产后抑郁症与甲状腺功能关系的研究进展

产后抑郁症(Postpartum depression,PPD)发病率高,是生育常见的并发症之一,对产妇、婴儿、家庭和社会均可造成不可估量的损害。多种因素可引起PPD的发生,目前多项研究表明下丘脑-垂体-甲状腺(Hypothalamuspituitary-thyroid,HPT)轴功能紊乱参与PPD的发生,但两者间的具体联系尚未明确。本文从妊娠期甲状腺功能变化、促甲状腺激素(Thyroid stimulating hormone,TSH)、游离三碘甲状原氨酸(Free triiodothyronine,FT3)、游离甲状腺素(Free thyroxine,FT4)水平变化对PPD的影响、甲状腺自身抗体与PPD的关系以及抗PPD治疗对甲状腺功能影响等方面对PPD与甲状腺功能关系研究进展做一综述,以期为深入了解和治疗PPD带来新的启示。     

Coinfection by Talaromyces marneffei and Mycobacterium abscessus in a human immunodeficiency virus-negative patient with anti-interferon-γ autoantibody: a case report

Patients with anti-interferon (IFN)-γ autoantibodies have weakened immune defenses against intracellular pathogens. Because of its low incidence and non-specific symptoms, diagnosis of anti-IFN-γ autoantibody syndrome is difficult to establish during the early stages of infection. Here, we report a patient with high titers of serum anti-IFN-γ autoantibodies suffering from opportunistic infections. The patient presented with intermittent fever for 2 weeks. During his first hospitalization, he was diagnosed with Talaromyces marneffei pulmonary infection and successfully treated with antifungal therapy. However, multiple cervical lymph nodes subsequently became progressively enlarged. Mycobacterium abscessus infection was confirmed by positive cervical lymph node tissue cultures. High-titer serum anti-IFN-γ antibodies were also detected. Following anti-M. abscessus therapy, both his symptoms and lymph node lymphadenitis gradually improved. Anti-IFN-γ autoantibody syndrome should be considered in adult patients with severe opportunistic coinfections in the absence of other known risk factors.     

原发性胆汁性胆管炎患者肝脏雌激素受体与外周血细胞因子及自身抗体的相关性分析

目的 探讨原发性胆汁性胆管炎（PBC）患者肝脏雌激素受体（ER-α）与外周血Th1、Th2细胞因子及自身抗体的相关性。方法 选择2015年12月—2017年12月南京市第二医院收治的PBC患者62例（PBC组）、自身免疫性肝炎患者60例（AIH组）及同期门诊体检健康者50例（对照组）为研究对象。酶联免疫吸附试验（ELISA）检测受试者外周血Th1细胞因子［干扰素（INF-γ）、白细胞介素-2（IL-2）］、Th2细胞因子［白细胞介素-4（IL-4）、白细胞介素-10（IL-10）］的质量浓度和自身抗体（AMA-M2、抗LKM-1抗体、抗LC1抗体、抗GP210抗体、抗SLA抗体、抗SP100抗体）的阳性情况。免疫组织化学（IHC）检测PBC组、AIH组肝组织中ER-α表达情况。Pearson法分析ER-α与Th1/Th2细胞因子、自身抗体的相关性。结果 3组INF-γ、IL-2、IL-4、IL-10质量浓度的比较,差异有统计学意义（P <0.05）,PBC组均高于AIH组（P <0.05）,AIH组均高于对照组（P <0.05）。PBC组和AIH组ER-α的阳性表达比较,差异有统计学意义（P <0.05）,PBC组以高表达为主（53.23%）,AIH组以低表达为主（75.00%）。PBC组ER-α与血清AMA-M2、抗GP210抗体、抗SP100抗体阳性率呈正相关（r =0.530、0.602和0.652,P <0.05）,与外周血INF-γ、IL-2、IL-4、IL-10呈正相关（r =0.615、0.593、0.558和0.601,均P <0.05）,与抗LKM-1抗体、抗LC1抗体、抗SLA抗体无关（r =0.135、0.068和0.095,均P >0.05）。结论 PBC患者肝组织中ER-α阳性表达升高,INF-γ、IL-2、IL-4、IL-10质量浓度升高,AMA-M2、抗LKM-1抗体、抗LC1抗体、抗GP210抗体、抗SP100抗体阳性表达升高,ER-α与INF-γ、IL-2、IL-4、IL-10呈正相关,ER-α与AMA-M2、抗GP210抗体、抗SP100抗体表达呈正相关。ER-α阳性表达可能是PBC发病原因之一。     

