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1.
报道阿达木单抗成功治疗一例坏疽性脓皮病,并进行文献复习。患者,男,53岁。左股内侧红斑、丘疹6个月,溃疡3个月。组织病理示:符合坏疽性脓皮病。给予雷公藤多苷片、沙利度胺片治疗3天,仍有新发红斑、丘疹,于第3天、第10天分别给予皮下注射阿达木单抗80 mg、40 mg,后每2周皮下注射阿达木单抗40 mg,注射第4剂阿达木单抗时溃疡已愈合。半年后随访,皮损未复发。  相似文献   

2.
患者男,14岁,枕部、双侧腋窝、腹股沟出现红色疼痛性丘疹、结节、脓肿半年。皮肤科情况:颈部、双侧腋窝和腹股沟处可见不规则的天鹅绒样增厚的色素沉着斑块,散在蚕豆大小的暗红色结节,部分结节破溃,表面伴有脓性分泌物,部分贯通形成窦道及瘘管。男孩身高140 cm,体重75 kg, BMI值38.3 kg/m2(肥胖)。实验室检查显示胰岛素抵抗和尿酸增加。诊断:毛囊闭锁三联征;肥胖相关性黑棘皮病;胰岛素抵抗;高尿酸血症。予糖皮质激素0.3 mg/(kg·d)治疗5 d、异维A酸20 mg/d治疗1个月、光动力治疗3次、局部创面护理并饮食控制治疗,但皮损改善不明显,且出现新病灶。遂采用肿瘤坏死因子(TNF-α)抑制剂阿达木单抗联合异维A酸20 mg/d及局部创面护理,阿达木单抗3次(80 mg、40 mg、40 mg, 1次/周)治疗后,病灶迅速消减,不再出现新病灶,但是患者出现全身骨痛,不得已终止阿达木单抗治疗。停止阿达木单抗治疗后1周,骨痛症状逐渐消退,偶有新发皮损。该患者仍然在随访中。  相似文献   

3.
【摘要】 目的 回顾性分析阿达木单抗联合阿维A治疗儿童泛发性脓疱型银屑病的临床疗效及安全性。方法 选取2019年10月至2020年8月就诊于天津市儿童医院皮肤科的5例泛发性脓疱型银屑病患儿,入院予口服0.5 mg·kg-1·d-1阿维A,待相关检查结果回报后,第0周(首剂)、第1周及此后每2周给予皮下注射阿达木单抗20/40 mg,日本皮肤科协会(JDA)评分改善50%后阿维A减量至0.3 mg·kg-1·d-1,改善75%后停用阿维A,于阿达木单抗治疗0、1、2、4、8、12、24周时观察并记录患者病情,治疗过程中监测不良反应。结果 5 例患者均接受至少40周疗程的药物治疗,2周时3例达JDA50;4周时4例达JDA75,1例JDA100;8周时5例均达到JDA100。至2021年6月,5例患儿均已接受至少40周随访,期间病情未见反复,均未出现感染或恶性肿瘤等严重不良反应。结论 阿达木单抗联合阿维A治疗儿童泛发性脓疱型银屑病起效较快,安全性较高。  相似文献   

4.
【摘要】 报道2017年8月至2019年12月第四军医大学西京皮肤医院收治的4例化脓性汗腺炎,年龄20 ~ 45岁,均为男性,皮损表现为腋窝、臀部、腹股沟的窦道、脓肿、瘢痕,Hurley分期Ⅱ~Ⅲ期。既往使用抗生素、糖皮质激素、维A酸类药物、中药等多种治疗方案,改善均不明显。予静脉滴注英夫利西单抗5 mg/kg,第0、2、6周各1次,后每间隔8周1次;或皮下注射阿达木单抗,第0、2周各80 mg/次,后每间隔2周40 mg/次。2例静脉滴注英夫利西单抗后出现输液反应,改用阿达木单抗。3例达到化脓性汗腺炎临床反应(HiSCR),1例无效。  相似文献   

