甲状腺乳头状癌中Galectin－3、CK19和HBME－1的表达变化及意义

目的观察甲状腺乳头状病变组织中Galectin-3、cytokeratin19（CK19）和HBME-1的表达变化,并探讨其意义。方法采用免疫组化SP法检测112例甲状腺乳头状病变组织（其中甲状腺乳头状癌72例,良性增生40例）中的Galectin-3、CK19和HBME－1。结果Galectin-3、CK19和HBME－1在甲状腺乳头状癌中均呈中至强阳性表达,而在甲状腺良性乳头状增生中均为阴性或弱阳性表达。其中HBME－1和Galectin－3联合检测诊断甲状腺乳头状癌的敏感性、特异性和诊断正确率分别为95．2％、94．1％和94．8％;三者联合检测分别为100％、96．7％和98．8％。结论甲状腺乳头状癌组织中Galeetin-3、CK19和HBME－1表达较甲状腺良性乳头状增生组织明显升高。三者是检测甲状腺乳头状癌较为可靠的标志物,三者的联合检测有助于提高甲状腺乳头状癌的诊断准确性。     

CK34βE12、p63表达在乳腺癌和前列腺癌诊断中的应用价值

目的探讨CK34βE12、p63表达在乳腺、前列腺良恶性病变鉴别诊断中的价值。方法采用免疫组化方法,观察CK34βE12、p63在乳腺、前列腺良恶性病变中的表达情况。结果乳腺良恶性病变组织中肌上皮细胞CK34βE12的标记敏感度低、特异性差,p63着色特异、敏感度高。在乳腺良性病变的腺泡和导管周围可见连续的p63阳性反应的肌上皮细胞围绕;乳腺导管内癌组织p63显示肌上皮呈不连续阳性;乳腺浸润性癌p63染色呈阴性,显示肌上皮消失。良性前列腺增生及低度前列腺上皮内肿瘤形成（PIN）的大多数腺泡和导管周围可见连续的CK34βE12和p63阳性表达,少数呈间断阳性（即部分细胞不着色）,尤以CK34βE12染色明显;高度PINCK34βE12、p63染色呈不连续阳性或阴性反应;前列腺癌20例中19例CK34βE12、p63染色呈阴性,1例CK34,SEl2、p63显示局灶性阳性反应。结论CK34βE12不宜作为标记乳腺肌上皮细胞的抗体在临床使用;p63对乳腺肌上皮细胞和前列腺基底细胞反应特异、敏感,有助干乳腺痛和前列腺癌的诊断。     

CK34βE12和PSA顺序免疫组化双染色在前列腺病变中的表达

目的探索免疫组化前列腺特异性抗原(PSA)、高分子量角蛋白(CK34βE12)双重染色法,并观察二者在前列腺增生性病变、癌前病变、癌及易被误为前列腺癌的精囊腺组织中的表达差异。方法采用PSA、CK34βE12顺序免疫组化双重染色法,选择良性前列腺增生症8例、腺病6例、萎缩后增生4例、基底细胞增生4例、高级别上皮内瘤6例、前列腺癌30例及精囊腺4例,观察染色变化。结果本染色方法稳定、结果分辨清晰。PSA在良性前列腺增生症、腺病、高级别上皮内瘤的分泌上皮、和绝大多数前列腺癌细胞中强表达,在萎缩后增生中不表达或弱表达,基底细胞增生、精囊腺不表达。CK34βE12在前列腺癌中完全缺失,而在增生性病变、癌前病变呈完整或断续状,精囊腺中表达完整。结论CK34βE12和PSA顺序免疫组化双染色在前列腺良、恶性、癌前性病变的诊断和鉴别诊断中是个可行而有用的辅助手段。     

