卡马西平超敏综合征

1例59岁男性患者因耳鸣服用卡马西平0.1 g,1～2次/d,服药7 d后出现双下肢一过性皮疹。停用卡马西平后皮疹消失,但随后耳鸣症状加重,遂入院,给予卡马西平0.1 g,2次/d口服;甲钴胺1 mg,3次/d口服。入院第2天患者体温39.2℃;第3天面颊部、躯干及双侧膝关节处出现红色斑丘疹。血生化检查示丙氨酸转氨酶359 U/L,天冬氨酸转氨酶137 U/L,γ-谷氨酰转移酶506 U/L,乳酸脱氢酶273 U/L。停用卡马西平及甲钴胺,给予甲泼尼龙及抗过敏治疗。2 d后体温恢复正常,5 d后皮疹、肝功能逐渐好转。入院第9天患者再度发热,体温38.1℃,随后皮疹再次出现,且逐渐增多,遍布全身。实验室检查:白细胞13.78×10~9/L,嗜酸粒细胞0.113;丙氨酸转氨酶187 U/L,天冬氨酸转氨酶45 U/L,γ-谷氨酰转移酶374 U/L,乳酸脱氢酶239 U/L。诊断为卡马西平所致药物超敏综合征,给予甲泼尼龙加用人免疫球蛋白治疗,皮疹症状及肝功能逐渐好转。入院第16天患者双下肢再次出现皮疹,经甲泼尼龙及对症治疗后缓解。     

左氧氟沙星致重症多型红斑型药疹一例

1 病例报告 患者 男,75岁.主因皮疹7d,于2007年6月23日入院.患者36 d前因咯血3d就诊于我院,查胸CT示右上肺空洞,诊断为:继发性右上肺结核复发,痰涂片阴性,给予异烟肼、利福平、乙胺丁醇抗结核及双环醇保肝治疗,22 d前好转出院.8 d前门诊复查时发现肝功能损害,丙氨酸转氨酶(ALT)124 U/L,天冬氨酸转氨酶(AST)95U/L,门诊停用利福平给予左氧氟沙星0.2 g/次,每日2次联合异烟肼、乙胺丁醇抗结核治疗加量双环醇保肝.     

甲状腺功能亢进合并肝功能损害48例临床分析

目的分析甲状腺功能亢进（以下简称甲亢）合并肝功能损害患者的临床特点及治疗措施。方法回顾性分析48例甲亢合并肝功能损害患者的临床特点、治疗措施及预后。结果 48例患者均给予保肝治疗,其余低碘饮食及补充维生素及普萘洛尔等治疗,肝功能轻度异常者在保肝治疗的同时使用抗甲状腺药物,每1周复查肝功能1次,治疗4周大部分患者甲功逐渐好转,最终恢复正常,同时肝功能逐渐减轻直至恢复正常。对3例肝功能损害严重者在使用保肝治疗后,2例肝功能好转后行131I治疗,1例肝功能各项指标基本正常后,使用抗甲状腺药物治疗。结论甲亢合并肝功能损害可保肝治疗同时尽早应用抗甲状腺药物治疗。对重症肝损害患者先明确肝损害原因并保肝治疗,肝功能出现好转后行131I治疗甲亢。     

甲苯磺酸索拉非尼致晚期肝癌患者高热伴皮疹

男性患者,56岁,因晚期原发性肝癌服用推荐剂量的索拉非尼(0.4 g,q12h)治疗。用药8 d后出现发热,体温最高至39.3℃。用药11 d开始出现皮疹,再次入院。入院后停用索拉非尼并给予抗过敏治疗,5 d后症状消退。随后给予低剂量索拉非尼(0.2 g,q12h),未出现发热及皮疹。5 d后索拉非尼加至0.4 g,q12h,治疗1 d后再次出现高热及新发皮疹。遂再次停用索拉非尼,高热及皮疹渐退。停用3 d后再次降低剂量至0.2 g,q12h。患者生命体征平稳、无畏寒、发热,无新发皮疹,病情稳定。该病例可为临床医生诊断索拉非尼引起的药物热及处理方法提供借鉴。     

