Qureshi A I, Cook A A, Mishu H P, Krendel D A
Department of Neurology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Muscle Nerve. 1997 Aug;20(8):1002-7. doi: 10.1002/(sici)1097-4598(199708)20:8<1002::aid-mus10>3.0.co;2-x.
Both humoral and cell-mediated autoimmune mechanisms have been implicated in the pathogenesis of Guillain-Barré syndrome (GBS). Therefore, its occurrence in severely immunocompromised patients is not expected. We identified 3 severely immunocompromised patients who developed GBS. Two of the 3 patients had acquired immunodeficiency syndrome with CD4 counts of 5 and 4 cells/mm3, respectively. One post-cardiac transplant patient was taking azathioprine and cyclosporine at the time of onset of GBS. In all 3 patients, immunocompromise was induced by infectious or chemotherapeutic agents which preferentially suppress T-lymphocyte responses. All 3 had severe lymphocytopenia and incomplete recovery. We conclude that GBS can occur in patients with severe t-cell suppression. Although no conclusion regarding prognosis can be drawn from our small group of patients, their incomplete recovery is consistent with the idea that T-cells are important for recovery.
体液免疫和细胞介导的自身免疫机制均与吉兰-巴雷综合征(GBS)的发病机制有关。因此,预计该疾病不会在严重免疫功能低下的患者中出现。我们识别出3例发生GBS的严重免疫功能低下患者。3例患者中有2例患有获得性免疫缺陷综合征,其CD4细胞计数分别为5个/mm³和4个/mm³。1例心脏移植术后患者在GBS发病时正在服用硫唑嘌呤和环孢素。在所有3例患者中,免疫功能低下是由优先抑制T淋巴细胞反应的感染性或化疗药物引起的。所有3例患者均有严重淋巴细胞减少且恢复不完全。我们得出结论,严重T细胞抑制的患者可能发生GBS。虽然从我们这一小群患者中无法得出关于预后的结论,但他们恢复不完全与T细胞对恢复很重要这一观点相符。