免疫球蛋白 G4相关性淋巴结病误诊为 Castleman 病一例

患者男性,43岁。因发现颈部肿物2个月入院。患者2个月前无意中发现右侧颈部肿物,大小2 cm×3 cm,质硬,活动,无压痛,无发热和盗汗,无皮肤瘙痒,体质量无减轻。当时血常规：白细胞计数（WBC）7.93×109／L,血红蛋白（Hb）147 g／L,血小板计数（Plt）39×109／L,颈部彩色超声示颈部双侧多发肿大淋巴结（右锁骨上最大者3.9 cm×2.2 cm,左锁骨上最大者2.3 cm×1.2 cm）。     

ⅣA期周围型肺癌免疫治疗降期转化后手术治疗1例

<正>患者女性,47岁,因“发现左侧颈部淋巴结肿大2日”于2020年5月就诊于甘肃省人民医院。颈部触诊发现左锁骨上窝一枚约1.5 cm×1.3 cm×1.0 cm肿大淋巴结,形态规则,边缘光滑,无触痛,无融合,对侧淋巴结未触及。颈部淋巴结彩色多普勒超声显示：双侧锁骨上窝淋巴结异常肿大,左侧大者为1.4 cm×1.4 cm,右侧大者为1.0 cm×0.83 cm（图1A）。胸部CT：右肺中叶周围型肺癌（约4.2 cm×3.5 cm）,纵隔及锁骨上窝多发淋巴结转移（图2A）。肿瘤标志物肺癌5项异常（图3）。     

桥本甲状腺炎并发甲状腺黏膜相关淋巴瘤1例报告

1病例报告患者女性,55岁。因"发现颈部肿物1周"于2009年7月入我院。查体:左侧颈部可触及一肿物,大小约2 cm×2 cm,质软,边缘清晰,活动度可,可随吞咽上下移动,无压痛,未闻及血管杂音;颈部、锁骨上、腋窝未触及肿大淋巴结。辅助检查:血FT4 21.74 pmol/L,FT4 4.21 pmol/L,TSH 1.4μIU/mL,CEA0.01 ng/mL,TGAb+,TPOAb+。颈部及上胸部CT平扫+增强:左侧甲状腺下极结节影(1.8 cm×1.5 cm),考虑腺瘤可能。     

原发性甲状腺血管肉瘤二例

1 患者男,60岁.颈前右侧无痛性肿物渐进性增大2个月,门诊以甲状腺右叶肿物性质待查收住院.入院查体:颈前右侧弥漫性隆起,甲状腺右叶触及约6.0 cm×6.5 cm大小的肿物,质硬,表面不光滑,边界不清,无压痛,吞咽时上下活动度欠佳,肿物下极突入胸骨后未能扪及,未闻及血管杂音及震颤,无声音嘶哑及饮水呛咳,颈部双侧未触及肿大淋巴结.心、肺、腹部未见明显异常.胸部X线片示右肺结节,考虑为钙化灶.     

Castleman病1例报告

1临床资料患者,女性,53岁.因发现腹股沟肿物1个月,右颈部肿物1d入院.查体:体温36.2℃,双颈部、双侧腋窝及腹股沟淋巴结肿大,质韧,无压痛,活动欠佳.右肺呼吸音低,双肺呼吸音清,未闻及干湿性罗音.心腹部检查无异常.实验室检查:白细胞2.45×109/L,中性粒细胞1.94×109/L,C反应蛋白8.97mg/L,血清乳酸脱氢酶(LDH)290.50 U/L,血沉44mm/h.胸部CT:右肺上叶纵隔旁占位;右肺门及纵隔多发肿大淋巴结,右侧锁骨下及双侧腋下多发肿大淋巴结;心包积液、双侧胸腔积液.颈部和双腋下彩超:双侧颈部、腋下多发肿大淋巴结.腹部彩超:腹腔多发实性占位,考虑肿大淋巴结;脾大;腹水.骨髓细胞学检查:骨髓增生减低,M/E=2.9/1,粒系58％,红系20％,血小板数量正常.左腋下淋巴结活检病理:淋巴组织高度增生,结合病史及免疫组化结果符合Castleman病(系统性),其中部分淋巴细胞侵至淋巴结被膜外脂肪.     