利福平引起剥脱性皮炎及肝功能损害1例

患者男, 24岁,因发热、咳嗽、左胸痛 1月,全身皮肤瘙痒 3d入院。曾于入院前 1月因发热、咳嗽、左胸痛在当地县医院就诊,诊断为左侧结核性胸膜炎,予异烟肼 0.3g/d、利福平 0.45g/d口服,链霉素 0.75g/d肌肉注射以及强的松等治疗,上述症状逐渐好转;两周后感全身皮肤瘙痒并出现红色丘疹,肝功能显示谷丙转氨酶 (ALT)168U/L、谷草转氨酶 (AST)220U/L、黄疸指数 38U/L,当地县医院考虑为结核药物所致,立即停用所有抗结核药物,并给予地塞米松、维生素 C静脉注射,口服赛庚啶等抗过敏及保肝治疗, 5d后皮肤瘙痒及红色丘疹逐渐减轻,…     

依巴斯汀相关肝损害

1例69岁男性患者,因过敏性皮炎服用依巴斯汀10 mg,1次/d;0.05%倍氯米松乳膏及0.3%乳酸环丙沙星乳膏外用.15 d后皮疹加重,肝功能示ALT 173 U/L,AST 120 U/L.停用依巴斯汀及乳酸环丙沙星乳膏,给予抗过敏与护肝治疗.1周后皮疹减轻,肝功能恢复正常.     

安乃近片相关中毒性大疱性表皮松解症

1例50岁男性患者因感冒、发热口服头孢氨苄胶囊0.25 g,3次/d和安乃近片0.5 g,3次/d治疗,服药后体温降至正常.次日,患者全身皮肤出现红斑、皮疹、瘙痒,继而出现水疱伴灼痛,并再次发热,高达40℃.入院后查体见面部、躯干及四肢有红斑及水疱,皮损面积达体表50%,结膜重度充血.实验室检查:WBC 18.9×109/L,N 0.78,L 0.12,M 0.10,ALT 74 U/L.诊断为中毒性大疱性表皮松解症.立即停用头孢氨苄和安乃近,给予地塞米松、酮替芬,头孢哌酮钠-舒巴坦钠,甘草酸二铵治疗.5 d后皮损有所好转,体温降至38.5℃.入院第6天,患者因发热再次服用安乃近0.5 g,2次/d,红斑再次加重.立即停药,再行抗过敏等治疗.10 d后皮肤症状消褪.     

拉莫三嗪致严重剥脱性皮炎及肝损害

1例10岁4个月男性患儿因癫痫给予拉莫三嗪12.5 mg,1次/d;丙戊酸钠0.13 g,3次/d口服.4 d后患儿全身出现红色皮疹伴瘙痒,遂停用拉莫三嗪,症状渐消失.再次使用拉莫三嗪,上述症状复现,并伴发热.虽再次停用拉莫三嗪,皮疹未好转,且逐渐增多,患儿出现全身皮肤潮红、肿胀、皲裂、破溃及大量鳞屑.经治疗无效,患儿出现反复发热,巩膜黄染.肝功能检查:ALT 408 U/L,AST 228U/L,γ-GT 336 U/L,TBil 162.4 μmol/L,DBil 112.4 μmol/L,IBil 50 μmol/L.尿常规:尿胆原(+),胆红素(++).经抗感染、抗过敏等治疗后病情逐渐好转.     

