yxoid adrenal cortical adenoma -the first case reported in China

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ARID1B基因变异致Coffin-Siris综合征1例报告并文献复习

doi:10.3969/j.issn.1000-3606.2021.04.014ARID1B基因变异致Cofﬁn-Siris综合征1例报告并文献复习徐欣汤健张丽陆芬李红英南京医科大学附属儿童医院康复科（江苏南京 210008）摘要：目的探讨ARID1B基因变异致Cofﬁn-Siris综合征的临床及遗传特征。

方法回顾分析1例ARID1B基因变异致Cofﬁn-Siris综合征患儿的临床资料及分子遗传学检测结果，并复习相关文献。

结果患儿，男，2岁8个月，因智力运动发育落后就诊。

患儿生后就有喂养困难，体质量增长不良，特殊面容（头皮毛发稀疏、发际低、拱形浓眉、长睫毛、鼻翼宽、鼻梁低、上唇薄、下唇厚而外翻、唇毛明显），四肢肌张力低下，右足趾甲小。

全外显子测序显示ARID1B基因存在c.6257T>C （p.Leu2086Pro）杂合错义变异，父母未发现上述变异，为新生变异。

文献共检索到已报道因ARID1B基因所致Cofﬁn-Siris 综合征患者86例，患儿临床特征与已报道病例基本相符。

结论 Cofﬁn-Siris综合征为罕见的常染色体显性遗传病，可累及多个系统，基因检测可协助诊断。

关键词： Cofﬁn-Siris综合征；ARID1B基因；变异Coffin-Siris syndrome caused by ARID1B mutation: a case report and literature review XU Xin, TANG Jian, ZHANG Li, LU Fen, LI Hongying (Department of Rehabilitation, Children’s Hospital of Nanjing Medical University, Nanjing 210008, Jiangsu, China)Abstract: Objective To explore the clinical and gene characteristics of Coffin-Siris syndrome caused by ARID1B mutation. Methods The clinical data and molecular genetic test results of Coffin-Siris syndrome caused by ARID1B gene mutation in a child were retrospectively analyzed, and the relevant literature was reviewed. Results A 2-year- and 8-month-old was brought to clinic for psychomotor retardation. He had difficulties in feeding and poor weight gain after birth. He presenteda distinctive facial appearance including sparse scalp hair, low frontal hairline, arched shaggy eyebrows, long eyelashes, broadnasal tip, flat nasal bridge, thin upper lip, a thick and everted lower lip and thick lip hair. He had hypotonia and small toenails in right foot. A heterozygous missense mutation of c. 6257T>C (p.Leu2086Pro) in ARID1B gene was found in the child by whole exome sequencing, which was not found in his parents and was a new variant. A total of 86 reported cases of Coffin-Siris syndrome caused by ARID1B gene mutation were retrieved through literature search. The clinical characteristics of the patients were basically consistent with the reported cases. Conclusion Coffin-Siris syndrome is a rare autosomal dominant genetic disease that can involve multiple systems, and genetic testing can help diagnose.Key words:Coffin-Siris syndrome; ARID1B gene; mutationCoffin-Siris综合征（Coffin-Siris syndrome，CSS，OMIM135900）是一种罕见的常染色体显性遗传疾病，主要表现为智力运动发育迟缓、多毛症、粗糙的面部特征、肌张力低下、指骨/指甲发育不全等[1]。

朗格汉斯细胞组织细胞增生症1例

朗格汉斯细胞组织细胞增生症1例
廖昕;陈卫国
【期刊名称】《中国医学影像技术》
【年(卷),期】2006(022)005
【摘要】患者女,25岁.因2年中下颌牙齿逐渐脱落,脱落时无疼痛感或出血,伴左侧颈部包块、腹胀及多饮、多尿入院.查体：整个背部、胸部及下腹部见散在红色丘疹,部分融合成片,搔痒,无水泡,皮肤无破损.下颌部凹陷,左侧颈部可触及一个10 cm×10cm肿块,光滑、固定,与皮肤无粘连,无触痛,右颈部触及多个肿大淋巴结.腹部膨隆,移动性浊音明显.实验室检查：血沉快、80 mm/第1小时,垂体功能检查示分泌功能异常.
【总页数】1页(P685-685)
【作者】廖昕;陈卫国
【作者单位】南方医科大学附属南方医院放射科,广东,广州,510515;南方医科大学附属南方医院放射科,广东,广州,510515
【正文语种】中文
【中图分类】R814.4
【相关文献】
1.朗格汉斯细胞与朗格汉斯细胞组织细胞增生症病理与临床 [J], 杨林军;冯丹
2.联合阿糖胞苷治疗难治性朗格汉斯细胞组织细胞增生症临床分析 [J], 唐文静;于洁
3.朗格汉斯细胞组织细胞增生症累及中枢神经系统1例 [J], 邹珍;赵康艳
4.成人朗格汉斯细胞组织细胞增生症临床特征以及预后因素分析 [J], 凌彦弢;李亚荣;龚玉萍
5.儿童朗格汉斯细胞组织细胞增生症发病机制及靶向治疗研究进展 [J], 周婵
因版权原因，仅展示原文概要，查看原文内容请购买。

脑脊液抗GFAP抗体阳性的原发性中枢神经系统淋巴瘤1例报告

脑脊液抗GFAP抗体阳性的原发性中枢神经系统淋巴瘤1例报告殷翔1，关鸿志2，任海涛2，范思远2，崔俐1摘要：本文报道1例原发性中枢神经系统淋巴瘤（PCNSL）病例。

患者为青年男性，亚急性起病，病情迁延8月余，主要表现为逐渐加重的头痛及头晕，头部核磁影像提示脑室扩张、脑积水，脑膜强化；早期脱水降颅压后头痛症状可缓解；脑脊液中抗GFAP抗体阳性，经激素治疗后症状一度好转，然而激素减量后头痛症状再次加重；最终经脑脊液细胞学、脑脊液免疫细胞化学染色得以明确诊断PCNSL。

关键词：原发性中枢神经系统淋巴瘤；　脑脊液细胞学；　GFAP抗体中图分类号：R739 文献标识码：APrimary central nervous system lymphoma with positive anti-GFAP antibody in cerebrospinal fluid：a case re⁃port YIN Xiang，GUAN Hongzhi，REN Haitao，et al.（Department of Neurology，The First Hospital of Jilin University，Changchun 130021，China）Abstract：This article reports a case of primary central nervous system lymphoma （PCNSL）.The patient was a young man with subacute onset， and the disease lasted for more than 8 months and had the main manifestations of gradu⁃ally aggravated headache and dizziness.Cranial MRI showed ventricular dilatation，hydrocephalus，and meningeal en⁃hancement. Dehydration treatment aiming to reduce intracranial pressure alleviated the symptom of headache in the early stage of the disease；the cerebrospinal fluid was tested positive for anti-GFAP antibodies，and the symptoms were im⁃proved temporarily after hormone treatment.However，the symptom of headache aggravated again after hormone reduc⁃tion. Finally， the patient was diagnosed with PCNSL based on cerebrospinal fluid cytology and cerebrospinal fluid immuno⁃cytochemistry staining.Key words：　Primary central nervous system lymphoma；　Cerebrospinal fluid cytology；　Anti-GFAP antibody原发性中枢神经系统淋巴瘤（primary central nervous system lymphoma，PCNSL）仅累及中枢神经系统，多为非霍奇金淋巴瘤，临床少见，仅脑膜受累的PCNSL则更是十分罕见［1-3］。

