孤独症与精神分裂症患者异常淋巴细胞的对照研究

目的了解孤独症患者免疫功能状况以及孤独症和精神分裂症在免疫指标上是否存在联系。方法采用随机、双盲法检测２４例孤独症和１５例精神分裂症患者外周血中的异常淋巴细胞。患者均未服过抗精神病药，精神分裂症为首次发作。结果孤独症和精神分裂症患者外周血中Ｐ型异常淋巴细胞分别为１２．７％±９．２％、１７．６％±８．７％，均较各自正常对照组（分别为３．２％±２．３％、５．１％±４．３％）显著增多（Ｐ＜０．０１），而孤独症组与精神分裂症组之间差异无显著性（Ｐ＞０．０５）。结论孤独症存在免疫功能异常，且在免疫指标上与精神分裂症存在某些相似的异常表现     

住院精神分裂症患者血清甲状腺素放射免疫学测定初步分析

作者应用放射免疫学技术，对１９０例住院精神分裂症患者的血清Ｔ３、Ｔ４及ＴＳＨ浓度进行测定。结果发现，这三种物质总的均值属正常范围，但男性高于女性且有显著差异（Ｐ＜０．０５）。２２．６３％患者Ｔ３值低于正常，４７．４％高于正常；５４．２１％患者Ｔ４值低于正常，６．３２％高于正常；１．５８％的ＴＳＨ值低于正常。男性病程短的（≤５年）Ｔ４值低于病程长的（＞２０年），有显著差异（Ｐ＜０．０１）；抗精神病药物日低剂量者Ｔ３值低于大剂量者有显著差异（Ｐ＜０．０５）。有精神病家族史者Ｔ３值和Ｔ４值明显高于无家族史者，均有显著差异（Ｐ＜０．０１）。作者认为，部分患者出现甲状腺素分泌量的异常是很难找到甲状腺机能障碍的可靠临床象，表明精神分裂症与甲状腺功能之间虽有联系却非因果关系。推测可能受患者情绪行为障碍及临床上不易觉察到的心理应激反应影响，使甲状腺分泌功能发生短暂的异常，一般无须特殊处理则可恢复正常，男性激素可起有一定的促进作用。大部分抗精神病药对甲状腺分泌功能具有间接的影响。     

孤独症患者T淋巴细胞功能及其亚群的研究

为研究孤独症患者免疫学方面的异常，探索孤独症的病理学机制，对２７例孤独症、１６例精神发育迟滞（ＭＲ）和１８名正常儿童进行了Ｔ淋巴细胞增殖反应及其亚群的测定，应用ｔ检验进行统计学处理。结果显示：孤独症组的ＣＤ４阳性细胞百分数明显低于其它两组（ｔ值分别为２．６４，２．２１；Ｐ平均值＜０．０５），孤独症ＣＤ３阳性细胞也较ＭＲ组显著为低（ｔ＝２．４７４，Ｐ＜０．０２）。在淋巴细胞增殖反应方面，孤独症组也较对照组明显降低（ｔ＝２．１７５，Ｐ＜０．０５）。提示ＣＤ４阳性细胞数下降与孤独症的发病有关，并讨论了孤独症与Ｔ淋巴细胞功能间的联系     

脑出血患者与外周血淋巴细胞rDNA转录活性的临床研究

为了探讨脑出血患者免疫状态,我们测定３２例脑出血患者外周血Ｔ淋巴细胞ｒＤＮＡ转录活性及其Ｔ淋巴细胞亚群与正常人作对照研究,结果发现：脑出血患者ｒＤＮＡ转录活性及Ｔ淋巴亚群明显低于正常对照组（Ｐ〈０．０１或Ｐ〈０．０５）,说明脑出血患者存在明显细胞免疫功能低下。     

老年人急性脑血管病免疫功能变化及其临床意义

目的　了解老年人急性脑血管病免疫功能的变化及临床意义。方法　检测１２８ 例患者外周血Ｔ淋巴细胞亚群和免疫球蛋白水平，并观察急性期与恢复期的动态变化。结果　脑梗死组和脑出血组外周血Ｔ细胞亚群有异常变化，ＣＤ４ 水平较正常对照组升高（Ｐ＜ ０．０５），其中脑梗死组升高更明显，６０～６９ 岁组与７０ 岁及７０ 岁以上组比较无差异，而ＣＤ８ 在脑梗死７０ 岁及以上组较６０～６９ 岁组明显下降（Ｐ＜ ０．０５）；脑出血组与脑梗死组之间外周血Ｔ淋巴细胞亚群水平的差异比较无显著意义。ＩｇＧ、ＩｇＭ 水平在两组患者中均有明显下降，与正常对照组有显著或非常显著性差异（Ｐ＜０．０５ 或Ｐ＜ ０．０１），在脑出血组下降更明显，恢复期有明显改善。结论　老年人急性脑血管病患者存在免疫功能的改变，脑梗死患者以Ｔ细胞亚群改变较明显，而脑出血患者则以免疫球蛋白改变更明显，早期预防动脉粥样硬化、改善患者的免疫功能对防治脑血管病具有一定的意义     

