"Giant" senile sebaceous hyperplasia.

Although the usual size of senile sebaceous hyperplasia is 2 to 3 mm in diameter, we report one "giant" nodular case on the face. The patient is a 75-year-old Japanese man with a dome-shaped, skin-colored nodule on his right cheek. The lesion was 10 mm in diameter and had multiple small umbilications on its surface. He also had several small, yellow-colored, asymptomatic papules with central umbilication on his cheeks. Histologically, the giant nodule and the papule on the right cheek showed the same architectural pattern, a sharply demarcated hyperplasia of grouped mature sebaceous glands with a sebaceous converging duct, whose opening to the surface epithelium corresponded to the clinical umbilication. The reason for the giant growth of this senile sebaceous hyperplasia in our case is obscure; the patient had not been stressed by inductive agents or factors such as systemic corticosteroid and hemodialysis except for electrocoagulation on the lesion. In spite of the extraordinarily large size of the nodule, the conservative proliferating pattern seemed to show the benign hyperplastic character of senile sebaceous 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."     

Diffuse (presenile) hyperplasia of the sebaceous glands, a new entity? Successful treatment with 13-cis-retinoic acid

We report the case of a young man with extreme sebaceous gland hyperplasia that occurred in a diffuse pattern of aggregated papular lesions involving the entire face, neck and upper chest, together with marked seborrhoea oleosa. Oral therapy with 13-cis-retinoic acid (isotretinoin) resulted in remarkable improvement within a few weeks. Parallels from our case are drawn to familial sebaceous hyperplasia, reported by Dypre et al. in 1980 [6], and to a case of a young man with severe sebaceous gland hyperplasia and facial seborrhoea, reported by de Villez et al. in 1982. We suggest that these types of seboglandular proliferative disorders be classified as diffuse (presenile) sebaceous gland hyperplasia in contrast to the well-defined senile circumscribed variant, and that they be regarded as a separate entity.     

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.     

Sebaceous gland hyperplasia on rabbit pinna induced by tetradecane

To investigate the pathologic changes of sebaceous glands during comedo formation induced by topically applied substances in a rabbit pinna model, purified tetradecane was inuncted on the ventral aspect of the rabbit pinnas once a day for a week. Histologically, a marked hyperplasia of sebaceous glands, epidermis, and follicular epithelium was seen. These remarkably enlarged sebaceous glands were examined histochemically and ultrastructurally. The acinus size and cell population of the hyperplastic sebaceous gland were significantly increased over those of the normal sebaceous gland. By N-(7-dimethylamino-4-methyl-3-coumarinyl)maleimide staining, normal distribution patterns of sulfhydryl (SH) and disulfide (SS) were seen in the peripheral to differentiating layers in the hyperplastic sebaceous glands. In the terminally differentiated layer, the brilliant SH fluorescence was gradually decreased and the SS fluorescence was gradually increased in intensity, indicating that most SH groups in the sebaceous cells were converted to SS linkages before holocrine secretion. By transmission electron microscopy, several cell layers of undifferentiated sebaceous cells were observed at the periphery of the large sebaceous gland. The differentiating sebaceous cells produced a large number of lipid droplets, which were produced in either rough or smooth endoplasmic reticulum. These cells were abruptly converted into homogeneously electron-dense cells which formed several layers. These homogeneous cells gradually lost their electron density before holocrine secretion. These findings indicate that the sebaceous cells in the hyperplastic sebaceous glands undergo a magnified step-by-step cell differentiation and play a role in slightly modified lipid formation, and that there may be an increased production of sebum in the rabbit pinna model. This is the first report of sebaceous hyperplasia induced by a topically applied substance on skin surface, except for androgens. The hyperplastic sebaceous glands could serve as a model for investigations of sebaceous cell differentiation and lipid formation.     

Circumscribed sebaceous gland hyperplasia: autoradiographic and histoplanimetric studies

Circumscribed sebaceous gland hyperplasia (sebaceous hyperplasia) is a common benign facial tumor found in adults and aged. Seventeen biopsies of sebaceous hyperplasia from 10 patients, females and males aged 57-87 years were secured which were injected 45 min or up to 15 days prior with tritiated thymidine, and prepared for autoradiography. Specimens were evaluated by cell counts (labeling index, labeled total cells), and histoplanimetric techniques (sagittal section areas and circumference of sebaceous hyperplasia, of sebocytes, and of sebocyte nuclei). Controls were uninvolved sebaceous follicles from the same subjects, from an age-matched group, and from young male adults. In sebaceous hyperplasia the labeling index of basal cells is low with 5.7% +/- 2.3 vs uninvolved sebaceous follicles from the same subject (8.6% +/- 2.4) and the younger subjects with a value of 10.1% +/- 2.0). Labeled cells are retained in the acini much longer than in young adults (slowed down transit and turnover time). The glands of sebaceous hyperplasia are very large, their sebocytes are small, and many more basal cells are found per unit basement membrane length.     