肾上腺节细胞性神经瘤一例

肾上腺节细胞性神经瘤一例
周勇;石木兰
【期刊名称】《临床放射学杂志》
【年(卷),期】1998(17)5
【摘要】患者女，４４岁。

阵发性高血压病史２５年，血压为１４０～１８０／９０～１３０ｍｍＨｇ。

近２年曾出现３次晕厥，伴有腹泻、心悸、视物不清等症状，在外院曾行ＣＴ检查见右肾上腺肿物，拟诊嗜铬细胞瘤。

近日感右腰、腹痛入院，查体无明显阳性体征。

实验室检查：儿茶酚胺...
【总页数】1页(P283-283)
【关键词】肾上腺肿瘤;节细胞性神经瘤;神经瘤;病例报告
【作者】周勇;石木兰
【作者单位】大连市第五人民医院放射科;北京中国医学科学院中国协和医科大学肿瘤医院影像诊断科
【正文语种】中文
【中图分类】R736.6
【相关文献】
1.肾上腺节细胞性神经瘤伴血儿茶酚胺异常一例 [J], 赵鸿;杨鲲;吴忠;丁强;张元芳
2.儿童肾上腺节细胞神经瘤一例 [J], 向芹;李红;胡耀红
3.右侧肾上腺脂肪瘤样节细胞神经瘤一例 [J], 王林省;王皆欢;李磊
4.嗜铬细胞瘤合并肾上腺节细胞神经瘤一例 [J], 付莉;杨川
5.肾上腺混合性嗜铬细胞瘤-节细胞神经瘤一例报告 [J], 张勤;刘贵秋;马喆;张传山因版权原因，仅展示原文概要，查看原文内容请购买。

肾上腺髓样脂肪瘤的CT诊断和鉴别诊断

肾上腺髓样脂肪瘤的CT诊断和鉴别诊断【摘要】目的：探讨肾上腺髓样脂肪瘤的CT表现及鉴别要点。

方法：收集10例临床及病理资料齐全的肾上腺髓样脂肪瘤，回顾性分析其CT表现。

结果：本组10例肾上腺髓样脂肪瘤，均为单侧发病，瘤体直径为4～10cm，呈圆形或类圆形，边界光整。

瘤体为脂肪密度3例；密度不均匀者7例，其中以脂肪为主3例，以软组织为主3例，1例伴肿瘤出血。

增强后所有病例软组织成分均轻至中度强化，脂肪成分均无强化。

3例见点、条状钙化，1例伴出血者为血管样钙化。

结论：肾上腺髓样脂肪瘤的CT表现较具特征性，一般可在术前作出诊断。

【关键词】肾上腺肿瘤髓样脂肪瘤 CT 诊断CT Diagnosis and Differential Diagnosis of Adrenal Myelolipoma【Abstract】 Purpose：To study the CT features and differential points of adrenal myelolipoma. Methods：10 cases of adrenal myelolipoma which contained clinical and pathologic information were retrospectively reviewed about CT features. Results：The 10 masses ，all of which were occurred unilaterally， were 4cm to 10cm in diameter with sharp margin，round or oval shaped. In 3 cases the tumors were full of fat density. Inhomogenous density was showed up in the other 7 cases with fat dominating in 3 cases， soft tissue dominating in 3 cases and tumor apoplexy in 1 case. There was mild-to-moderate enhancement in the soft tissue in all tumors after administration of contrast medium， as oppose to the fat tissue no enhancement. There were dot and stripecalcification in 3 cases， among which one bleeding case was vascular calcification. Conclusion：The CT manifestations of adrenal myelolipoma were characteristic features and the diagnosis could be usually reached before operation.【Keywords】 Adrenal neoplasm Myelolipoma CT Diagnosis肾上腺髓样脂肪瘤（adrenal myelolipoma）是一种罕见的无功能性肾上腺良性肿瘤，由脂肪组织和骨髓成分按不同比例混合构成[1]。

