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突发性感音神经性听力损失中的自身免疫异常:与抗心磷脂抗体的关联。

Autoimmune aberration in sudden sensorineural hearing loss: association with anti-cardiolipin antibodies.

作者信息

Toubi E, Ben-David J, Kessel A, Podoshin L, Golan T D

机构信息

Division of Clinical Immunology, Bnai Zion Medical Center, Haifa, Israel.

出版信息

Lupus. 1997;6(6):540-2. doi: 10.1177/096120339700600611.

Abstract

In view of the presence of autoantibodies against inner ear antigens, the pathogenesis of sudden deafness (SD) and progressive sensorineural hearing loss (PSNHL) is suggested to be of an autoimmune nature. However, microthrombosis of the inner ear may result from pathogenic anti-cardiolipin antibody (aCL) activity. We studied 30 patients (17 females and 13 males, age range 20-52 y), of whom 11 suffered from SD and 19 from PSNHL. All were clinically and serologically evaluated for association with autoimmune disorders (serological examination included: aCL, ANA, ENA, ANCA, proteinelectrophoresis, and complement levels). Twenty healthy matched subjects served as controls. None of the control group were aCL positive, whereas 8 out of 30 (27%) patients demonstrated low-moderate titers (P < 0.02), of whom 5 out of 8 suffered from SD. In addition, 2 aCL negative patients with PSNHL demonstrated hypergammaglubolinemia accompanied by hypocomplementemia, whereas none with SD had such abnormalities. Our data suggests that aCL is detected in patients with sudden sensorineural hearing loss and therefore may play an important role in the pathogenesis of this disability. If sustained by additional studies, these findings would warrant the consideration of anticoagulant therapy.

摘要

鉴于存在针对内耳抗原的自身抗体,突发性耳聋(SD)和进行性感音神经性听力损失(PSNHL)的发病机制被认为具有自身免疫性质。然而,内耳微血栓形成可能源于致病性抗心磷脂抗体(aCL)的活性。我们研究了30例患者(17例女性和13例男性,年龄范围20 - 52岁),其中11例患有突发性耳聋,19例患有进行性感音神经性听力损失。所有患者均进行了临床和血清学评估,以确定与自身免疫性疾病的关联(血清学检查包括:aCL、ANA、ENA、ANCA、蛋白电泳和补体水平)。20名健康匹配受试者作为对照。对照组中无一例aCL阳性,而30例患者中有8例(27%)表现出低 - 中度滴度(P < 0.02),其中8例中有5例患有突发性耳聋。此外,2例aCL阴性的进行性感音神经性听力损失患者表现出高丙种球蛋白血症伴低补体血症,而突发性耳聋患者中无一例有此类异常。我们的数据表明,在突发性感音神经性听力损失患者中检测到aCL,因此其可能在这种残疾的发病机制中起重要作用。如果进一步的研究证实,这些发现将有必要考虑抗凝治疗。

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