系统性红斑狼疮病人活性氧基与自身抗体变化的观察

对比观察６０例ＳＬＥ病人血浆脂质过氧化物（ＬＰＯ）、红细胞超氧化物歧化酶（ＳＯＤ）及过氧化氢酶（ＣＡＴ）含量与ＡＮＡ、ｄｓ－ＤＮＡ、Ｓｍ和Ｕ１ＲＮＰ自身抗体的变化。活动期病人活性氧基（ＯＲ）水平增高，以致ＳＯＤ及ＣＡＴ活性下降，ＬＰＯ含量增高；非活动期ＳＯＤ及ＣＡＴ活性相对增高，ＬＰＯ含量降低，提示体内ＯＲ水平下降。抗ｄｓ－ＤＮＡ抗体滴度与红细胞ＳＯＤ、ＣＡＴ、血浆ＬＰＯ含量及疾病的严重程度密切相关。内源性ＯＲ的增加可导致Ｔ抑制细胞功能下降，Ｂ淋巴细胞异常增殖，以致体内产生多种自身抗体，诱发免疫炎症反应     

系统性红斑狼疮患者外周血淋巴细胞bcl-2的表达及临床意义

目的 为了探讨ｂｃｌ－２基因在系统红斑狼疮（ＳＬＥ）发病机制中的作用及临床意义。方法 应用逆转录－聚合酶链反应（ＲＴ－ＰＣＲ）检测３１例ＳＬＥ患者外周血单一核细胞（ＰＢＭＣ）ｂｃｌ－２ｍＲＮＡ表达水平和流式细胞仪双标记法分析其Ｔ、Ｂ细胞ｂｃｌ－２蛋白表达。结果 活动期ＳＬＥ患者ＰＢＭＣｂｃｌ－２ｍＲＮＡ表达水平明显升高,占５５．６％,且活动期ＳＬＥ患者ＣＤ３＾＋、ＣＤ４＾＋和ＣＤ８＾＋Ｔ细胞亚群Ｐ     

用MDT后麻风病人及其接触者血中的抗PGI IgM抗体检测

推广应用ＭＤＴ后用ＮＴ－Ｏ－ＢＳＡ－ＥＬＩＳＡ检测了１７１５名麻风接触者和６例新病人血中的抗ＰＧＩ－ＩｇＭ抗体。１７１５例接触者中的抗体阳性率分别为：开始ＭＤＴ前３３．４％，用ＭＤＴ２－２４个月３２．８２％，用ＭＤＴ后４８个月２１．８４％（Ｐ＜０．００１）；６例新病人在推广ＭＤＴ５年时ＯＤ下降７２．７４％；连续观察２４３例抗体阳性的接触者，２－５年共发病７例（ＢＴ１例，ＢＬ４例，ＬＬ２例）。结果说     

系统性红斑狼疮患者外周血单一核细胞CD23的表达

为了揭示Ｂ细胞中ＣＤ２３的表达与ＳＬＥ发生发展的关系及在ＳＬＥ发病机理中可能的作用，我们应用ＡＢＣ免疫组化法和斑点核酸杂交技术对ＳＬＥ患者外周血单一核细胞（ＰＢＭＣ）ＣＤ２３蛋白和ｍＲＮＡ表达进行了检测。结果显示：３０例ＳＬＥ患者ＰＢＭＣＣＤ２３蛋白表达显著增高（Ｐ＜０．０１），且与疾病活动呈正相关关系（ｒｓ＝０．３８１４，Ｐ＜０．０５）；具有不同ＡＮＡ、抗ｄｓＤＮＡ抗体水平，有无伴肾损、脑损的ＳＬＥ患者，ＰＢＭＣＣＤ２３表达均无显著性差异（Ｐ均＞０．０５）；单纯使用皮质类固醇激素治疗或和其它免疫抑制剂联合治疗的ＳＬＥ患者，ＰＢＭＣＣＤ２３表达亦无显著性差异（Ｐ＞０．０５）。２０例ＳＬＥ患者ＰＢＭＣＣＤ２３ｍＲＮＡ表达较正常人显著增高（Ｐ＜０．０１）。经治疗病情稳定后，ＣＤ２３蛋白和ｍＲＮＡ表达均降至正常（Ｐ均＞０．０５）。提示在ＳＬＥ活动期Ｂ细胞高度激活、增殖并大量表达ＣＤ２３，且该种表达与ＡＮＡ、抗ｄｓＤＮＡ抗体产生水平无直接关系     