论文 pathology research and practice

This article appeared in a journal published by Elsevier.The attached copy is furnished to the author for internal non-commercial research and education use,including for instruction at the authors institutionand sharing with colleagues.Other uses,including reproduction and distribution,or selling or licensing copies,or posting to personal,institutional or third partywebsites are prohibited.In most cases authors are permitted to post their version of thearticle(e.g.in Word or Tex form)to their personal website orinstitutional repository.Authors requiring further informationregarding Elsevier’s archiving and manuscript policies areencouraged to visit:/copyrightPathology –Research and Practice 207 (2011) 192–196Contents lists available at ScienceDirectPathology –Research andPracticej o u r n a l h o m e p a g e :w w w.e l s e v i e r.d e /p rpTeaching casesNon-functional adrenocortical adenoma:A unique case of combination with myelolipoma and endothelial cystsSohsuke Yamada a ,∗,Akihide Tanimoto a ,b ,Ke-Yong Wang a ,Yan Ding a ,Xin Guo a ,Shohei Shimajiri a ,Hironobu Sasano c ,Yasuyuki Sasaguri aaDepartment of Pathology and Cell Biology,School of Medicine,University of Occupational and Environmental Health,1-1Iseigaoka,Yahatanishi-ku,Kitakyushu 807-8555,Japan bDepartment of Molecular and Cellular Pathology,Kagoshima University Graduate School of Medical and Dental Sciences,Kagoshima,Japan cDepartment of Pathology,Tohoku University Graduate School of Medicine,Sendai,Japana r t i c l e i n f o Article history:Received 17May 2010Received in revised form 20July 2010Accepted 21July 2010Keywords:Adrenal glandAdrenocortical adenoma Myelolipoma Endothelial cyst Degenerationa b s t r a c tA case of non-functioning adrenocortical adenoma combined with myelolipoma and endothelial cysts is reported.A 72-year-old Japanese female was noticed to have right renal and left adrenal tumors by an abdominal CT scan.At surgery,the mildly enlarged left adrenal gland contained a well-demarcated tumor.Macroscopically,it was yellowish to dark red or grayish in color,and was characterized by geo-graphic appearance on the cut surface.Histopathological examination revealed a solid proliferation of clear or compact cells and a normal rim of adrenal gland,coexisting with vascular multiple cysts and myelolipomas.The cysts were ﬁlled with clotted blood,ﬁbrinous material,or thrombi,and were partially lined with ﬂattened endothelial cells with focal papillary hyperplasia,which were immunohistochemi-cally positive for CD31and CD34.These cystic walls were often thickened with hyalinized ﬁbrosis and calciﬁcation,and were connected to myelolipomatous elements.To our knowledge,this is the ﬁrst case report of adrenocortical adenoma associated with myelolipoma and endothelial cysts.It is probable that the extensive degeneration in adenoma might induce myelolipomatous metaplasia and cystic vascular formation.© 2010 Elsevier GmbH. All rights reserved.IntroductionAdrenal myelolipoma,characterized by a benign tumor-like lesion composed of mature fat admixed with variable hematopoi-etic elements,is now well recognized because it is easily recognized as an incidentaloma by CT or MRI.However,this is a relatively rare incidence,estimated to affect 0.08–0.2%of the general pop-ulation,based on autopsy studies [1,2].Adrenal cysts are also common among adrenal incidentalomas.These account for approx-imately 6%,a rate almost similar to that of myelolipoma (7%)[3,4].Histopathologically,these are classiﬁed into four types:(a)parasitic cysts (7%),(b)epithelial cysts (9%),(c)hemorrhagic cysts or pseudo-cysts (39%),and (d)endothelial cysts (45%)[5].More recently,the two latter types of cysts have been considered variants of vascular adrenal cysts,accounting for the majority of non-neoplastic lesions [5,6].The present case had an incidental adrenocortical adenoma,which is very common in autopsy series,with reported preva-lences of 2–9%[7].However,the present case was very uncommon because of a combination with myelolipomatous elements and∗Corresponding author.Tel.:+81936917426;fax:+81936038518.E-mail address:sousuke@med.uoeh-u.ac.jp (S.Yamada).endothelial cysts.Our case is also rare owing to a coexistence with clear cell carcinoma on the opposite side of the kidney.Only a few cases of co-localization of renal cell carcinoma and adrenal cor-tical adenoma have been reported [8,9].Most of these occurred in Japan,but there may be many unreported ones.This is the ﬁrst case report of adrenocortical adenoma in combination with myelolipoma and endothelial cysts,associated with renal cell car-cinoma.We here report a rare case of non-functioning adrenocortical adenoma with myelolipoma and endothelial cysts.It is well known and accepted that adrenal cortical metaplasias,in response to any stimulus,are proposed etiologies of adrenal myelolipoma [10].In addition,it has been reported that vascular cysts of the adrenal gland often occur in the context of local circulatory failure,char-acterized by repeating cycles of hemorrhage,thrombus formation,and recanalization [11,12].Therefore,it is probable that the exten-sive degeneration in adrenocortical adenoma might be complicated by myelolipomatous metaplasia and cystic formation.Clinical summaryA 72-year-old Japanese female had a 23-year history of hep-atitis C virus (HCV)-positive chronic hepatitis.She underwent a0344-0338/$–see front matter © 2010 Elsevier GmbH. All rights reserved.doi:10.1016/j.prp.2010.07.008S.Yamada et al./Pathology–Research and Practice207 (2011) 192–196193Fig.1.(A)Abdominal CT scan image.An approx.3cm×3cm mass protrudes from the right kidney(arrowhead).Moreover,a well-demarcated and approx.2cm×2cm nodule is noted in the contralateral left adrenal gland,consisting of non-enhanced and low-density areas(arrows).(B)Grossﬁndings of the resected tumor.The left adrenal gland,measuring3.7cm×2.7cm×2.5cm,contains an encapsulated nodular lesion(inset).On the cut surface,the solid adrenal nodule is yellowish to dark red or grayish incolor,and is characterized by geographic appearance.Adjacently,normal adrenal cortex tissue is compressed by the tumor to form a normalrim.Fig.2.Histological examination of renal clear cell carcinoma.(A)Low-power view of the right renal tumor shows a solid proliferation of atypical clear cells,arranged predominantly in an alveolar or trabecular growth pattern with foci of hemorrhage and necrosis,and focal hyalinized stroma(H&E stains,Original magniﬁcation×40).(B) In high-power view,these proliferating epithelioid cells contained abundant clear cytoplasm and small,regular,and uniform round nuclei,almost comparable in size to the red blood cells seen in thisﬁeld,with inconspicuous nucleoli.No mitoticﬁgures are seen(H&E stains,original magniﬁcation×200).total hysterectomy due to leiomyoma of uterus when she was49 years old.On the abdominal follow-up CT scan(Fig.1A),right renal and left adrenal tumors were found incidentally.There was no history of immunosuppressive disorders,use of immunosuppres-sive medications,or unusual infections,and her family history was unremarkable.On admission,physical examination revealed no remarkable ﬁndings,and no hypertension was boratory data, including blood cell count and chemistry,were within normal lim-its,except for high levels of AST(96IU/L)and ALT(79IU/L).The plasma cortisol level was9.8␮g/dL(normal range:4.0–18.3␮g/dL) with a normal diurnal rhythm.The plasma aldosterone level was71.9pg/mL(normal range:35.7–240.0pg/mL),plasma ACTH was13.8pg/mL(normal range: 4.4–48.0pg/mL),and plasma active renin concentration(ARC)was0.8ng/mL/h(normal range: 0.5–2.0ng/mL/h).The plasma epinephrine and norepinephrine concentrations were within normal limits,42pg/mL(normal range:<100pg/mL),and mildly high,540pg/mL(normal range: 100–450pg/mL),respectively.An abdominal CT scan(Fig.1A)revealed an enhanced mass, measuring3cm×3cm,protruding from the right kidney(arrow-head).Moreover,a well-demarcated nodule,2cm×2cm in size, was located in the contralateral left adrenal gland,consisting of non-enhanced and low-density areas(arrows).CT scans of the chest and abdomen disclosed no evidence of metastasis in the lymph nodes or other organs.Clinically,right renal cell carcinoma and left adrenal myelolipoma were suspected.Therefore,right nephrectomy and left adrenalectomy were performed.TherightFig.3.Histological examination of adrenocortical adenoma combined with myelolipoma and endothelial cysts.