5.
目的 观察阿达木单抗治疗儿童中重度斑块状银屑病的疗效及安全性。方法 选取2020年3月-2021年7月就诊于新疆维吾尔自治区人民医院皮肤性病科的11例中重度斑块状银屑病患儿。体重<30 kg者,首次给予皮下注射阿达木单抗20 mg,之后1、3、5、7、9、11、13、15周注射20 mg;体重≥30 kg者,首次治疗予皮下注射阿达木单抗40 mg,之后第1、3、5、7、9、11、13、15周注射40 mg,于第4、8、12、16周时记录患儿银屑病皮损面积和严重度指数(PASI)及儿童皮肤病生活质量指数(CDLQI)。治疗过程密切监测不良反应。结果 治疗16周PASI及CDLQI与治疗前比较均显著下降(P<0.05)。4周时,4例PASI改善率可达50%(PASI50);8周时,7例达PASI75;12周时,11例均达PASI75,其中5例达PASI90;16周时,8例达PASI90,其中1例达PASI100。11例患者均未发生感染、肿瘤等严重不良反应,其中1例患儿出现肝功能轻度异常。结论 隔周皮下注射阿达木单抗治疗儿童中重度银屑病临床疗效显著,同时需密切关注不良反应的发生。  相似文献   

6.
【摘要】 目的 观察阿达木单抗治疗重度斑块状银屑病的疗效及安全性。方法 选取2018年6月至2019年4月就诊于河南省人民医院皮肤科的20例重度斑块状银屑病患者,首次治疗予皮下注射阿达木单抗80 mg,之后第1、3、5、7、9、11周注射40 mg,于第4、8、12周时观察并记录患者银屑病皮损面积和严重度指数(PASI),采用反射式共聚焦显微镜观察皮损的演变情况。治疗过程中监测不良反应。结果 4周时,12例PASI改善率达50%(PASI50);8周时,14例达PASI75;12周时,20例达PASI 75,其中5例达PASI90,2例达PASI100。治疗前,RCM下皮损区域基底层黑素较皮损周围正常皮肤减少,治疗4周时较治疗前逐渐恢复;12周时基本恢复正常水平。20例患者均未发生感染、肿瘤等相关不良反应。结论 隔周皮下注射阿达木单抗治疗重度银屑病临床疗效显著,相关不良反应少。  相似文献   

7.
目的:观察阿达木单抗联合甲氨蝶呤治疗银屑病的临床疗效。方法:应用阿达木单抗联合甲氨蝶呤治疗3例中重度银屑病患者,对其皮损及关节治疗的有效程度进行临床观察。结果:3例患者的皮损及关节症状均明显改善,治疗8周后患者皮损改善可达PASI 50以上,治疗18周可达PASI 75以上。结论:阿达木单抗联合甲氨蝶呤治疗银屑病,对患者皮肤损害有明显疗效,同时可改善银屑病合并结膜炎等不适症状。  相似文献   

8.
本文报道种球蛋白联合阿达木单抗治疗单纯疱疹病毒(HSV)相关的复发性多形红斑1例并复习相关文献。患儿,男,9岁。口唇反复糜烂、渗出15个月,全身反复红斑8个月。皮肤科查体:口唇糜烂,背部、四肢散在暗红色斑片,局部周边可见松弛水疱。病理检查符合多形红斑,单纯疱疹病毒I型IgG滴度444.72 RU/mL。诊断为单纯疱疹病毒感染相关多形红斑,给予伐昔洛韦抗病毒治疗的同时,给予阿达木单抗联合人免疫球蛋白治疗,2周后皮损消退,单纯疱疹病毒I型IgG滴度明显下降。  相似文献   

9.
目的:明确阿达木单抗治疗斑块型银屑病患者的疗效.方法:收集2020年9月至2021年3月经阿达木单抗治疗的斑块型银屑病患者,分析经阿达木单抗治疗0、4、8、12周的PASI评分变化及相关性.结果:共收集20例患者,其中1例中断治疗,19例患者中伴和不伴代谢综合征患者分别为11例和8例.经阿达木单抗治疗12周后,19例患...  相似文献   

10.
目的 观察阿达木单抗治疗重度银屑病的临床疗效及安全性。方法 在2015 年12月至2017年8月就诊于南京医科大学附属无锡第二医院的重度银屑病患者中选择传统治疗无效的患者14例,给予阿达木单抗单药皮下注射治疗,初始剂量80 mg,1周时给予40 mg,以后每2周给予40 mg,分别于第4、8、12周时记录患者银屑病皮损面积和严重度指数(PASI)及疾病严重程度评分(PGA)改善情况,观察临床疗效及药物不良反应。合并关节病性银屑病患者的关节改善采用美国风湿病协会(ACR)有关类风湿关节炎改善的ACR20作为评价指标。结果 14 例患者均接受至少12 周疗程的药物治疗。4 周时,8 例达PASI 50;8周时,8例达PASI 75,其中2例达PASI 90;12周时,14例达PASI 75,其中7例达PASI 90,3例达PASI 100。治疗前14例患者PGA为(4.92 ± 0.02)分,12周时下降至(1.21 ± 0.02)分。3 例合并关节病性银屑病患者,关节症状改善明显,8周时2例达ACR20,12周时3例达ACR20。所有患者均未出现严重感染或恶性肿瘤等严重的药物不良反应。3例患者出现荨麻疹,给予抗组胺药后症状缓解。结论 阿达木单抗隔周皮下注射治疗重度银屑病疗效显著,不良反应较少,为传统治疗无效的重度银屑病患者的治疗提供了新选择。  相似文献   