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     

卡介菌多糖核酸对尖锐湿疣患者外周血淋巴细胞mIL－2R表达及sIL－2R水平的影响

采用ＩＩＦ和ＥＬＩＳＡ法分别检测了２２例尖锐湿疣（ＣＡ）患者和１６例正常对照者外周血淋巴细胞（ＰＢＬ）上膜白细胞介素２受体（ｍＩＬ－２Ｒ）表达水平及其培养上清中可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）的含量，同时观察了卡介菌多糖核酸（ＢＣＧ－ＰＳＮ）在体外对这两项指标的影响。结果发现，患者ＰＢＬ上ｍＩＬ－２Ｒ表达下降，而培养上清中ｓＩＬ－２Ｒ含量明显增高；一定浓度的ＢＣＧ－ＰＳＮ能在体外使患者淋巴细胞ｍＩＬ－２Ｒ表达增强，以及降低培养上清中ｓＩＬ－２Ｒ的含量。这表明ＣＡ患者存在细胞免疫缺陷，ＢＣＧ－ＰＳＮ能在体外调节患者细胞免疫功能。     

红斑狼疮皮损中浸润细胞免疫表型和角质形成细胞HLA-DR抗原表达的研究

应用抗ＨＬＡＤＲ、ＣＤ３、ＣＤ４、ＣＤ８、ＣＤ２０的单克隆抗体和ｓｔｒｅｐｔｒａｖｉｄｉｎｐｅｒｏｘｉｄａｓｅｓｔａｉｎｉｎｇ（ＳＰ）技术对１０名正常人皮肤,１６例ＳＬＥ皮损和１９例ＤＬＥ皮损进行了免疫组化研究。观察到正常人皮肤角质形成细胞未见ＨＬＡＤＲ抗原表达,而ＳＬＥ（６／１６）,ＤＬＥ（８／１９）皮损处角质形成细胞可以表达ＨＬＡＤＲ抗原。在ＳＬＥ、ＤＬＥ真皮内浸润细胞主要为Ｔ淋巴细胞（ＣＤ３＋浸润细胞）,且以ＴＨ细胞（ＣＤ４＋浸润细胞）占优势。另外,还发现在两种ＬＥ表皮角质形成细胞表达ＨＬＡＤＲ抗原处,真皮内可见ＣＤ３＋浸润细胞和激活的Ｔ淋巴细胞（ＨＬＡＤＲ＋浸润细胞）。讨论了ＬＥ皮损角质形成细胞ＨＬＡＤＲ抗原表达及其与病损内浸润细胞免疫表型的关系。ＬＥ皮损处ＨＬＡＤＲ＋角质形成细胞可能具有抗原递呈作用,而角质形成细胞异常表达ＨＬＡＤＲ抗原则可能与真皮内浸润单个核细胞或淋巴细胞释放的ＩＦＮα,ＴＮＦγ等有关。     

卡介菌多糖核酸对尖锐湿疣患者外周血淋巴细胞mILI—2R表达及sIL—2…

采用ＩＩＦ和ＥＬＩＳＡ法分别检测了２２例尖锐湿疣（ＣＡ）患者和１６例正常对照者外周血淋巴细胞（ＰＢＬ）上膜白细胞介素２受体（ｍＩＬ－２Ｒ）表达水平及其培养上清中可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）的含量，同时观察了卡介菌多糖核酸（ＢＣＧ－ＰＳＮ）在体外对这两项指标的影响。结果发现，患者ＰＢＬ上ｍＩＬ－２Ｒ表达下降，而培养上清中ｓＩＬ－２Ｒ含量明显增高；一定的浓度的ＢＣＧ－ＰＳＮ能在体外使患者淋巴     