TURP术后标本CK34βE12、p63和p504S检测及意义

目的探讨经尿道前列腺切除术（TURP）术后组织标本中CK34βE12、p63和p504S变化及在判断前列腺疾病性质中的价值。方法免疫组化法检测32例前列腺腺癌患者和40例良性前列腺增生患者TURP术后组织标本（分别为恶性组及良性组）中CK34βE12、p63和p504S表达。结果良性组未见p504S表达,恶性组p504S阳性率为96.88%,P〈0.01;良性组CK34βE12和p63均阳性表达,恶性组仅2例呈弱阳性表达或无表达。结论 TURP切除组织标本CK34βE12、p63联合p504S检测可提高前列腺腺癌的确诊率。     

混合型抗体EZH2/34βE12/p63在前列腺穿刺标本中的诊断意义

目的探讨混合型抗体EZH2/34βE12/p63在不同前列腺病变穿刺标本中的表达及其意义。方法在一张切片上采用免疫组织化学方法同时检测EZH2、34βE12、p63在前列腺癌(PCa)、良性前列腺增生(BPH)、高度上皮内瘤变(HGPIN)、非典型腺瘤样增生(AAH)中的表达。结果 52例PCa标本中,EZH2主要表达于前列腺腺上皮细胞核,阳性率为98.1%。60例BPH、10例HGPIN和14例AAH标本中,34βE12主要表达于前列腺基底细胞胞质,在上述病变中的阳性率分别为96.7%、100.0%和85.7%;p63主要表达于前列腺基底细胞胞核,在上述病变中的阳性率分别为98.3%、90.0%和92.9%。EZH2、34βE12和p63在PCa中表达与BPH、HGPIN、AAH中两两比较差异均有统计学意义(P0.05)。结论联合检测混合型抗体EZH2/34βE12/p63 3种免疫学指标,在前列腺穿刺标本中对PCa与其他病变的鉴别诊断具有一定参考价值。     

桥本甲状腺炎不典型增生甲状腺上皮细胞的组织病理学研究

目的 探讨桥本甲状腺炎(HT)中不典型增生甲状腺上皮细胞(thyroid epithelial cells,TEC)的组织病理学改变及其与甲状腺乳头状癌(PTC)的关系.方法 从存档病例中选取30例HT不典型增生TEC病例和50例PTC,以甲状腺瘤旁滤泡和HT中的相对正常滤泡为对照组(各40例),进行常规形态学观察和细胞角蛋白19(CK19)、增殖细胞核抗原(PCNA)以及B细胞淋巴瘤因子2(Bcl-2)免疫组化标记(Max-Vision法),结果用x<'2>检验进行分析.结果 HT中不典型增生TEC有一定异型性,细胞排列拥挤,核增大,出现毛玻璃样改变.HT中不典型增生TEC和PTC上皮均明显表达CK19、PCNA和Bcl-2,与对照组相比差异有统计学意义(P<0.05),但前两组内差异无统计学意义(P>0.05).结论 HT中不典型增生TEC呈现某些PTC的形态学、免疫学表型特征,表达PTC特异的CK19,可能是HT癌变过程的中间环节,应引起高度重视.     

CK34βEl2和PSA顺序免疫组化双染色在前列腺病变中的表达

目的 探索免疫组化前列腺特异性抗原(PSA)、高分子量角蛋白(CK34βEl2)双重染色法，并观察二者在前列腺增生性病变、癌前病变、癌及易被误为前列腺癌的精囊腺组织中的表达差异。方法 采用PSA、CK34βE12顺序免疫组化双重染色法，选择良性前列腺增生症8例、腺病6例、萎缩后增生4例、基底细胞增生4例、高级别上皮内瘤6例、前列腺癌30例及精囊腺4例，观察染色变化。结果 本染色方法稳定、结果分辨清晰。PSA在良性前列腺增生症、腺病、高级别上皮内瘤的分泌上皮、和绝大多数前列腺癌细胞中强表达，在萎缩后增生中不表达或弱表达，基底细胞增生、精囊腺不表达。CK34βEl2在前列腺癌中完全缺失，而在增生性病变、癌前病变呈完整或断续状，精囊腺中表达完整。结论CK34βEl2和PSA顺序免疫组化双染色在前列腺良、恶性、癌前性病变的诊断和鉴别诊断中是个可行而有用的辅助手段。     

