皮脂腺痣并发皮脂腺瘤

报告1例皮脂腺痣并发皮脂腺瘤.患儿男,13岁.头顶部一椭圆形淡黄色疣状新生物13年.皮肤科检查:头顶部见一约2cm×3cm椭圆形淡黄色斑块,边界清楚,表面呈轻度疣状.皮损组织病理检查:表皮棘层增生肥厚,轻度乳头瘤样增生,真皮浅中部见增生的皮脂腺及不成熟的毛囊结构,并可见异位大汗腺,真皮中部还可见多个大小不等肿瘤团块,肿瘤团块由基底样细胞和少许成熟的皮脂腺细胞组成,但未形成皮脂腺小叶样结构,团块周边细胞未见栅状排列及收缩间隙.诊断为皮脂腺痣并发皮脂腺瘤.     

浅表上皮瘤伴皮脂腺分化

报告1例浅表上皮瘤伴皮脂腺分化。患者女,53岁。颈部黄色扁平斑块1年,皮损渐增大,无不适。皮损组织病理检查示浅表上皮性肿瘤,表皮多个部位向下增生,增生的细胞团块部分为嗜碱性细胞,部分细胞有明显的胞质,呈皮脂腺分化,细胞无异形性。结合临床及组织病理特点诊断为浅表上皮瘤伴皮脂腺分化。     

早熟性皮脂腺增生1例

患者男,20岁。胸前区散在分布多个直径约为1~3mm的皮色或淡黄色丘疹13年余,偶觉轻微瘙痒。皮损组织病理示:表皮大致正常,真皮浅层可见由多个成熟的皮脂腺小叶组成的团块,中心有扩大的皮脂腺导管。诊断:早熟性皮脂腺增生。     

巨大毛囊皮脂腺囊性错构瘤

报告1例巨大毛囊皮脂腺囊性错构瘤。患者男,15岁。右臀部丘疹,结节15年。体格检查示右臀部多个大小不一的丘疹及结节、部分融合成硬斑块。组织病理检查示毛囊扩张畸形,其上端为毛囊漏斗部扩张,形成囊性结构,下端为增生的皮脂腺,周围胶原增生硬化,且在真皮浅层及中部可见散在成熟的脂肪组织。诊断：巨大毛囊皮脂腺囊性错构瘤。     

传染性软疣并发表皮囊肿1例

表皮囊肿又称角质囊肿、皮脂腺囊肿、表皮样囊肿,是最常见的皮肤囊肿之一.笔者诊治1例传染性软疣并发表皮囊肿,现报告如下. 患者男,39岁.阴囊出现丘疹2个月余.2个月前患者无意中发现阴囊上一黄豆大丘疹,无自觉症状,皮损无明显增长,于2007年12月4日来我科就诊.     

巨大毛囊皮脂腺囊性错构瘤

报告1例巨大毛囊皮脂腺囊性错构瘤。患者男,29岁,左眼眶外侧及颞部出现红色丘疹20年,增大为结节和斑块8年。皮肤科检查:左眼眶外侧暗红色结节,部分与额部暗红色斑块相连,结节和斑块表面见多处凹陷,质地软,无触痛,无内容物挤出。左眼眶外侧结节组织病理检查:真皮中部可见多个畸形的毛囊结构,毛囊漏斗部扩张,与增生的皮脂腺小叶相连,周围有增生硬化的胶原,真皮浅中层可见增生的毛细血管。诊断:巨大毛囊皮脂腺囊性错构瘤。     

皮脂腺痣17例临床病理分析

目的　探讨皮脂腺痣与表皮及皮肤附属器错构瘤样结构的关系。方法　收集 17例皮脂腺痣 ,分析、总结其临床病史 ,病理学改变特点。结果　 14例 (82 %)初生时发病 ,男女之比为 1.3 0∶1(9∶8) ,本病主要表现为毛囊发育不良和皮脂腺增生 ,4例伴有表皮痣 ,1例伴有基底细胞癌 ,1例伴表皮样囊肿 ,6例伴有大汗腺异位。结论　皮脂腺痣是一种错构瘤样增生 ,常伴有其他表皮或皮肤附属器错构瘤样结构存在。     

