患者男性,28 岁,体检发现右肾上腺占位,当地医院复查腹部彩超,考虑"肾上腺肿瘤"可能.腹部 CT不能除外"肝脏占位",腹部MRI示"右侧肝肾间隙富含脂质肿瘤性占位,考虑起源于右肾上腺可能性大",因肝功能异常,住院保肝治疗25 天后以"右肾上腺占位:嗜铬细胞瘤"出院.为求进一步手术治疗来我院就诊,门诊以"右肾上腺占位:嗜铬细胞瘤"收治;行全麻下机器人辅助后腹腔镜右侧腹膜后肿瘤切除术.

0引言 口腔原发性皮脂腺癌(sebaceous carcinoma,SC)是一种极其少见的恶性肿瘤,检索国内外文献报道仅10余例,其主要发生于颊黏膜[1-5],其次为口底、唇黏膜、舌和上颌牙龈[6-11],仅见1例报道发生于下颌牙龈黏膜[12].本文现报道1例发生于下颌牙龈黏膜的原发性SC,回顾性分析其临床病理特征,并复习相关文献,旨在提高对该疾病的认识,有利于正确诊断.

十二指肠乳头癌临床少见,而以急性胰腺炎起病者更为罕见.对于急性胰腺炎患者要进一步明确其病因,尤其有胰管、胆管扩张时,需要内镜检查明确十二指肠乳头部有无病变.现将我院2例以急性胰腺炎起病的十二指肠乳头癌报道如下.

目的:探讨脾脏硬化性血管瘤样结节性转化(SANT)的临床病理特征.方法:对8例SANT的临床特点、病理特征进行分析并复习相关文献.结果:6例无明显症状,1例为左上腹不适,1例为右上腹胀痛不适.肉眼均可见脾脏内边界相对清楚的孤立性病灶,中央为灰白色瘢痕样.镜下病变呈多结节状,结节中心为裂隙样、不规则形血管腔隙,周边为环形排列的梭形、卵圆形细胞、增生的胶原纤维及散在的炎性细胞.免疫组化显示结节内血管内皮细胞CD34阳性,CD30同样高表达,结节间梭形细胞Vimentin、SMA阳性.Masson染色显示结节周边环绕亮绿色增生的胶原纤维.EBER原位杂交结果均阴性.结论:SANT是一种罕见、良性的多克隆反应性病变,发病机制尚不清楚,形态易与血管瘤、炎性假瘤、窦岸细胞血管瘤等混淆,手术切除即可治愈.

目的:观察巨脾大部切除后残脾VEGF、VEGFR-2、CD34的表达,探讨残脾微血管密度(MVD)变化.方法:选取门静脉高压脾肿大患者13例,术后切取脾组织为巨脾组,术后8年穿刺获取脾组织为残脾组,另设外伤性脾组织13例为对照组.应用免疫组织化学方法,并对残脾MVD进行定量分析.结果:残脾组红髓MVD为(12.54±1.32)个/高倍视野,脾实质为(16.64±1.10)个/高倍视野;巨脾组红髓MVD为(16.72±1.41)个/高倍视野,脾实质为(21.20±1.52)个/高倍视野;对照组红髓MVD为(9.65±1.47)个/高倍视野,脾实质为(13.56± 1.14)个/高倍视野.巨脾组MVD值与残脾组、对照组比较明显增高,差异有统计学意义(P＜0.01);残脾组MVD值与对照组比较明显增高,差异有统计学意义(P＜0.01).在脾脏组织CD34表达阳性,VEGF和VEGFR-2表达阴性.结论:巨脾大部切除后残脾MVD减少,VEGF和VEGFR-2阴性表达.

