Biomedical subjects
Publications and source records attributed to K Klepzig.
In 3 patients suffering from follicular center-cell-derived B-cell lymphoma with primary cutaneous manifestation, antiadult T-cell leukemia-associated antigen antibodies were detected by the ELISA. In one of the patients, the husband and the dog had died from thymoma and from malignant lymphoma, respectively.
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A survey is given on 23 patients (10 of our own, 13 reported in personal communications and in the literature) suffering from lymphoproliferative diseases and treated with acyclovir (ACV). In 5 patients (3 of 18 with cutaneous T-cell lymphomas, 2 of 5 with lymphomatoid papulosis) partial remission could be achieved. Since herpes simplex virus, cytomegalovirus and viruses like Epstein-Barr and varicella-zoster do not play an etiologic role and since HTLV-I virus, due to its lack of thymidine kinase, cannot activate ACV, the following mechanisms should be discussed regarding the possible effectiveness of ACV in lymphoproliferative diseases: a direct cytopathic effect; activation of ACV by the thymidine kinase of viruses not yet detected in cutaneous lymphoproliferative disorders; ACV activation by cellular thymidine kinase, which has been found to be elevated in lymphoproliferative disorders. Preliminary clinical observations suggest that ACV may exhibit an antiproliferative effect intravenously in some patients with lymphomatoid papulosis.
Atypical cells resembling Reed-Sternberg cells are a characteristic histologic feature of lymphomatoid papulosis. Thus far no consistent data are available on the nature of these cells, or a possible antigenic relationship between them and Reed-Sternberg cells. Twenty-four biopsy specimens from 14 patients with lymphomatoid papulosis were immunolabeled with antibodies against Ki-1 and other Reed-Sternberg cell-associated antigens. In all cases a proportion of the large, atypical cells expressed the Ki-1 antigen. In contrast, in 20 biopsy specimens of benign inflammatory skin lesions or mycosis fungoides, Ki-1-positive cells were absent or only occasionally present. Furthermore, the large atypical cells of lymphomatoid papulosis also expressed other antigens (for example, T3, T4, HLA-DR, IL-2 receptors) that have previously been demonstrated on Reed-Sternberg cells. Our findings, together with the observation that the Ki-1 antigen can be induced on peripheral blood lymphocytes after prolonged phytohemagglutinin stimulation, suggest that the Ki-1-positive cells in lymphomatoid papulosis are activated T cells closely related to the Reed-Sternberg cells of Hodgkin's disease.
The various morphologic and functional subtypes of nodal B-cell lymphomas can also be found in the skin. These reflect the various steps of lymphocyte differentiation including maturation from the pre-B lymphocyte to the well-differentiated B2 lymphocyte or plasma cell in the peripheral blood. The subtypes of cutaneous B-cell lymphomas have been discussed (Kiel classification); the percentages indicate the frequencies of the subtypes among a total of 736 cutaneous lymphomas of both T-cell and B-cell origin: Lymphocytic lymphoma (7 per cent). Immunoglobulin-producing lymphomas, including the rate plasmacytoma of the skin, lymphoplasmacytoid immunocytoma, which represents the largest group of cutaneous B-cell lymphoma (12 per cent), and immunoblastic lymphoma, which is the most aggressive form in this group (8 per cent). Cutaneous B-cell lymphoma arising from or related to follicular center cells, including centrocytic lymphoma (7 per cent), mantle-cell lymphoma, centroblastic/centrocytic lymphoma (6 per cent), the highly malignant centroblastic lymphoma (4 per cent), and lymphoblastic lymphoma, Burkitt type. The Ann Arbor staging system is not applicable to cutaneous B-cell lymphoma; therefore, a TNM staging system has been proposed. The diagnosis of cutaneous B-cell lymphoma is based primarily on cytomorphologic features. Differentiation of cutaneous B-cell lymphoma from pseudolymphoma of the skin cannot be based on a single criterion; a spectrum of characteristic features must be evaluated. Analysis of the infiltrating cells in cutaneous B-cell lymphoma using monoclonal antibodies demonstrates that the proliferation of the neoplastic clone is accompanied by a mixture of accessory cells of various origins, including T cells, macrophages, and dendritic reticulum cells. As in nodal B-cell lymphomas, several factors may be involved in the generation of cutaneous B-cell lymphoma, including persistent antigenic stimulation and loss of regulatory mechanisms for lymphocyte proliferation and differentiation in conjunction with environmental and other factors.
We report on a keratinization disorder in four brothers in a family in which members had been affected in three generations. Clinical signs and genetic, histopathologic, autoradiographic and ultrastructural examinations all support the diagnosis of hystrixlike, proliferative ichthyosis with cornoid lamellae and autosomal dominant inheritance. The relationship of the disorder to other hystrixlike genetic keratinization disorders is discussed.
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Immediately after the argon laser impact one finds necrosis of epidermis and superficial dermis. Dilated vessels down to a depth of 0.8 mm are filled with coagulated erythrocytes. After 2 days there is initial restoration of epidermis, and dilated vessels are filled with agglutination thrombi. With and after the 6th day fibroblasts and capillary blood vessels grow into the thrombi, and later on vessels are completely replaced by granulation tissue and after 2-4 weeks by newly formed fibrous tissue.