伴皮脂腺增生的结缔组织增生性毛发上皮瘤一例

【摘要】 患者男,67岁,因头顶部皮损1年余来院就诊。体检：头顶部一淡红色环形斑块,约1.5 cm × 1cm,中央凹陷,边缘见淡黄色丘疹样突起,表面无毛发生长。皮损组织病理检查：表皮轻度增生,表面部分区域凹陷,真皮内见多个皮脂腺融合增生;真皮浅层见较多条索状嗜碱性上皮细胞及角囊肿,周围胶原纤维明显增生。免疫组化结果：CD34阳性（毛源性间质）,上皮膜抗原、细胞角蛋白20阳性,bcl?2、P53、CD56、Ⅳ型胶原纤维均阴性,增殖指数Ki67 2% ~ 5%。病理诊断：结缔组织增生性毛发上皮瘤伴皮脂腺增生。     

单发性早熟性皮脂腺增生一例

报道一例单发性早熟性皮脂腺增生。患者女,17岁,因左颊部丘疹2年余就诊,无自觉症状。左颊部一黄豆大小皮色丘疹,分叶、表面光滑、触之质硬。组织病理：表皮角化过度伴角栓形成,棘层肥厚,表皮突伸长增宽。真皮可见增生的皮脂腺小叶,皮脂腺多为成熟期。诊断单发性早熟性皮疹腺增生。     

阴囊多发性钙化上皮瘤1例

阴囊多发性钙化上皮瘤１例余昌勇航天部七一二医院（邮政编码６３６４５０）患者男，２３岁。因阴囊多发性肿块４年余人院。肿块初位阴囊左侧，绿豆大小，两枚，后渐增多增大，且累及右侧，伴病痒。曾诊断为“阴囊皮脂腺囊肿”、“阴囊结核”。体检：用囊部结节一１４ｇｂ...     

Sebaceous glands changes following topical application of citral

The long-lasting effect of a flavour cosmetic constituent on male rat skin was studied. Topical daily application of citral (15.4%) solution for 3 months produced an increase in the number of sebaceous gland lobules and hyperplasia of sebaceous cells in each gland. It is suggested that the mechanism of this hyperplasia might be activation of the testosterone 5 alpha-reductase which induces the formation of dihydrotestosterone, the mediator of sebaceous gland activity.     

Giant sebaceous gland hyperplasia of the vulva

BACKGROUND: Sebaceous gland hyperplasia is an epithelial tumour with sebaceous differentiation. Genital involvement is rare. In this paper, we report a new case of sebaceous gland hyperplasia of the vulva. CASE REPORT: A 27 year-old woman presented multiple polypoid lesions of the lower third of left labium majus. The lesions were soft to the touch, measured 5 cm in length and were painless. The cutaneous biopsy confirmed the diagnosis of sebaceous gland hyperplasia of the vulva. Surgical excision was performed in two separate procedures and was successful. DISCUSSION: This case was unusual in terms of the site, the clinical appearance and the weeping seen due to the high concentration of hyperplasic sebaceous glands.     

丹参酮ⅡA磺酸钠抗金黄地鼠皮脂腺增生的研究

目的 探讨丹参酮ⅡA磺酸钠（STS）外用对动物模型皮脂腺增生的影响。方法 选用成年雄性金黄地鼠侧腹皮脂腺斑作为动物模型,采用自身对照法,分别予丹参酮ⅡA磺酸钠、生理氯化钠溶液外涂一侧皮脂腺斑,一天3次,随机分用药0、10、20、30 d 4个时间组。在各时间点用游标卡尺测定两侧皮脂腺斑的面积。HE染色法观察皮脂腺斑组织结构的变化,取组织切片用免疫组化方法检测皮脂腺细胞增殖细胞核抗原（PCNA）的表达,TUNEL法检测皮脂腺细胞的凋亡情况。结果 用药前,两侧皮脂腺斑大小比较差异无统计学意义（P > 0.05）,皮脂腺结构完整,排列紧密,皮脂腺细胞的增殖与凋亡比较差异均无统计学意义（P > 0.05）。随着用药时间的延长,与生理氯化钠溶液对照侧比较,STS侧金黄地鼠皮脂腺斑的面积缩小（P < 0.05）;皮脂腺数目减少,体积变小,排列疏松,用药至30 d时,皮脂腺呈明显萎缩状态;皮脂腺细胞PCNA表达明显下调（P < 0.01）,用药至10 d、20 d时更为明显（P < 0.01）;皮脂腺细胞凋亡亦增加（P < 0.01）,用药至20 d时凋亡显著（P < 0.01）,且皮脂腺中央部细胞的凋亡较周围更为明显。结论 丹参酮ⅡA磺酸钠能缩小金地鼠皮脂腺斑的面积,改变皮脂腺斑的显微结构,可抑制皮脂腺增生。     