OBJECTIVE:To establish an animal model of sulfur mustard (SM)-induced acute lung injury in rats through different routes and compare the morphological changes in lung tissue and cells.METHODS:One hundred and thirty-six male rats were selected and randomly divided into 5 groups, namely peritoneal cavity SM group (n=32), trachea SM group (n=32), peritoneal cavity propylene glycol group (n=32), trachea propylene glycol group (n=32), and normal control group (n=8). The rats in peritoneal cavity SM group were injected intraperitoneally with diluted SM (0.1 ml, 8 mg/kg), and the rats in trachea SM group were injected intratracheally with diluted SM (0.1 ml, 2 mg/kg). Once the rats were sacrificed at 6, 24, 48, and 72 h after SM treatment, morphological changes in lung tissue and cells were observed by light and electron microscopy.RESULTS:In the peritoneal cavity SM group, the epithelial cells of bronchioles maintained intact with increased exudate and bleeding in alveolar cavity and large areas of pulmonary consolidation under the light microscope. In the tracheal SM group, focal ulcer formed in the epithelial cells of bronchioles with increased exudate and bleeding in alveolar cavity, partial pulmonary consolidation, and compensatory emphysema in peripheral alveolar space under the light microscope. The alveolar interval areas were widened obviously in both groups in a time-dependent manner. Under the electron microscope, we observed local loss of cellular membrane in type I alveolar epithelium, broken or lost microvilli in cells of typeⅡalveolar epithelium and fuzzy mitochondrial crista as well as the appearance of ribosome detached from rough endoplasmic reticulum in both two groups. Compared with those in the trachea SM group and the control group, the ratio of the alveolar septum average area to the visual field area in the peritoneal cavity SM group at 6, 24, 48, and 72 h was significantly higher (P<0.05).CONCLUSION:The lung tissue injury through the intraperitoneal route is more severe than that through the tracheal route, while focal ulceration of bronchioles epithelial cells appears in the case of tracheal route. The degree of injury increases over time in both groups, and the cellular damage is approximately the same in both groups.

Objective To establish animal model of acute lung injury induced by sulfur mustard (SM) in rats,in order to observe the histomorphologic change of lung,protein content and cell numbers in bronchoalveolar lavage fluid (BALF),and serum inflammatory factors reaction in different time phases.Methods 72 male rats were selected,then randomly divided into three groups:SM group (n =32),propylene glycol group (n =32),and control group (n =8).The rats in SM group were injected intratracheally diluted SM (2 mg/kg,0.1 ml),the rats in propylene glycol group were injected intratracheally propylene glycol 0.1 ml,and status quo was kept with the control group.BALF,serum,and lung tissue were obtained in 6h,24h,48h,and 72h respectively.HE and immunohistochemistry staining were used to observe histomorphologic change and inflammatory cell infiltration.The alveolar interval area,content of inflammatory factor in serum,total albumen and cell number in BALF were measured.Results SM group:①The epithelium cells of the damaged bronchioles were shed,and the focal ulcer formed.②Dilatating and congestive vessels were observed in pulmonary interstitial,and lymphocyte is the main element of the inflammatory infiltration.③Inflammatory exudate and inflammatory cells appeared in alveolar cavity,which the albumen content and cell number in BALF peaked in 48 hours.④The content of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in serum peaked in 24 hours.⑤ The alveolar interval area widened obviously,and the damage degree was time dependent.Results in the propylene glycol group was the same with those in the control group.Conclusions SM (2 mg/kg) can induce histomorphologic change similar to acute respiratory distress syndrome.Lymphocyte is the main element of inflammatory infiltration.BALF and serum results suggest there was temporary inflammation,and the damage degree is time dependent.

Objective To establish an animal model for rat respiratory tract injury due to sulfur mustard (SM),and observe the morphologic changes of tracheal tissues and epithelial cells in SM-induced injury.Methods Male SD rats (n =72)were randomly divided into three groups (SM group,propylene glycol group,and normal group).The rats in the SM (2 mg/kg)group were injected intratracheally with diluted SM (0.1 ml).Histomorphologic and cytomorphogic changes of the specimen were observed under light and electron microscopy.Results In the SM group,histomorphologic changes included shed tracheal epithelial cells,focal ulcer formation,deranged cilia,increased glands in the lamia propria mucosae,and inflammatory cells invading the submucosa.The cytomorphologic changes were as follows:the cellular membranes lacking,medullary changes in the mitochondria with difficult to discern mitochondrial cristae appeared in goblet cells,and difficult to discern karyotheca,karyopyknosis,and margination of the nuclear chromatin in cilia,basal cells,fibroblasts.The structure of tracheal tissue and epithelial cells of the propylene glycol group was the same as the control group.Conclusions SM (2 mg/kg)can cause acute injury of tissues and multi-epithelial cells of the rat trachea.The degree of injury is positively correlated to the duration of time.SM mainly affects the cellular membranes and organelles of goblet cells,as well as nuclear chromatin of cilia,basal cells,and fibroblasts.

