A. Cırık, M. Evcimik, G. Ülfer, Turkan Yigitbasi, Öztürk Aktaş
{"title":"Bell’s麻痹患者的缺血修饰白蛋白水平","authors":"A. Cırık, M. Evcimik, G. Ülfer, Turkan Yigitbasi, Öztürk Aktaş","doi":"10.4103/indianjotol.indianjotol_4_22","DOIUrl":null,"url":null,"abstract":"Background: Although several causes have been regarded as possible including viral, autoimmune, inflammatory, and vascular ischemia, the accurate etiology and pathophysiology of Bell's palsy (BP) remain unclear. The aim of the present article was to determine whether serum levels of ischemia-modified albumin (IMA) are associated with BP and if there is a posttreatment change in IMA levels. Materials and Methods: This was a prospective study enrolling 23 patients (10 males and 13 females; mean age: 44.71 ± 16.72 years; and range, 20–57 years) and 23 healthy individuals (12 males and 11 females; mean age: 37.91 ± 9.16 years; and range, 9–73 years) as the control group. Blood samples were obtained from the antecubital vein from all of the volunteers. Albumin cobalt binding test was used to obtain the IMA levels. Results: The mean IMA level was 0.38 ± 0.06 absorbance units in the study group at the time of diagnosis, 0.35 ± 0.07 absorbance units at the posttreatment period, and 0.35 ± 0.06 absorbance units in the control group. IMA levels of patients in posttreatment period were lower than the onset of illness. The result was statistically significant (P = 0.01). Conclusion: The data demonstrate that IMA decreased in BP with treatment. This is a preliminary study and we could not obtain results that clearly support the ischemic hypothesis of pathogenesis of BP; we think it gives an idea for further studies.","PeriodicalId":44304,"journal":{"name":"Indian Journal of Otology","volume":"28 1","pages":"139 - 143"},"PeriodicalIF":0.2000,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ischemia-Modified Albumin Levels in Patients with Bell's palsy\",\"authors\":\"A. Cırık, M. Evcimik, G. Ülfer, Turkan Yigitbasi, Öztürk Aktaş\",\"doi\":\"10.4103/indianjotol.indianjotol_4_22\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: Although several causes have been regarded as possible including viral, autoimmune, inflammatory, and vascular ischemia, the accurate etiology and pathophysiology of Bell's palsy (BP) remain unclear. The aim of the present article was to determine whether serum levels of ischemia-modified albumin (IMA) are associated with BP and if there is a posttreatment change in IMA levels. Materials and Methods: This was a prospective study enrolling 23 patients (10 males and 13 females; mean age: 44.71 ± 16.72 years; and range, 20–57 years) and 23 healthy individuals (12 males and 11 females; mean age: 37.91 ± 9.16 years; and range, 9–73 years) as the control group. Blood samples were obtained from the antecubital vein from all of the volunteers. Albumin cobalt binding test was used to obtain the IMA levels. Results: The mean IMA level was 0.38 ± 0.06 absorbance units in the study group at the time of diagnosis, 0.35 ± 0.07 absorbance units at the posttreatment period, and 0.35 ± 0.06 absorbance units in the control group. IMA levels of patients in posttreatment period were lower than the onset of illness. The result was statistically significant (P = 0.01). Conclusion: The data demonstrate that IMA decreased in BP with treatment. This is a preliminary study and we could not obtain results that clearly support the ischemic hypothesis of pathogenesis of BP; we think it gives an idea for further studies.\",\"PeriodicalId\":44304,\"journal\":{\"name\":\"Indian Journal of Otology\",\"volume\":\"28 1\",\"pages\":\"139 - 143\"},\"PeriodicalIF\":0.2000,\"publicationDate\":\"2022-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Indian Journal of Otology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4103/indianjotol.indianjotol_4_22\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"OTORHINOLARYNGOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Indian Journal of Otology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/indianjotol.indianjotol_4_22","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"OTORHINOLARYNGOLOGY","Score":null,"Total":0}
Ischemia-Modified Albumin Levels in Patients with Bell's palsy
Background: Although several causes have been regarded as possible including viral, autoimmune, inflammatory, and vascular ischemia, the accurate etiology and pathophysiology of Bell's palsy (BP) remain unclear. The aim of the present article was to determine whether serum levels of ischemia-modified albumin (IMA) are associated with BP and if there is a posttreatment change in IMA levels. Materials and Methods: This was a prospective study enrolling 23 patients (10 males and 13 females; mean age: 44.71 ± 16.72 years; and range, 20–57 years) and 23 healthy individuals (12 males and 11 females; mean age: 37.91 ± 9.16 years; and range, 9–73 years) as the control group. Blood samples were obtained from the antecubital vein from all of the volunteers. Albumin cobalt binding test was used to obtain the IMA levels. Results: The mean IMA level was 0.38 ± 0.06 absorbance units in the study group at the time of diagnosis, 0.35 ± 0.07 absorbance units at the posttreatment period, and 0.35 ± 0.06 absorbance units in the control group. IMA levels of patients in posttreatment period were lower than the onset of illness. The result was statistically significant (P = 0.01). Conclusion: The data demonstrate that IMA decreased in BP with treatment. This is a preliminary study and we could not obtain results that clearly support the ischemic hypothesis of pathogenesis of BP; we think it gives an idea for further studies.