银屑病合并大疱性类天疱疮1例

报道寻常型银屑病合并大疱性类天疱疮1例。患者男,56岁,既往银屑病史40余年反复未愈,现全身弥漫性水疱、大疱10 d。皮肤科情况:躯干四肢见粟粒至1元硬币大红斑,上见银白色鳞屑,刮去鳞屑可见发亮的薄膜及点状出血,同形反应阳性。于红斑及正常皮肤上见粟粒至核桃大水疱,疱壁紧张,疱液清亮,尼氏征阴性。组织病理及免疫荧光检查均符合大疱性类天疱疮。诊断:寻常型银屑病合并大疱性类天疱疮。     

大疱及疱疹性皮肤病

20070886大剂量静脉注射用人免疫球蛋白辅助治疗大疱性皮肤病3例；20070887 大疱性类天疱疮皮损糖皮质激素受体α和β表达的研究；20070888 米诺环素联合烟酰胺治疗25例大疱性类天疱疮；20070889 免疫抑制剂联合糖皮质激素治疗寻常型天疱疮疗效观察；[编按]     

激素联合环孢素治疗寻常型银屑病伴发大疱性类天疱疮1例并文献复习

银屑病和大疱性类天疱疮是有显著临床及病理特征的慢性炎症性皮肤病,二者同时发生在同1例患者身上却不多见,在治疗上存在矛盾。笔者应用激素联合环孢素治疗1例寻常型银屑病病史10余年后伴发大疱性类天疱疮的患者,并随访近1年,至投稿时环孢素已停用4个月,激素减量至阿赛松4 mg/d,未见大疱性类天疱疮复发,未见红皮型或脓疱型银屑病出现,寻常型银屑病在停用环孢素后2周后稍有出现。     

45例大疱性类天疱疮初次住院患者临床回顾性分析

目的总结45例初次住院的大疱性类天疱疮患者的临床特点及治疗经验。方法分析2009年8月—2014年12月45例住院治疗的大疱性类天疱疮患者临床表现、组织病理、免疫病理、治疗方案及并发症等方面的情况。结果 45例住院患者86.67%为老年人,均表现为瘙痒性紧张性大疱,普通组织病理表现为表皮下水疱,直接免疫荧光检查见IgG和(或)C3在基膜带呈线状沉积。6例患者转科或自动出院,入院时均存在低白蛋白血症。余39例患者好转或临床治愈出院,总有效率为86.67%。39例患者中9例单纯使用糖皮质激素治疗,30例糖皮质激素联合免疫抑制剂治疗(主要为甲氨蝶呤)。单纯糖皮质激素治疗组的住院天数显著少于糖皮质激素联合免疫抑制剂治疗组(P0.05)。糖皮质激素联合使用免疫抑制剂治疗感染发生率更高(P0.05)。结论系统使用糖皮质激素是大疱性类天疱疮患者住院治疗的首选,视病情联合免疫抑制剂治疗可以增加疗效,但感染发生率会增加,要警惕低白蛋白血症的危险性。     

红斑型天疱疮治疗过程中合并银屑病1例

临床常见银屑病合并自身免疫性疾病,但合并自身免疫性疱病的报道并不多,目前国内外所见的报道都是在寻常型银屑病治疗后出现免疫性疱病的病例,而我科收治的1例红斑型天疱疮患者在治疗过程中出现寻常型银屑病,实属罕见。     

结节性类天疱疮

结节性类天疱疮是大疱性类天疱疮的罕见型,多见于老年患者,主要临床表现是结节、水疱,病理、直接免疫荧光、间接免疫荧光显示大疱性类天疱疮特征。治疗上需系统应用皮质类固醇激素,有时需合并使用免疫抑制剂。免疫印迹试验发现多数PN患者血清与230kD的表皮抗原相结合。     