(A)A scan magniﬁcation of the left adrenal nodule shows multiple cystsﬁlled with clotted blood orﬁbrinous material(#),and a small amount of myelolipomatous or lipomatous elements(*)surrounded by adrenocortical tumor with a thinﬁbrous capsule( ).A normal rim of left adrenal gland tissue is seen adjacently( ).(H&E stain).(B)High-power view of the adrenocortical adenoma shows a solid proliferation of bland-looking clear or compact cells having mildly to moderately enlarged nuclei with no mitotic activity(H&E stains,Original magniﬁcation×200).194S.Yamada et al./Pathology –Research and Practice207 (2011) 192–196Fig.4.Immunohistochemical analysis of steroidogenic enzymes in the adrenocortical adenoma.(A–C)The adenoma is immunopositive for cytochrome P45017␣-hydroxylase (P450c17)(A)and 3␤-hydroxysteroid dehydrogenase (3␤HSD)(B),and in addition,is focally positive for DHEA-sulfotransferase (DHEA-ST)(C).(D)However,in the zona reticularis of the attached normal adrenal cortex,DHEA-ST expression is almost suppressed immunohistochemically.renal solid mass measured 3.1cm ×2.7cm ×2.5cm,and the cut surface was yellow to tan in color.The left adrenal gland measured 3.7cm ×2.7cm ×2.5cm,and contained an encapsulated nodular lesion (Fig.1B,inset).On the cut surface,the solid adrenal nodule measured 2.7cm ×2.5cm,and was yellowish to dark red or grayish in color,and was characterized by geographic appearance (Fig.1B).Adjacently,normal adrenal cortex tissue was compressed by the tumor to form a normal rim.Pathological ﬁndingsA histological examination of the right renal tumor showed a relatively well-demarcated nodular lesion composed of a solid proliferation of atypical clear cells,arranged predominantly in an alveolar or trabecular growth pattern with foci of hemorrhage and necrosis,and focal,hyalinized stroma (Fig.2A).These proliferat-ing epithelioid cells contained abundant clear cytoplasm,as well as small,regular,and uniform round nuclei,almostcomparableFig.5.Histological examination of myelolipoma and endothelial cysts.(A–C)The adrenal endothelial cysts are occasionally ﬁlled with thrombi (A,H&E stains),and are lined with ﬂattened endothelial cells without atypia,focally displaying a papillary hyperplasia (B,H&E stains),which are immunohistochemically positive for CD31(C).(D)The adrenal myelolipomas are made up of three series of hematopoietic cells with less than 40%cellularity,admixed with mature fat components (inset).S.Yamada et al./Pathology–Research and Practice207 (2011) 192–196195to the red blood cells as regards size,with inconspicuous nucleoli (Fig.2B).No mitoticﬁgures were seen.Therefore,nuclear Grade 1was estimated,according to the4-tiered nuclear grading sys-tem[13].Immunohistochemically,these atypical clear cells were positive for cytokeratin(AE1/AE3;Chemicon International,Tamec-ula,CA,USA)and Cam5.2(Becton Dickinson Immunocytometry Systems,San Jose,CA,USA)(not shown).Moreover,there was no evidence of vascular permeation or surrounding fat invasion.These features were consistent with renal clear cell carcinoma,the TNM classiﬁcation of which was T1a,N0,and M0[14].A scanning magniﬁcation of the left adrenal nodule(Fig.3A) demonstrated multiple and dilated small to medium-sized cysts ﬁlled with clotted blood orﬁbrinous material(#),which were surrounded by adrenocortical tumor with a thinﬁbrous cap-sule( ).A normal rim of left adrenal gland tissue was noted ( ),which was partially compressed by the tumor,but was not apparently atrophic,and not hypertrophic.Histologically,the well-demarcated adrenocortical tumor consisted of a solid proliferation of bland-looking clear or compact cells in almost equal propor-tion,having mildly to moderately enlarged nuclei with no mitotic activity,estimated to be of nuclear Grades1–2[13],arranged pre-dominantly in alveolar structures without evidence of necrotic foci(Fig.3B).Ki67(MIB-1;Epitomics,Inc.,CA,USA,1:2000)label-ing index was less than1%,and neither vascular nor capsular invasion was seen.Therefore,this tumor was assigned the low-est level(0),according to Weiss’s criteria[15],and it appeared to be a benign adrenocortical adenoma.In addition,immunohis-tochemical analysis of steroidogenic enzymes(all from Sasano H, previously described[16])revealed the expression of cytochrome P45017␣-hydroxylase(P450c17),3␤-hydroxysteroid dehydro-genase(3␤HSD),and DHEA-sulfotransferase(DHEA-ST)in the adenoma(Fig.4A–C),although it was likely that this adrenocortical adenoma did not function on the basis of the clinical and histologi-calﬁndings described above.Despite the difﬁculties in performing an accurate analysis due to the coagulation artifacts of surgery, DHEA-ST expression was most likely suppressed in the zona retic-ularis of the attached normal adrenal cortex(Fig.4D),suggesting autonomous hyperfunctioning of the adrenocortical adenoma,i.e., subclinical Cushing’s syndrome.Moreover,these adenoma cells were negative for epithelial markers(AE1/AE3and Cam5.2)(not shown),distinguishing the clear cells in the adrenal adenoma from those in the renal cell carcinoma.The dilated cysts were occasionallyﬁlled with thrombi(Fig.5A),and were lined withﬂat-tened endothelial cells without atypia,focally displaying a papillary hyperplasia(Fig.5B).They were immunohistochemically positive for CD31(Dako Cytomation Co.,Kyoto,Japan,1:20)(Fig.5C)and CD34(IMMUNOTECH,Marseille,France,1:50),but negative for D2-40(Nichirei Bioscience Co.,Tokyo,Japan,1:1).The endothelial cyst walls were often thickened with extensively hyalinizedﬁbrous tis-sue and calciﬁcation,being continuous with a small amount of myelolipomatous or lipomatous elements(*in Fig.3A).The myeloid tissue consisted of three series of hematopoietic cells with less than40%cellularity(Fig.5D),admixed with mature fat components (Fig.5D,inset).There were scattered hemorrhagic foci,whereas no focus of necrosis,inﬂammatory cell inﬁltration,or amyloid depo-sition was recognized in the left adrenal tumor.There were no anomalous vascular channels within or around the adrenal gland.On the basis of these features,we diagnosed clear cell car-cinoma of the right kidney,and non-functioning adrenocortical adenoma with myelolipoma and endothelial cysts of the left adrenal gland.DiscussionAdrenal adenomas are relatively common in adults,and are frequently encountered incidentally on abdominal CT scans[4,7].However,the present case is very uncommon because the adrenal myelolipomas and endothelial cysts were located in a non-functioning adrenocortical adenoma.A similar case has not yet been reported in the available English literature,although there are several cases with combined tumors such as adrenal cortical adenoma and myelolipoma[1,17–19],or adrenal cortical adenoma and endothelial cysts[12].Adrenal myelolipoma is a benign and hormonally inactive tumor that is composed of mature adipose and hematopoietic tissues varying in proportion[20].Moreover,myelolipoma has been reported as an isolated adrenal mass,but also in associa-tion with other adrenal pathological conditions at a frequency of5–15%[1,2,10,17–19,21],such as non-functioning adrenal adenoma,adrenocortical carcinoma,pheochromocytoma,adeno-matoid tumor,primary aldosteronism,Cushing syndrome,Conn’s syndrome,and congenital adrenal hyperplasia.The other reported conditions coexisting with