良性苔藓样角化症和扁平苔藓临床及病理比较分析

良性苔藓样角化症,又名扁平苔藓样角化症(lichen planus like keratosis,LPLK),临床上不多见。我科自1988年以来遇到14例患者,临床诊断各异,均由病理确诊为LPLK。因该病病理与扁平苔藓(lichen planus,LP)相似,故又收集了同期48例LP患者的资料以作比较。     

角化性皮肤病

毛囊角化病样发疹性汗管瘤1例，扁平苔藓样角化病2例，持久性豆状角化过度症1例，乳头乳晕角化过度症伴黑棘皮病1例，残毁性掌跖角皮症伴鱼鳞病1例，     

慢性苔藓样角化病5例临床病理分析

报告5例慢性苔藓样角化病。男4例,女1例,年龄13～50岁。3例皮损为带状或网状分布的紫红色丘疹,2例皮损呈疣状。皮损多无自觉症状,但有1例患者皮损伴有剧烈的瘙痒。组织病理改变主要为表皮角化过度伴局灶性角化不全,局部颗粒层增厚,棘层不规则肥厚,表现为棘层肥厚和萎缩相间,基底细胞液化变性。真皮浅层炎性细胞呈带状浸润,主要为淋巴细胞和组织细胞,并可见少量嗜酸性粒细胞和浆细胞。4例患者的毛囊和真皮血管周围也有炎性细胞浸润。本病需与扁平苔藓和扁平苔藓样角化病等鉴别。     

扁平苔藓样角化病2例

报告2例扁平苔藓样角化病。均为老年患者,分别因右肩部黑褐色丘疹10年余及左大腿内侧淡褐色斑50年,增大,颜色加深伴瘙痒1个月就诊,皮疹均为单发,组织病理检查为表皮角化过度,颗粒层增高,基层灶性液化变性,真皮浅层可见带状炎症细胞浸润,手术切除皮损后治愈。     

日光性雀斑样痣、脂溢性角化病及扁平苔藓样角化病皮肤镜特征专家共识

【摘要】 日光性雀斑样痣、脂溢性角化病及扁平苔藓样角化病是常见的良性表皮增生性疾病,其皮肤镜特征对于明确诊断、与其他皮肤肿瘤相鉴别、避免不必要的活检和手术以及动态监测皮损变化等都有一定帮助。本共识对这3种疾病的皮肤镜特征进行了总结。日光性雀斑样痣的皮肤镜特征主要为皮损边界清晰、虫蚀状边缘、模糊的色素网、指纹模式、棕色均质模式、假性网络。脂溢性角化病的皮肤镜特征主要为皮损边界清晰、粟粒样囊肿、粉刺样开口、脑回状模式、发夹样血管、摇晃试验中皮损整体移动。扁平苔藓样角化病的皮肤镜特征主要为胡椒粉样或颗粒模式以及周围可见日光性雀斑样痣、脂溢性角化病或光线性角化病的皮肤镜特征。     

痣样乳头乳晕角化过度症四例

目的 报道4例痣样乳头乳晕角化过度症.方法 收集和分析4例痣样乳头乳晕角化过度症患者的临床资料和组织病理学资料.结果 4例患者中,女3例,男1例,平均年龄32岁,平均病程4.5年,均表现为乳头和(或)乳晕角化过度和疣状增生.组织病理检查:表皮角化过度,乳头瘤样增生,皮突延长.结论 痣样乳头乳晕角化过度症是乳头乳晕角化过度症的一种亚型,临床较为少见,好发于年轻女性,临床和组织学都有一定特点.     

类天疱疮样扁平苔藓1例

目的：报告和分析一例少见的类天疱疮样扁平苔藓病例。方法：取患背部皮损活检组织部分行组织病理和免疫病理检查。结果：活检组织切片,HE染色示：表皮角化过度伴角化不全,颗粒层不规则增厚,基底细胞液化严重已融合成表皮下大疱,无大疱区域表皮和真皮分界不清。有较多淋巴细胞在此区域以及血管周浸润,可见“色素失禁”现象。直接免疫荧光显示基底膜有IgG、C3、IgM呈线状沉积。符合类天疱疮样扁平苔藓。经治疗后痊愈,随访一年未见复发。结论：类天疱疮样扁平苔藓临床表现和病理结果不同于大疱性扁平苔藓和大疱性类天疱疮,是一个独立的疾病。可采用灰黄霉素、四环素和烟酰胺治疗。     

孤立性扁平苔藓样角化病

孤立性扁平苔藓样角化病(Solitary lichenplanus-like keratosis,SLPLK)与扁平苔藓、红斑狼疮、光泽苔藓、苔藓样药疹、热带扁平苔藓都属于苔藓样组织反应性疾病。本病在组织学方面与扁平苔藓的一种单发性角化性疾病极其相似。现将最近5年间我们对此病的8例组织学与临床所见报告如下:     

慢性苔藓样角化病的研究进展

慢性苔藓样角化病为一种少见的角化性皮肤病,临床上表现为面部、躯干、四肢角化性丘疹、斑块,需要与扁平苔藓、扁平苔藓样角化病,红斑狼疮等相鉴别。本病治疗困难,局部使用钙泊三醇、PUVA、NB-UVB、光动力,或口服维A酸类药物,可改善病情。本文对慢性苔藓样角化病的病因、发病机制、临床表现、诊断和治疗的研究进展进行综述。     

阿维A诱发药疹1例

正阿维A可抑制角质形成细胞增殖并调节其分化,临床上可用于治疗角化异常性皮肤病,如银屑病、扁平苔藓、扁平苔藓样角化病、汗孔角化病等。我们应用阿维A治疗1例经组织病理确诊的扁平苔藓患者,治疗20 d后出现皮疹,考虑为阿维A所诱发,由阿维A诱发的药疹国内外罕见报道,现报告如下。     

Large-cell acanthoma is a solar lentigo.