大疱及疱疹性皮肤病

寻常型天疱疮患者外周血调节性T淋巴细胞数量及Foxp3基因表达；中药联合免疫抑制剂治疗大疱性类天疱疮1例；     

表现为环状红斑水疱的自身免疫性表皮下水疱病25例回顾性分析

目的总结表现为环状红斑水疱的自身免疫性表皮下水疱病的临床、组织病理、免疫血清学及治疗特点。方法回顾性分析2015—2022年就诊于中国医学科学院皮肤病医院表现为环状红斑水疱的自身免疫性表皮下水疱病患者的资料。结果共纳入患者25例, 男10例、女15例, 年龄(39.21 ± 24.65)岁, 包括线状IgA大疱性皮病9例, 大疱性类天疱疮7例, 抗P200类天疱疮5例, 获得性大疱性表皮松解症4例, 20例(80%)有不同程度瘙痒。15例(60%)出现真皮组织嗜酸性粒细胞浸润, 11例(44%)外周血嗜酸性粒细胞计数增加, 7例(28%)同时有嗜酸性粒细胞组织浸润和外周血嗜酸性粒细胞升高。盐裂皮肤-间接免疫荧光及免疫印迹实验显示, 9例同时存在抗基底膜带IgG及IgA抗体, 包括4例大疱性类天疱疮、1例线状IgA大疱性皮病、2例抗P200类天疱疮、2例获得性大疱性表皮松解症;5例同时存在多种抗基底膜带靶抗原的抗体。7例大疱性类天疱疮均予系统糖皮质激素治疗, 其中5例联合免疫抑制剂, 2例联合米诺环素;线状IgA大疱性皮病、抗P200类天疱疮、获得性大疱性表皮松解症患者对抗炎药物及氨苯砜...     

寻常性银屑病合并结节性类天疱疮1例并文献复习

报告1例寻常性银屑病合并结节性类天疱疮。患者男，56岁，既往有银屑病病史8年。全身红斑、风团反复发作1年余，双上肢丘疹伴瘙痒1个月。皮肤科检查：头皮散在红斑，上覆鳞屑；背部及四肢散在红色斑块，边界清楚，上覆银白色鳞屑；躯干及四肢大片红斑、风团；头部、背部及四肢暗褐色丘疹、结节，未见水疱、大疱及脓疱。皮损组织病理检查：角化过度，角化不全，表皮不规则增生，表皮下可见裂隙，真皮浅层血管周围可见淋巴细胞及少量嗜酸性粒细胞浸润。间接免疫荧光：IgG沉积于真表皮交界处。酶联免疫吸附试验（ELISA）：抗大疱性类天疱疮抗原1(BP230)抗体和抗大疱性类天疱疮抗原2(BP180)抗体阳性。诊断：寻常性银屑病合并结节性类天疱疮。     

银屑病并发免疫性大疱性皮肤病11例临床分析

目的:对银屑病并发免疫性大疱性皮肤病患者的临床相关因素及其临床特征进行回顾性分析.方法:收集11例银屑病并发免疫性大疱性皮肤病患者资料,对其临床特征、大疱病的诱发因素、免疫病理以及治疗等方面进行回顾性分析;并对部分患者的特异性致病性抗体进行检测.结果:11例患者中1例为女性,10例为男性,平均年龄(70.55±11.08)岁.患者在银屑病发生后平均(15.36±9.19)年出现大疱性皮肤病;4例患者在出现大疱病前有明确的窄谱中波紫外线(NB-UVB)照射史.7例患者并发天疱疮,4例并发类天疱疮.7例天疱疮患者中4例免疫荧光检查阳性,而阴性的2例患者中外周血检出高滴度抗Dsg1抗体,另有1例结果不详;4例类天疱疮患者中3例患者免疫荧光检查阳性,2例患者抗BP180抗体阳性.这些患者应用小剂量糖皮质激素联合免疫抑制剂,对并发的免疫性大疱病均有较好疗效,对原有的银屑病亦有一定的疗效.结论:银屑病并发免疫性大疱性皮肤病临床上较为罕见,对该病的正确认识,有助于早期合理的临床治疗,尽早控制病情.     