p63、角蛋白及肌动蛋白在乳腺导管增生性病变中的表达及应用价值

目的 探讨p63、角蛋白及肌动蛋白在乳腺增生性病变中的表达,并比较它们及不同类型细胞角蛋白(CK5/6、34βE12和CK8)在乳腺导管增生性病变诊断及鉴别诊断中的应用价值.方法 对24例普通型导管增生(UDH)、20例不典型导管增生(ADH)、35例导管原位癌(DOS)、52例浸润性导管癌(IDC)患者及16例正常乳腺对照者的组织进行p63、CK5/6、34βE12、CK8、Actin免疫组化染色.结果 正常乳腺、ADH、DCIS、IDC腺体基底膜侧及癌巢周围肌上皮中p63、Actin、CK5/6、34βE12连续和(或)不连续表达,表达率分别为87.50％、70.00％、95.00％、0,100％、75.00％、94.30％、0,93.75％、65.00％、94.30％、0,87.50％、75.00％、42.86％、0,四种抗体在IDC和前三者之间表达差异有统计学意义(P均＜0.05);CK8表达均为0;在UDH、ADH、DCIS、IDC增生腺上皮细胞中CK5/6、34βE12表达率分别为95.80％、20.00％、2.90％、9.62％和91.20％、30.00％、22.90％、13.46％,二者在UDH和其他三组表达差异有统计学意义(P均＜0.05);CK8表达分别为95.8％、100％、94.3％、90.3％,Actin和p63表达均为0,各组之间表达差异无统计学意义(P均＞0.05).结论 联合检测p63、角蛋白及肌动蛋白有助于乳腺导管增生性病变的鉴别诊断,其中p63和CK5/6分别优于Actin和34βE12; CK5/6优于34βE12,有助于UDH和ADH/DCIS鉴别诊断,UDH细胞为多克隆增生,包括定向干细胞、腺中间细胞和腺终端细胞等.ADH、DCIS、IDC表现为单克隆增生.     

TPO mRNA和HGF/c-Met在甲状腺良恶性结节中的表达及意义

目的 探讨甲状腺过氧化物酶(TPO)mRNA和肝细胞生长因子及其受体蛋白(HGF/c-Met)在良恶性甲状腺结节中的表达及意义.方法 应用逆转录聚合酶链反应技术检测55例甲状腺结节新鲜标本的TPO mRNA丰度,采用免疫组织化学法检测600例甲状腺结节石蜡标本HGF/c-Met的表达.结果 甲状腺癌HGF/c-Met表达率显著高于甲状腺良性结节,乳头状癌高于滤泡型癌(P<0.01).甲状腺恶性结节TPOmRNA的阳性表达率显著低于甲状腺良性病变.结论 HGF/c-Met和TPO的联合检测在良恶性甲状腺病变的鉴别中有一定应用价值.     

高分子量角蛋白抗体表达在甲状腺乳头状癌与乳头状增生鉴别诊断中的价值

目的为甲状腺乳头状癌（PTC）与结节性甲状腺肿伴乳头状增生（NGWPH）的鉴别诊断提供可靠分子标志物。方法用免疫组化EnVision法测定50例PTC（PTC组）及50例NGWPH组织中（NGWPH组）高相对分子质量角蛋白抗体（34βE12）表达情况,计算34βE12用于鉴别诊断的评价指标。结果PTC组34βE12表达阳性46例（92．2％）,NGWPH组表达均为阴性。两组阳性率比较有显著差异（P〈0．05）;3413E12用于PTC与NGWPH鉴别诊断的敏感度为92％,特异度为100％,准确度为96％,阳性预测值为100．00％,阴性预测值为92．59％。结论34βE12可作为鉴别PTC与NGWPH的重要参考标志物。     