On the basis of a study of 54 specimens each of large-cell acanthoma, solar lentigo, reticulated seborrheic keratosis, and lichen planus-like keratosis, it is concluded that clinically, histopathologically, and biologically, large-cell acanthoma is a variant of solar lentigo, and solar lentigo (including the large-cell variant) is a stage in the evolution of reticulated seborrheic keratosis and of lichen planus-like keratosis.     

A case of lichen planus-like keratosis: deposition of IgM in the basement membrane zone

An 81-year-old woman presented with a round erythematous macule with keratotic scales on her left hand. The skin specimen histologically showed hypergranulosis and apoptotic keratinocytes in the epidermis with lichenoid infiltration of lymphocytes. Parakeratosis seen in the hyperkeratotic cornified layer indicated lichen planus-like keratosis, as distinguished from lichen planus. Direct immunofluorescence study revealed the linear deposition of IgM in the basement membrane zone; IgG, IgA and C3 were not detected.     

Lentigo senilis and its evolutions.

Histologic studies have shown the evolution of lentigo senilis and have established the relationship between lentigo senilis, solitary lichen planus-like keratosis, and the reticulated form of seborrheic verruca. Histologic differentiation can be made between lentigo senilis and the early light-brown stage of lentigo maligna.     

Documented evolution of a solar lentigo into a solitary lichen planus-like keratosis

The purpose of this communication is to report the evolution of a solar (senile) lentigo into a solitary lichen planus-like keratosis (SLPLK). This case is unique because this evolution was documented by biopsies taken from the same lesion nearly 5 years apart. The pathogenesis of SLPLK is discussed.     

Demonstration of antibody to 230 kDa bullous pemphigoid antigen in lichen planus-like keratosis.

We describe a 67-year-old man with lichen planus-like keratosis associated with anti-230 kDa bullous pemphigoid antigen (BPAG1) autoantibody. The patient had noticed solitary dark brown macule more than 6 years previously on his left chest. Histological findings showed hypergranulosis, irregular acanthosis, liquefaction degeneration of basal cells, band-like infiltration of lymphocytes at the subepidermal portion, and a cleft at the basement membrane zone (BMZ), resulting in the formation of subepidermal blisters. Direct immunofluorescence findings of perilesional skin showed a linear deposition of IgG at BMZ. On indirect immunofluorescent study using normal human skin, circulating IgG autoantibody to BMZ was present in the patient's serum at a titer of 1:80. The antigen located on the epidermal site of normal skin split by 1M NaCl was reacted with the patient's serum. Immunoblot analysis using epidermal extracts demonstrated the presence of IgG antibody directed to BPAG1 in the patient's serum. These observations suggest that the presence of an antibody to BPAG1 could be caused by the damage of basal cells following lichen planus-like keratosis.     

Key points in dermoscopic differentiation between lentigo maligna and solar lentigo

A clinical diagnosis of lentigo maligna at an early stage is often difficult even for experienced dermatologists. Differential diagnoses would include solar lentigo, early lesions of seborrheic keratosis, lichen planus-like keratosis, pigmented actinic keratosis and melanocytic nevus. Dermoscopy has been shown to have higher diagnostic accuracy, especially in the diagnosis of pigmented skin lesions, in the past two decades. To aim of the present study was to review the diagnostic key points on dermoscopy in the published work to differentiate lentigo maligna from other differential diagnoses and reassess these important features on dermoscopy for specificity by describing the findings in detail. Diagnostic key points for lentigo maligna/lentigo maligna melanoma on dermoscopy are asymmetrical pigmented follicular openings, rhomboidal structures, annular-granular structures and gray pseudo-network. Lentigo maligna, at first, seems to occur as asymmetrical pigmented follicular openings and/or annular-granular structures, then expand and develop into the rhomboidal structures. Annular-granular structures and gray pseudo-network seem to be observed also in regressive areas of solar lentigo/initial seborrheic keratosis, lichen planus-like keratosis and pigmented actinic keratosis. The four important criteria on dermoscopy for the diagnosis of lentigo maligna have been reviewed, and the former two criteria seem to be more specific, but it might be difficult to recognize these findings without misinterpretation. The latter two seem to be not so specific as they would also be demonstrated in other pigmented epidermal lesions, although the distribution of the structures in these disorders would be inclined to be more homogeneous than that of lentigo maligna.     

Lentigo Maligna: Review of Salient Characteristics and Management

Lentigo maligna is a melanocytic neoplasm, often regarded as ‘melanoma in situ,’ which may progress to lentigo maligna melanoma. Lentigo maligna clinically presents as a pigmented, asymmetric macule that originates on the head and neck and spreads slowly. The preferred method for diagnosing lentigo maligna is excisional biopsy. Histology shows proliferation of atypical melanocytes at the epidermal–dermal junction in small nests or single cells. The differential diagnosis includes solar lentigo, seborrheic keratosis, lichen planus-like keratosis, pigmented actinic keratosis, and melanocytic nevus. Stains used in diagnosis include hematoxylin and eosin, HMB-45, MART-1/Melan-A, Mel-5, and S-100. Surgical excision is the preferred treatment for lentigo maligna. Second-line techniques include medical (topical imiquimod) and destructive therapy.