SummaryBackgroundDermatitis artefacta (DA) is a dermatologicopsychiatric illness that is a conscious self-infliction of lesions to accessible regions of the body. The lesions usually do not resemble those of any know skin disease and there are no specific diagnostic tests to recognize them. This makes dermatitis artefacta a very slow, challenging and expensive disease to diagnose.Case ReportWe present 5 different clinical cases of dermatitis artefacta treated in the Department of Dermatology, Venereology and Allergology, Medical University of Gdańsk in 2011. Detailed anamnesis and physical examination were performed at the day of admission. All patients had biochemical and hematological blood tests, skin biopsies and swabs for bacteriological examination, and photographs were taken. Psychiatric consultation was recommended in all cases.Clinical symptoms before diagnosis lasted from 1 to 10 years. The female-to-male ratio is 1:0.7, with age range of 57–62 years. Of our patients, only 2 refused a psychiatric consultation. Three out of 5 patients denied self-mutilation (2 of those 3 patients finally admitted to self-manipulations). Lesions were usually within the reach of the dominant hand. Two patients have other personality disorders. In 4/5 cases visible improvement after treatment with occlusive dressings were observed.ConclusionsWe discuss and attempt to depict issues associated with collaboration between dermatologists and psychiatrists, reasons for poor recognition of the disease, very long diagnosis and high costs. To conclude, we found that close collaboration between dermatologists and psychiatrists is important in diagnosing and treating DA patients.
Objectives The primary mechanism for bone marrow failure in aplastic anemia (AA) is autoimmune hematopoietic stem cell destruction. AA can be cured with antithymocyte globulin (ATG) treatment, and some smaller studies have indicated that the number of regulatory T cells (Tregs) may be predictive of response. Additionally, AA patients appear to have elevated numbers of Th17 cells and bone marrow macrophages, but outcome data are missing. Methods We performed immunohistochemistry on bone marrow biopsies from 121 ATG‐treated AA patients and 14 healthy controls, using antibodies against FOXP3 (for Tregs), IL‐17 (for Th17), CD68 (for pan‐macrophages) and CD163 (for M2 type macrophages) to study their possible relation to ATG response and AA prognosis. Results AA patients had significantly fewer Tregs and Th17 cells but significantly more macrophages compared with controls. Treg, Th17 and pan‐macrophage cell numbers were not associated with ATG response or differences in survival. Patients with higher levels of M2 macrophages had improved 5‐year overall survival: 79.6% versus 57.4% (p = .017), and this benefit was primarily seen in AA patients with non‐severe disease. Conclusions We found that Treg and Th17 cell numbers did not predict ATG response or survival, whereas M2 macrophages may be associated with improved survival.
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