68例白癜风患者血清β2—微球蛋白与免疫球蛋白水平的检测

测定６８例白癜风患者血清β２－微球蛋白（β２－Ｍ）与免疫球蛋白ＩｇＧ、ＩｇＡ、ＩｇＭ水平。测定结果，寻常型进展期与稳定期白癜风血清β２－Ｍ水平均显著性升高，以进展期尤甚（Ｐ＜０．０１），节段型白癜风血清β２－Ｍ水平无显著性改变（Ｐ＞０．０５）；寻常型白癜风血清免疫球蛋白ＩｇＧ、ＩｇＡ、ＩｇＭ均显著高于对照组（Ｐ＜０．０１），节段型白癜风除血清ＩｇＧ升高外（Ｐ＜０．０５），ＩｇＡ、ＩｇＭ无显著性变化（Ｐ＞０．０５）。提示β２－Ｍ与白癜风自身免疫发病学说之间有一定的关系。     

抗心磷脂抗体在银屑病表皮细胞异常增殖中作用机理探讨—附4…

测定了４６例寻常型银屑病患者血清抗心磷脂抗体（ＡＣＡ），以及血浆６－酮－前列腺素Ｆ１α（６－Ｋ－ＰＧＦ１α）和血栓烷（ＴＸＢ２），发现患者循环ＡＣＡ、６－Ｋ－ＰＧＦ１α及ＴＸＢ２水平低下，与皮炎－湿疹组及正常人比较差异非常显著（Ｐ＜０．０１）。相关回归分析显示患者的ＡＣＡ－ＩｇＧ与６－Ｋ－ＰＧＦ１α有一定的相关性（γ＝０．２９０，Ｐ≤０．０５）。对它们之间的关系及其在表皮细胞异常增殖中的作用进行了     

花斑癣患者血清中抗糠秕马拉色菌IgG、IgM、IgA抗体的检测及其意义

目的：探讨机体体液免疫在花斑癣发病中的作用和意义。方法：以糠秕马拉色菌（Ｍ．ｆｕｒｆｕｒ）整菌（ＷＭＦ）为抗原,用间接酶联免疫吸附试验（ＥＬＩＳＡ）方法,检测６８例花斑癣患者和４１例正常人血清中的抗ＷＭＦ抗体。结果：正常人血清中存在高滴度的抗ＷＭＦ抗体,花斑癣患者血清中抗ＷＭＦＩｇＧ抗体明显低于正常对照组（Ｐ〈０．０１）,男性患者血清中ＩｇＧ抗体低于女性患者（Ｐ〈０．０１）,病程１年以上者血清中特异的ＩｇＧ抗体低于病程不到１年者（Ｐ〈０．０１）。结论：机体血清抗Ｍ．ｆｕｒｆｕｒ抗体可能是人体内天然抗体,且特异的ＩｇＧ抗体具有保护作用。支持花斑癣的发病与免疫缺陷有关。     

用PGL—1和LAM—β对麻风复发做血清学监测

选３５例单用ＤＤＳ治愈平均已１８．６年的病人，相隔一年取两次耳垂血；１９９４和１９９５年共取血清７０份，分别用ＰＧＬ－１和ＬＡＭ－β抗原做ＥＬＩＳＡ。ＩｇＧ－ＬＡＭ－βＯＤ值〉）．１８，ＩｇＭ＿ＰＧＬ－１〉０．１６为阳性，ＩｇＧ－ＬＡＭ－β，ＢＬ－ＬＬ组２３份阳性（４８％）ＢＴ－ＴＴ组５份阳性（２３％）。ＩｇＭ－ＬＡＭ－１，ＢＬ－ＬＬ组２４份阳性（５０％），ＢＴ－ＴＴ组６份阳性（２７．６％）。所有     

McAb－BA－ELISA检测人血清青霉素特异性IgE

利用单克隆抗体及生物素亲和素系统，建立ＭｃＡｂ－ＢＡ－ＥＬＩＳＡ检测人血清青霉素特异性ＩｇＥ。２７例青霉素Ｉ型变态反应患者中，６例青霉素特异性ＩｇＥ（２２．２％）阳性；而１００例非青霉素过敏者均阴性，且随机使用青霉素无反应。结果尚表明青霉素特异性ＩｇＧ并未明显影响青霉素特异性ＩｇＥ的检测（Ｐ＞０．０５）。     

