药物超敏综合征8例临床分析

分析8例药物超敏综合征患者的临床特点和治疗。结果：8例患者均以发热、度疹为首发症状，于用药后2～6周发生；其中伴浅表淋巴结肿大者4例，肝功能损害者8例，肾损害者3例，8例患者的自细胞均升高，嗜酸粒细胞升高7例，4例出现异型淋巴细胞。致敏药物分别为：解热镇痛剂3例、磺胺类2例、卡马西平2例、别嘌醇1例。皮损类型为：重症多形红斑型（Stevens—Johnson综合征）3例，麻疹样型2例，剥脱性皮炎型2例，中毒性表皮坏死松解症1例。1例自动出院、3例好转、4例痊愈出院。糖皮质激素与免疫球蛋白联用是治疗药物超敏综合征的有效疗法，中西医结合疗法可能有助于缩短病程及糖皮质激素用药时间。     

药物超敏综合征23例临床分析

回顾分析23例药物超敏综合征(DHS)的临床资料.总结药物超敏综合征的临床特点及治疗.结果:23例患者均有发热、泛发性皮疹、白细胞升高,20例浅表淋巴结肿大,19例肝功能损害,21例嗜酸粒细胞升高,10例见异型淋巴细胞.18例患者糖皮质激素1.5～2 mg/(kg·d)能控制病情,有异型淋巴细胞者加用更昔洛韦.DHS应与传染性单核细胞增多症鉴别,除用糖皮质激素治疗外,酌情加用免疫球蛋白和更昔洛韦.     

药物超敏反应综合征55例临床分析

目的分析55例药物超敏反应综合征的临床表现、实验室检查。方法回顾分析55例药物超敏反应综合征患者的临床资料。结果 41例可确定可疑致敏药物,最常见的前三位是抗菌药、解热镇痛药、抗惊厥药。51例患者以皮疹和发热为首发症状,发疹潜伏期为10~42天。其中肝功能损害者48例,血嗜酸粒细胞增多者39例,白细胞升高者24例,肾损害者18例,肺损害者11例,伴浅表淋巴结大者9例。治疗多单独使用糖皮质激素或联合丙种球蛋白。结论药物超敏反应综合征潜伏期长,如在临床用药过程中出现发热、血细胞异常、全身性皮疹和内脏损害者特别是迟发性和长时间的肝功能异常应高度警惕其发生,可使用足量糖皮质激素或联合丙种球蛋白治疗。     

药物超敏综合征21例临床表现及治疗转归

目的：探讨药物超敏综合征的临床表现及治疗。方法：回顾性分析我科病房收治的2l例药物超敏综合征患者的诊疗情况。结果：21例中可疑致敏药物分别为别嘌呤醇13例,卡马西平5例,解热镇痛药（对乙酰氨基酚）1例,甲硝唑1例,别嘌呤醇加卡马西平1例。发疹潜伏期为13～45d,均伴发热,肝功能异常。同时伴有浅表淋巴结肿大16例,白细胞增高17例,急性肾功能衰竭1例,糖皮质激素治疗均有效。20例患者痊愈或好转出院,1例皮疹控制后因突发脑血管意外,家人放弃治疗后自动出院次日死亡。结论：临床用药过程中出现发热、全身皮疹伴有内脏损害、血液系统损害等应警惕药物超敏综合征的发生。治疗上早期、足量糖皮质激素或联合大剂量免疫球蛋白有效,无常规应用抗生素必要,但要注意患者相关病毒学的检测及作相应抗病毒治疗。     

药物超敏综合征误诊传染性单核细胞增多症1例

报告药物超敏综合征误诊传染性单核细胞增多症1例。患者女,38岁,全身皮疹18天,高热5天,全身浅表淋巴结肿大,肝、脾肿大,尿蛋白(+),EBV抗体IgG阳性,白细胞升高,末梢血及骨髓片中嗜酸粒细胞明显增高,异常淋巴细胞达48%。     

药物超敏反应综合征26例临床分析

目的探讨药物超敏反应综合征的临床特点及治疗。方法回顾分析26例药物超敏反应综合征患者的临床资料。结果 26例中可疑致敏药物分别为别嘌醇12例,非甾体类抗炎药(NSAIDs)4例(氨酚加敏2例、保泰松1例、氨酚伪麻分散片1例),中成药4例,抗癫痫药3例(卡马西平2例、奥卡西平1例),甲硝唑、磺胺类药(柳氮磺吡啶)、美西律各1例。发疹潜伏期为13~60 d,均伴肝功能异常,伴发热18例,伴浅表淋巴结增大者19例,肾功能异常者15例,白细胞升高者25例,血嗜酸粒细胞增多者24例。结论药物超敏反应综合征潜伏期长,临床表现多样,若病程中出现发热、皮损伴有内脏受累、血液系统损害等应警惕药物超敏反应综合征的发生,系统应用糖皮质激素联合免疫球蛋白大剂量冲击治疗对药物超敏综合征疗效较好。     