myelolipoma include hypertention, obesity,diabetes mellitus,cardiovascular disease,and acquired immunodeﬁciency syndrome[2,22,23].Although the pathogen-esis of adrenal myelolipoma still remains to be clariﬁed,there are,historically,at least3theories regarding the etiology[2,10]. Myelolipomas are derived from bone marrow embolization or embryonic primitive mesenchymal cells,or arise from metaplastic transformation of adrenal(or other sites)stromal cells.Currently, the third is the most accepted theory according to which necrosis, infection,and stress could induce the formation of myelolipoma [10].Previously,Selye and Stone have demonstrated that the tis-sue of rat adrenal gland could be experimentally transformed into myelolipomatous elements by injecting necrotic tumor or extracts of corticotropine and testosterone[24].Bennet et al.also suggested that myelolipomatous change might be induced by excessive stim-ulation with ACTH[25].According to the report of Goetz et al., the hormonal microenvironment might have played an impor-tant role in the development of those myelolipomatous foci[20]. Therefore,in the present case,it is very likely that stimuli by mul-tiple adrenal cyst formation related to thrombi,hemorrhage,or probably infarction might result in myelolipomatous formation. In addition,hormonal effects could also be related more closely to myelolipomatous change,because the adrenocortical adenoma may function subclinically,strongly supported by the immuno-histochemical positivity of steroidogenic enzymes.Moreover,we cannot exclude the possibility that adrenal cortical disruption associated with adrenal cyst formation might induce localized hor-monal elevations.It is also supposed that necrotic foci from the right renal cell carcinoma might be one of the sources of any stimu-lus.In addition,adrenal tumors are more likely to become centrally ischemic,leading to low steroid hormone levels[9,25],which can cause extensive degeneration such as myelolipomatous or cystic change.Indeed,it is well known that functional adenomas are less susceptible to degeneration as compared with non-functional ones, because higher levels of steroid hormones secreted by the tumors may be capable of suppressing the production of various inﬂam-matory cytokines and neovascularization[25].The pathogenesis of an adrenal endothelial cyst formation within an adrenocortical adenoma is also an enigmatic issue.Sev-eral theories have been suggested that the cyst may originate from a preexisting vascular hamartoma[5,6],ectatic lymphatic chan-nels[26],or secondary to intraparenchymal hemorrhage[11,12]. As immunohistochemical analysis conﬁrms the endothelial nature of the lining cells,it is not probable that there is a lymphatic ori-gin in the present case.Moreover,no apparent anomalous vascular channels have been identiﬁed within or around the endothelial cysts.Recently,vascular cysts of the adrenal gland have been reported to occur often in the context of local circulatory fail-ure by repeating cycles of thrombus formation and recanalization [12],possibly leading to infarction and/or hemorrhage.Our case196S.Yamada et al./Pathology–Research and Practice207 (2011) 192–196also shows extensively hyalinized or focally calciﬁed degenera-tion in the cyst walls,which were associated with thrombi and hemorrhage.The most important differential diagnosis of adrenal vascular cysts is adrenal neoplasms with cystic degeneration.It is well known that large adenomas could often demonstrate hem-orrhage or cystic degeneration due to central ischemia and low hormonal effects[7,25].However,no residual adenoma cells with or without necrotic change were recognized in the cystic part of the present case.It is probable that the extensive degeneration in adrenocortical adenoma might induce not only myelolipomatous metaplasia but also cystic formation.In summary,we herein reported a rare case of non-functioning adrenocortical adenoma combined with myelolipoma and endothelial cysts.It is very likely that the extensive degenera-tion in the adrenocortical adenoma caused both myelolipomatous metaplasia and cystic formation.References[1]T.Matsuda,H.Abe,M.Takase,et al.,Case of combined adrenal cortical adenomaand myelolipoma,Pathol.Int.54(2004)725–729.[2]E.R.Timonera,M.E.Paiva,J.M.Lopes,et al.,Composite adenomatoid tumor andmyelolipoma of adrenal gland.Report of2cases,b.Med.132 (2008)265–267.[3]F.Mantero,M.Terzolo,G.Arnaldi,et al.,A survey on adrenal incidentaloma inItaly Study Group on adrenal tumors of the Italian society of endocrinology,J.Clin.Endocrinol.Metab.85(2000)637–644.[4]Y.Aso,Y.Homma,A survey on incidental adrenal tumors in Japan,J.Urol.147(1992)1478–1481.[5]E.Carvounis,A.Marinis,N.Arkadopoulos,et al.,Vascular adrenal cysts.A briefreview of the literature,b.Med.130(2006)1722–1724.[6]C.Torres,J.Y.Ro,M.A.Batt,et al.,Vascular adrenal cysts:a clinicopathologic andimmunohistochemical study of six cases and a review of the literature,Mod.Pathol.10(1997)530–536.[7]J.H.Newhouse,C.S.Heffess,B.J.Wagner,et al.,Large degenerated adrenal ade-nomas:radiographic-pathologic correlation,Radiology210(1999)385–391.[8]T.Ebina,S.Umemura,K.Sugimoto,et al.,Adrenal tumors associated with renalcell carcinoma,Nippon Jinzo Gakkai Shi32(1990)841–847.[9]A.Hirose,Y.Okada,A.Fukushima,et al.,A rare case of primary aldostero-nism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma,J.UOEH27(2005)315–323.[10]E.Bisho,J.N.Eble,L.Cheng,et al.,Adrenal myelolipomas show nonrandomX-chromosome inactivation in hematopoietic elements and fat:support for a clonal origin of myelolipomas,Am.J.Surg.Pathol.30(2006)838–843.[11]L.Bonati,P.Rubini,Hemorrhagic pseudocyst of adrenal gland:a case report,G.Chir.18(1997)286–289.[12]T.Nigawara,S.Sakihara,K.Kageyama,et al.,Endothelial cyst of the adrenalgland associated with adrenocortical adenoma:preoperative images simulate carcinoma,Intern.Med.48(2009)235–240.[13]S.A.Fuhrman,sky,C.Limas,Prognostic signiﬁcance of morphologicparameters in renal cell carcinoma,Am.J.Surg.Pathol.6(1982)655–663. [14]J.N.Eble,G.Sauter,J.I.Epstein,et al.(Eds.),World Health Organization Classi-ﬁcation of Tumours.Tumours of the Urinary System and Male Genital Organs: Pathology and Genetics,IARC Press,Lyon,2004.[15]L.M.Weiss,Comparative histologic study of43metastasizing and nonmetas-tasizing adrenocortical tumors,Am.J.Surg.Pathol.8(1984)163–169.[16]H.Sasano,Localization of steroidogenic enzymes in adrenal cortex and its dis-orders,Endocr.J.41(1994)471–482.[17]H.Murayama,M.Kikuchi,T.Imai,Myelolipoma in adenoma of accessoryadrenal gland,Pathol.Res.Pract.164(1979)207–213.[18]M.Vyberg,L.Sestoft,Combined adrenal myelolipoma and adenoma associatedwith Cushing’s syndrome,Am.J.Clin.Pathol.86(1986)541–545.[19]R.Armand,A.R.Cappola,R.B.Horenstein,et al.,Adrenal cortical adenoma withexcess black pigment deposition,combined with myelolipoma and clinical Cushing’s syndrome:a case report and review of the literature,Int.J.Surg.Pathol.12(2004)57–61.[20]S.P.Goetz,T.H.Niemann,R.A.Robinson,et al.,Hematopoietic elements asso-ciated with adrenal glands.A study of the spectrum of change in nine cases, b.Med.118(1994)895–896.[21]P.J.Kenney,B.J.Wagner,P.Rao,et al.,Myelolipoma:CT and pathologic features,Radiology208(1998)87–95.[22]A.Angeles-Angeles,E.Reyes,L.Munoz-Fernandez,et al.,Adenomatoid tumorof the right adrenal gland in a patient with AIDS,Endocr.Pathol.8(1997)59–64.[23]F.Rodriguez-Vallejo,F.J.Gomez-Perez,Two siblings with untreated CYP21deﬁciency and giant myelolipomas:case report and review of the literature, Endocrinologist16(2006)172–178.[24]H.Selye,H.Stone,Hormonally induced transformation of adrenal into myeloidtissue,Am.J.Pathol.26(1950)211–233.[25]B.D.Bennett,T.J.Mckenna,A.J.Hough,et al.,Adrenal myelolipoma associatedwith Cushing’s disease,Am.J.Clin.Pathol.73(1980)443–447.[26]L.A.Erickson,R.V.Lloyd,R.Hartman,et al.,Cystic adrenal neoplasm,Cancer101(2004)1537–1544.。