11.
患者,男,65岁.因腹泻1个月,全身红斑、大疱、血疱5天伴发热入院.皮肤组织病理示:表皮角化过度,局部表皮缺失,表皮下疱形成,真皮乳头高度水肿,真皮浅中层多数中性粒细胞浸润.结肠组织病理特征符合克罗恩病改变.结合临床及病理表现诊断为大疱性Sweet综合征合并克罗恩病.治疗:给予甲泼尼龙40 mg/d,发热逐渐消退,皮疹...  相似文献   

12.
A 56-year-old-man who had refractory anemia with an excess of blasts underwent an allogeneic peripheral blood stem cell transplantation (PBSCT) from his brother after preparation with melphalan and fludarabin. He received GvHD (graft-vs.-host disease) prophylaxis with cyclosporine from day -1 at a daily dose of 5 mg/kg of body weight. The daily dosage was tapered gradually from day +20. On post-PBSCT day 68 he developed acute cutaneous GvHD grade 3 and acute gastrointestinal GvHD grade 2-3, which was resolved with a daily dose of 1 mg/kg of body weight of prednisone. The patient was discharged in good clinical condition and without signs of GvHD, and he started tapering his immunosuppressive treatment. By day 160 he developed oral lichen planus-like changes, with several reticulate white lesions on the oral mucosa. A biopsy specimen was microscopically consistent with lichenoid GvHD (Fig. 1). By day 150 after PBSCT, when he was being treated with CsA 100 mg once daily and prednisone 10 mg once daily, his fingernails started to grow abnormally and gradually became dystrophic and painful. Two months later his toenails became similarly affected. Although affecting all finger and toe nails, the lesions were especially important in both thumbs. Physical examination revealed multiple findings on his nails (Fig. 2): thickening, fragility, onycholysis, longitudinal striations, and even pterygium. The micological cultures were negative. A biopsy specimen showed an sparse papillary dermis lymphoid infiltrate with focal exocytosis and presence of isolated multiple necrotic keratinocytes (Fig. 3). These findings were interpreted as a lichenoid GvHD with oral and nail involvement. The patient did not have other associated cutaneous lesions. He did not develop signs or symptoms consistent with hepatic GvHD. In May 2000 thalidomide was added to the immunosuppressive therapy, at a daily dose from 100 to 300 mg according to tolerance (constipation, sedation, ...). The lesions on the oral mucous showed a substantial improvement, but the nail changes remained more or less stable. Thalidomide was discontinued after 7 months because the patient displayed numbness and tingling in the hands and feet consistent with a peripheral neuropathy. Twenty days later he stopped taking thalidomide and the oral lichenoid lesions worsened, resulting in difficulty in eating. He also developed periungueal erythema, swelling and intense pain after minimal trauma. The daily dose of prednisone increased to 20-30 mg with moderate improvement. However, the dose could not be increased because of the secondary immunosuppressive effects. Twenty-three months post-PBSCT the patient remains with intense oral and nail lichenoid lesions.  相似文献   

13.
患者,男,69岁,皮损表现为躯干、四肢密集或散在紫红色扁平斑丘疹40天,以四肢末端为著,伴瘙痒,近2年间断口服酒石酸美托洛尔片(β受体阻滞剂)。病理检查符合扁平苔藓样药疹诊断。停用酒石酸美托洛尔片,给予口服阿维A,30mg,日1次,共1个月,外用3%水杨酸软膏、0.1%他克莫司软膏,皮损消退,效果明显。  相似文献   

14.
报道一例使用阿达木单抗治疗泛发型环状肉芽肿并复习相关文献.患者,男,76岁.躯干、四肢泛发型环状红斑、丘疹,境界清楚,组织病理示:表皮轻度增生,真皮内见上皮样肉芽肿,中央胶原纤维变性、坏死,肉芽肿周围组织细胞、淋巴细胞浸润,胶原纤维增生,胶原间散在单一核细胞浸润.诊断为泛发型环状肉芽肿.第0周给予阿达木单抗注射液80 ...  相似文献   

