Introduction: Alopecia areata (AA) is disease characterized by focally, nonscarring hair loss on the scalp or other parts of the body. It affects 1-2% population of both genders and occurs at all age groups. The etiology is unknown, although most evidence supports the hypothesis that AA is a T-cell-mediated autoimmune disease of the hair follicle and that cytokines play an important role. Objective: The aim of our study was to evaluate serum concentrations of IL-1α and IL-1β in patients with AA and healthy subjects and also to asses a possible association between these cytokines and duration of the disease. Methods: Forty six patients with AA and 20 healthy controls were enrolled in the study. Serum concentrations of IL-1α and IL-1β were measured using enzyme-linked immunoassay techniques. Results: The serum level of IL-1α in patients with AA was significantly higher than that in the control group (4.34±0.86 pg/mL vs 3.66±0.35 pg/mL, respectively). IL-1β levels were greater in patients with AA than in controls (2.35±0.17 pg/mL vs 2.24±0.30, respectively) but the difference was not significant (p>0.05). No correlations were found between duration of disease and the serum levels of IL-1α and IL-1β. Conclusion: Our results have demonstrated the importance of determining IL-1a concentration in serum in patients with AA. This research could contribute to the interpretation of insufficiently well known views of the pathogenesis role and significance of IL-1α in AA. Streszczenie Wstep: Łysienie plackowate to choroba charakteryzująca sie ogniskowym, niebliznowaciejącym lysieniem skory glowy lub tez innych okolic ciala. Choroba ta dotyka 1-2% populacji, bez predylekcji plci ani tez wieku. Etiologia choroby pozostaje nieznana, jednakze najwiecej dowodow potwierdza hipoteze, ze AA jest chorobą autoimmunologiczną mediowaną za pomocą komorek T, zajmującą korzen wlosa oraz ze cytokiny pelnią w tym procesie wazną role. Cel: Celem naszego badania bylo oszacowanie stezenia w surowicy interleukin: IL-1α i IL-1β u pacjentow z AA oraz u osob zdrowych by wykazac mozliwe związki pomiedzy tymi cytokinami a dlugością trwania choroby. Metody: Do badania zakwalifikowano 46 pacjentow z AA oraz 20 osob zdrowych. Stezenia cytokin IL-1α i IL-1β byly mierzone za pomocą techniki EIA. Wyniki: Poziomy IL-1α u chorych na AA byl znacznie wyzszy niz ten w grupie kontrolnej (4.34±0.86 pg/mL vs 3.66±0.35 pg/mL, odpowiednio). Poziomy IL-1β byly wieksze u pacjentow z AA niz w grupie kontrolnej (odpowiednio 2.35±0.17 pg/mL vs 2.24±0.30) jednak statystycznie nieistotne (p>0.05). Nie znaleziono korelacji pomiedzy trwaniem choroby a poziomami interleukin IL-1α i IL-1β w surowicy krwi. Wnioski: Nasze wyniki badan dowodzą wagi pomiaru stezenia IL-1a w surowicy krwi osob chorych na AA. To badanie moze przyczynic sie do nie do konca poznanej roli IL-1α w patogenezie oraz odkryciu pelnego znaczenia w Alopecia Areata.

FOUCAULT, Michel. Do governo dos Vivos – Curso no College de France, 1979-1980 (excertos). Traducao, transcricao, notas e apresentacao de Nildo Avelino, Rio de Janeiro Achiame, 2010.

Background: Neonatal dried blood spots (Guthrie cards) have been used to demonstrate a prenatal origin of clonal leukemia-specific genetic aberrations in several subgroups of childhood acute lymphoblastic leukemia (ALL). One hypothesis suggests that an infectious agent could initiate genetic transformation already in utero. In search for a possible viral agent, Guthrie cards were analyzed for the presence of 3 newly discovered polyomavirus Karolinska Institutet polymavirus (KIPyV), Washington University polyomavirus (WUPyV), and Merkel cell polyomavirus (MCPyV). Methods: Guthrie cards from 50 children who later developed ALL and 100 matched controls were collected and analyzed by standard or real-time polymerase chain reaction for the presence of the VP1 region of KIPyV, WUPyV, and MCPyV, and the LT region for MCPyV. Results and Conclusions: DNA from KIPyV, WUPyV, and MCPyV was not detected in neonatal blood samples from children with ALL or controls. Prenatal infections with these viruses are not likely to be etiological drivers for childhood leukemogenesis.