抑郁症病人细胞免疫和血超氧化物歧化酶含量的研究

目的探讨生物学因素与抑郁症病因病理的关系。方法对内源性抑郁１３例、非内源性抑郁１１例和１３例健康人进行自然杀伤细胞（ＮＫ）、淋巴细胞转化率、血超氧化物歧化酶（ＳＯＤ）测定。结果病人组ＮＫ细胞均明显降低（Ｐ＜００１），淋巴细胞转化率及ＳＯＤ含量与正常人无明显差别（Ｐ均＞００５）。结论抑郁症病人存在免疫参数异常，但这种异常可能不是其特异性生物学指标，而是一种状态标志；抑郁症病人不存在自由基活动增强。     

精神分裂症白细胞介素2和CD4 细胞的相关研究

目的　探讨精神分裂症患者 Ｃ Ｄ４ ＋ 细胞与白细胞介素２（ Ｉ Ｌ２） 之间的关系。方法　对３０ 例精神分裂症和２５例正常对照分别采用碱性磷酸酶抗碱性磷酸酶桥联酶标法、放射免疫法进行外周血 Ｃ Ｄ４ ＋ 细胞、 Ｉ Ｌ２ 分泌细胞数和 Ｉ Ｌ２ 含量检测。结果　精神分裂症组外周血 Ｃ Ｄ４ ＋ 细胞、 Ｉ Ｌ２ 分泌细胞和 Ｉ Ｌ２ 含量均显著低于正常组（ Ｐ＜ ００５） ；正常组血 Ｃ Ｄ４ ＋细胞数与外周 Ｉ Ｌ２ 含量显著正相关（ Ｐ＜ ００５） ，病人组无相关。结论　精神分裂症可能存在免疫激活，与其自身免疫假说相符；同时，分泌 Ｉ Ｌ２ 的 Ｔ 细胞也可能存在自身缺陷。     

产科并发症和抽动秽语综合征

目的探讨产科并发症（ＯＣ）和抽动秽语综合征（ＴＳ）的关系。方法对分娩期和孕期有ＯＣ的（ＴＳ）患者各３０例分别与无ＯＣ的ＴＳ患者３０例作对照比较。结果研究组发病年龄早于对照组（Ｐ＜０．０１）；治疗前及治疗后的症状评分大于对照组（Ｐ＜０．０１）；脑电图异常例数要多于对照组（Ｐ＜０．０５）。结论ＯＣ是导致ＴＳ发病的重要危险因素，并对ＴＳ的预后有一定影响     

精神病患者血清中腺苷脱氨酶活性的研究

对３２１例精神病患者进行了血清ＡＤＡ活性测定，发现精神分裂症和情感性精神病患者高干对照组（ｐ＜０．０１）．而神经症患者与对照组无异常（Ｐ＞０．０５），服用与未服精神病药物及家族史阳性与阴性患者之间无明显差异（Ｐ＞０．０５）．根据上述结果，推测精神分裂症和情感性精神病患者ＡＤＡ增高可能与精神病患者免疫功能障碍有关，提高精神病治愈事和纠正免疫功能障碍，注意纠正ＡＤＡ活性可能是一个有效的途径。     