非霍奇金淋巴瘤1例

女性,47岁。主因颈部肿物1个月而入院。患者于入院前无意中发现颈部肿物,后渐增大,无发热、消瘦、疼痛、声音嘶哑、多汗、易饥、心悸、易激动等症状。查体：颈前右侧皮肤局限性隆起,甲状腺右叶下极可触及一约5cm×4cm×3cm大小肿物,质中,界清,随吞咽活动上下移动,无压痛。颈右侧胸锁乳突肌后缘中部可触及一约1cm×1cm×0．7cm大小的肿大淋巴结。胸大片未见异常。血常规：WBC 5．5×109／LL 20％。B超：甲状腺右叶实性占位伴颈部淋巴结肿大。ECT：甲状腺右叶下极冷结节。甲状腺功能：T3 2．390．7～2．3μg／LT4 1694…     

原发性乳腺神经内分泌癌一例报告

1 病例报告 患者,女,65岁.2011-11查体发现右侧乳房肿块1个月就诊.查体:双侧乳腺发育正常,乳头无偏斜、凹陷,乳房皮肤无红肿、隆起和凹陷;右侧乳头下方可触及一肿物,大小1.5 cm×1.0 cm,质硬,界限清晰,有压痛,与皮肤、胸壁无粘连.双侧腋窝及锁骨上未触及肿大淋巴结.B超检查示,右侧乳腺实性占位.钼靶显示,左侧乳房肿块.行穿刺活检示,增生的纤维结缔组织内见异性细胞浸润,核有异性,隐约见核分裂像,意见为乳腺浸润性癌.     

多发性骨软骨瘤骶骨病灶恶变一例报告

临床资料 患者,男,41岁.发现左下腹无痛性肿物20余年,进行性增大2个月入院.查体:右前外侧胸壁第10肋外缘可触及8cm×6cm×3cm大小肿物(图1),局部皮温正常,质硬,无压痛,边界清楚,活动度差;腹平坦,左下腹部可触及大小约12cm×8cm×8cm肿物,质硬,无压痛,活动度差,边界尚清,表面粗糙;双侧胫骨近端可触及骨性肿物,右侧大小约2cm×3cm×1cm,左侧大小约2cm×2cm×1cm,质硬,不活动,无压痛.     

甲状腺原发性非霍奇金淋巴瘤1 例

患者,女,75岁,因左颈部肿物2个月于2007年5月12日入院.患者伴声音嘶哑及轻度吞咽困难.体检:左颈前隆起,甲状腺左叶可触及大小约9cm×8cm肿物,质硬,边界不清,轻度压痛,能随吞咽上下移动,气管受压向右侧移位.右侧甲状腺未触及肿物.全身浅表淋巴结无肿大.颈部CT示:甲状腺左叶区域可见类圆形软组织密度肿块影,与周围组织边界不清,大小约9.5cm×5.5cm×8.0cm,密度均匀,挤压气管向右侧移位,颈部骨质未见明显破坏,考虑甲状腺左叶区域占位性病变.气管正位片:气管明显右移.肿瘤标志物CA125 67.24 μ/L,甲状腺功能检查正常.     

以深静脉血栓为首发表现的胃癌1例

1病案摘要 患者男性,38岁,因咳嗽发热2月余,发现左侧颈部肿块5天于2006年12月7日入院。患者于2个月前出现咳嗽、发热,体温最高38．5℃,在门诊就诊,结核菌素试验阴性,给予抗炎治疗热退,仍偶有咳嗽,5天前发现左侧颈部无痛性肿块,经超声检查示左侧颈内静脉血栓形成。入院给予尿激酶、低分子肝素、华法林治疗,左侧颈内静脉血栓消失出院。2007年1月29日患者再次因左颈部、左腋窝无痛性肿块伴右下肢水肿来院就诊。入院后查体：体温36．2℃,血压120／80mmHg。左颈部、锁骨上、腋窝、胸壁及左上肢轻度水肿。左颈部可触及多个肿块,约花生米大小,质韧,无压痛,活动度差,左侧腋窝可触及1枚淋巴结,约2．0cm×1．5cm,质韧,无压痛,活动度欠佳。心肺无明显异常。腹软,无压痛,肝脾未触及,墨菲氏征阴性。右下肢轻度凹陷性水肿。     