Chronological ageing and photoageing of the human sebaceous gland

The human sebaceous gland undergoes both extrinsic and intrinsic ageing. The latter is associated with morphological changes and alteration in the sebaceous gland activity. The high androgen-dependent sebum secretion in neonates falls during childhood, starts to rise again during puberty and reaches its maximum in young adults. While the number of sebaceous glands remains the same during life, sebum levels tend to decrease after menopause in females, whereas no major changes appear until the eighth decade of life in men. Reduced androgen levels in aged individuals lead to a slow cellular turnover in the sebaceous glands resulting in hyperplasia of the facial sebaceous glands in advanced age. Ultraviolet radiation and immune suppression (cyclosporin A with corticosteroids) represent cofactors for the development of sebaceous gland hyperplasia. Current molecular findings indicate that overexpression of the ageing-associated gene Smad7 and parathormone-related protein correlate with sebaceous gland hyperplasia, whereas c-myc overexpression is associated with enhanced sebum production. On the other hand, down-regulation of the mismatch repair genes hMLH-1 and hMSH-2 may promote the development of sebaceous gland carcinoma. In addition to spontaneous single tumours, sebaceous gland carcinomas have been reported in immune-suppressed transplant recipients (azathiorpine, cisplatin, cyclosporin A) and in association with the Muir-Torre syndrome. Microsatellite instability with a loss of the mismatch repair gene hMSH-2 has been detected in immune suppressed patients and under photo-induced DNA damage. Topical and systemic oestrogens offer treatment options for skin xerosis in menopausal females. A combination of isotretinoin and interferon-alpha may prevent tumour development in patients with Muir-Torre syndrome.     

皮脂腺痣皮肤镜及反射式共聚焦显微镜特征分析

【摘要】 目的 探讨不同年龄患者皮脂腺痣的皮肤镜及反射式共聚焦显微镜特征。方法 2016年1 - 12月将武汉市第一医院皮肤科门诊经组织病理学确诊的83例皮脂腺痣患者,按年龄分成4组,采集、分析其皮肤镜及反射式共聚焦显微镜图像特征。结果 < 10岁组21 例,皮损在皮肤镜下表现为橘色背景下独立分布、较为一致的黄红色、球块状结构,似鹅卵石样排列,伴血管增生、扩张;反射式共聚焦显微镜下可见皮脂腺发育不全, 仅见幼稚毛囊。10 ~ 20岁组28例,皮肤镜下可见聚集分布、与毛囊无关、大小不同的黄色圆形、卵圆形结构,伴毛细血管扩张;反射式共聚焦显微镜下可见,真表皮交界处及真皮浅层葡萄串样皮脂腺结构,中央为管状/柄样结构,外周为簇集分布、鱼籽/蛙卵样增生的皮脂腺小叶,其上方表皮往往呈疣状/乳头瘤样增生。21 ~ 59岁组30例,影像学表现同10 ~ 20岁组。≥ 60岁组4例,影像学特征主要为乳头瘤样增生。结论 皮脂腺痣是一种动态发展的疾病,不同年龄阶段影像学表现不尽相同;在皮肤镜及反射式共聚焦显微镜下均具有特征性结构,可作为有效的无创性诊断方法。     

Giant solitary sebaceous gland hyperplasia clinically simulating epidermoid cyst

We report an unusual case of sebaceous gland hyperplasia manifested clinically as a large solitary intracutaneous nodule, which was at first diagnosed as an epidermoid cyst. Histologically, the nodule consisted of a single large central cavity connected with numerous fully-matured sebaceous glands. We discuss the unique clinical appearance and its histopathological differential diagnosis including sebaceous adenoma, sebaceous trichofolliculoma, organoid nevus and sebaceous gland hyperplasia.     