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.     

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.     

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.     

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.     

阴囊皮脂腺增生1例

报告1例阴囊皮脂腺增生,患者男,20岁。阴囊散在多个皮色或淡黄色粟粒大兵疹1年,无自觉症状,皮肤组织病理显示表皮正常,真皮浅层可见单个增生、成熟的由18个皮脂腺小叶组成的团块,中心有扩大的皮脂腺导管,未见明显的细胞异形性。     

Bonbon toffee sign: a new dermatoscopic feature for sebaceous hyperplasia

Introduction Sebaceous hyperplasia is a benign proliferation of the sebaceous gland. In this study, we tried to define the dermatoscopic features of sebaceous hyperplasia, which will help to minimize misdiagnoses. Material and method Seventeen patients with 30 sebaceous hyperplasia lesions were included in the study. All the lesions were evaluated dermatoscopically. Results Cumulus sign, crown vessels, and milia‐like cysts were detected in 100%, 86.6%, 53.3% of the lesions, respectively. In 80% of the lesions, the bonbon toffee sign was detected. Conclusion During this study, we observed a feature with central umbilication surrounded by cumulus sign in 80% of our cases, and we named this entity as the ‘Bonbon toffee sign’, which resembled us ‘bonbon toffee’. We think the ‘bonbon toffee sign’ is a simple and easily recognizable phrase, and it can be used as a new terminology in dermatoscopic diagnosis of sebaceous hyperplasia.     

Areolar sebaceous hyperplasia with underlying primary duct carcinoma of the breast in a woman with Donohue syndrome (leprechaunism)

Areolar hyperplasia is only reported when exaggerated, and even so, exaggerated areolar sebaceous hyperplasia is rare. We have recently seen a case of areolar sebaceous hyperplasia in a 32-year-old woman with Donohue syndrome (leprechaunism), who also had an invasive ductal carcinoma in the same breast. The patient showed typical "elfin-like" face with wide nostrils and thick lips, large and low-set ears, and dysplastic nails. The areola showed a yellowish thickened plaque of 5-cm diameter that corresponded to a hyperplasia of the sebaceous glands. Immunohistochemistry for the mismatch repair proteins (MLH1, MSH2, MSH6, and PMS2) was performed on the sebaceous hyperplasia and on the breast carcinoma, and no lack of expression of the markers was evidenced. We have found no other reported case of areolar sebaceous hyperplasia either in cases of breast carcinoma or in cases of leprechaunism.     

Complex adnexal tumor of the primary epithelial germ with distinct patterns of superficial epithelioma with sebaceous differentiation, immature trichoepithelioma, and apocrine adenocarcinoma.

A 60-year-old man came for treatment of a sharply outlined erythematous plaque on the gluteal area (45 x 20 mm) of 20 years' duration. Eccentrically located on the plaque was a nodule, 20 mm in diameter. Histological study of the plaque showed a superficial platelike tumor with basaloid bland cytology and sebaceous gland differentiation. Histologic study of the nodule found an undifferentiated adenocarcinoma whose ductlike glandular structures opened to the skin surface and infiltrated the whole depth of the dermis. Study of other areas of the lesion detected two more neoplasms. A nodule of squamous cell carcinoma was found within the superficial band of the benign sebaceous tumor. The fourth neoplastic pattern consisted of epithelial islands composed of basaloid cells within a fibroblastic stroma. There was prominent palisading of epithelial cell nuclei at the periphery of the islands, which usually were surrounded by a sheath of mesenchymal cells. In this complex adnexal tumor of the primary epithelial germ, sebaceous and follicular differentiation both simulate neoplastic patterns recently described as separate entities: superficial epithelioma with sebaceous differentiation and immature trichoepithelioma. The undifferentiated adenocarcinoma may represent differentiation toward the third component of the germ, that is, the apocrine gland.     

