脂水肿性头皮伴脂水肿性脱发

报告1例脂水肿性头皮伴脂水肿性脱发.患者女,53岁.因头皮增厚、头顶部弥漫性脱发、无明显不适3个月就诊.皮损组织病理检查示表皮大致正常,毛囊数量减少,毛囊周围及皮下脂肪层脂肪组织增生,阿新蓝染色阴性.B超检查示头顶部头皮厚度增加,皮下脂肪组织增厚.     

脂水肿性脱发1例

 报告1例脂水肿性头皮伴脂水肿性脱发。患者女,44岁,因头皮肿胀、增厚伴脱发5年余就诊。皮肤专科检查：患者头顶部可见一面积约9 cm×18 cm的梭形毛发稀疏区域,残留断发＜2 cm,脱发区头皮呈黄褐色,稍隆起,明显增厚,触之柔软,似海绵状;拉发试验阴性。头部MRI示头皮下脂肪层不均匀增厚。皮损组织病理示：毛囊数量减少,毛囊由增生的纤维组织替代,少许淋巴细胞浸润。诊断为脂水肿性头皮伴脂水肿性脱发。患者及家属拒绝治疗,随访半年余,病情未进展。     

脂肿性头皮伴脂肿性脱发一例

患者,女,52岁.头皮肿胀增厚伴脱发3个月余就诊.皮肤科查体:头皮明显肿胀增厚,头顶部增厚区域界限清楚的脱发斑.皮肤镜检查见脱发区毛囊明显减少,毛囊周围见褐色环状结构.组织病理示:皮下脂肪组织明显增厚,位置上移,由成熟脂肪细胞组成.诊断:脂肿性头皮及脂肿性脱发.     

Brocq假性斑秃1例

患者女,31岁。头皮部出现多个瓷白色脱发斑2年。皮损组织病理示:表皮轻度萎缩,真皮血管周围见少许淋巴细胞浸润,真皮纤维组织增生伴胶原化,毛囊数量减少。诊断:Brocq假性斑秃。     

硬化性粘液水肿1例

患者,男,54岁,以颜面及肢体反复水肿性红斑、苔癣样丘疹为主要临床表现,无系统损害,相关实验室检查无明显异常。组织病理学示:表皮萎缩,表皮突消失,真皮成纤维细胞增多和胶原纤维增粗,部分毛囊萎缩;真皮网状层较大量阿辛蓝染色阳性的黏蛋白弥漫性沉积;血管周围淋巴组织细胞浸润。根据临床表现、组织病理及阿辛蓝染色等诊断为硬化性粘液水肿。     

毛囊黏蛋白病二例并文献复习

报道2例毛囊黏蛋白病并进行文献复习.患者1,男,44岁,颈项部局限性浸润性红斑伴疼痛2个月,组织病理示:真皮毛囊水肿,毛囊内外淋巴组织细胞浸润,个别嗜酸粒细胞.阿新蓝染色:毛囊黏蛋白阳性.患者2,男,32岁,左面部浸润性暗红斑45天,组织病理示:表皮大致正常,毛囊上皮水肿,淡蓝色黏液样物质沉积,毛囊内及毛囊周围较多嗜酸...     

黏液水肿性苔藓1例

报告1例黏液水肿性苔藓或硬化性黏液水肿。患者男，45岁。面部皮肤弥漫性肿胀、硬化并有多发隆起性斑块，鼻根部斑块隆起明显，形成一纵行皮嵴，颈部、躯干、双上肢近端泛发苔藓样丘疹。常规实验室检查无异常。皮肤组织病理示真皮内胶原纤维及成纤维细胞增多，胶原束间黏蛋白沉积。     

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。     

黏液水肿性苔藓1例

患者男,55岁。双前臂肤色丘疹7年余。有糖尿病史。组织病理检查示真皮中上部较多黏蛋白沉积,粘蛋白阿新蓝染色阳性。诊断:黏液水肿性苔藓。     

硬化性黏液水肿性苔藓1例

报告1例硬化性黏液水肿性苔藓。患者男,45岁。因全身密集苔藓样丘疹,浸润性斑块伴瘙痒1年余就诊。皮肤科检查见双眉间、鼻梁及下颌两侧呈硬性隆起。组织病理学检查示真皮上部胶原稀疏、水肿,胶原束排列紊乱,胶原束间隙增宽,成纤维细胞增生,阿新蓝染色阳性。系统检查无异常。     

Lipedematous Alopecia in an Asian Woman: Is It an Advanced Stage of Lipedematous Scalp?

Lipedematous alopecia (LA) is a rare disease entity that manifests as increased thickness of subcutaneous fatty tissue in the scalp with a variable degree of acquired, non-scarring alopecia. Although the pathogenesis of alopecia in LA is not clear, it is assumed that the increased thickness of subcutaneous fat retards hair growth by disturbing the peripheral microenvironment of the hair bulb. LA is clinically distinguishable from lipedematous scalp (LS) in that LS is not associated with any hair abnormalities, while LA is characterized by variable degree of hair loss. However, both LA and LS share increased scalp thickness. Here, we describe a rare case of LA on the frontal scalp of an Asian woman, further characterize the clinical and histologic features, and suggest applying an integrated diagnosis as lipedematous diseases of the scalp.     