系统性红斑狼疮患者外周血单个核细胞中IL-6与TNF-α的表达

目的：探讨系统性红斑狼疮（ＳＬＥ）中某些具炎症介质作用细胞因子的自然表达。方法：用逆转录－多聚酶链反应（ＲＴ－ＰＣＲ）法检测了１０例正常人和１５例活动期ＳＬＥ患者外周血单个核细胞（ＰＢＭＣ）中白介素６（ＩＬ－６）和肿瘤坏死因子α（ＴＮＦ－α）ｍＲＮＡ表达的水平。结果：与正常人相比,活动期ＳＬＥ患者ＰＢＭＣ中ＩＬ－６和ＴＮＦ－αｍＲＮＡ的表达水平均增高（均Ｐ〈０．０１）。结论：ＳＬＥ患者中ＩＬ－６与ＴＮＦ－α的表达上调,可能在发病机制中起一定作用。     

活动性系统性红斑狼疮患者外周血单个核细胞白介素6信使RNA（IL－6mRNA）表达水平的研究

应用反转录／聚合酶链反应（ＲＴ／ＰＣＲ）方法检测了２１例ＳＬＥ患者及１４例正常人外周血单个核细胞（ＰＢＭＣｓ）中白介素６信使ＲＮＡ（ＩＬ－６ｍＲＮＡ）表达水平，结果表明活动性ＳＬＥＰＢＭＣｓ中ＩＬ－６ｍＲＮＡ表达明显高于非活动性患者及正常对照，而非活动期ＳＬＥ与正常组比较无显著统计学差异，提示ＩＬ－６可能参与活动性ＳＬＥ的发病机制。     

Levels of serum IgE, serum soluble-Fc epsilon RII, and Fc epsilon RII(+) peripheral blood lymphocytes in atopic dermatitis.

Levels of serum IgE, serum soluble-Fc epsilon RII (S-Fc epsilon RII), and Fc epsilon RII(+) peripheral blood lymphocytes (PBL) were examined in 73 patients with atopic dermatitis (AD) and 17 control subjects with no atopic disease, in order to investigate the correlation of these parameters with AD. AD patients showed increases in IgE, S-Fc epsilon RII and Fc epsilon RII(+)PBL as compared with control subjects. In AD patients, levels of serum IgE and Fc epsilon RII(+)PBL increased as the extent of dermatitis became more severe, while levels of serum S-Fc epsilon RII showed no correlation with the extent of dermatitis. In 8 of the 73 AD patients who showed an improvement in their symptoms with treatment with topical corticosteroids or antihistamine, IgE, Fc epsilon RII(+)PBL, and S-Fc epsilon RII were measured before and after treatment. Fc epsilon RII(+)PBL correlated with disease activity; IgE and S-Fc epsilon RII did not show any such correlation. Patients with elevated IgE levels (IgE greater than 5,000 U/ml) showed low levels of S-Fc epsilon RII. Severely affected cases with a history of respiratory atopy also showed decreased S-Fc epsilon RII levels. It is believed that S-Fc epsilon RII binds to IgE in serum and may neutralize or down-regulate IgE mediated allergic reactions. A low level of S-Fc epsilon RII may cause an elevation of IgE and an exacerbation of the disease.     

Reduced proliferative responses of peripheral blood mononuclear cells specifically toCandida albicans antigen in patients with atopic dermatitis — comparison with their normal reactivity to bacterial superantigens

Although reduced cutaneous reactivities toCandida, albicans have been reported in patients with atopic dermatitis (AD), there is still controversy as to whether the in vivo lymphocyte proliferation response is normal or reduced. We have also reported that patients with AD manifest a decreased cutaneous response only toC. albicans antigen in scarification patch tests. The purpose of this study was to examine whether patients with AD show normal lymphocyte transformation responses toC. albicans antigen. Peripheral blood leucocytes (PBL) from 21 patients with AD and 14 healthy control (HC) subjects were cocultured with optimal concentrations ofC. albicans antigen and of superantigens (staphylococcal enterotoxin A and B). PBL from the patients with AD showed a significantly lower response toC. albicans antigen, but there was no statistically significant difference, in PBL responses to superantigens between the patients with AD and the HC subjects. This decreased proliferative response of PBL was particularly noticeable in those whose RAST scores forC. albicans antigen were high. These results suggest the development of a specific anergy toC. albicans antigen in patients with AD.     