精神分裂症患者血清催乳素和生长激素水平研究

目的　探讨精神分裂症患者血清催乳素（ Ｐ Ｒ Ｌ） 、生长激素（ Ｇ Ｈ） 基础水平与正常人的差异及治疗前后 Ｐ Ｒ Ｌ、 Ｇ Ｈ 水平的变化，以及利培酮对 Ｐ Ｒ Ｌ、 Ｇ Ｈ 的影响。方法　采用放射免疫法对６２ 例精神分裂症患者治疗前和治疗后第２ 、４ 、６ 周末的 Ｐ Ｒ Ｌ、 Ｇ Ｈ 水平进行测定，并与３２ 名正常人对照，同时分为利培酮组３２ 例和氯丙嗪组３０ 例进行对照分析。结果　精神分裂症患者总样本的基础 Ｐ Ｒ Ｌ、 Ｇ Ｈ 水平与对照组无差异（ Ｐ＞ ０ ．０５） ，用抗精神病药物治疗后 Ｐ Ｒ Ｌ 显著升高（ Ｐ＜ ０ ．０１） ， Ｇ Ｈ 无显著变化（ Ｐ＜ ０ ．０５） 。女性患者治疗后 Ｐ Ｒ Ｌ 水平升高明显，为男性的２３ 倍。利培酮治疗后６ 周末 Ｐ Ｒ Ｌ 水平为（１２２ ．３３ ±７３ ．２７）μｇ／ Ｌ，较治疗前明显增高（ Ｐ＜ ０ ．０１） ，较氯丙嗪组 Ｐ Ｒ Ｌ 水平（１０２ ．０６ ±６５ ．６１）μｇ／ Ｌ为高，但无显著差异（ Ｐ＞ ００５） 。结论　结果支持精神分裂症的多巴胺功能亢进假说，抗精神病药物所致 Ｐ Ｒ Ｌ 升高有明显的性别差异，利培酮有明显的致 Ｐ Ｒ Ｌ 升高的作用，有较强的拮抗中枢多巴胺作用。     

Subsets of lymphoid cells in blood and thymus in myasthenia gravis : Monoclonal Antibody Analysis

Lymphoid cell subpopulations in peripheral blood and thymus were analyzed in patients with myasthenia gravis (MG) using monoclonal antibodies. The proportion of lymphocytes of T lineage (OKT 3 +, OKT 4 +, OKT 8 + cells) in peripheral blood of 11 MG patients, was significantly decreased in comparison with controls, but the ratio of OKT 4+/OKT 8+ cells was not different. Thymus cells were studied in 9 patients. The percentage of OKIa 1 + cells was significantly higher in MG thymus than in control thymus (P < 0.0005). There were no significant differences in the proportions of T lymphocyte subsets between MG and control thymuses.     

Medication effect on lymphocyte morphology in schizophrenia

Past studies on the occurrence of atypical lymphocytes in the blood of individuals with schizophrenia are contradictory; some researchers have argued that such cells are a genetic marker of the disease while others have explained the cells simply as an effect of antipsychotic drugs. The present study blindly measured atypical lymphocytes in 14 schizophrenics on medication for at least 6 weeks and off medication for at least 4 weeks, ten Huntington's disease patients on antipsychotic medication, and ten normal controls. The patients with schizophrenia (P less than 0.05) and those with Huntington's disease (P less than 0.02) both had significantly more atypical lymphocytes than the normal controls. However no difference was found in the percentage of atypical lymphocytes in patients with schizophrenia on and off medication. The authors cite the need for studies of first-admission, never-tested patients to definitively settle this question.     

Lymphocyte subpopulations in peripheral blood from schizophrenic patients

Patients with acute and chronic schizophreniz were examined for T andFc receptor-bearing lymphocytes in blood by means of rosette techniques. The patients had normal numbres of peripheral blood lumphocyte. The percentage iof T lymphocytes in patients with acute schizophrenia was reduced (60 ± 2%) comlpared with controls (66 ± 1 %) and patients with chronic schizophrenia (67 ± 3 %). The total number of T lymphocytes was significantly decreased in patients with acute schizophrenia (1, 238 ± 89 cells/mm³, p<0.02) compared with controls (1, 538 ± 157 cells/mm³), while patients with chronic schizophrenia had slightly elevated numbers (1, 778 ± 200 cells/mm³). the percentage and total numbers of Fc receptor-bearing lumphocutes were normal in both patients groups. Both immune mechanisms and the neuroplepic drug treatment may be of importance of the observed decrease in T lymphocyte numbers in blood from patients with acute schizophrenia.     

Monoclonal antibody analysis of blood T-cell subsets in myasthenia gravis

Analysis of peripheral blood T-cell subsets and B-cells in patients with myasthenia gravis was performed using monoclonal antibodies and antibody against surface immunoglobulins (SIg) in an immunofluorescent technique. We found a modest but significant decrease in percentages of OKT3- and OKT8-positive cells (thought to represent total T-cells and T-suppressor/cytotoxic cells, respectively) in myasthenics as a group. The percentage of OKT3-positive cells was significantly decreased in patients with late-onset disease (>35 years old), while the percentage of OKT8-positive cells was significantly reduced in those with early-onset myasthenia (<35 years old). Both thymectomized and nonthymectomized patients exhibited a decreased percentages of SIg-positive cells in myasthenics and controls. Our results suggest that only modest imbalances of circulating immunoregulatory lymphocytes occur in myasthenia gravis; however, it is conceivable that the small differences observed in this study may reflect pathogenetically important reductions in a functionally distinct lymphocyte subpopulation.     