缬沙坦对糖尿病肾病并高血压AT1自身抗体阳性患者血压和糖化血红蛋白的影响

[目的]探讨抗血管紧张素Ⅱ受体拮抗剂缬沙坦对糖尿病肾病(DN)合并高血压抗AT1受体自身抗体阳性患者血压和糖化血红蛋白的影响.[方法]以合成的AT1受体多肽片段为抗原,应用酶联免疫吸附测定(ELISA)技术,检测196例DN合并高血压患者血清抗AT1受体自身抗体.①糖尿病肾病合并高血压136例(1组,治疗组)抗AT1受体自身抗体阳性组和阴性组均在原胰岛素降糖方案治疗基础上均给予尼群地平30 mg/d,缬沙坦(Valsartan)80～160 mg/d,肠溶阿司匹林100 mg/d口服,观察受体自身抗体阳性和阴性组降压疗效;2,6,12周为一疗程.②2组糖尿病肾病合并高血压60例(对照组)不给缬沙坦,余治疗同上,观察不给缬沙坦对此类病人糖化血红蛋白的影响.治疗前及治疗3个月测糖化血红蛋白.[结果]①高血压合并DN治疗组和对照组抗AT1受体自身抗体阳性率分别为52.2%(71/136)和51.7%(60/71);②抗AT1受体自身抗体阳性组缬沙坦治疗2、6、12周降压疗效达标,与抗AT1受体自身抗体阴性组比较,具有显著的统计学意义(P＜0.05,P＜0.01);③糖尿病肾病合并高血压患者治疗组缬沙坦治疗后对糖化血红蛋白达标率明显优于对照组.[结论]对于高血压合并糖尿病肾病抗AT1受体自身抗体阳性组,缬沙坦治疗降压效果和糖化血红蛋白达标率明显优于对照组,靶向治疗具有重要的临床意义.     

Regional brain metabolism in a murine systemic lupus erythematosus model

Systemic lupus erythematosus (SLE) is characterized by multiorgan inflammation, neuropsychiatric disorders (NPSLE), and anti-nuclear antibodies. We previously identified a subset of anti-DNA antibodies (DNRAb) cross-reactive with the N-methyl-D-aspartate receptor, present in 30% to 40% of patients, able to enhance excitatory post-synaptic potentials and trigger neuronal apoptosis. DNRAb+ mice exhibit memory impairment or altered fear response, depending on whether the antibody penetrates the hippocampus or amygdala. Here, we used 18F-fluorodeoxyglucose (FDG) microPET to plot changes in brain metabolism after regional blood–brain barrier (BBB) breach. In DNRAb+ mice, metabolism declined at the site of BBB breach in the first 2 weeks and increased over the next 2 weeks. In contrast, DNRAb− mice exhibited metabolic increases in these regions over the 4 weeks after the insult. Memory impairment was present in DNRAb+ animals with hippocampal BBB breach and altered fear conditioning in DNRAb+ mice with amygdala BBB breach. In DNRAb+ mice, we observed an inverse relationship between neuron number and regional metabolism, while a positive correlation was observed in DNRAb− mice. These findings suggest that local metabolic alterations in this model take place through different mechanisms with distinct time courses, with important implications for the interpretation of imaging data in SLE subjects.     

自身免疫性肝炎44例分析

目的　探讨自身免疫性肝炎(autoimmunehepatitis,AIH)的免疫学实验诊断特点。方法　观察 44例AIH的临床表现,并分析有关实验室检查资料。结果　本组患者临床症状不典型,肝功能各项指标普遍异常,有 38例患者抗核抗体 (antinuclearantibodies,ANA)阳性, 29例抗平滑肌抗体 (smoothmuscleantibodies,SMA)阳性, 22例抗线粒体抗体 (antimitochondrialantibodies,AMA)阳性(其中 1例M2阳性), 2例抗肝肾微粒体(anti liver/kidneymicrosomalantibodies,anti- LKM)- 1抗体阳性, 4例抗可溶性肝抗原抗体(anti solubleliverantigenantibodies,anti- SLA)阳性。结论　AIH无典型临床症状,患者可以通过自身抗体的检测结合临床表现获得诊断。     

Anti-GOR in hepatitis D: specific association with hepatitis C virus superinfection

Summary A group of 113 patients with chronic hepatitis D was investigated for the presence of anti-GOR and liver kidney microsomal antibodies. Eight patients were anti-GOR positive and also positive for hepatitis C virus-infection. In sera from 16 patients liver-kidney microsomal antibodies were detectable by immunofluorescence. They were classified as LKM-3 due to their fluorescence pattern. Two of the LKM-3-positive sera were also anti-hepatitis C virus and anti-human immunodeficiency virus positive. None of these patients were positive for anti-GOR. Fourteen sera from LKM-3-positive patients reacted in Western blot with a microsomal protein at 55 kDa that differs from the 50-kDa LKM-1 (cytochrome P450IID6) antigen. Our studies demonstrate that hepatitis D virus itself does not induce an autoimmune reaction against the GOR antigen and that autoimmunity to the LKM-3 antigen induced by hepatitis D virus infection does not correlated with anti-GOR. These studies support the specificity of the anti-GOR response for hepatitis C virus infection.