Nerve growth factor and substance P are useful plasma markers of disease activity in atopic dermatitis

BACKGROUND: Neurogenic components, such as neurotrophic factors and neuropeptides, are probably involved in the pathogenesis of atopic dermatitis (AD) via the neuroimmunocutaneous system. Numerous in vitro and in vivo studies have shown that nerve growth factor (NGF), the best-characterized member of the neurotrophin family, modulates the synthesis of the neuropeptide substance P (SP), both of which may be associated with the pathogenesis of human allergic diseases. OBJECTIVES: To evaluate the levels of NGF and SP in the plasma of patients with AD and to examine their possible correlation with disease activity. METHODS: We measured plasma levels of NGF by an immunoenzymatic assay and of SP by aradioimmunoassay in 52 patients with AD, and compared them with 35 normal non-atopic controls. The severity of the disease in AD patients was evaluated using validated clinical scoring systems. RESULTS: Patients with AD had significant increases in plasma levels of NGF and SP compared with controls (P < 0.0005 and P < 0.0001, respectively). A positive correlation between the plasma levels of NGF and SP was found in AD patients (correlation coefficient, Cc = 0.920, P < 0.0001). There was a significant correlation of plasma NGF and SP levels with disease activity evaluated using three different scoring systems: the grading system of Rajka and Langeland (P < 0.001 and P < 0.01, respectively), the objective Severity Scoring of AD (Cc = 0.656, P < 0.005 and Cc = 0.752, P < 0.0005, respectively) and the Eczema Area and Severity Index (Cc = 0.740, P < 0.001 and Cc = 0.765, P < 0.005, respectively). CONCLUSIONS: These data represent the first reported evidence of increased plasma levels of NGF and SP in an allergic human skin disease. They suggest that these neurogenic factors systemically modulate the allergic response in AD, probably through interactions with cells of the immune-inflammatory component. In addition, NGF and SP may be useful markers of disease activity in patients with AD.     

Serum Levels of Eosinophil Cationic Protein Reflect the State of In vitro Degranulation of Blood Hypodense Eosinophils in Atopic Dermatitis

In patients with atopic dermatitis (AD), serum levels of eosinophil cationic protein (ECP) have been shown to be a good reflector of disease severity. To elucidate what serum levels of ECP actually reflect, ECP levels in serum and plasma and cytological aspects of blood eosinophils were examined in AD patients (n=27) and compared to healthy subjects (n=12). Significantly elevated levels of serum ECP were noted in AD patients, while plasma ECP were uniformly recorded at nadir levels in both AD patients and normal subjects. In addition to blood eosinophilia, AD patients had significantly increased numbers of hypodense eosinophils (HEo) with morphological characteristics consistent with an activated state. Serum ECP levels strongly correlated with HEo numbers rather than with total eosinophil counts. These results indicate that elevated levels of serum ECP may be a consequence of in vitro degranulation of “activated” HEo, not of ECP supplementation from lesional skin. In addition, the dynamic correlations of eosinophil-associated parameters (total eosinophil counts, HEo numbers, and serum ECP levels) with AD severity suggest that inflammatory events in lesional skin may be involved in causing not only eosinophilopoiesis in bone marrow, but also development of HEo in the periphery, whose degree in turn may be mirrored in the levels of serum ECP in vitro.     

Synergistic effects of interleukin 4 and interferon-gamma on monocyte phosphodiesterase activity.

Patients with atopic dermatitis (AD) have elevated leukocyte cyclic AMP-phosphodiesterase (PDE) activity and increased in vitro IgE synthesis compared to normal (NL) subjects. Interleukin 4 (IL-4), interferon-gamma (IFN-gamma), and PDE inhibitor have been shown to regulate in vitro IgE synthesis. This study investigated whether soluble T-cell factors such as IL-4 and IFN-gamma could account for elevated PDE activity in patients with AD. Both rhIL-4 and IFN-gamma significantly increased normal monocyte PDE activity to a maximum of 188% (n = 6, p less than 0.05) and 315% above control (n = 3, p less than 0.05), respectively. At concentrations below 0.1 units/ml IL-4 and IFN-gamma had synergistic effects on activation of monocyte PDE. AD and NL T-cell culture supernatants also significantly stimulated normal monocyte PDE activity, but the stimulatory activity was not significantly greater in the AD T-cell supernatants. The effect of both cytokines and T-cell supernatants on normal monocytes was inhibited by antibodies against IL-4 and IFN-gamma, respectively. This study demonstrates that IL-4 and IFN-gamma can increase PDE activity in normal monocytes. Though the levels of IL-4 and IFN-gamma in T-cell supernatants are undetectable with an enzyme-linked immunosorbent assay (ELISA) assay, the concentration of these cytokines below the detectable level can significantly increase PDE activity of monocytes in a synergistic and dose-dependent manner. These results suggest that cytokine-mediated activation of monocytes can increase PDE activity. Furthermore, lymphokines may play an important role in modulating the cyclic nucleotide regulatory pathway.     

