS patient fulfilling diagnostic criteria whosuffered from both keloids and pilomatricoma. We also performed a literature search, which identified the possible involvement of the Wnt/ß-catenin signaling pathway in the pathogenesis of these two skin lesions.
Subject(s)
Keloid/genetics , Pilomatrixoma/genetics , Rubinstein-Taybi Syndrome , Adult , Cyclic AMP Response Element-Binding Protein/genetics , Cyclic AMP Response Element-Binding Protein/metabolism , Humans , Keloid/pathology , Male , Rubinstein-Taybi Syndrome/genetics , Signal Transduction , Wnt Proteins/metabolism , beta Catenin/metabolismABSTRACT
A 29-year-old man diagnosed as having pulmonary sarcoidosis in 2008, and hypothyroidism secondary to thyroidectomy for Basedow's disease was admitted to our hospital with pustular psoriasis in November 2010. He experienced high fever (38°C) and headache in late October 2010. Gadolinium-enhanced T1-weighted image showed multiple micronodular lesions with leptomeningeal enhancement, mainly in the brainstem. Cerebrospinal fluid (CSF) analysis revealed pleocytosis, raised protein level and hypoglycorrhachia (7 mg/dl). The patient was also found to have osteonecrosis of the left femoral head. Antituberculous treatment and steroid pulse therapy were started, but produced no improvement of either the symptoms or the laboratory data. Finally, the patient was diagnosed as having meningeal disseminated sarcoidosis by meningeal biopsy in late March 2011. He was started on treatment with 60 mg prednisolone per day, which resulted in marked clinical improvement. It should be borne in mind that marked hypoglycorrhachia in the CSF can also be seen in meningeal disseminated sarcoidosis.
