Home About us Contact | |||
Painful Lesions (painful + lesion)
Selected AbstractsA clonal cutaneous CD30+ lymphoproliferative eruption in a patient with evidence of past exposure to hepatitis EINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2000Freddye M. Lemons-Estes CDR, MC USN The patient was a 52-year-old white man who had worked in remote areas of the world during the past 2 years, including an extended period in rural areas of Central Africa and in Central and South America. He had no acute illnesses during the 2-year period except for rare, mild, upper respiratory tract infections. For approximately 1 year, however, he had developed recurrent, papular-vesicular, slightly painful lesions on the fingers and palms, that spontaneously healed over weeks to months ( Fig. 1). The patient had no other concurrent illnesses and no abnormal laboratory findings, except for positive enzyme-linked immunoabsorbent assay (ELISA) for immunoglobulin G (IgG) antibodies for hepatitis E virus (HEV) using a recombinant expressed HEV antigen (Genelabs Technologies, Inc., San Antonio). Prolonged treatment with minocycline did not appear to moderate the lesions. At approximately 2.5 years after the development of his first cutaneous lesion, however, the patient reported that he had had no new lesions for over 3 months. Figure 1. Vesicular ,lesion on the finger which regressed over a period of weeks A biopsy specimen showed an intraepidermal vesicle with prominent epidermal necrosis and reticular degeneration ( Fig. 2). Within the epidermis, there was a dense infiltrate of lymphoid cells. The majority of these cells were pleomorphic with prominent nucleoli and frequent mitotic figures ( Fig. 3). Sheets of atypical cells were found in the subjacent dermis. The infiltrate extended down into the reticular dermis. With extension into the dermis, the infiltrate became more polymorphous with more small lymphoid cells, large numbers of eosinophils, and some plasma cells located more deeply. Figure 2. Intraepidermal ,blister showing reticular degeneration and marked epidermotrophism of large atypical cells with extension into the dermis with a mixed infiltrate containing eosinophils and plasma cells (30×) Figure 3. Intraepidermal ,infiltrate of large atypical cells with extension into the dermis with a mixed infiltrate containing eosinophils and plasma cells (400×) Immunohistochemical stains for CD3 (DAKO), CD4 (Becton Dickinson), CD8 (Becton Dickinson), CD15 (LeuM1, Becton Dickinson), CD20 (L-26, DAKO), CD30 (Ber-H2, DAKO), CD45RO (UCHL1, DAKO), S-100 protein (DAKO), T-cell intracellular antigen (TIA) (Coulter), epithelial membrane antigen (EMA) (DAKO), KP-1 (CD68, DAKO), MAC-387 (DAKO), Epstein,Barr virus (EBV) latent membrane antigen-1 (LMP-1, DAKO), and EBV-encoded nuclear antigen 2 (EBNA2, DAKO) were performed on formalin-fixed tissue using the ABC method with DABA as the chromagen. CD3 showed diffuse membrane staining of the large atypical lymphoid cells, as well as the majority of the small lymphoid cells ( Fig. 4). CD4 showed positive membrane staining of the large atypical lymphoid cells and the majority of the small lymphoid cells. CD8 showed only scattered light membrane staining of small lymphoid cells. CD15 was negative, and CD20 showed foci of groups of small lymphoid cells mainly within the reticular dermis. CD30 showed positive membrane and paranuclear staining of the large atypical cells, most abundant within the epidermis and papillary dermis ( Fig. 5). CD45RO showed positive membrane staining of the large atypical cells and the majority of the small lymphoid cells. S-100 protein showed increased dendritic cells within the surrounding viable epidermis and the subjacent papillary dermis ( Fig. 6). TIA showed granular staining in the large atypical lymphoid cells and only rare staining in small lymphoid cells ( Fig. 7). EMA staining was essentially negative. KP-1 showed only scattered positive cells mainly in the lower papillary and the reticular dermis. MAC-387 showed membrane staining in the viable epidermis ( Fig. 8). LMP-1 and EBNA2 for EBV were negative within the lymphoid cells as well as within the overlying epidermis. Figure 4. Immunohistochemical ,staining for CD3 showing diffuse staining of lymphoid cells within the epidermis and dermis (150×) Figure 5. Immunohistochemical ,staining for CD30 showing membrane and paranuclear staining of large atypical lymphoid cells within the epidermis and papillary dermis (a, 150× b, 400×) Figure 6. Immunohistochemical ,staining for S-100 protein within the epidermis and in the papillary dermis (a, 150× b, 300×) Figure 7. Immunohistochemical ,granular staining of large atypical lymphoid cells for TIA (200×) Figure 8. Immunohistochemical ,staining for MAC-387 showing epidermal staining (100×) Gene rearrangement studies showed a ,-T-cell receptor gene rearrangement. The monoclonal band was detected with VJ1, VJ2, and D1J2 primer sets. The T-cell