NERVE GROWTH FACTOR, NEUROPEPTIDES AND CUTANEOUS NERVES IN ATOPIC DERMATITIS

Introduction:

Neurogenic components, as neurotrophic factors and neuropeptides, are probably involved in the pathogenesis of atopic dermatitis (AD) with the neuroimmunocutaneous system as they modify the functions of immunoactive cells in the skin. Nerve growth factor (NGF) is the best-characterized member of the neurotrophin family. Both NGF and neuropeptides (NPs) may be associated with the disease pathogenesis.

Aim:

This study aims to evaluate the plasma level of NGF and NPs in AD patients and correlate them with the disease activity and nerve changes in the skin by electron microscopy.

Materials and Methods:

Plasma levels of NGF and vasoactive intestinal peptide (+VIP) were measured by an immunoenzymatic assay while plasma levels of calcitonine gene related peptide (CGRP) and neuropeptide Y (NPY) were measured by radioimmunoassay in 30 AD patients in comparison to 10 normal non-atopic controls. Electron microscopic study was done in 10 AD patients.

Results:

It has been found that there is significant increase of plasma levels of NGF and NPs in AD patients compared with controls. There is a positive correlation between the plasma levels of NGF and disease activity (correlation coefficient = 0.750, P<0.005). There is a significant correlation between the number of Schwann axon complex, evidenced by electron microscopic examination and plasma level of NGF in AD patients.

Conclusion:

It has been concluded that these neurogenic factors; NGF and NPs modulate the allergic response in AD, probably through interactions with cells of the immune-inflammatory component. NGF might be considered as a marker of the disease activity.     

IL-4/IL-13 antagonist DNA vaccination successfully suppresses Th2 type chronic dermatitis

Background  Atopic dermatitis (AD) is a chronic disease with a Th2-type-cytokine dominant profile. Several cytokines and related peptides have been used for the treatment of AD but they were ineffective because of their limited biological half-life. We have recently developed a highly efficient mouse dominant negative interleukin (IL)-4/IL-13 antagonist (IL-4DM), which blocks both IL-4 and IL-13 signal transductions.
Objective  To examine the effects of IL-4DM in vivo in an AD model induced by the repeated exhibition of oxazolone (OX).
Methods  Plasmid DNA was injected intraperitoneally to cause an experimental AD-like dermatitis. The effect was evaluated by ear thickness, histological findings, and mast cells counts in the inflamed skin. The plasma IgE and histamine levels were measured. Cytokine production in skin and splenocytes were also analysed.
Results  Mice treated with control plasmid developed marked dermatitis with mast cells and eosinophil infiltration, and had increased plasma IgE and histamine levels with a Th2 type splenocyte cytokine profile. Treatment with mouse IL-4 DNA augmented the ear swelling and thickness with an increased dermal eosinophil count, plasma histamine level, and production of splenocyte IL-4. However, IL-4DM treatment successfully controlled the dermatitis, decreased the mast cell and eosinophil count, and suppressed plasma IgE and histamine levels. Splenocytes produced an increased level of IFN-γ.
Conclusion  These data showed that the simultaneous suppression of IL-4/IL-13 signals successfully controlled Th2-type chronic dermatitis. IL-4DM DNA treatment is a potent therapy for AD and related diseases.     

Defective monocyte and polymorphonuclear leukocyte chemotaxis and clinical characteristics in atopic dermatitis

Summary Using highly purified cell suspensions, monocyte (MO) and polymorphonuclear leukocyte (PMN) chemotaxis was measured by the ⁵¹Cr-labeled cells technique in 30 adult patients with atopic dermatitis (AD). MO chemotaxis was depressed in 60% of the patients; in one-third both MO and PMN chemotaxis was impaired. All patients with normal MO chemotaxis had normal PMN chemotaxis. The defective chemotaxis was related to the presence of cutaneous infection and to the activity of the disease. Cutaneous infection was observen in 70% of the patients with low MO and PMN chemotaxis. We found no relation between the chemotaxis defects and serum IgE levels. Presence of asthma in addition to AD did not influence the results. Preincubation of normal leukocytes with AD plasma did not alter the chemotactic responses. Plasma from atopics had a lower capacity for inducing migration than normal plasma using leukocytes from healthy subjects as test cells.     