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Ｒｅｃｅｉｖｅｄ：７　Ｓｅｐｔｅｍｂｅｒ　２００６／Ｒｅｖｉｓｅｄ：１　５　Ｓｅｐｔｅｍｂｅｒ　２００６／Ａｃｃｅｐｔｅｄ：３０　Ｓｅｐｔｅｍｂｅｒ　２００６　Ａｂｓｔｒａｃｔ　Ｍｙｘｏｉｄ　ａｄｒｅｎａＩ　ｃｏｒｔｉｃａＩ　ａｄｅｎｏｍａ　ｉｓ　ａ　ｒａｒｅ　Ｉｕｍｏｒ　ａｎｄ　ＩｉｌＩ　ｎｏｗ　ｏｎｌｙ　９　ｃａｓｅｓ　ｈａｖｅ　ｂｅｅｎ　ｐｒｅｓｅｎｔｅｄ　ｉｎ　Ｉｈｅ　ｗｏｒｌｄ．Ｗｅ　ｈｅｒｅ　ｒｅｐｏｒｔ　ａｎｏｔｈｅｒ　ｃａｓｅ　ｏｆ　ｍｙｘｏｉｄ　ａｄｅｎｏｍａ　ｏｆ　Ｉｈｅ　ａｄｒｅｎａＩ　ｇｌａｎｄ　ｉｎ　ａ　４５一ｙｅａｒ－ｏｌｄ　Ｃｈｉｎｅｓｅ　ｍａｎ　ｗｈｏ　ｗａｓ　ａｄｍｉｔｔｅｄ　Ｉｏ　ｈｏｓｐｉｔａＩ　ｂｅｃａｕｓｅ　ｏｆ　Ｉｈｅ　ｒｉｇｈｔ　ａｄｒｅｎａＩ　ｍａｓｓ　ａｎｄ　ｍｉｌｄ　ｈｙｐｅｒｔｅｎｓｉｏｎ．ＡＩ　ｓｕｒｇｅｒｙ．Ｉｈｅ　ｍａｓｓ　ｗａｓ　ｗｅｌｌ—ｃｉｒｃｕｍｓｃｒｉｂｅｄ．ｍｅａｓｕｒｅｄ　３．３　ｃｍ　ｉｎ　ｄｉａｍｅｔｅｒ．Ｌ＿ｑｈｆ－ｍｉｃｒ０ｓｃｏｐｉｃ　ｆｉｎｄｉｎｇｓ　ｓｈｏｗｅｄ　ｍｏｓＩ　ｏｆ　Ｉｈｅ　Ｉｕｍｏｒ　ｒｅｇｉｏｎ　ｗｉｔｈ　ｍｙｘｏｉｄ　ｓｔｒｏｍａ，ａｎｄ　Ｉｈｅ　Ｉｕｍｏｒ　ｃｅｌｌｓ　ｗｅｒｅ　ｂｅｎｉｇｎ—ｌｏｏｋ．　ｉｎｑ．ＩｍｍｕｎＯｈｉｓＩＯｃｈｅｍｉｃａＩ　ｓｔｕｄｙ　ｓｈｏｗｅｄ　Ｉｈｅ　Ｉｕｍｏｒ　ｈａｄ　Ｉｈｅ　ｐｏｓｉｔｉｖｉｔｙ　ｆｏｒ　ｖｉｍｅｎｔｉｎ，ｓｙｎａｐｔｏｐｈｙｓｉｎ，ｎｅｕｒｏｎ　ｓｐｅｃｉｆｉｃ　ｅｎｄｏｌａｓｅ　ｂｕＩ　ｎｅｇａｔｉｖｅ　ｗｉｔｈ　ｃｙｔｏｋｅｒａｔｉｎ　ａｎｄ　ｅｐｉｔｈｅｌｉａＩ　ｍｅｍｂｒａｎｅ　ａｎｔｉｇｅｎ．Ｍｏｒｅｏｖｅｒ．ｉｔ　ｗａｓ　ｎｅｇａｔｉｖｅ　ｗｉｔｈ　ａｌｐｈａ—ｉｎｈｉｂｉｎ　ＩｈａＩ　ｉｓ　ｎｏＩ　ｉｎ　ａｃｃｏｒｄａｎｃｅ　ｗｉｔｈ　ｔｈｏｓｅ　ｒｅｐｏｒｔｅｄ．Ｔｈｅｒｅ　ｗａｓ　ｎｏ　ｆｉｎｄｉｎｇ　ｃｏｒｒｅｓｐｏｎｄｉｎｇ　ｔｏ　ｍａｌｉｇｎａｎｃｙ．　

