Subject(s)
Genital Diseases, Female/etiology , Genital Diseases, Male/etiology , HIV Infections/complications , Skin Diseases/etiology , Female , Genital Diseases, Female/diagnosis , Genital Diseases, Female/therapy , Genital Diseases, Male/diagnosis , Genital Diseases, Male/therapy , Humans , Immunocompromised Host , Male , Skin Diseases/diagnosis , Skin Diseases/therapyABSTRACT
We review the clinical features, histopathology, and immunohistochemistry in three cases of eosinophilic histiocytosis, comparing lymphomatoid papulosis and eosinophilic histiocytosis. Each of the patients presented with self-healing recurrent papules and ulcerative nodules that were associated with pruritus. Disease duration was 5 months to 9 years. Histologically, the lesions demonstrated spongiosis and lymphocytic exocytosis, epidermal hyperplasia, papillary dermal edema, and a superficial and deep mixed perivascular inflammatory infiltrate. The infiltrate showed numerous eosinophils, histiocytoid cells, lymphocytes, and large mononuclear cells with atypical hyperchromatic nuclei. Most of the lymphocytes and large mononuclear cells with atypical nuclei marked with UCHL-1 (T-cell marker). The histiocytoid cells marked with S-100 and were dendritic both in the epidermis and the dermis. Eosinophilic histiocytosis appears to differ from classic lymphomatoid papulosis. It presents with recurrent papules and nodules associated with marked pruritus. Eosinophilic histiocytosis uniformly has more eosinophils and does not have the Reed-Sternberg cells often observed in lymphomatoid papulosis type A. Eosinophilic histiocytosis does not have cells that mark with Ki-1 and shows numerous S-100-positive histiocytoid cells that are most likely Langerhans cells, unlike lymphomatoid papulosis. However, eosinophilic histiocytosis may be an unusual Ki-1-negative variant of lymphomatoid papulosis with histopathologic changes not typical of type A or type B. In addition, eosinophilic histiocytosis lacks multinucleated histiocytes and the atypical histiocyte with a reniform nucleus, findings that are characteristic of histiocytosis X. Further studies are needed to define the pathophysiology and prognosis of this apparently distinct entity more accurately.
Subject(s)
Eosinophilia/pathology , Histiocytosis/pathology , Skin Diseases, Papulosquamous/pathology , Adult , Aged , Aged, 80 and over , Chromatin/ultrastructure , Dendritic Cells/pathology , Edema/pathology , Eosinophilia/metabolism , Eosinophils/pathology , Epidermis/pathology , Exocytosis , Female , Histiocytosis/metabolism , Humans , Hyperplasia , Immunohistochemistry , Leukocytes, Mononuclear/pathology , Lymphocytes/pathology , Lymphomatoid Papulosis/pathology , Male , Pruritus/pathology , Recurrence , S100 Proteins/analysis , Skin Diseases, Papulosquamous/metabolism , T-Lymphocytes/pathologyABSTRACT
Squamous syringometaplasia, squamous metaplasia of eccrine glands, is considered to be an important component of pseudoepitheliomatous hyperplasia, which can be a response to a variety of conditions. Recently, squamous syringometaplasia was described as occurring in lobular panniculitis, pancreatic panniculitis, and pyoderma gangrenosum. We report a case of annular elastolytic granuloma with associated squamous syringometaplasia. The initial biopsies were superficial, and the squamous syringometaplasia extended to the base of the specimen, closely resembling squamous cell carcinoma. Immunohistochemical stains for carcinoembryonic antigen outlined eccrine structures. The special stains and an excisional biopsy helped confirm the diagnosis. In addition, the clinical course has been consistent with the diagnosis of annular elastolytic granuloma. It is postulated that the dense granulomatous inflammatory infiltrate in annular elastolytic granuloma damages the eccrine structures, and this damage initiates the process.
