伴有肺部损害的多中心网状组织细胞增生症1例

报道1例伴有肺部损害的多中心网状组织细胞增生症。患者男、43岁。其临床特征为全身皮肤多发性丘疹和结节,毁损性关节炎和肺部多发性小结节。皮肤及肺结节组织病理示大量浆呈伊红和毛玻璃样外观的组织细胞和多核巨细胞浸润;免疫组化染色：CD68（＋）,S－100（－）,HHF35（－）,AE1／AE3（－）。     

皮肤窦性组织细胞增生症一例并文献复习

报道1例皮肤窦性组织细胞增生症并对文献进行复习。患者,女,56岁,右上肢暗红色结节、斑块2年余,无系统受累。组织病理：真皮内大量组织细胞、淋巴细胞,可见组织细胞伸入现象。免疫组化：S-100（+）、CD68（+）、CD1a（-）。外用卤米松等治疗后皮损范围已明显缩小。     

朗格汉斯组织细胞增生症1例并文献复习

报告1例以皮肤损害就诊的朗格汉斯组织细胞增生症.患儿男,2岁半,因头面、躯干、下肢红斑、丘疹、脓疱一年半入院.皮肤组织病理检查:大量单个核细胞弥漫分布于真皮乳头层并向表皮侵入,单个核细胞体积较大,胞质淡染,核折叠成肾形,中央空泡化,可见线状沟,呈咖啡豆样外观.免疫组织化学法:CD1α及 S-100染色阳性.诊断为朗格汉斯组织细胞增生症.同时结合相关文献对朗格汉斯组织细胞增生症的临床表现、诊断和预后等进行分析.     

硬皮病样皮肤转移性恶性纤维组织细胞瘤1例

报告1例硬皮病样皮肤转移性恶性纤维组织细胞瘤。患者男,60岁。面颊及颈部皮肤硬韧1个半月。病理检查示:真皮浅中层胶原纤维间见散在或密集的类似成纤维细胞样细胞、组织细胞样细胞浸润,细胞核大而深染,呈长梭形及圆形,小血管腔内也见核大深染的细胞及多核巨细胞。免疫组化示:CD68(+),CD34,CK,SMA均阴性。诊断:皮肤转移性恶性纤维组织细胞瘤。     

多中心网状组织细胞增生症 1例

患者,男，65岁。手部皮色丘疹结节伴关节痛3月余，组织病理示：真皮可见大量组织细胞和多核巨细胞，胞体大，胞浆丰富，部分胞浆红染，呈“毛玻璃”样。PAS染色阳性，免疫组化Vimentin（+），CD68（+），CD1a（-），S100（-）。诊断：多中心网状组织细胞增生症。经“强的松、甲氨蝶呤、雷公藤”联合口服治疗后皮疹和关节症状明显改善。     

皮肤窦性组织细胞增生症

报告1例皮肤窦性组织细胞增生症（CSH）。患者女,48岁,仅表现为左面颊部有一斑块。皮损的组织病理特征为真皮及皮下有以组织细胞和淋巴细胞为主的浸润,可见吞噬现象。免疫组化染色组织细胞S-100蛋白和CD68阳性,CD1a标记阴性。阿维A试验性治疗有效。     

皮肤型Rosai-Dorfman病1例

患者男,44岁,右侧面部及右鼻背皮损1年。皮损组织病理示:真皮全层组织细胞淡染区和炎性细胞浸润的深染区形成深、淡相间分布,部分组织细胞内吞噬淋巴细胞、浆细胞及中性粒细胞。免疫组织化学示:S-100蛋白阳性、CD68阳性、CD1a阴性。诊断:皮肤型Rosai-Dorfman病。     

多中心网状组织细胞增生症1例

患者女,35岁。全身红斑、丘疹、结节伴瘙瘁7个月,双手指间关节、腕关节、肘关节肿痛2个月。肌电图示左三角肌、右股二头肌肌源性损害。右前臂皮疹组织病理示：真皮可见大量组织细胞和多核巨细胞,细胞体积大,胞浆丰富、嗜酸性,均质或细颗粒状,呈“毛玻璃”样,瘤细胞Vimentin（＋）,CD68（＋）,CD163（＋）,S-100（-）,CD1a（-）。诊断：多中心网状组织细胞增生症。经“甲泼尼龙、MrD（、羟氧喹”联合治疗后皮疹和关节症状明显改善．     