儿童药物超敏综合征9例临床分析

目的探讨儿童药物超敏综合征的临床特点。方法回顾性分析了9例住院儿童药物超敏综合征的临床资料和随访结果。结果9例患儿均出现发热、全身皮疹、浅表淋巴结肿大和内脏损害。致敏药物苯巴比妥6例、卡马西平4例、磺胺嘧啶和阿司匹林各1例。随访时均已痊愈。结论儿童药物超敏综合征以发热、皮疹、淋巴结肿大和内脏损害为特征,致敏药物以抗惊厥药为主。     

药物超敏综合征的临床研究进展

药物超敏综合征是一种严重的药物不良反应,又称药疹伴嗜酸粒细胞增多和系统症状,常累及多个脏器并伴发多种疾病.血液学异常表现为白细胞增多常伴有异形淋巴细胞和嗜酸粒细胞增多,肝脏损害最常见,表现为丙氨酸氨基转移酶显著增加,药物超敏综合征患者可因巨细胞病毒性溃疡而发生突发性消化道出血,可出现肾功能不全,肺损害会出现间质性肺炎伴嗜酸粒细胞增多,心血管受损表现为药物超敏综合征相关性心肌炎,神经系统并发症主要包括脑炎和脑膜炎.药物超敏综合征痊愈后可伴发多种自身免疫性疾病,包括Ⅰ型糖尿病、甲状腺疾病、硬皮病样表现、系统性红斑狼疮和自身免疫大疱性疾病.药物超敏综合征治疗包括系统应用糖皮质激素治疗、抗病毒药物、环磷酰胺和根据受累器官和伴发疾病来进行对症治疗.     

药物超敏综合征16例临床分析

分析16例药物超敏综合征(DHS)的临床特点和治疗。结果:16例中致敏药物分别为别嘌醇8例、卡马西平5例、苯巴比妥2例、氨苯砜1例,发疹潜伏期14～42d,平均(23.1±10.0)d,所有患者均伴发热,其中伴浅表淋巴结肿大10例,白细胞升高13例,嗜酸粒细胞升高11例,肝功能异常12例,肾功能异常6例。早期、足量应用糖皮质激素或联合大剂量丙种球蛋白治疗有效。     

氨苯砜超敏反应综合征5例临床分析

目的探讨氨苯砜超敏反应综合征的临床特征和治疗方法。方法回顾分析5例氨苯砜超敏反应综合征临床资料。结果5例氨苯砜超敏综合征用药潜伏期较长,为20～42天,均以发热或皮疹为首发症状,皮疹呈多形性,为麻疹样型、多形红斑型和红皮病型,所有患者均有浅表淋巴结肿大,肝肿大,1例脾肿大,并伴有血液学异常和肝功能受损,治疗时间平均58天,4例痊愈出院,1例死于肺部感染。结论氨苯砜超敏综合征表现为发热、皮疹、黄疸、淋巴结肿大、肝损害和溶血性贫血。根据DDS用药史,排除微生物感染和其他发疹性疾病可诊断本病,治疗应遵循重症药疹治疗原则。     

氨苯砜综合征8例临床分析

目的:探讨氨苯砜(DDS)综合征的临床特点。方法:回顾分析8例DDS综合征患者的临床资料。结果:8例患者均在服用DDS21～40d后起病,以皮损或发热为首发症状,都伴有皮肤或巩膜黄染;均有浅表淋巴结增大,6例有肝大,3例脾大;3例有胸腔或腹腔积液;血常规示6例嗜酸性粒细胞升高,2例出现异形淋巴细胞,3例单核细胞增多;8例均有肝功能异常和贫血。结论:DDS综合征的临床特征为发热、皮损、黄疸、淋巴结增大、贫血及肝脏损害等,其治疗遵循重症药疹的治疗原则。开始要足量使用糖皮质激素,减量不宜过快。     

别嘌醇致药物超敏综合征23例临床分析

目的探讨别嘌醇致药物超敏综合征(DHS)的临床特征。方法回顾分析了23例别嘌醇致DHS患者的临床表现、实验室检查、治疗、并发症及预后。结果别嘌醇致DHS潜伏期长,疹型多,以发疹型为主,常伴紫癜样斑疹、皮肤肿胀及反复脱屑。均有发热,常见浅表淋巴结肿大及血液学异常,脏器受累以肝肾为主,糖皮质激素治疗有效。结论DHS为具有特征性表现的临床综合征,病程迁延,早期、足量地应用糖皮质激素有助于预后的改善。     

DRESS syndrome associated with carbamazepine and phenytoin

Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) syndrome reflects a serious hypersensitivity reaction to drugs. Its clinical manifestations include diffuse maculopapular rash, exfoliative dermatitis, facial edema, lymphadenopathy, fever, multivisceral involvement and it is associated with a high mortality rate. We report a 62-year-old patient suffering from epilepsia presenting erythroderma following carbamazepine intake. Blood tests revealed eosinophilia, leukocytosis, elevated liver enzymes and high levels of Eosinophil Cationic Protein (ECP). We applied systemic steroids and anticonvulsant therapy was switched to phenytoin, which had been taken previously without adverse reactions. The skin eruptions persisted and the patient developed fever. Anticonvulsant medication was discontinued and skin eruptions finally resolved under steroid application. This case report demonstrates that cross reactivity between carbamazepine and phenytoin may not only lead to the development but also to the worsening of DRESS syndrome. ECP blood levels may represent a sufficient parameter to monitor the development of DRESS syndrome.     