卡瑞利珠单抗联合阿帕替尼致严重皮肤不良反应1例★

1例80岁男性患者因左肺腺癌行6周期化疗后进展，采用免疫治疗，给予卡瑞利珠单抗0.2 g静脉滴注（d1，21 d为1个周期）。首次静脉滴注卡瑞利珠单抗后1周，患者躯干部出现多处皮疹伴瘙痒，对症治疗后好转。继续第2周期卡瑞利珠单抗联合阿帕替尼治疗后5 d，患者头面部、躯干及四肢再次出现大面积皮疹伴瘙痒，诊断为发疹型药疹。停用卡瑞利珠单抗及阿帕替尼，给予糖皮质激素和抗过敏药物等治疗，10 d后皮疹基本消退。     

丙基硫氧嘧啶与左旋咪唑的少见不良反应

1 丙基硫氧嘧啶致关节疼痛 阳××,男,43岁,住院号443068.4个月前被确诊为"甲亢",服用他巴唑治疗,两个月后发现肝功能异常,故停药.不久,甲亢症状再次复发,查T3、T4升高,遂入院.入院后即给予护肝降酶治疗,并于1998年11月28日起应用丙基硫氧嘧啶0.1 po q6h.12月2日晚,患者突感右肩关节剧烈疼痛、彻底不眠.次日肩关节X线片无异常.12月6日起双膝关节也受累,虽用非甾体消炎药亦不能完全缓解.疼痛部位外观无变化,活动尚可.既往无类似病史.考虑此反应可能由"丙基硫氧嘧啶"所致,故于12月8日停用,停药的第2天,关节疼痛消失,且未见反复.     

别嘌醇致肝损伤2例

2例患者（例1男性,32岁;例2女性,27岁）,应用抗结核药物治疗期间肝功能均正常,因尿酸水平升高加用别嘌醇0．1g,3次／d口服。2周后出现发热、皮疹。实验室检查：例1丙氨酸转氨酶（ALT）1182U／L,天冬氨酸转氨酶（AST）595U／L,总胆红素25．9mmol／L;例2A坍1452U／L,AST1942U／L。停用别嘌醇及抗结核药,接受保肝治疗。2例患者肝功能分别于治疗后14、25d后基本恢复正常。例1继续抗结核治疗,随访4个月肝功能正常。例2因病情稳定停止抗结核治疗。     

替考拉宁与盐酸万古霉素致严重水疱型药疹

1例74岁男性患者,因直肠癌根治术后出现咳嗽、咯痰、发热约1个月,先后给予拉氧头孢钠、比阿培南、莫西沙星、替考拉宁、盐酸万古霉素、利柰唑胺和达托霉素治疗。在应用替考拉宁12d后换用莫西沙星,应用莫西沙星的第4天,患者四肢及躯干部位出现充血性皮疹伴瘙痒感。停用莫西沙星、改用盐酸万古霉素并给予抗过敏对症治疗后患者皮疹好转。应用盐酸万古霉素第8天,患者四肢再次出现红疹,停用盐酸万古霉素并换用替考拉宁。应用替考拉宁第5天患者皮疹加重,部分皮疹表面出现水泡并连接成片,换用利奈唑胺并继续抗过敏治疗,陈旧水泡逐渐吸收,未再出现新发水疱。考虑可能为替考拉宁引起的迟发型过敏反应,不排除还存在与盐酸万古霉素交叉过敏的可能。     

Acute hepatic failure associated with oral minocycline: a case report.

A 39-year-old woman was evaluated for possible liver transplantation due to rapidly developing hepatic failure 4 weeks after initiation of oral minocycline 100 mg twice a day for the treatment of acne. The patient developed a maculopapular rash, malaise, fever, nausea, and vomiting 2 weeks prior to admission to the hospital. On admission, her symptoms rapidly progressed to liver failure characterized by rapidly rising liver enzyme levels, worsening encephalopathy, and coagulopathy. Viral hepatitis serologies and blood cultures were all negative. After intensive supportive care for 2 weeks, the patient's condition gradually improved and she was discharged with mildly elevated liver enzyme levels and pruritus, without need of liver transplantation. Minocycline-induced hepatic injury is an idiosyncratic reaction with a sensitization period that appears to be 3-4 weeks in duration. The characteristic features include rash, fever, lymphadenopathy, and eosinophilia, as well as severe alterations in liver function. The high liver enzyme levels and the significant prolongation of the prothrombin time suggest massive hepatocellular damage. In light of the profound liver damage that occurs with this adverse reaction, care should be taken in administering minocycline to patients who have concomitant liver disease. It is recommended that patients should be instructed as to the possible signs and symptoms of toxicity and be monitored for evidence of idiosyncratic reaction or liver failure.     