卵巢透明细胞癌临床治疗效果研究

背景与目的:卵巢透明细胞癌相比于其他卵巢上皮性癌,其预后较差,本文对本院卵巢透明细胞癌患者生存率作分析比较,探讨CAP[表柔比星(E-ADM)、顺铂(DDP)加环磷酰胺(CTX)]方案加用丝裂霉素(MMC)后的治疗效果。方法:对本院于1999年1月1日至2002年12月31日接受治疗的卵巢透明细胞癌共33例(A组),同时随机取37例卵巢其他上皮性癌的患者作对照(B组)。Ⅰ期患者行全子宫 双附件 大网膜切除 阑尾切除 淋巴结分期术),2例患者需要生育的卵巢癌患者行患侧附件切除 对侧卵巢活检 大网膜切除 阑尾切除术术。Ⅱ期以上的患者行肿瘤减灭术(tumor reductive surgery,TRS)尽可能使残余灶<1cm,2组患者均在术后化疗均采用CAP方案(静脉应用),但A组患者CAP方案中加用了丝裂霉素。A组患者与仅用CAP方案的透明细胞癌患者(C组)Ⅰ/Ⅱ期15例及Ⅲ/Ⅳ期9例相比较。结果:术前A组与B组Ⅰ/Ⅱ血清CA125差异有显著性,卵巢透明细胞癌血清CA125水平值较低,Ⅲ/Ⅳ期血清CA125差异无显著性。在3次及6次化疗后与化疗前Ⅰ/Ⅱ期A组及B组血清CA125差异有显著性,而Ⅲ/Ⅳ期血清CA125下降水平差异无显著性。A组卵巢透明细胞癌患者中有11例有子宫内膜异位症(33.33%),有7例患者出现深静脉血栓(21.21%),有深静脉血栓的患者与生存率无直接关系(P=0.26)。Ⅰ/Ⅱ期患者的平均生存时间分别为:A组38.3±2.4个月,B组38.3±2.7个月,Ⅰ/Ⅱ期患者A组与B组用Log Rank检验相比较4年生存率差异无显著性(P=0.471),Ⅲ/Ⅳ期患者的平均生存时间分别为:A组20±3个月,B组34±4个月,Ⅲ/Ⅳ期患者A组与B组相比较用Log Rank检验4年生存率差异有显著性(P<0.05)。C组患者Ⅰ/Ⅱ期15例,平均生存时间为:30±3个月,与A组用MMC的透明细胞癌患者Ⅰ/Ⅱ期23例比较生存率差异有显著性(P<0.05)。C组患者Ⅲ/Ⅳ期9例,均死亡。平均生存时间为18±3个月。与A组用MMC的透明细胞癌患者Ⅲ/Ⅳ期10例比较生存率差异无显著性(P=0.430)。结论:卵巢透明细胞癌术前及化疗后血清CA125水平值较低,用CAP加丝裂霉素的规则化疗治疗透明细胞癌对Ⅰ/Ⅱ期患者有一定的治疗效果,对Ⅲ/Ⅳ期患者治疗效果不佳。卵巢透明细胞癌疾病的复发率及死亡率仍然较高。     

The relation between the aging of the steroid generating system and the geneses of cancers of the stomach, the breast and the uterine cervix