Cuero cabelludo lipedematoso

Lipedematous scalp is a rare condition first described by Cornbleet in 1935. An increased thickness of subcutaneous tissue in the scalp gives rise to a soft spongy appearance of the surface and occasionally causes pruritus and pain in the affected area. When hair loss is also associated with the condition, it is described as lipedematous alopecia. To date, 10 cases of lipedematous scalp and 13 of lipedematous alopecia have been reported.We present the case of a 77-year-old white women who developed dysesthesia on her scalp 5 months after the death of her husband. Biopsy revealed subcutaneous tissue thickening that even extended to the dermis. Computed tomography showed thickening of subcutaneous tissue at the vertex and in the occipital region. We diagnosed a new case of lipedematous scalp in a white women. This case highlights the importance of differential diagnosis in cases of dysesthetic syndrome of the scalp.     

Lipedematous alopecia of the scalp

Lipedematous scalp is a rare disorder, mainly described in adult African-American females. We report 2 adult caucasian males with lipedematous scalp associated with androgenetic alopecia. Patients were studied by dermoscopy and histopathology; they were treated with finasteride 1 mg. In our patients, lipedematous scalp affected the occipital and the vertex areas and pathologically exhibited mild edema and thickening of the adipose subcutaneous layer. At videodermoscopy, lipedematous scalp areas showed linear areas of teleangiectasia within the scalp creases, possibly caused by compression of the superficial blood capillaries by the increased volume of the subcutaneous fat layer within the thickened scalp. Finasteride at a dose of 1 mg per day for 1 year induced mild improvement of androgenetic alopecia in one patient and stabilization of the disease in the other. The lipedematous scalps remain unchanged. Lipedematous scalp is apparently a rare disease even though the condition is probably underdiagnosed. As a matter of fact, we diagnosed lipedematous scalp in our patients during a clinical examination for androgenetic alopecia, which was the patients' complaint. The association of lipedematous scalp and androgenetic alopecia in our two patients appears to be coincidental.     

Hyperplasia of the subcutaneous adipose tissue is the primary histopathologic abnormality in lipedematous scalp

A 51-year-old white woman presented with thickening of the scalp located at the vertex and left lateral occiput without hair abnormalities or alopecia. Skin biopsies of the thickened scalp showed thickening of the subcutaneous tissue with proliferation of mature subcutaneous fat cells but no signs of inflammation or hair abnormalities. During 2.5 years of follow-up, scalp thickening progressed over the entire hair-bearing scalp and persisted without signs of further progression at 3.5 year follow-up. Lipedematous scalp is an extremely rare diagnosis. It is defined by a thickening of the subcutaneous layer of the scalp and can be distinguished from lipedematous alopecia, in which subcutaneous thickening is associated with diffuse alopecia and shortening of scalp hairs. A total of seven cases of lipedematous alopecia and two cases of lipedematous scalp have been reported. We report the third case of lipedematous scalp in a 51-year-old white woman associated with early symptoms of meningitis. Additional features described in the literature include pruritus, pain, and paresthesia of the scalp as well as associated medical problems such as hyperelasticity of skin and laxity of joints, renal failure, and diabetes mellitus. This sporadic disorder is predominantly located at the vertex and occiput. The etiology and pathogenesis of lipedematous scalp and alopecia remain unclear. The treatment is symptomatic.     

A case of lipedematous alopecia occurring in a male patient

A 30-year-old Japanese man presented with a thickening of the scalp and diffuse alopecia on the vertex. A skin biopsy specimen of the thickened scalp showed an increased thickness of subcutaneous adipose tissue and a marked decrease in the number of hair follicles. By an MRI examination, the irregularly thickened subcutaneous fatty tissue was visualized. These findings indicated that the patient had been suffering from lipedematous alopecia. This is a rare condition characterized by diffuse alopecia due to the thickening of the layer of adipose tissue covering the scalp. Only 4 female cases of lipedematous alopecia have been reported previously. MRI is thought to be useful for the differentiation of lipedematous alopecia from lipoma. The present case is considered to present the first male patient with lipedematous alopecia.     

Lipedematous alopecia: spongy scalp syndrome

Lipedematous scalp and lipedematous alopecia are rare and closely related entities of unknown etiology Almost all cases have occurred in black women. We report a case of lipedematous alopecia that is characterized by a boggy spongy thickening of the scalp, an increase in subcutaneous fat, short hairs, patchy alopecia, scarring, atrophy, and depigmentation. The histologic finding of an increase in subcutaneous adipose tissue is notable.     

Congenital Lipedematous Alopecia: Adding to the Differential Diagnosis of Congenital Alopecia

Lipedematous alopecia is a rare condition of unknown etiology characterized by a thick boggy scalp with varying degrees of hair loss. It is usually seen in adult African-American females, and a case in a 9-year-old was the youngest patient reported thus far. We report on the appearance of this condition in two children, a 6-year-old child and a 10-year-old child. Each presented with congenital patchy hair loss on the occipital area and the left temple. A boggy hairless scalp with soft swelling was detected in both patients. Histological examination showed increased thickness of the subcutaneous fat tissue with a decrease in hair follicles. These features were consistent with a diagnosis of lipedematous alopecia. We report two cases of congenital lipedematous alopecia, which has not been reported previously. Although congenital, these distinct clinical features should be kept in mind in the diagnosis of alopecic hair loss.