receptor , rearrangement assay has a sensitivity of 61% and a specificity of 94% for the detection of a monoclonal rearrangement in T-cell lymphomas for which amplifiable DNA can be recovered. Electron microscopy was performed on formalin-fixed material, positive-fixed with 2.5% phosphate-buffered glutaraldehyde and further with 1% osmium tetroxide by standard techniques. Intracellular, 50,60-nm, cytoplasmic, spherical, viral-like particles were identified ( Fig. 9). Figure 9. Electron ,microscopy showing 50,60-nm diameter, intracellular, viral-like particles (arrows) (70,000×) [source] The natural history of hidradenitis suppurativaJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 5 2000JM Von Der Werth Abstract Aim,To investigate aspects of the natural history of hidradenitis. Background,The natural history of hidradenitis suppurativa (HS) is not well known. There is incomplete published data on the average age of disease onset, progression of the disease, average monthly incidence and duration of boils, and factors that relieve or exacerbate disease symptoms. Study design,Questionnaire-based survey among HS patients identified from hospital records of three hospitals in Nottinghamshire, UK. Results,One hundred and ten of 156 questionnaires (70.5%) were returned, 93 from females and 17 from males. The average patient's age was 40.1 years and the average reported age of disease onset was 21.8 years. At the time of the survey patients had suffered an average disease duration of 18.8 years. Most patients (98 of 110) still had experienced active disease within the past year. There was some evidence that in women the condition has a tendency to ease or subside after the menopause. Forty-four per cent of women felt that their condition was aggravated by menstruation. Thirty-eight per cent of patients gave a positive family history of the disorder. The average duration of painful boils was 6.9 days. In addition, 62% of patients acknowledged the presence of permanently painful boils that failed to subside. Patients developed a median of two boils per month. Factors that could aggravate the condition were primarily sweating or heat, stress or fatigue and tight clothing or friction. Factors that could improve the condition consisted largely of a variety of medical treatments and a number of life-style measures, such as swimming or baths. Twenty-four per cent of patients had failed to find anything at all to help their condition, despite an average disease duration of almost 19 years. Conclusions,The study highlights several of the factors that make HS one of the most distressing dermatological diseases, such as the average monthly incidence of painful lesions, their average duration and the chronicity of the disease. It seems striking that the mean duration of an HS boil (6.9 days) roughly equals the duration of an average course of antibiotics. The postulated response of HS to oral antibiotics may thus simply have its explanation in the natural history of the condition itself. [source] Oral ulcers: clinical aspects.CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2009A tool for dermatologists. Summary Oral ulcers are generally painful lesions that are related to various conditions developing within the oral cavity. They can be classified as acute or chronic according to their presentation and progression. Acute oral ulcers are be associated with conditions such as trauma, recurrent aphthous stomatitis, Behçet's disease, bacterial and viral infections, allergic reactions or adverse drug reactions. Chronic oral ulcers are associated with conditions such as oral lichen planus, pemphigus vulgaris, mucosal pemphigoid, lupus erythematosus, mycosis and some bacterial and parasitic diseases. The correct differential diagnosis is necessary to establish the appropriate treatment, taking into account all the possible causes of ulcers in the oral cavity. In this second part of this two-part review, chronic oral ulcers are reviewed. [source] Oral ulcers: clinical aspects.CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 3 2009A tool for dermatologists. Summary Oral ulcers are generally painful lesions that are related to various conditions developing within the oral cavity. They can be classified as acute or chronic according to their presentation and progression. Acute oral ulcers are be associated with conditions such as trauma, recurrent aphthous stomatitis, Behçet's disease, bacterial and viral infections, allergic reactions or adverse drug reactions. Chronic oral ulcers are associated with conditions such as oral lichen planus, pemphigus vulgaris, mucosal pemphigoid, lupus erythematosus, mycosis and some bacterial and parasitic diseases. The correct differential diagnosis is necessary to establish the appropriate treatment, taking into account all the possible causes of ulcers in the oral cavity. In the first part of this two-part review, acute oral ulcers are reviewed. [source] |