Is “Premature Sebaceous Hyperplasia” Really a Sebaceous Hamartoma? Report of a Case with Neonatal Onset

Sebaceous hyperplasia is a common benign proliferation of the sebaceous gland. It commonly presents in middle-aged people as soft, yellow papules with central umbilication on the face, particularly on the forehead. We report a newborn with striking unilateral sebaceous hyperplasia and suggest that this may represent a unique sebaceous hamartoma rather than "premature sebaceous hyperplasia."     

Frequency of microsatellite instability in unselected sebaceous gland neoplasias and hyperplasias

Sebaceous gland neoplasias are the cutaneous manifestation of the Muir-Torre syndrome, which is known to be a phenotypical variant of hereditary nonpolyposis colorectal cancer. Both hereditary nonpolyposis colorectal cancer and Muir-Torre syndrome are caused by inherited DNA mismatch repair defects. As a prominent molecular genetic feature, all tumors associated with a DNA mismatch repair defect exhibit high microsatellite instability. So far, the frequency of DNA mismatch repair defects in patients selected solely on the basis of a sebaceous gland tumor has never been determined. In order to estimate this frequency, we assessed microsatellite instability with up to 10 microsatellite markers in a newly collected unselected series of 25 sebaceous gland neoplasias (six sebaceous adenomas, 16 sebaceous epitheliomas, three sebaceous carcinomas) in comparison to 32 sebaceous gland hyperplasias from unrelated patients. As many as 15 of the 25 sebaceous gland neoplasias (60%), but only one of the 32 sebaceous gland hyperplasias (3%), exhibited high microsatellite instability. Thus, in our study, the majority of patients with a sebaceous gland neoplasia in contrast to patients with a sebaceous gland hyperplasia are highly suspicious for an inherited DNA mismatch repair defect. On the basis of the subsequently collected tumor histories, nine of the 15 patients with a high microsatellite unstable sebaceous gland neoplasia were identified to have Muir-Torre syndrome. In none of these cases, however, were the clinical Amsterdam criteria for diagnosing hereditary nonpolyposis colorectal cancer fulfilled. In the sebaceous tumors of the remaining six patients, high microsatellite instability was an incidental finding. In two of these six patients, single relatives were known to be affected with internal cancer; however, their family histories were not suggestive of Muir-Torre syndrome or hereditary nonpolyposis colorectal cancer. In comparison with microsatellite instability screening studies in a variety of other randomly selected tumors, our study identifies sebaceous gland neoplasias as tumors with the highest frequency of high microsatellite instability reported so far, whereas sebaceous gland hyperplasia rarely exhibits high microsatellite instability. Therefore, screening for microsatellite instability in sebaceous gland neoplasias will be of great value in the detection of an inherited DNA mismatch repair defect, which predisposes to various types of internal cancers.     

Coexistence of Basal Cell Carcinomas and Multiple Sebaceous Gland Hyperplasias in a Cyclosporine (Ciclosporin)-Treated Renal Transplant Recipient

A 55-year-old man presented with multiple, asymptomatic, yellowish papules on his face with a 4-year history, and two non-healing tumoral lesions on his nose with a 7-month history. He was a renal transplant recipient and had been treated with cyclosporine (ciclosporin) for 9 years. A biopsy from the asymptomatic, yellowish papule on the face showed sebaceous gland hyperplasia, and biopsies from the lesions on the nose revealed basal cell carcinomas. The lesions on the nose were excised. Sebaceous gland hyperplasia and skin cancers are among the cutaneous neoplasms observed in renal transplant recipients receiving cyclosporine. To our knowledge, this is the third reported case of the coexistence of basal cell carcinomas and multiple sebaceous gland hyperplasias in a cyclosporine-treated renal transplant recipient.     

Sebaceous gland hyperplasia following topical application of citral. An ultrastructural study

Topical application of citral on male rat skin induces hyperplasia of the sebaceous glands. Ultrastructural study showed that this hyperplasia is manifested by an increase in number of the partially differentiated cells of the gland. Citral was found in fat droplets of the mature differentiated and partially differentiated cells. Because citral causes an increase in testosterone level, we conclude that the sebaceous gland hyperplasia is related to androgen activity.