Ｋｅｙ　ｗｏｒｄｓ　ａｄｒｅｎａｌ　ｇｌａｎｄ；ｍｙｘｏｉｄ　ａｄｒｅｎａｌ　ｃｏｒｔｉｃａｌ　ａｄｅｎｏｍａ；ｄｉｆｆｅｒｅｎｔｉａｌ　ｄｉａｇｎｏｓｉｓ　

Ｍｙｘｏｉｄ　ｎｅｏｐｌａｓｍｓ　ｏｆ　ｔｈｅ　ａｄｒｅｎａｌ　ｃｏｒｔｅｘ　ａｒｅ　ｅｘｔｒｅｍｅｌｙ　ｒａｒｅ［”．Ｔｏ　ｏｕｒ　ｋｎｏｗｌｅｄｇｅ，ｔｈｅｒｅ　ｗｅｒｅ　ｏｎｌｙ　１９　ｃａｓｅｓ　ｔｈａｔ　ｈａｖｅ　ｂｅｅｎ　ｒｅｐｏｒｔｅｄ　ｔｈｕｓ　ｆａｒ，ｉｎｃｌｕｄｉｎｇ　１０　ｃａｒｃｉｎｏｍａｓ　ａｎｄ　９　ａｄｅｎｏｍａｓ．Ａｓ　ｆｏｒ　ｔｈｅ　ｌａｔｅｒ　ｉｔ　ｗａｓ　ｔｙｐｉｃａ１　ｔｏ　ｎｏｔｉｃｅ　ｔｈｅ　ｌａｃｋ　ｏｆ　ａｔｙｐｉａ，ｍｏｒｅ　ｏｒ　ｌｅｓｓ　ｔｈｅ　ｍｙｘｏｉｄ　ｃｏｍｐｏｎｅｎｔ　ａｎｄ　ｈｅｔｅｒｏｇｅｎｅｏｕｓ　ｇｒｏｗｔｈ　ｐａｔｔｅｒｎｌ２Ｉ＿Ｗｅ　ｈｅｒｅ　ｐｒｅｓｅｎｔ　ａｎｏｔｈｅｒ　ｃａｓｅ　ｏｆ　ｍｙｘｏｉｄ　ａｄｒｅｎａｌ　ｃｏｒｔｉｃａｌ　ａｄｅｎｏｍａ　ｔｈａｔ　ｗａｓ　ｔｈｅ　ｆｉｒｓｔ　ｃａｓｅ　ｒｅｐｏｒｔｅｄ　ｉｎ　Ｃｈｉｎａ．Ｈｉｓｔｏｌｏｇｉｃａｌｌｙ　ｉｔ　ｗａｓ　ａｌｉｋｅ　ｔｈｏｓｅ　ｒｅｐｏｒｔｅｄ　ｔｈａｔ　ｔｈｅ　ｂｅｎｉｇｎ—ｌｏｏｋｉｎｇ　ｔｕｍｏｒ　ｃｅｌｌｓ　ａｒｒａｎｇｅｄ　ｉｎ　ｐｓｅｕｄｏｇ１ａｎｄｕ１ａｒ　ｐａｔｔｅｒｎ　ｗｉｔｈ　ａｂｕｎｄａｎｔ　ｍｙｘｏｉｄ　ｓｔｒｏｍａ，　ｂｕｔ　ｉｍｍｕｎｏｈｉｓｔｏｃｈｅｍｉｃａｌｌｙ　ｉｔ　ｈａｄ　ａ　ｌｉｔｔｌｅ　ｄｉｆｆｅｒｅｎｔ　ｃｈａｒ—　ａｃｔｅｒｉｓｔｉｃｓ　ｓｉｎｃｅ　ｉｔ　ｗａｓ　ｎｅｇａｔｉｖｅ　ｔｏ　ａｌｐｈａ—ｉｎｈｉｂｉｎ．　Ｃａｓｅ　ｒｅｐｏｒｔ　Ａ　４５一ｙｅａｒ—ｏｌｄ　ｍａｎ　ｗａｓ　ａｄｍｉｔｔｅｄ　ｔｏ　ｏｕｒ　ｈｏｓｐｉｔａ１　ｉｎ　Ｄｅ—　ｃｅｍｂｅｒ　２００４　ｓｉｎｃｅ　ｈｅ　ｈａｄ　ａ　ｒｅｃｅｎｔ　ｍｉｌｄ　ｈｙｐｅｒｔｅｎｓｉｏｎ．Ｔｈｅ　ｐａｔｉｅｎｔ　ｈａｄ　ｎｏ　ｏｔｈｅｒ　ｃｏｍｐｌａｉｎｔｓ．Ｕｌｔｒａｓｏｕｎｄ　ａｎｄ　ｃｏｍ—　ｐｕｔｅｄ　ｔｏｍｏｇｒａｐｈｙ　ｓｃａｎ　ｒｅｖｅａｌｅｄ　ａ　４－ｃｍ　ｓｏｌｉｄ，ｈｙｐｅｒｄｅｎｓｅ　ｍａｓｓ　ｉｎ　ｔｈｅ　ｒｉｇｈｔ　ａｄｒｅｎａｌ　ｇｌａｎｄ　ａｎｄ　ｎｏ　ｍｅｔａｓｔａｓｅｓ　ｗｅｒｅ　ｆｏｕｎｄ　ｅｌｓｅｗｈｅｒｅ．Ｌａｂｏｒａｔｏｒｙ　ｔｅｓｔｓ　ｓｈｏｗｅｄ　ｏｎｌｙ　ｔｈｅ　ｍｅｔａ—　ｎｅｐｈｒｉｎｅｓ　ａｎｄ　ｎｏｒｍｅｔａｎｅｐｈｒｉｎｅｓ　ｉｎ　ｐｌａｓｍａ　ｗｅｒｅ　ｓｌｉｇｈｔｌｙ　ｉｎｃｒｅａｓｅｄ．Ｈｅ　ｗａｓ　ｓｕｓｐｅｃｔｅｄ　ｏｆ　ｈａｖｉｎｇ　ａ　ｐｈｅｏｃｈｒｏｍｏｃｙ—　ｔｏｍａ　ａｎｄ　ｌａｐａｒｏｓｃｏｐｉｃ　ａｄｒｅｎａｌｅｃｔｏｍｙ　ｗａｓ　ｐｅｒｆｏｒｍｅｄ．Ａｆ－　ｔｅｒ　ｔｈｅ　ｓｕｒｇｅｒｙ，ｈｉｓ　ｈｙｐｅｒｔｅｎｓｉｏｎ　ｄｉｓａｐｐｅａｒｅｄ，ａｎｄ　ｎｏｗ　ｔｈｅ　ｐａｔｉｅｎｔ　ｉｓ　ｆｒｅｅ　ｏｆ　ｄｉｓｅａｓｅ　ｆｏｒ　ｏｖｅｒ　２０　ｍｏｎｔｈｓ．　Ｔｈｅ　ｒｅｓｅｃｔｅｄ　ｓｐｅｃｉｍｅｎ　ｗａｓ　ｐｒｏｃｅｓｓｅｄ　ｒｏｕｔｉｎｅｌｙ　ｔｏ　ｈａｖｅ　ｓｅｃｔｉｏｎｓ　ｓｔａｉｎｅｄ　ｗｉｔｈ　ｈｅｍａｔｏｘｙｌｉｎ　ａｎｄ　ｅｏｓｉｎ，Ａｌｃｉａｎ　ｂｌｕｅ　ｗｉｔｈ　ｈｙａｌｕｒｏｎｉｄａｓｅ　ｄｉｇｅｓｔｉｏｎ，ｔｈｅ　ｐｅｒｉｏｄｉｃ　ａｃｉｄ—Ｓｃｈｉｆｆ　ｒｅａｃｔｉｏｎ　ａｎｄ　ｔｈｅ　ａｎｔｉｂｏｄｉｅｓ　ａｇａｉｎｓｔ　ｅｐｉｔｈｅｌｉａ１　ｍｅｍｂｒａｎｅ　ａｎｔｉｇｅｎ（ＥＭＡ），ｃｙｔｏｋｅｒａｔｉｎ（ＣＫ），ｖｉｍｅｎｔｉｎ，ｎｅｕｒｏｎ　ｓｐｅ—　ｃｉｆｉｃ　ｅｎｄｏｌａｓｅ，ｓｙｎａｐｔｏｐｈｙｓｉｎ，ｃｈｒｏｍｏｇｒａｎｉｎ　Ａ，Ｓ一１００　ａｎｄ　Ｃｏｒｒｅｓｐｏｎｄｅｎｃｅ　ｔｏ：Ｈｏｎｇｋａｉ　Ｚｈａｎｇ．Ｅｍａｉｌ：ｚｈｋ０４８４＠ｓｉｎａ　ｃｏｒｎ　ａｌｐｈａ—ｉｎｈｉｂｉｎ．　Ｍａｃｒｏｓｃｏｐｉｃ　ａｎａｌｙｓｉｓ　ｒｅｖｅａｌｅｄ　ｔｈａｔ　ｔｈｅ　ｔｕｍｏｒ　ｗａｓ　ｗｅｌｌ　