Amiodarone and the thyroid

Amiodarone is an iodine-rich drug widely used for the management of cardiac arrhythmias. During long-term amiodarone therapy drug toxicity may occur and a substantial proportion of amiodarone-treated patients develop either hypothyroidism or thyrotoxicosis. Several mechanisms are involved in amiodarone-induced thyroid dysfunction: defective thyroid auto-regulatory mechanism in presence of excessive iodine offer, immunological factors and cytotoxicity. Approximately 50% of patients taking amiodarone present abnormal thyroid function. Therefore, for adequate clinical follow up of these patients, it is critical a careful monitoring of thyroid hormones and TSH, before and during treatment.     

Age and the thyroid

Thyroid diseases are common in elderly patients, but their clinical manifestations are more subtle and often are hidden by a background of intercurrent disease. Therapy for thyroid disease in the elderly can also be more problematic because of increased risks of complications.     

Amiodarone and the thyroid

Among the drugs affecting the thyroid gland, no drug has puzzled, and at the same time fascinated, endocrinologists more than amiodarone. Amiodarone is a potent class III anti-arrhythmic drug that also possesses beta-blocking properties. It is very rich in iodine, with a 100-mg tablet containing an amount of iodine that is 250 times the recommended daily iodine requirement. Amiodarone produces characteristic alterations in thyroid function tests in euthyroid patients. Understanding these alterations is crucial in avoiding unnecessary investigations and treatment. Amiodarone-induced thyroid dysfunction occurs because of both its iodine content and the direct toxic effects of the compound on thyroid parenchyma. Amiodarone-induced hyperthyroidism is more common in iodine-deficient regions of the world, whereas amiodarone-induced hypothyroidism is usually seen in iodine-sufficient areas. In contrast to amiodarone-induced hypothyroidism, amiodarone-induced thyrotoxicosis is a difficult condition to diagnose and treat. In this review, we discuss the alterations in thyroid function tests seen in euthyroid subjects, the epidemiology and mechanism of amiodarone-induced thyroid dysfunction, treatment options available, and the consequences of amiodarone use in pregnancy and lactation; and finally, we propose a follow-up strategy in patients taking amiodarone.     

Smoking and the thyroid

The effects of smoking on the thyroid gland have been studied for years. The consequences of smoking on thyroid function and size are however still controversial. It is accepted that an increase in serum thyiocyanate, a potent inhibitor of iodine transport, may contribute to the development of thyroid dysfunction, particularly in geographical areas with borderline iodine deficiency. In the general population, smoking is associated with normal thyroid hormone levels, with a tendency to lower TSH levels and enlargement of thyroid size. There is an increased risk of developing over thyroid disease. The relationship between smoking and relapse of Graves' disease and the incidence and severity of Graves' ophthalmopathy are constantly reported. Smoking also has a potent nodular goitrigenic effect in low iodine areas. Despite the fact that smoking decrease both thyroid secretion and thyroid hormone action, hypothyroidism does not appear to be more frequent. Smoking does however increase the metabolic effects of hypothyroidism. Active and passive smoking have proven deleterious effects on the fetal thyroid. Paradoxically, there is evidence of reduced risk for thyroid cancer in smokers.     

Evidence that both long-acting thyroid stimulator and long-acting thyroid stimulator-protector stimulate the human thyroid gland.

Thyroid-stimulating immunoglobulins were prepared from two potent sera, one contained long-acting thyroid stimulator (LATS) and the other contained both LATS and LATS-protector (LATS-P). The potencies of the immunoglobulin G (IgG) preparations were estimated in the McKenzie assay. The accumulation of cyclic AMP in mouse thyroid lobes was stimulated only by LATS--IgG; LATS-P--IgG was inactive. In contrast, both LATS-IgG and LATS-P--IgG were equally effective in slices of human thyroid.