McAb－BA－ELISA检测人血清青霉素特异性IgE

利用单克隆抗体及生物素亲和素系统，建立ＭｃＡｂ－ＢＡ－ＥＬＩＳＡ检测人血清青霉素特异性ＩｇＥ。２７例青霉素Ｉ型变态反应患者中，６例青霉素特异性ＩｇＥ（２２．２％）阳性；而１００例非青霉素过敏者均阴性，且随机使用青霉素无反应。结果尚表明青霉素特异性ＩｇＧ并未明显影响青霉素特异性ＩｇＥ的检测（Ｐ＞０．０５）。     

寻常性银屑病患者血浆肿瘤坏死因子水平检测

检测４０例银屑病患者血浆ＴＮＦ含量和ＩｇＡ、ＩｇＧ、ＩｇＭ、Ｃ_３水平。结果：银屑病组血浆ＴＮＦ较正常组显著升高，男性高于女性（Ｐ＜０．０５），进行期高于静止期，伴甲部损害者ＴＮＦ明显升高，ＴＮＦ水平与病情严重程度呈正相关，与ＩｇＡ、ＩｇＧ、ＩｇＭ、Ｃ_３无明显线性关系。结果分析表明ＴＮＦ参与银屑病病理生理变化过程，是其进展中重要影响因素。     

检测血清中沙眼衣原体IgG IgM抗体对泌尿生殖道感染的诊断价值

目的探讨检测血清中沙眼衣原体ＩｇＧ、ＩｇＭ抗体的应用价值。方法应用间接免疫荧光技术（ＩＦＡ）,检测三组共６０例血清标本中沙眼衣原体ＩｇＧ、ＩｇＭ抗体水平,其中实验组、阳性对照组和正常对照组各２０例。结果实验组和阳性对照组血清ＩｇＧ、ＩｇＭ抗体效价分别与正常血清对照组进行比较,均有显著性差异（Ｐ＜０．０５）。结论用免疫荧光技术检测血清中沙眼衣原体ＩｇＧ、ＩｇＭ抗体可为泌尿生殖道感染的诊断和评价病情提供有价值的依据。     

北方汉族白癜风患者HLA－Ⅰ类抗原相关性研究

目的 探讨中国北方汉族人群中白癜风与ＨＬＡ－Ⅰ类抗原的相关性。方法 白癜风患者９５例，采用ＨＬＡ血清学分型技术检测ＨＬＡ－Ａ、Ｂ位点的抗原特异性，并与１００例正常人进行比较。结果 ①白癜风患者ＨＬＡ－Ａ２、Ａ１０、Ａ３０＋３１、Ｂ１３、Ｂ１５抗原频率显著增高（Ｐｃ〈０．０１）；ＨＬＡ－Ａ２８、Ｂ４６抗原频率显著降低（Ｐｃ〈０．０１）。②有明确家族史的白癜风患者ＨＬＡ－Ａ１０、Ｂ１３、Ｂ１５抗原频率     

表皮下大疱病的鉴别诊断和抗原表达区域性差别的研究

通过间接免疫荧光和盐裂皮损周围皮肤直接免疫荧光（简称盐裂ＤＩＦ），分别研究正常人皮肤、类天疱疮（ＢＰ）及获得性大疱性表皮松解症（ＥＢＡ）抗原表达的区域性差别和表皮下大疱病鉴别诊断。 窝、肘窝、上背、下背、股内侧和下腹部皮肤ＢＰ抗原表达率较高；膝、阳窝、足背、肘、肘窝和下腹部皮肤ＥＢＡ抗原表达率较高。皮肤ＤＩＦ显示２５例表皮下大疱病中１６例（６４％）基底膜带有Ｃ３或ＩｇＧ或伴Ｃ３和ＩｇＡ沉积；盐裂ＤＩＦ表明２５例（１００％）均有ＩｇＧ或伴Ｃ３和ＩｇＡ沉积在表皮侧或真皮侧。结果提示，ＢＰ抗原高表达率与皮损好发部位相一致；ＥＢＡ抗原高表达率一部分与皮损好发部位一致。盐裂ＤＩＦ不仅提高ＤＩＦ阳性率，而且根据免疫反应物沉积部位可以鉴别出ＢＰ与ＥＢＡ以及大疱性系统性红斑狼疮。     

Immune Thrombocytopenia Due to Tranilast (Rizaben®): Detection of Drug-dependent Platelet-associated IgG

Tranilast (Rizaben®)-induced thrombocytopenia occurring in a 17-year-old man was reported. After withdrawal of the drug, he recovered within a week with oral prednisolone administration. Serological examination revealed no anti-platelet antibody, but platelet-associated IgG (PAIgG) was found. After incubation of peripheral blood of the patient with the drug in vitro, the level of PAIgG was significantly increased. These findings suggest the presence of a drug-dependent anti-platelet IgG in the patient's serum. This is the first report of immune thrombocytopenia caused by Tranilast. Our method for detecting drug-dependent platelet antibody in vitro is safe and useful for diagnosing drug-induced thrombocytopenia.     