The purpose of the present study is to test the validity of the steroid carcinogenesis hypothesis in humans by investigating the problem whether or not a cancer-specific change of the hormonal milieu emerges at a specified stage of life where the growth rate of cancer risk is at its zenith. A case-control study of 14 urinary steroid excretions was conducted for each of 3 human neoplasias. The identification and the size (in parenthesis) of the population units used in this study were,given as follows: a) the male gastric cancer group (421); b) the male control group (104); c) the female breast cancer group (245); d) the cervical cancer group (345); e) the female control group (127). Two kinds of steroid parameters were employed for the statistical analysis of hormonal data: a) the logarithm of a steroid excretion figure (mu g/day), as expressed by log x; b) the logarithm of a relative weight of a given steroid to tetrahydrocortisol, as expressed by log x/THF. The case-control difference for each parameter was expressed in terms of a t-value of Student's t-test. The steroid deviation profile was prepared for each neoplasia and for each of the log x data set and the log x/THF data set. The results obtained are as follows: a) the 2 steroid parameters (log x and log x/THF) for each of 14 urinary steroids were both subject to change with the progress of host age. The rate of age-dependent change was different for each steroid parameter and for each population unit. b) The above differential age dependency of the steroid parameters gave rise to a continual transition of the steroid deviation profile in the course of aging. c) The hormonal traits of male gastric cancer, female breast cancer and cervical cancer were described each as a complex of androgen depression and glucocorticoid stimulation (male gastric cancer), a sequential emergence of premenopausal progestin depression and postmenopausal predominance of glucocorticoid over androgen (female breast cancer), and a complex of androgen-glucocorticoid depression over progestin (cervical cancer). d) The emergence of the above cancer-specific steroid disorders chronologically coincided with the quasiexponential growth phase of cancer risk (and slow growth phase of cancer risk in postmenopausal breast cancer). e) The usefulness of the log x/THF type deviation profile for the assessment of the hormonal milieu of the host was verified by both theoretical approach to the problem and its application to the real data of a case-control study. f) The age dependent decline of androgens was generally much faster in their progressions than that of glucocorticoids - a finding to suggest the possibility that the production of a cancer-specific steroid deviation profile might have taken the form of the stress shift of Hans Selye, since both phenomena share depletion of gonadal steroids relative to glucocorticoid in common. The etiological relevancy of the 3 cancer-specific steroid changes to the geneses of 3 cancers:was discussed in the light of the experimental pathology studies in our laboratory as well as in other laboratories.     

大肠腺癌组织MDR1表达与肠系膜淋巴结转移关系的研究

目的　探索大肠腺癌组织多药耐药基因 (MDR1)表达与大肠腺癌分化程度及肠系膜淋巴结转移之间的关系。方法　以光敏生物素标记MDR1cDNA探针 ,链亲和素胶体金为检测系统做原位杂交 (ISH SAG)检测大肠癌MDR1mRNA表达 ,同时用LSAB法对P 糖蛋白进行免疫组织化学检测。结果　大肠腺癌MDR1mRNA表达阳性的肠系膜淋巴结转移率与MDR1表达阴性的肠系膜淋巴结转移率两者有显著性差异 (P <0 0 5) ,大肠癌MDR1表达阳性率与分化程度无显著性差异(P >0 0 5)。结论　MDR1表达高低与大肠腺癌肠系膜淋巴结转移呈正相关 ,MDR1阳性表达与细胞分化程度比较无统计学意义。MDR1表达的检测对判定化疗疗效及预后有一定的意义。     

大肠腺癌组织MDR1表达与肠系膜淋巴结转移关系的研究

 目的　探索大肠腺癌组织多药耐药基因(MDR1)表达与大肠腺癌分化程度及肠系膜淋巴结转移之间的关系。方法　以光敏生物素标记MDR1 cDNA探针,链亲和素胶体金为检测系统做原位杂交(ISH-SAG）检测大肠癌MDR1 mRNA表达,同时用LSAB法对P-糖蛋白进行免疫组织化学检测。结果　大肠腺癌MDR1 mRNA表达阳性的肠系膜淋巴结转移率与MDR1表达阴性的肠系膜淋巴结转移率两者有显著性差异(P<0.05),大肠癌MDR1表达阳性率与分化程度无显著性差异(P>0.05)。结论　MDR1表达高低与大肠腺癌肠系膜淋巴结转移呈正相关,MDR1阳性表达与细胞分化程度比较无统计学意义。MDR1表达的检测对判定化疗疗效及预后有一定的意义。