自身免疫性大疱病合并银屑病20例临床分析

收集2011年1月1日至2021年9月30日就诊于四川大学华西医院的自身免疫性大疱病合并银屑病患者的资料,对其临床表现、组织病理、免疫病理、血清学特异性抗体、治疗和转归等进行回顾性分析。共分析20例自身免疫性大疱病合并银屑病患者,男14例,女6例,平均年龄(64.75±13.13)岁,其中17例患者表现为银屑病先于自身免疫性大疱性疾病发生,平均时间(18.03±14.69)年。治疗上采用糖皮质激素和(或)免疫抑制剂治疗,15例患者皮损控制良好,病情较稳定,4例患者失访,1例死亡。自身免疫性大疱病合并银屑病临床少见,临床工作中应警惕两种疾病并发的情况。     

Pemphigus vulgaris with psoriasis vulgaris successfully treated with methotrexate and low‐dose methylprednisolone

Psoriasis and pemphigus are clinically well‐characterized chronic, inflammatory skin diseases. Many case reports have described the coexistence of psoriasis and bullous pemphigoid. However, the present report is about a rare case of pemphigus vulgaris in a patient with psoriasis vulgaris. We had a 68‐year‐old male psoriatic patient who developed blisters lesions and erosions on the trunk and extremities. The histopathology of a blister lesion showed the intraepidermal blisters that contained serous fluid and inflammatory cells. Both of desmoglein core protein 1 antibody and desmoglein core protein 3 antibody were detected. Diagnoses of pemphigus vulgaris and psoriasis vulgaris were made. The patient was treated with methotrexate (12.5 mg/week) and methylprednisone (16 mg/day) after his admission. Two weeks after admission, the patient's lesions gradually subsided. This case reminds us that the therapeutic effect of pemphigus vulgaris may be related to the incidence of psoriasis.     

Concomitant psoriasis and bullous pemphigoid: coincidence or pathogenic relationship?

Psoriasis vulgaris and bullous pemphigoid represent two clinically well-characterized, chronic, inflammatory skin diseases. The concomitant occurrence of these two entities in a patient is rare, and the pathogenic implications of this phenomenon are unknown. We describe a 55-year-old woman with a 25-year history of plaque-type psoriasis who presented with disseminated tense bullae. Skin biopsies showed the typical histologic and immunohistochemical traits of bullous pemphigoid, and she had circulating immunoglobulin G (IgG) antibodies against the basement membrane zone, specifically the BP180 antigen. The bullous eruption was successfully treated with oral methylprednisolone and dapsone. Bullous pemphigoid is the autoimmune blistering disease that has most often been associated with psoriasis. Forty cases have been described in the literature. Classical psoriasis and psoriasis associated with bullous pemphigoid are identical. The pathogenic relationship between psoriasis and bullous pemphigoid is unclear. It has been postulated that the autoimmune process responsible for bullous pemphigoid lesions may be induced by ultraviolet light therapy, topical corticosteroids, and/or the inflammatory processes that occur in psoriasis. Immunomodulatory therapy may positively influence shared as well as distinct inflammatory mechanisms in patients who have psoriasis and bullous pemphigoid.     

Bullous pemphigoid. Occurrence in psoriasis treated with psoralens plus long-wave ultraviolet radiation.

The occurrence of bullous pemphigoid during treatment for psoriasis has been described in the literature. We saw a case of psoriasis that was complicated by bullous pemphigoid in a patient receiving orally administered psoralen followed by long-wave ultraviolet radiation (PUVA) therapy. In our patient the localization of bullous lesions to psoriatic plaques demonstrates that the PUVA-treated psoriatic skin may have a decreased threshold for the development of clinical bullous pemphigoid. This suggests factors other than simple coexistence of the two diseases. Therapy with PUVA might induce bullous pemphigoid in psoriasis, either primarily or by facilitating the expression of a previously existing subclinical form of the bullous disorder.     

Possible paraneoplastic syndrome case of bullous pemphigoid with immunoglobulin G anti‐BP180 C‐terminal domain antibodies associated with psoriasis and primary macroglobulinemia