目的:观察高流体静力压对大隐静脉和脾静脉管壁滋养血管的影响.方法:收集曲张大隐静脉和高压性脾静脉标本(疾病组),以及正常大隐静脉和脾静脉标本(正常对照组).采用CD34免疫组化染色与Masson染色,计算各组管壁滋养血管的数量和平均截面积,并定量分析.结果:形态学观察显示,两个疾病组管壁滋养血管均较各自的对照组明显增生.定量分析显示,两个疾病组的滋养血管数量、平均截面积在中膜或外膜,均明显大于各自的正常对照组(均P＜0.05);脾静脉外膜滋养血管数量疾病组与其正常对照组差值明显大于大隐静脉,大隐静脉外膜滋养血管疾病组与其正常对照组平均截面积差值明显大于脾静脉(均P＜0.05),但两种血管间以上差值在中膜中的差异均无统计学意义(均P＞0.05).结论:高流体静力压下大隐静脉和脾静脉管壁滋养血管明显增生,两者变化存在异质性,大隐静脉中以管径增大为主,脾静脉中以数量增多为主.

目的 观察大隐静脉和脾静脉滋养血管内皮细胞超微结构变化,探讨高流体静力压和缺氧对滋养血管内皮细胞的影响.方法 收集曲张大隐静脉和高压性脾静脉管壁标本34例,另设对照组为正常大隐静脉和脾静脉34例.采用HE染色光镜下观察大隐静脉和脾静脉外膜层滋养血管,半薄切片定位.再采用超薄切片,透射电镜下观察滋养血管内皮细胞的超微结构变化.结果 大隐静脉曲张组和病脾静脉组滋养血管内皮细胞细胞核结构完整,染色质分布正常;部分线粒体基质深染,嵴模糊、嵴断裂.结论 高流体静力压和缺氧下大隐静脉和脾静脉管壁滋养血管内皮细胞的超微结构会出现重塑现象,二者改变相同.

Objective To establish rat model of pulmonary injury induced by sulfur mustard (SM) to investigate the apoptosis and oxidative stress in the injured lung.Methods 72 male rats were selected,then randomly divided into SM group (n =32),propylene glycol group (n =32),and normal control group (n =8).The rats in SM group were injected intratracheally diluted SM (2 mg/kg,0.1 ml),the rats in propylene glycol group were injected intratracheally propylene glycol 0.1 ml,meanwhile the status quo was kept with the normal control group.Then the SM-induced apoptosis and oxidative stress were observed by electron microscope,immunohistochemical staining,and bronchoalveolar lavage fluid (BALF) examination.Results SM group:①The content of lactate dehydrogenase and glutathione peroxidase in BALF peaked in 6h.②There was local defect of cellular membrane in alveolar epithelial type Ⅰ cells,while microvilli missed as well as disarranged in alveolar epithelial type Ⅱ cells.The appearance of ribosome detached from rough endoplasmic reticulum,and illegibility of mitochondrial cristae were observed in both types of cells.③Apoptosis was observed significantly increasing in the alveolar septum.Results in the propylene glycol group was the same with those in the normal control group.Conclusions Apoptosis and oxidative stress are two main mechanism characteristics of SM (2 mg/kg) induced pulmonary injury in rats.

<正>硬化性血管瘤样结节性转化(sclerosing angiomatoid nodular transformation,SANT)是一种近年来才得到命名的罕见的脾脏良性病变,临床和病理医师对其缺乏足够的认识,临床存在过度治疗风险,病理诊断存在差异。现对3例SANT患者的临床表现、病理特征及免疫组化表型进行分析,并通过文献复习,探讨该病变的临床特点和发生机制。1资料与方法

1 病例报告 患者女,65岁.因右乳房无痛性多发包块5d于2011-10-22入院.查体:右乳房内上象限触及2个自乳头放射状分布包块,分别约1.8 cm×1.0 cm和1.5 cm×0.8 cm,相距约1.5 cm,质硬,表面欠光滑,边界不清,无触痛,表面皮肤无橘皮样变,基底部可活动,同侧腋窝未触及肿大淋巴结.血常规、肝肾功和胸片未见异常.彩色多普勒超声检查示,右乳腺内上象限可见2个不均质回声包块,约1.7 cm×1.0 cm和1.4 cm×0.7 cm,相距约1.6 cm,边界不清,形态不规则,内有强弱不均匀回声,较大者内部可见斑点状强回声及明显血流信号(图1).

早期细支气管肺泡癌误诊为肺结核一例报告于敏，王美红，刘昌起患者女性，４７岁１９９０年１２月１４日，因低热、咳嗽伴少量痰，摄胸片后发现左上阴影（图１），按肺结核治疗，１９９１年４月２日复查胸片示肺内病变无改变（图２），当时已无任何症状即开始恢复工作。未...