寻常型白癜风临床特征及遗传传递方式分析

目的 分析中国汉族寻常型白癜风的临床特征及家族遗传特征,探索其可能的遗传传递方式。方法 以调查表的形式收集患者的临床资料及家系资料,用Epi Info 5.0及SPSS 10.0软件包进行统计学分析,用SAGE3.1进行遗传传递方式的复合分离分析。结果 寻常型白癜风的发病年龄为(19.02±12.58)岁,无性别差异(P=0.54);男女先证者疾病轻重程度(P=0.66)、发病季节分布(P=0.302)差异亦无统计学意义;女性患者的伴发疾病率显著高于男性(P=0.03),尤以甲亢为著(P=0.02)。患者亲属中白癜风患病率较一般人群显著增高。寻常型白癜风符合多基因累加遗传传递方式(P>0.05)。结论 寻常型白癜风的发生无性别差异,但存在明显的家族聚集性,该病的发生可能是由多基因累加遗传效应及环境因素共同作用的结果。     

Familial aggregation of vitiligo in the French West Indies (Isle of Martinique).

Environmental factors are thought to influence the genetic transmission of vitiligo, and may change in families of different extraction. Most studies on vitiligo have been performed in occidental countries or in India, therefore, our purpose was to study the familial vitiligo aggregation in Martinique (French West Indies). Data on 16 families were collected from 1995 to 1999. Information was compared to 36 controls affected with sporadic vitiligo, using the chi(2) test. The prevalence among relatives of patients was 7%, as compared to 0.34% in the general population (p < 0.001). The age of onset of vitiligo was 31 in family cases and 33 in controls. Vitiligo occurred before the age of 20 in 19% of family cases and in 36% of controls. Most families (75%) have no more than 2 affected members. No difference was observed in triggering and environmental factors in family cases and controls. Our observations are in agreement with the literature data, leading to the assumption that the environmental factors involved in the expression of vitiligo in our island do not differ from other areas.     

1005例白癜风患者遗传因素的调查

目的 探讨白癜风患者发病过程中遗传因素所起的作用。方法 采用问卷调查方法收集1997年9月至2009年3月于我科门诊就诊的1005例白癜风确诊患者的临床资料,应用SPSS 13.0软件对所得数据进行统计学分析。结果 本调查的1005例白癜风先证者中,有家族史者206例,占20.5%。家族史阳性者的平均发病年龄（24.45 ± 15.87岁）比家族史阴性者（28.12 ± 16.88岁）小（P < 0.05）。家族史阳性者皮损双侧分布的比例比家族史阴性者高（71.3%比60.8%）（P < 0.05）。家族史阳性者以B型血居多（19.9%）,家族史阴性者以O型血居多（16.8%）（P > 0.05）。结论 ①白癜风的发病符合多基因遗传规律,具有家族聚集性,且血缘关系愈近,其发病率愈高。②白癜风的发病与性别无关。③家族史阳性者的平均发病年龄较家族史阴性者小,父系或母系遗传对发病年龄无影响。④家族史阳性者皮损双侧分布的比例较家族史阴性者高,而对其他临床表现无影响。     

SLE患者血小板功能障碍与红细胞减少相关性分析

分析了系统性红斑狼疮患者在小血小板数量处于正常水平时,红 减少对血小板功能的影响。结果显示ＳＬＥ患者在血小板数量处于正常范围时,随着红细胞的减少,血小板的聚集、粘附功能亦明显减低,红细胞计数,红细胞压积的变化与血小板聚集,粘附功能以及ＧＭＰ－１４０、５－ＨＴ的改变成正相关。     

Exogenous arachidonic acid metabolism in platelets from psoriatic patients

Several reports have been published on platelet hyperaggregation in psoriatic patients, which might be related to alterations in arachidonic acid (AA) metabolism by platelets. We have studied the AA metabolism pattern, total eicosanoid formation and biosynthesis rate in platelet from psoriatic patients and from normal subjects after incubation with exogenous AA. We have found no difference in the metabolic pattern of platelets. Total formation of 12-HETE was higher in the control group (p less than 0.01). The rate of synthesis of cyclooxygenase products was higher in the psoriatic group, but only that of thromboxane B2 was statistically significant (p less than 0.02). There was a close correlation between thromboxane B2 formation rate and the lag time of platelet aggregation in response to 1 mM AA (p less than 0.01). The percentage of aggregation of platelets from psoriatics was significantly higher than that from normal subjects (p less than 0.05) and the lag time was lower in psoriatic group, but the difference was not statistically significant.     