A 61‐year‐old Japanese man developed bullous skin lesions during topical therapy for psoriasis vulgaris. Physical examination demonstrated numerous tense bullae and scaly erythemas on the trunk and extremities. Histopathology of the skin biopsy demonstrated subepidermal bullae and lymphocytic infiltration with eosinophils in the dermis. Direct immunofluorescence revealed linear deposits of immunoglobulin (Ig)G, IgA and C3 along the basement membrane zone. Indirect immunofluorescence of 1 mol/L NaCl‐split skin showed IgG reactivity with both epidermal and the dermal sides. IgM reactivity with both the epidermal and dermal sides was also detected. Enzyme‐linked immunosorbent assays showed negative results for both BP180 and BP230. Immunoelectrophoresis of serum and bone marrow aspiration revealed underlying primary macroglobulinemia with M‐proteinemia of IgM‐κ type. Immunoblot analysis revealed IgG, but not IgM, antibodies to recombinant protein of BP180 C‐terminal domain. We diagnosed the present case as bullous pemphigoid with IgG anti‐BP180 C‐terminal domain autoantibodies associated with primary macroglobulinemia and psoriasis vulgaris. Systemic administration of prednisolone 30 mg/day resulted in dramatic improvement of both bullous and psoriatic skin lesions. When the bullous and psoriatic lesions relapsed, DRC chemotherapy (dexamethasone, rituximab and cyclophosphamide) for macroglobulinemia was performed. Then, the psoriatic lesions improved and the bullous lesions disappeared. We suggested that the present case may be paraneoplastic syndrome of bullous pemphigoid associated with primary macroglobulinemia and psoriasis vulgaris.     

Delayed onset of bullous pemphigoid after PUVA and sunlight treatment of psoriasis

The coexistence of bullous pemphigoid and psoriasis has previously been noted. In most patients, the bullous lesions start during PUVA or UVB therapy of psoriasis. We report on a psoriatic patient who developed bullous pemphigoid approximately three to four weeks after discontinuing PUVA treatment, and then three to four weeks after exposure to natural sunlight. Delayed induction of bullous pemphigoid has not been previously reported, and it raises the question of ultraviolet therapy inducing subclinical or latent bullous pemphigoid in psoriatic patients.     

A case of bullous pemphigoid limited to psoriatic plaques

Psoriasis occurs with increased incidence in patients with bullous pemphigoid (BP). In this article, we describe the seventh reported English literature case in which the bullous lesions were limited to psoriatic plaques, and we discuss the pathophysiologic mechanisms that might explain this phenomenon. Treatment with acitretin quickly cleared both psoriatic and bullous lesions, suggesting a direct link between the psoriatic inflammatory process and the evolution of bullous lesions.     

Evidence of an association between bullous pemphigoid and psoriasis

The medical records of 62 consecutive patients with bullous pemphigoid and 62 case-matched leg ulcer controls were examined to determine whether psoriasis and bullous pemphigoid are associated. Psoriasis occurred in seven of the pemphigoid patients (11%) but in none of the controls. The prevalence of psoriasis in the pemphigoid sample was significantly higher than expected (P less than 0.01, Poisson distribution). This difference, together with the clinical course, suggests that there may be an association between pemphigoid and psoriasis.     

A biological approach in a patient with psoriasis and bullous pemphigoid associated with losartan therapy

Several cases of psoriasis associated with bullous disorders have been reported, and it is clearly recognized that bullous pemphigoid (BP) is the most common bullous disorder observed in association with psoriasis, especially after ultraviolet (UV)B and psoralen UVA therapy. Moreover, other medications have been repeatedly reported to induce bullous diseases, especially pemphigus vulgaris. We report for the first time a case of BP possibly induced by losartan, an angiotensin II antagonist, in a patient with a severe psoriatic background. Angiotensin II type 1 receptor antagonists belong to a new class of drug for hypertension or congestive heart failure with established efficacy and few side-effects. Coexistence of psoriasis vulgaris with bullous diseases represents also a difficult therapeutic challenge. This rare case of psoriasis and generalized BP triggered by a sartan drug was treated with rituximab and etanercept.     

Psoriasis vulgaris coexistent with epidermolysis bullosa acquisita

Summary Autoimmune bullous diseases, such as bullous pemphigoid or pemphigus vulgaris. occasionally develop in psoriatic patients. In addition, a novel subepidermal bullous disease with autoantibodies against a lower lamina lucida antigen of 200kDa has recently been reported in association with psoriasis. We describe here a patient with psoriasis vulgaris who developed epidermolysis bullosa acquisita (EBA). Direct immunofluorescence revealed linear deposition of IgCl and C3 at the basement membrane zone. The patient's serum bound to the dermal side of salt-split normal human skin. However, immnumohlol analysis demonstrated that the patient's serum reacted with an EBA antigen of 290 kDa. EBA should be included in the list of autoimmune diseases associated with psoriasis vulgaris.