误诊为环状肉芽肿的多中心网状组织细胞增生症1例

报道1例误诊为环状肉芽肿的多中心网状组织细胞增生症。女性患者，42岁，双手足指（趾）背面、关节和侧缘等泛发圆形的质坚实的丘疹和结节，“串珠状”外观，部分发生破溃，曾误诊为环状肉芽肿。经多次病理检查，最后结果显示表皮增生，少许嗜中性白细胞侵入表皮，真皮较多嗜中性白细胞和组织细胞样细胞浸润，免疫组化染色：组织细胞样细胞Mac387（＋）、CD68（＋）、S-100（-）、EMA（-），诊断为多中心网状组织细胞增生症。     

皮肤Rosai-Dorfman病2例并文献复习

例1女,44岁,背部结节并斑块半年。例2女,25岁,面部结节1个月。皮损组织病理均显示:真皮内病变区域呈深染区和浅染区相间分布,可见组织细胞"伸入运动"。免疫组织化学示:组织细胞CD68及S100(+),CD1a(-)。诊断:皮肤Rosai-Dorfman病。采取手术切除皮损治疗,随访2年,未见复发。     

皮肤型恶性组织细胞增生症肿瘤细胞的电镜观察

报告3例皮肤型恶性组织细胞增生症特异性皮损肿瘤细胞超微结构改变.肿瘤细胞分为3种:分化好的组织细胞,分化差的组织细胞和异形组织细胞,后者又可分为巨核异形组织细胞和畸形核异形组织细胞.异形组织细胞的吞噬能力比分化好的组织细胞差.电镜观察容易发现肿瘤细胞内所含有的光镜观察不到的胞质碎片.     

进行性结节性组织细胞瘤

目的描述进行性结节性组织细胞瘤临床、细胞结构及亚细胞结构的特征。方法 活检组织HE染色、免疫组织化学染色显微镜观察及电镜观察。结果镜下可见活检皮损与周围组织界限清晰,并见多核巨细胞、泡沫样组织细胞和组织细胞,部分区域可见席纹状排列梭形细胞,多核巨细胞、梭形细胞、泡沫样组织细胞、组织细胞CD68、溶酶体标志物染色阳性,S-100蛋白染色阴性。冰冻组织切片苏丹黑染色可见泡沫样组织细胞内脂滴。电镜下未发现Birbeck颗粒和Caputo小体。结论本病应与多发性幼年性黄色肉芽肿、网状组织细胞增生症、发疹性组织细胞瘤、播散性黄瘤病鉴别,该病例可以确立进行性结节性组织细胞瘤诊断。     

A case of non-selective phagocytosis of hemosiderin and melanin of dermal histiocytes in stasis dermatitis

A case study was undertaken to determine whether or not the same dermal histiocytes could phagocytose both melanin and hemosiderin simultaneously. A biopsy specimen was taken from a pigmented lesion of the lower leg of a 57-year-old woman with stasis dermatitis. The specimen was processed for histology, conventional transmission electron microscopy and electron-probe X-ray microanalysis. Histologically, numerous histiocytes with their cytoplasm packed with either Prussian blue-positive granules or Fontana-Masson-positive granules were distributed almost equally in the dermis. Electron microscopically, the dermis had many histiocytes with their cytoplasm containing solitary or compound electron-dense substances. The electron-dense substances were classified into three types according to their degree of electron density. By electron-probe X-ray microanalysis, these electron-dense substances were classified into iron-containing and non-iron-containing substances. Both substances were seen in the cytoplasm of the same histiocytes and even in the same compound electron-dense substance. The former were siderosomes and the latter were probably melanosomes. These results show that the same dermal histiocytes probably phagocytose non-selectively both hemosiderin and melanin granules.     

皮肤Rosai-Dorfman病1例

患者男,28岁。左小腿内侧暗红色结节4月。皮损组织病理示:示真皮全层及皮下组织中有大量组织细胞浸润,其间有淋巴细胞及浆细胞,并可见组织细胞内吞噬淋巴细胞及浆细胞。免疫组化结果示淡染的组织细胞S-100蛋白阳性、CD68阳性。诊断:皮肤Rosai-Dorfman病。     

