Meakins J L, Pietsch J B, Bubenick O, Kelly R, Rode H, Gordon J, MacLean L D
Ann Surg. 1977 Sep;186(3):241-50. doi: 10.1097/00000658-197709000-00002.
Primary failure of host defense mechanisms has been associated with increased infection and mortality. Anergy, the failure of delayed hypersensitivity response, has been shown to identify surgical patients at increased risk for sepsis and related mortality. The anergic and relatively anergic patients whose skin tests failed to improve had a mortality rate of 74.4%, whereas those who improved their responses had a mortality rate of 5.1% (P < 0.001). This study documents abnormalities of neutrophil chemotaxis, T-lymphocyte rosetting in anergic patients and the effect of autologous serum. These abnormalities may account for the increased infection and mortality rates in anergic patients. Skin testing with five standard antigens has identified 110 anergic (A) or relatively anergic (RA) patients in whom neutrophil chemotaxis (CTX) and bactericidal function (NBF), T-lymphocyte rosettes, mixed lymphocyte culture (MLC), cell-mediated lympholysis (CML), and blastogenic factor (BF) were studied. The MLC, CML and BF were normal in the patients studied, and were not clinically helpful. Neutrophil CTX in 19 controls was 117.5 +/- 1.6 u whereas in 40 A patients, neutrophils migrated 81.7 +/- 2.3 u and in 15 RA patients 97.2 +/- 3.8 u (P < 0.01). In 14 patients whose skin tests converted to normal, neutrophil migration improved from 78.2 +/- 5.4 u to 107.2 +/- 4.0 u (P < 0.01). Incubation of A or control neutrophils in A serum reduced migration in A patients from 93 +/- 3.7 u to 86.2 +/- 3.5 u (P < 0.01) and in normals from 121.2 +/- 1.6 u to 103.6 +/- 2.6 u (P < 0.001). The per cent rosette forming cells in 66 A patients was 42.5 +/- 3.1 compared to 53.6 +/- 2.8 in normal responders (P < 0.02). Incubation of normal lymphocytes in anergic serum further reduced rosetting by 30%. Restoration of delayed hypersensitivity responses and concurrent improvement in cellular and serum components of host defense were correlated with maintenance of adequate nutrition and aggressive surgical drainage.
宿主防御机制的原发性衰竭与感染增加及死亡率升高有关。无反应性,即迟发型超敏反应的缺失,已被证明可识别出脓毒症及相关死亡率风险增加的外科手术患者。皮肤试验未改善的无反应性及相对无反应性患者的死亡率为74.4%,而反应性改善的患者死亡率为5.1%(P<0.001)。本研究记录了无反应性患者中性粒细胞趋化性、T淋巴细胞玫瑰花结形成的异常情况以及自体血清的影响。这些异常情况可能解释了无反应性患者感染率和死亡率的增加。用五种标准抗原进行皮肤试验,已识别出110名无反应性(A)或相对无反应性(RA)患者,对其研究了中性粒细胞趋化性(CTX)和杀菌功能(NBF)、T淋巴细胞玫瑰花结、混合淋巴细胞培养(MLC)、细胞介导的淋巴细胞溶解(CML)和母细胞形成因子(BF)。所研究患者的MLC、CML和BF均正常,在临床上并无帮助。19名对照者的中性粒细胞CTX为117.5±1.6单位,而40名A组患者的中性粒细胞迁移率为81.7±2.3单位,15名RA组患者为97.2±3.8单位(P<0.01)。在14名皮肤试验转为正常的患者中,中性粒细胞迁移率从78.2±5.4单位提高到107.2±4.0单位(P<0.01)。将A组或对照者的中性粒细胞在A组血清中孵育,可使A组患者的迁移率从93±3.7单位降至86.2±3.5单位(P<0.01),正常者从121.2±1.6单位降至103.6±2.6单位(P<0.001)。66名A组患者的玫瑰花结形成细胞百分比为42.5±3.1,而正常反应者为53.6±2.8(P<0.02)。将正常淋巴细胞在无反应性血清中孵育可使玫瑰花结形成率进一步降低30%。迟发型超敏反应的恢复以及宿主防御的细胞和血清成分的同时改善与维持充足营养和积极的手术引流相关。