An updated review of the sebaceous gland and its role in health and diseases Part 1: Embryology,evolution, structure,and function of sebaceous glands

Sebaceous glands are sebum‐secreting components of pilosebaceous units. The embryological development of the sebaceous gland follows that of the hair follicle and epidermal tissue, beginning between weeks 13 and 16 of fetal development. New sebaceous glands do not normally develop following birth, but their size increases with age. Sebocytes express a multitude of hormone receptors and are heavily regulated to secrete sebum by androgens. There is a large increase of sebum excretion at birth and again at puberty, until approximately age 17. In adulthood, sebum production remains stable and declines to zero in postmenopausal women and in men aged 60‐70. Besides the production and release of sebum, sebaceous glands function to lubricate the skin and hair, provide thermoregulation, and exhibit antimicrobial activity. Research has shown sebaceous glands to possess the cellular capability to transcribe genes necessary for androgen metabolism. Dysfunction of the sebaceous gland can be seen primarily in steatocystoma simplex and multiplex, sebaceous gland hyperplasia, sebaceoma, sebaceous adenoma, sebaceous carcinoma, nevus sebaceus, and folliculosebaceous cystic hamartoma. Sebaceous glands are secondarily involved in acne vulgaris, seborrheic dermatitis, and androgenic alopecia.     

Sebaceous carcinoma in children

Sebaceous carcinoma is a rare malignant tumor derived from the epithelium of sebaceous glands. It potentially may develop from any sebaceous gland, but most commonly occurs in the periorbital area. We report a case of sebaceous carcinoma in a 14-year-old girl who was first seen with an asymptomatic 2.5 x 2.3-cm firm, multilobulated cutaneous nodule on the anterior thorax, which had been present for 1 year. She was adopted, and no family history is available. A skin biopsy specimen revealed a poorly differentiated infiltrative carcinoma involving the dermis and subcutaneous fat and focally involving the epidermis. Tumor cells had sebaceous and squamous differentiation. A diagnosis of sebaceous carcinoma was made. She was treated by surgical excision with a 2-cm margin. Further work-up showed no evidence of Muir-Torre syndrome.     

Familial nevoid sebaceous gland hyperplasia affecting three generations of a family

Familial sebaceous gland hyperplasia is a benign entity with onset at puberty and a tendency to worsen with age. It is characterized by a nevoid symmetric pattern in the sebaceous areas of the face sparing the orbital, perinasal, preauricular and perioral areas showing prominent follicular openings and interfollicular dermal yellowish or white prominent skin. Usually, the face is affected, with the neck, column and thorax affected in a milder pattern. We describe a family with familial nevoid sebaceous gland hyperplasia in three consecutive generations. All the patients were successfully treated with oral isotretinoin. The pedigree suggests autosomal dominant inheritance with incomplete penetrance.     

皮脂腺肿瘤p53及bcl-2蛋白表达的研究

目的研究ｐ５３及ｂｃｌ ２基因在皮脂腺肿瘤中的作用。方法应用免疫组化方法对皮脂腺良、恶性肿瘤上述两种基因产物的表达进行了检测。结果５例皮脂腺癌、２例皮脂腺痣和２例皮脂腺增生症均不同程度表达ｂｃｌ ２蛋白,而ｐ５３蛋白仅表达于５例皮脂腺癌的癌细胞。两种蛋白表达强度无相关关系（ｒ’ｓ＝０．１０５,Ｐ＞０．０５）。结论ｐ５３基因突变在皮脂腺癌发生中起决定性作用,而ｂｃｌ ２基因则起协同促进作用。检测ｐ５３蛋白可用于鉴别皮脂腺良、恶性肿瘤。     

Muir-Torre syndrome: case report and review of the literature

Muir-Torre syndrome (MTS), a subtype of Lynch syndrome II, presents as at least one internal malignancy associated with at least one sebaceous skin tumor. This autosomal-dominant genetic disorder is thought to arise from microsatellite instability. Although not all patients with sebaceous tumors have MTS, even a single biopsy-proven sebaceous adenoma may warrant evaluation for MTS. We report the case of a 76-year-old man with a marked family history of colon cancer; a personal history of colon cancer status post-partial resection of the colon; and multiple cutaneous neoplasms including sebaceous adenomas, sebaceous gland hyperplasia, and basal and squamous cell carcinomas. We review the literature describing MTS and highlight the important role of dermatologists and dermatopathologists in the potential early detection and initial diagnosis of this familial or hereditary colon cancer in patients presenting with cutaneous sebaceous adenomas. Correct diagnosis may be lifesaving in patients with MTS and their at-risk relatives who would benefit from earlier colonoscopy, tumor surveillance, and potential early cancer detection. Muir-Torre syndrome represents yet another dermatologic symptom of an internal disease.