ABC免疫光镜及免疫电镜证实硬红斑皮损炎症区郎格罕细胞

应用Ｌｅｕ６、ＨＬＡ－ＤＲ、Ｓ１００抗体ＡＢＣ免疫光镜及免疫电镜方法对ＥＩ皮损内Ｓ１００蛋白阳性组织细胞性质进行了研究。８例ＥＩ免疫光镜观察显示ＥＩ真皮深部及皮下炎症区Ｓ１００蛋白阳性组织细胞其Ｌｅｕ６及ＨＬＡ－ＤＲ染色亦阳性，且多呈树枝状或椭圆形。３例ＥＩ免疫电镜观察显示Ｌｅｕ６十细胞其细胞核是卷曲的脑回状，胞浆内可见不典型的棒状样的郎格罕颗粒，部分阳性细胞超微结构有受损伤的表现。上述结果表明，ＥＩ皮损内所谓的Ｓ１００蛋白阳性组织细胞为ＬＣ，ＬＣ不仅存在于表皮及真皮，亦存在于皮下组织中，且可能介导了ＥＩ细胞免疫的发生。     

皮肤巨淋巴结病性窦组织细胞增生症

报告1例皮肤巨淋巴结病性窦组织细胞增生症。患者女,47岁。面颈部无痛性棕黄色斑块3年,无淋巴结增大及其他系统受累。皮损组织病理检查显示真皮全层及皮下组织中有大量组织细胞浸润,其间有淋巴细胞及浆细胞,并可见组织细胞内吞噬淋巴细胞及浆细胞。免疫组化染色结果示组织细胞S-100蛋白、DC68均阳性。皮损组织分枝杆菌PCR扩增、分枝杆菌培养及真菌培养均为阴性。诊断：皮肤巨淋巴结病性窦组织细胞增生症。     

Sea-blue histiocytes in mycosis fungoides.

A patient with tumor-stage mycosis fungoides and lymph node involvement had sea-blue (ceroid-containing) histiocytes in her bone marrow. Leukopenia, eosinophilia, and a mild type II beta-hyperlipoproteinemia were also features. Sea-blue histiocytes were demonstrated in the skin after the mycosis fungoides infiltrate had cleared with treatment. There is a possible interrelationship between the sea-blue histiocytes, the abnormal mycosis cells in the skin, and lipid metabolism.     

窦组织细胞增生伴巨大淋巴结病

报告1例窦组织细胞增生伴巨大淋巴结病.患者男,27岁.头皮、颈部、躯干部丘疹及结节半年,伴双侧颌下淋巴结肿大3个月.皮损组织病理检查示真皮内大量组织细胞增生,可见伸入运动.淋巴结组织病理检查示淋巴窦明显扩张,窦内可见大量组织细胞及伸人运动.免疫组化染色示S-100蛋白及CD68阳性,CD1a阴性.依据临床表现、组织病理改变和免疫组化检查,确诊为窦组织细胞增生伴巨大淋巴结病.     

A case of cutaneous involvement by sinus histiocytosis with massive lymphadenopathy

A 44-year-old woman developed an erythematous indurative plaque and papules on the right scapular region. Histological and ultrastructural findings were consistant with sinus histiocytosis with massive lymphadenopathy. However, lymphadenopathy was not demonstrated clinically and the lesion was limited to the skin. Immunohistochemical study showed that histiocytes were positive for S 100 protein and weakly positive to negative for lysozyme. We consider that the histiocytes in this cutaneous lesion of sinus histiocytosis with massive lymphadenopathy are “T-zone histiocytes” and related to an immunoreaction to unknown antigens.     

Small,freshly arrived histiocytes in cutaneous and mucosal herpetic lesions

We report on the predominance of a special type of small histiocyte in the inflammatory infiltrate accompanying herpetic bullae. These histiocytes, which have previously been taken to be neutrophils, are freshly arrived cells with a hitherto unknown function. Until now, they have been found only in Sweet’s syndrome and erythema nodosum where they form Miesscher’s radial granulomas. Similar small histiocytes were found in half of those herpetic lesions with intact bullae, and in over two-thirds of ulcerated lesions in which these cells formed a palisade in the fibrinoid material covering the floor of the ulcerated vesicles. Small histiocytes, admixed with neutrophils, were in close proximity to virally infected keratinocytes. Immunohistochemical analysis confirmed their histiocytic nature. With the exception of ecthyma contagiosum (orf), similar small histiocytes were not found in other viral infections or in nonspecific ulcers of the skin. In cases of herpetic folliculitis, small histiocytes showed massive epidermotropism towards hair follicle epithelium. We conclude that cutaneous and oral herpetic infections represent yet another disease in which small, freshly arrived histiocytes occur. They may be involved in antigen presentation, or in killing of infected keratinocytes. Received: 7 July 1995