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   尿毒症病患甲型免疫球蛋白低下的研究      ★★★ 【字体: 】  
尿毒症病患甲型免疫球蛋白低下的研究
收集整理:佚名    来源:本站整理  时间:2009-02-06 11:54:46   点击数:[]    

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论文类别】 毕业论文
【中文摘要】
感染是尿毒症病患主要的致死原因的一,而免疫系统的缺失是造成病患增加感染的主因。
本科曾发现两位长期血液透析病人患有反覆性皮肤及呼吸道感染,在探求其反覆感染的原
因时,意外发现两位病患均并有甲型免疫球蛋白(IgA)低下的现象。因此本研究的目的即
在筛检尿毒症患者发生血清IgA低下情形,及探讨产生IgA缺乏可能的机转。
首先选取250位正常人、56位慢性肾衰竭但尚未进行透析的病患、246位长期血液透析、及
40位腹膜透析病患,测定上述四群人血清IgG、IgA、IgM以了解尿毒症病患与正常人的差异
。结果发现长期血液透析或腹膜透析病患其血清IgA浓度相较于正常人、慢性肾衰竭病患皆
有明显的下降(225 ±100 mg/dl、217 ±97 mg/dl vs. 270 ±96mg/dl、296 ±137 mg/
dl,p

--------------------------------------------------------------------------------
【英文摘要】
Infection is one of the major causes of mortality and morbidity in uremic
patients. Impaired host defense is the important predisposing factor. We
experienced two hemodialysis (HD) patients with recurrent skin and
respiratory
tract infections in 1992 and 1995. Unexpectedly, we found both of them
were
IgA deficiency (IgAD). Therefore, we conducted the following studies to
survey
the prevalence and the mechanisms of IgAD in uremic patients. Serum
Immunoglobulin (Ig) G/A/M concentrations of 246 HD, 40 continuous
ambulatory
peritoneal dialysis (CAPD), 56 chronic renal failure (CRF) patients, and
250
normal controls were examined by Nephelometry. Lower serum IgA
concentrations
were found in HD and CAPD patients in comparison to normal controls and
CRF
patients ( 225 ±100 mg/dl, 217 ±97 mg/dl vs. 270 ±96 mg/dl, 296 ±137 mg/
dl; p
there was no such finding in CRF and normal groups. Partial IgAD were
found in
10 HD patients, 2 CAPD patients and 2 of controls.
The possibility of uremic toxin interfering with the measurement of IgA by
nephelometry was excluded by serial dilution of patients serum mixing
with
serum of normal control. The decrease of serum IgA concentrations did not
correlated with serum creatinine concentrations, nor with the HD duration.
There was no association between IgA deficiency and hepatitis B or C. To
explore the mechanisms of IgAD, the presence of anti-IgA antibody in
patients
serum was detected by double immunodiffusion and enzyme-linked
immunoabsorbant
assay (ELISA). And the numbers the B cell and IgA secreting B cell were
studied by Flow cytometry to know whether the IgAD was caused by
impairment of
IgA production. ELISA revealed positive result in 3 cases of IgAD, which
indicated the presence of IgG type anti-IgA autoantibody. By Flow
cytometry,
decreased numbers of B cell and IgA secreting B cell were detected.
In conclusion, the results showed 1) Serum IgA concentrations were lower
in
both HD and CAPD patients. 2) A higher prevalence of selective IgA
deficiency
in dialysis patients. 3) The clinical symptoms were more obvious in uremic
patients with IgAD, so the deficiency of serum IgA in uremic patients has
the
clinical significance. 4) Decreased serum IgA concentration in uremic
patients
was not related to the dialysis duration, serum creatinine level, and the
existence of hepatitis B or C. 5) Some of the uremic patients with IgAD
were
caused by the existence of circulating anti-IgA autoantibody, but some
were
caused by decrease of the numbers of B cell and IgA secreting B cell,
which
indicate that the mechanisms of IgA deficiency in uremic patients are
diversified.

--------------------------------------------------------------------------------
【 目 录 】
中文摘要------------------------------------------------------ 3
英文摘要-------------------------------------------------------5
第一章    前言------------------------------------------------7
第二章 尿毒症病患血清免疫球蛋白的浓度,及甲型免疫球蛋白缺乏的盛行率------------
----------------------------------------------9
一、 方法及材料------------------------------------------10
二、 结果------------------------------------------------12
第三章 尿毒症病患假型免疫球蛋白低下的临床意义----------------14
一、 尿毒症病患甲型免疫球蛋白低下与感染相关性------------15
二、 唾液的甲型免疫球蛋白的探讨--------------------------17
第四章 尿毒症病患甲型免疫球蛋白低下原因的探讨----------------18
一、 干扰因子的测定--------------------------------------19
二、 自体免疫抗体的侦测----------------------------------20
三、 IgA制造功能的探讨-----------------------------------25
第五章 综合讨论与结论---------------------------------------- 31
参考文献------------------------------------------------------36
表------------------------------------------------------------41
       
                   
       
       


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