特应性皮炎患者外周血CD4+CD25+调节性T细胞的检测

目的 探讨CD4+CD25+调节性T细胞（CD4+CD25+ Treg）在特应性皮炎（AD）发病中的作用机制及临床意义。方法 流式细胞仪分析AD患者外周血中CD4+CD25+ Treg细胞数量,实时荧光定量PCR检测外周血单核细胞（PBMC）中Foxp3 mRNA水平,ELISA检测血清中IL-2、IL-4、IL-10、IFN-γ水平。结果 AD患者外周血中CD4+CD25+ Treg细胞占CD3+ T细胞及CD4+ T细胞的比例均明显低于正常人对照组（t′ = 3.775、4.533,P值均 ＜ 0.01）;外周血中CD4+CD25+ Treg细胞占CD3+ T细胞比例在AD患者急性期明显低于慢性期（t = 2.217,P < 0.05）,而在急性期与亚急性期、亚急性期与慢性期之间差异均无统计学意义（t = 1.558、0.49,P值均 ＞ 0.05）。AD患者PBMC中Foxp3 mRNA的水平低于正常人对照组（z = -2.368,P ＜ 0.05）;其外周血中CD4+CD25+ Treg细胞与血清中IL-2和IL-10成正相关（r = 0.512、0.494,P值均 ＜ 0.05）,与IL-4和IFN-γ的相关性无统计学意义（r = -0.110、-0.237,P值均 ＞ 0.05）。结论 在AD患者中,外周血中CD4+CD25+ Treg细胞数量及Foxp3 mRNA水平均下降,从而可能减少对Th2细胞增生及其细胞因子分泌的抑制,使Th2占优势,参与AD的发病。     

Effective treatment of pruritus in atopic dermatitis using H1 antihistamines (second-generation antihistamines): changes in blood histamine and tryptase levels

BACKGROUND: Atopic dermatitis (AD) is a common chronic inflammatory and allergic skin disease that almost always begins in childhood and follows a course of remittance and flare-up. AD is characterized by intense pruritus and itchiness that can be triggered by an interplay of genetic, immunologic and environmental factors. Of the mediators, histamine is one of the most potent inducers of pruritus. Serum tryptase, which is also a mediator, may be used to examine allergic disease as well. The development of minimal sedation H1 antihistamines (second-generation antihistamines) has revolutionized treatment of allergic diseases. OBJECTIVE: The present study examines the efficacy of second-generation antihistamines in relieving pruritus due to AD. In addition, the relationship between AD pruritus and antihistamine therapy was analyzed by measuring the blood histamine and tryptase levels. METHODS: Thirty-two AD patients were recruited and underwent second-generation antihistamine therapy for 2 weeks. Seventeen received combined topical corticosteroid treatment (Group 1) and the other 15 did not receive steroid treatment (Group 2). The Severity Index and Pruritus Score were assessed as an AD clinical activity index and compared with baseline data. RESULTS: Both the Severity Index and Pruritus Score improved significantly in Group 1 (P<0.001, P<0.05). Group 2 demonstrated a significant improvement in Pruritus Score (P<0.05), but not in the Severity Index. Plasma histamine levels were significantly higher in AD at baseline compared with healthy controls. CONCLUSION: Following antihistamine therapy, these levels decreased significantly in both AD groups (P<0.05). There was a significant correlation between baseline blood histamine and typtase levels. However, this correlation was not evident following treatment. This may reflect insufficient detection capabilities of the measuring assay. The present results suggest that second-generation antihistamine therapy provides an effective clinical treatment for AD, with a notable improvement in pruritus. Furthermore, antihistamine therapy reduced plasma histamine levels in AD patients. These findings further suggest that high blood histamine and tryptase levels in AD patients contribute to the pathogenesis of this disorder, including the onset of pruritus.