15.
A 40-year-old man, an established pemphigus vulgaris patient in remission, reported with recurrence of extensive blisters over the skin and the mucous membranes. In addition, he had grand mal epilepsy for which he was being given 200 mg diphenylhydantoin and 60 mg phenobarbitone. In view of the severity of the condition, he was admitted and was administered 100 mg (20 tablets) of prednisolone daily in addition to antiepileptic treatment. Despite this, there was hardly any perceptible amelioration of his clinical picture. Instead, fresh lesions continued to add to its severity, resulting in extensive erosions of the skin and mucous membranes. We were impelled to increase the dose to 30 mg dexamethasone (=300 mg prednisolone), a dose so far never given to any other pemphigus patient in our institution. This too had no effect. At this point, interaction of antiepileptic drugs and steroids was believed to be responsible. Accordingly, antiepileptic drugs were gradually tapered over 7 days. Following their discontinuation, a dramatic improvement was noticed in the next 72 hours, which was characterized by the absence of new lesion and regression of old lesions. The further course of the disease was uneventful, and the lesions cleared completely in 15 days. Corticosteroids were gradually tapered off under the cover of cyclophosphamide 100 mg daily.  相似文献   

16.
Background While adalimumab is a mainstay of treatment for moderate to severe chronic plaque psoriasis, the data regarding optimal treatment intervals for therapeutic maintenance are limited. Objective We compared the clinical efficacy of biweekly maintenance administration of adalimumab with that of monthly treatment. Methods 17 psoriasis patients treated with adalimumab 40 mg every other week with initial loading dose of 80 mg until week 24 were assigned to the maintenance therapy with adalimumab 40 mg either every other week (n = 7), or every month (n = 10). The treatment efficacy was evaluated by the proportion of patients who achieved PASI 75 from the baseline at weeks 36, 48 and 60. There was no selection bias between the two groups. Results At week 24, all the patients except for one in each group achieved PASI 75. In both groups, all the patients who achieved PASI 75 at week 24 maintained PASI 75 responses at week 60. Regarding two patients who did not achieve PASI 75 at week 24, one biweekly treated patient experienced a gradual increase in therapeutic response while one monthly treated patient showed exacerbation after week 24. Conclusion Monthly adalimumab treatment seems to be a reasonable treatment option for patients who responded well to initial standard adalimumab treatment for 24 weeks. Since there are several limitations in this study, including the number of patients, observation period, and patients’ characteristics, large randomized controlled trials are needed to confirm these results.  相似文献   

17.
17 children suffering from neurodermatitis, aged 2 to 14 years, were treated with ketotifen at a dosage of 1 mg twice daily. In 7 children polyvalent therapy was given. Ketotifen therapy produced a pronounced alleviation of the itching within only two weeks and the patients became entirely itching free after 20 days on an average. The improvement of skin lesions appeared after two months of treatment. Patients became entirely skin lesions free between seven and nine months. In three patients the deterioration of skin lesions was triggered with infection. With regard to long-lasting of Ketotifen therapy, the side effects were not observed.  相似文献   

18.
The pathogenesis of erythema nodosum leprosum (ENL) involves both immune complex deposition and dysfunction of cell mediated immunity. Tumour necrosis factor-alpha (TNF-alpha) plays an important role in its pathogenesis. Thalidomide and corticosteroids are the mainstay of treatment for ENL. However, there are often severe limitations to their use. We report a case of recurrent ENL treated successfully with azathioprine. A 15-year-old unmarried girl with lepromatous leprosy had recurrent ENL for 2 years. She was treated with WHO-MB MDT and prednisolone in doses of 40-90 mg a day for 2-12 weeks. Her condition was inadequately controlled. The patient was therefore treated with thalidomide 300 mg and prednisolone 40 mg. The symptoms subsided after 5 days and ENL lesions healed in 2 weeks. Prednisolone was reduced by 10 mg per week and stopped, while thalidomide was reduced to 100 twice daily after 4 weeks. Azathioprine 100 mg (2 mg/kg per day) daily orally was added to prevent recurrences. Thalidomide was further reduced and stopped after another 4 weeks while she continued with azathioprine in the same doses for 8 months. There was no recurrence of ENL lesions and no side effects of the therapy. MB-MDT was stopped 1 year ago, and she is on follow-up without any relapse. Azathioprine, therefore, appears to be an effective and safe drug to prevent recurrences of ENL.  相似文献   

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