两种类型白癜风患者郎格罕细胞电镜观察

本文对皮节型和泛发型白癜风患者皮肤内郎格罕细胞进行了电镜比较观察。结果表明，两型白癜风患者皮肤内郎格罕细胞均存在着不同程度的形态学改变，以皮节型皮损区更为明显。作者认为白癜风皮肤郎格罕细胞可能受累，但这些改变主要见于皮节型白癜风皮损区。因此目前还难以肯定郎格罕细胞在白癜风发病机制中的作用     

Increased platelet aggregation in psoriasis

Platelet aggregation was measured in fasting platelet-rich plasma in 25 psoriatics, 6 of whom were diabetic, 50 normal controls, and 24 diabetics. The aggregating agents employed to induce platelet aggregation included ADP, epinephrine and collagen. Platelet aggregation was significantly increased in psoriatics compared with normal controls. An additive effect was observed when diabetes was associated with psoriasis, with platelet aggregation being further increased by ADP. Platelet aggregability was re-evaluated in 7 psoriatics after they presented with clearing of the rash. The increased platelet aggregation with ADP and epinephrine was significantly reduced when the skin lesions had cleared.     

Effect of psoralen and ultraviolet A on platelet functioning: an in vitro and in vivo study.

We investigated possible alterations induced by psoralen and ultraviolet A radiation (PUVA) on platelet function both in vitro and in vivo. In vitro, using conventional aggregometry and adenosine diphosphate (ADP), collagen, ristocetin and arachidonic acid as aggregating agents, platelet aggregation was determined on platelet-rich plasma (PRP) from normal subjects at basal conditions and following the addition of increasing concentrations of 8-methoxypsoralen (8-MOP) with and without exposure to ultraviolet A (UVA) light (5 J/cm2) and compared with UVA light exposure alone. At basal conditions and following exposure to UVA light alone, no changes in the normal platelet aggregation patterns were observed. Exposure to UVA light of PRP containing 8-MOP also demonstrated no abnormality in the platelet aggregation patterns at 8-MOP concentrations of 200 ng/ml. However, abnormal platelet aggregation as a response to ADP and collagen was observed at higher concentrations of 8-MOP, which was augmented upon exposure to UVA light. In vivo, platelet aggregometry was performed on PRP from 4 patients submitted to PUVA treatment at basal conditions, 2.5 h after oral ingestion of 8-MOP (0.6-0.8 mg/kg) and after 4 PUVA sessions. No patient showed modification of the platelet aggregation profile after either 8-MOP ingestion or PUVA treatment. Our study shows that 8-MOP at high concentrations in vitro impairs platelet aggregation by ADP and collagen augmented by UVA light exposure, but PUVA therapy causes no detectable abnormality in platelet function in vivo.     

Intravenous immunoglobulins induce CD32-mediated platelet aggregation in vitro

Background  Intravenous immunoglobulins (IVIg) and cytomegalovirus immunoglobulins (CMVIg) are currently finding increased acceptance in clinical states of high immune activity and in transplant recipients. A rare side-effect of their application is intravascular thrombosis, which is thought to be related to pre-existing hyperviscosity. In a previous study we have shown that rabbit antithymocyte globulin causes platelet aggregation in vitro via the Fc IgG receptor (CD32).
Objectives  To investigate if IVIg and CMVIg have the potential to cause CD32-dependent platelet aggregation.
Methods  The influence of CMVIg or IVIg on platelets pre-incubated with or without monoclonal antibody AT10 was studied in an aggregometer. Expression of platelet surface activation marker CD62P was determined by fluorescence-activated cell sorting analysis and presence of soluble CD40L (sCD40L) was evaluated by enzyme-linked immunosorbent assay. All in vitro experiments were performed using platelet concentrates from the blood bank, at therapeutic concentrations of immunoglobulins.
Results  Incubation of platelets with CMVIg and IVIg markedly induced platelet aggregation, and increased expression of CD62P and secretion of sCD40L. The capacity of CMVIg and IVIg to induce platelet aggregation was completely abrogated by adding the blocking antibody AT10 directed against the low-affinity Fc IgG receptor (CD32).
Conclusions  Our results suggest that CMVIg and IVIg solutions with activating Fc domains are able to bind CD32 on platelets and cause platelet aggregation in vitro . These results indicate a mechanism by which in vivo intravascular thrombosis may be explained and suggest caution with concomitant use of packed platelets and IVIg in autoimmune diseases in the clinical setting.