ｃｉｒｃｕｍｓｃｒｉｂｅｄ，ｍｅａｓｕｒｅｄ　３．３　ｃｍｘ２．８　ｃｍｘ２．７　ｃｍ．Ｏｎ　ｃｕｔ　ｓｕｒｆａｃｅ，ｔｈｅ　ｃｏｍｐｒｅｓｓｅｄ　ｎｏｒｍａｌ　ａｄｒｅｎａｌ　ｃｏｒｔｅｘ　ｗａｓ　ｓｅｅｎ　ａｔ　ｔｈｅ　ｐｅｒｉｐｈｅｒｙ　ｏｆ　ｔｈｅ　ｔｕｍｏｒ　ｗｉｔｈ　ｃａｎａｒｙ—ｙｅｌｌｏｗ　ｃｏｌｏｒ　ａｎｄ　ｈａｄ　ａ　ｃｌｅａｒ　ｄｅｍａｒｃａｔｉｏｎ　ｆｒｏｍ　ｔｈｅ　ｂｏｒｄｅｒｅｄ　ｔｕｍｏｒ．　Ｔｈｅ　ｔｕｍｏｒ　ｒｅｇｉｏｎ　ｗａｓ　ｇｒｅｙ。。ｙｅｌｌｏｗ——ｂｒｏｗｎ　ｗｉｔｈ　ｃｙｓｔｉｃ——　ｓｏｌｉｄ　ｓｕｒｆａｃｅ，ｔｈｅ　ｃｙｓｔｓ　ｗｅｒｅ　１－１．５　ｃｍ　ｉｎ　ｓｉｚｅ，ｃｏｎｔａｉｎｉｎｇ　ｂｒｏｗｎ　１ｉｑｕｉｄ　ｗｈｉｃｈ　ｗａｓ　ｔｈｉｎ　ｇｅｌａｔｉｎｏｕｓ．Ｔｈｅ　ｓｏｌｉｄ　ａｒｅａ　ｗａｓ　ｙｅｌｌｏｗ—ｇｒａｙｉｓｈ　ｃｏｌｏｒ　ｗｉｔｈ　ａ　ｆｉｒｍ　ｃｏｎｓｉｓｔｅｎｃｙ．Ａｔ　ｌｉｇｈｔ　ｍｉｃｒｏｓｃｏｐｙ，ｗｅ　ｎｏｔｉｃｅｄ　ｔｈａｔ　ｔｈｅ　ｔｕｍｏｒ　ｃｅｌｌｓ　ａｒｒａｎｇｅｄ　ｉｎ　ｃｏｍｐａｃｔ　ｃｏｒｄｓ　ａｎｄ　ｔｕｂｕｌｅｓ　ｍｕｃｈ　ｍｏｒｅ　ｗｈｅｎ　ｔｈｅｙ　ｗｅｒｅ　ｎｅａｒ　ｔｈｅ　ｃｏｍｐｒｅｓｓｅｄ　ｎｏｒｍａｌ　ｃｏｒｔｉｃａｌ　ｇｌａｎｄ　ｔｈａｎ　ｔｈｅｙ　ｗｅｒｅ　ａｔ　ｔｈｅ　ｃｅｎｔｅｒ　ｗｈｅｒｅ　ｔｈｅ　ｔｕｍｏｒ　ｃｅｌｌ　ｃｏｒｄｓ　ｗｅｒｅ　１ｏｏｓｅｌｙ　ａｎａｓ—　ｔｏｍｏｓｉｎｇ，ｏｒ　ｆｏｒｍｅｄ　ｔｈｅ　ｓｏ　ｃａｌｌｅｄ　ｐｓｅｕｄｏｇ１ａｄｕ１ａｒ　ｃｈａｒ—　ａｃｔｅｒｓｉｃｓ（Ｆｉｇ．１－２）．Ｎｅａｒｌｙ　ａｌｌ　ｏｆ　ｔｈｅ　ｔｕｍｏｒ　ｃｅｌｌｓ　ｗｅｒｅ　ｉｎ　ｇｅｌａｔｉｎｏｕｓ　ｓｔｒｏｍａ　ｗｈｉｃｈ　ｗｅｒｅ　ｓｌｉｇｈｔｌｙ　ｓｔａｉｎｅｄ　ｐｏｓｉｔｉｖｅ　ｔｏ　ＡＢ　ｏｎｌｙ＜２％ａｒｅａ　ｒｅｓｅｍｂｌｅｄ　ｔｈｅ　ｃｏｎｖｅｎｔｉｏｎａｌ　ｃｏｒｔｉｃａｌ　ａｄ—　ｅｎｏｍａ　ｃｈａｒａｃｔｅｒｉｓｔｉｃｓ．Ａｌｔｈｏｕｇｈ　ｔｈｅｒｅ　ｗｅｒｅ　ｓｅｖｅｒａｌ　ｃｙｓｔｓ　ａｔ　ｍａｃｒｏｓｃｏｐｉｃ　ｗｈｉｃｈ　ｃｏｎｔａｉｎｅｄ　ｔｈｅ　ｂｒｏｗｎ　１ｉｑｕｉｄ　ｗｅ　ｈａｄ　ｔｈｏｕｇｈｔ　ｂｌｏｏｄｉｎｇ，ｔｈｅｒｅ　ｗａｓ　ｎｏ　ｎｅｃｒｏｓｉｓ　ｓｅｅｎ　ｔｈｅｒｅ　ｅｘｃｅｐｔ　ｓｏｍｅ　ｒｅｄ　ｃｅｌｌｓ　ｃｏｕｌｄ　ｂｅ　ｓｅｅｎ　ｉｎ　ｔｈｅ　ｇｅｌａｔｉｎｏｕｓ　ｓｔｒｏｍａ．Ｔｈｅｓｅ　ｔｕｍｏｒ　ｃｅｌｌｓ　ｗｅｒｅ　ｎｅａｒｌｙ　ａｌ１　ｂｅｎｉｇｎ—ｌｏｏｋｉｎｇ，ｒｏｕｎｄ，ｏｖａ１　ｏｒ　ｐｏｌｙｇｏｎａｌ，ｍｅｄｉｕｍ　ｓｉｚｅｄ　ｗｉｔｈ　ｃｌｅａｒ　ｃｙｔｏｐｌａｓｍ，ｓｏｍｅ　ｍａｙ　ｈａｖｅ　ａｍｐｈｏｐｈｉｌｉｃ　ｃｙｔｏｐｌａｓｍ．Ｎｏ　ｏｂｖｉｏｕｓｌｙ　ｃｅｌｌ　ａｔｙｐｉａ，　ｍｉｔｏｔｉｃ　ｆｉｇｕｒｅｓ　ｏｒ　ｖａｓｃｕｌａｒ　ｉｎｖａｓｉｏｎ　ｏｒ　ｃａｐｓｕｌａｒ　ｉｎｖａｓｉｏｎ　ｗｅｒｅ　ｓｅｅｎ．Ｔｈｅ　ｉｍｍｕｎｏｐｈｅｎｏｔｙｐｅ　ｏｆ　ｔｈｉｓ　ｔｕｍｏｒ　ｓｈｏｗｅｄ　ｔｈｅ　ｐｏｓｍｖ］ｔｙ　ｆｏｒ　ｖｌｍｅｎｔｍ，ｓｙｎａｐｔｏｐｈｙｓｌｎ，ｎｅｕｒｏｎ　ｓｐｅｃｉｆｉｃ　ｅｎｄｏｌａｓｅ，ｎｅｇａｔｉｖｅ　ｔｏ　Ｓ一１００，ＣＫ　ａｎｄ　ＥＭＡ，ｃｈｒｏｍｏｇｒａｎｉｎ　Ａ　ａｎｄ　ａｌｐｈａ—ｉｎｈｉｂｉｎ（Ｆｉｇ．３）．　