Stimulated lymphocytes in schizophrenia

This study examines the effect of neuroleptic medication on the distribution of the reported atypical lymphocytes of schizophrenia. The predominant atypical type in schizophrenia was termed the P-type atypical lymphocyte to differentiate the cell from other types of peripheral lymphocytes. Such P cells showed stimulated features: clear cytoplasmic basophilia and an irregularly shaped nucleus with a leptochromatic structure and occasionally one or two nucleoli, but the cell size ranged from small to large. P cells were found in all 42 schizophrenic patients examined and ranged from 5% to 45% of lymphocytes. Patients receiving neuroleptic medication had a lower mean percentage of P cells (17.8%) compared with patients not receiving neuroleptic medication (28.7%). The findings indicate that neuroleptic medication in not likely to be inducing the P-cell reaction.     

The inflammatory process in polymyositis: monoclonal antibody analysis of muscle and peripheral blood immunoregulatory lymphocytes.

An analysis was made of the lymphocyte subpopulations in the muscle lesions and the peripheral blood of 25 patients with inflammatory myopathy, in the acute or chronic phase of the disease. Percentages of activated T lymphocytes (65% +/- 3.4), both helper and suppressor/cytotoxic, macrophages (25% +/- 3.2) and B cells (11% +/- 0.9) in the tissues were similar at all stages of the illness; T cells were, however, more common in acute polymyositis than in acute dermatomyositis, where B cells were significantly increased. A loss of circulating OKT8-positive lymphocytes in the peripheral blood was demonstrated, supporting other evidence of disturbed immunoregulation. It was concluded that the attack on muscle fibres is mediated by T cells, macrophages, and B cells, with the first two playing the major roles.     

T lymphocytes in cerebrospinal fluid from patients with neurological diseases.

T lymphocytes were determined according to their ability to form rosettes with sheep erythrocytes, in cerebrospinal fluid (CSF) from 120 patients, and in peripheral blood from 59 patients. Normal CSF contained 74.9 +/- 9.6% T lymphocytes. Increased T lymphocyte percentage was found in CSF from patients with active multiple sclerosis (MS), and Guillain-Barré syndrome, as well as the 2 patients with retrobulbar neuritis and the 1 with subacute sclerosing panencephalitis. Patients with stable MS showed no significant change in CSF T lymphocyte percentage. CSF from patients with viral meningo-encephalitis or meningo-radiculitis had a decreased T lymphocyte percentage. This decrease was also found in the 2 patients with malignant disease and the 2 with presenile dementia. An exceptionally low CSF T cell count (5%) was found in 1 patient with cerebellar ataxia.     

Search for atypical lymphocytes in schizophrenia.

The existence of atypical lymphocytes with specific morphological characteristics in the peripheral blood of schizophrenic patients has been suggested in several reports over the last 40 years. In our study this observation was examined not only by using the formerly applied method of light microscopy for general cell distribution and lymphocyte morphology but also by applying flow cytometry, a well established immunological method for lymphocyte patterns such as lymphocyte subgroups and lymphocyte activity. In contrast to the previously published data, our results demonstrated no differences in cell distribution (lymphocytes, polymorphonuclear cells, eosinophil and basophil granulocytes, monocytes), lymphocyte morphology ("atypical lymphocytes" vs. "normal lymphocytes"), distribution of lymphocyte-subtypes (T-cells (CD3(+)), T-helper-cells (CD3(+)/CD4(+)), cytotoxic T-cells (CD3(+)/CD8(+)), B-cells (CD19(+)), NK-cells (CD3(-)/CD56(+))) or state of T-lymphocyte activity (CD25(+) or HLA-DR(+)-cells) in schizophrenic patients compared to healthy controls. We suggest that possible immunological alterations in schizophrenia do not correlate with morphological characteristics of lymphocytes observable by light microscopy or an altered state activity of T-lymphocytes examined by flow cytometric parameters. Further studies should concentrate on intracellular and functional aspects of the different lymphocyte subgroups.     

Thymic and peripheral blood T- and B-cell levels in myasthenia gravis.

We have compared the percentage of T and B lymphocytes in the thymus and peripheral blood populations of patients with myasthenia gravis. There were significantly fewer thymic T cells in myasthenic hyperplastic thymus (MG-H), but not in myasthenia gravis-thymoma (MG-T), compared with normal thymus biopsies obtained at cardiac surgery. Conversely, B cells were increased in MG-H versus MG-T and normals. Peripheral blood T and B cells were not different in any group of myasthenic patients compared to normal populations. In vitro autologous mixed lymphocyte reactions between thymus and peripheral blood lymphocytes occurred in MG-H, but did not correlate with the degree of thymic B-cell increases in these patients.