抗惊厥药所致药物超敏综合征19例临床特征分析

目的：探讨抗惊厥药所致药物超敏综合征（DHS）的临床特征。方法：回顾分析19例抗惊厥药所致DHS患者的临床表现、实验室检查、治疗方法、并发症及预后。结果：抗惊厥药所致DHS潜伏期长,皮损形态多样,以发疹型为主,常伴有紫癜样斑疹、皮肤肿胀及反复脱屑,多有发热、黏膜损害、浅表淋巴结增大及血常规异常。脏器受累以肝脏为主,肾脏次之。糖皮质激素治疗有效。结论：DHS为具有特征性表现的临床综合征,病程较长,早期、足量地应用糖皮质激素有助于预后的改善。     

Phenytoin hypersensitivity reaction.

A clinically characteristic hypersensitivity reaction to phenytoin occurred in two patients three to four weeks after they started phenytoin therapy. It consisted of a characteristic rash, fever, tender generalized lymphadenopathy, leukocytosis with atypical lymphocytes, and eosinophilia. One patient had liver function abnormalities suggestive of hepatitis, as have most previously reported cases. The rash was pruritic and generalized; it consisted of irregular, ill-defined macular erythema in patches with superimposed follicular papules and massive edema of the face and periorbital region. Facial edema is characteristic of this syndrome. In one case the rash progressed to include follicular pustules and resolved with superficial desquamation. Histopathologic specimens from both cases showed a dense, superficial lymphohistiocytic infiltrate in the dermis and epidermal spongiosis. Intraepidermal pustules were present in one patient. The importance of recognizing this syndrome is stressed because it is potentially fatal.     

Toxic epidermal necrolysis as a dermatological manifestation of drug hypersensitivity syndrome

Drug hypersensitivity syndrome (DHS) is believed to be an adverse idiosyncratic drug reaction associated mainly with administration of aromatic antiepileptic drugs, such as phenytoin, carbamazepine, phenobarbital, lamotrigine. The syndrome is defined by the clinical triad of fever, skin rash and internal organ involvement and can be life-threatening condition. We describe three patients treated in our institution. The first was a 32-year-old man who developed toxic epidermal necrolysis (TEN) with pulmonary and liver involvement after initiation of lamotrigine therapy for concomitant epilepsy. The second 32-year-old man was treated with salazopyrine and omeprazole in order to relief the symptoms of inflammatory bowel disease, but as a result developed toxic epidermal necrolysis with elevated liver enzymes. The third patient was a 28-year-old man with long history of alcohol abuse who began treatment with carbamazepine and a few days later he was admitted to the clinic with symptoms of severe disseminated skin rash. The patients had peripheral eosinophilia. All the patients needed urgent life-saving therapy, intensive care and nursing. The culprit drug was discontinued and prompt systemic therapy with corticosteroids at an initial dose of 2 mg/kg/d and with broad spectrum antibiotics was started. Topical therapy included spraying Avène thermal water and local antiseptics. Resolution and epithelization of skin erosions were observed in about 4 weeks after the initiation of the therapy. Medications can give rise to certain adverse reactions including serious cutaneous and systemic involvement. TEN is a rare complication of DHS. Patients who develop DHS need optimal and adequate treatment. The concomitant use of corticosteroids and broad spectrum systemic antibiotics is essential. The local therapy plays an important part in relieving symptoms and should consist of mild preparations with minimally sensitizing potential.     

Allopurinol‐Induced DRESS Syndrome in an Adolescent Patient

Abstract: A 16‐year‐old male patient, with a history of essential hypertension enrolled in an experimental drug protocol using allopurinol, presented to our emergency department with a 10‐day history of fever. Initial laboratory evaluation revealed leukocytosis, eosinophilia, and transaminitis. After extensive work‐up and exclusion of infectious and oncologic etiologies, the diagnosis of allopurinol‐induced drug reaction and eosinophilia with systemic symptoms syndrome was carried out. The patient responded to administration of IV methylprednisolone, with complete resolution of symptoms and improvement of laboratory abnormalities. This case represents the first report of allopurinol‐induced drug reaction and eosinophilia with systemic symptoms syndrome in a pediatric patient.