Chronic salicylism in a patient with juvenile rheumatoid arthritis

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.     

Temozolomide-induced desquamative skin rash in a patient with metastatic melanoma

Temozolomide is an oral alkylating agent used in the treatment of metastatic melanoma. Commonly reported adverse effects of the drug include nausea and vomiting, constipation, headache, and fatigue, as well as myelosuppression, which may be dose limiting. Few reports have described dermatologic adverse effects such as rash and pruritus, and, to our knowledge, none have discussed the seriousness or extensiveness of the rash. We describe a 37-year-old woman who was receiving temozolomide for treatment of metastatic melanoma. After 6 weeks of therapy, the patient developed an unexplained fever. The drug was discontinued, and the fever resolved within 2 days. Temozolomide was restarted 2 months later; the patient again developed a fever. This time the fever was accompanied by a diffuse erythematous skin rash that progressed to an extensive, full-body, desquamative skin rash. The rash was treated with moisturizing cream along with intravenous and topical corticosteroids and antibiotics. Due to the severity of the rash, temozolomide was permanently discontinued. Even after its discontinuation, the patient experienced the rash on a long-term basis, with periodic exacerbations. However, none were as severe as the first rash. The patient's metastatic disease remained stable for the next 2 years. According to the Naranjo adverse drug reaction probability scale, the likelihood that temozolomide was responsible for the adverse drug reaction of fever was probable (score of 6). Clinicians should be aware that an erythematous and exfoliative rash may be induced by temozolomide, and be familiar with the pharmacologic and supportive measures necessary for its treatment.     

抗结核药致药物超敏反应综合征1例

1例34岁女性肺结核患者,予口服四联抗结核药治疗（异烟肼片,利福平胶囊,吡嗪酰胺片）,用药35天后出现皮疹,38天后出现发热、腹痛、皮疹加重。实验室检查：丙氨酸氨基转氨酶460 U/L,天冬氨酸氨基转氨酶533 U/L,γ-谷氨酰基转移酶80 U/L,胆碱酯酶3336 U/L。考虑为抗结核药导致的药物超敏反应综合征。停用所有抗结核药物,予支持对症治疗,患者腹痛逐渐缓解,仍反复发热,皮疹逐渐加重。后经保肝、激素冲击和免疫调节治疗后好转出院。     

Possible roxithromycin-induced fulminant hepatic failure in a child.

A pediatric formulation of roxithromycin is a relatively new addition to the antibiotic market in Australia. A previously healthy 5-year-old boy with no significant medical history was treated with roxithromycin 50 mg twice/day for cough, fever, and anorexia. After completing a 5-day course of the agent, he developed a nonpruritic, nonurticarial, erythematous, maculopapular, generalized rash and occasional vomiting. Three days later his symptoms included jaundice, dark urine, and pale stools. Laboratory results revealed acute hepatitis, and the patient was admitted to the hospital. His hepatic function continued to deteriorate, so the boy was transferred to a tertiary pediatric hospital. His condition continued to worsen, and 6 days after transfer, he underwent liver transplantation. Clinicians should be aware of potential hepatic complications associated with the use of roxithromycin.     

拉莫三嗪与丙戊酸钠先后致皮疹、红细胞巨幼化及高敏综合征

1 例64 岁男性患者,因癫痫反复发作口服丙戊酸钠（500 mg,bid）及拉莫三嗪（25 mg,qd）进行治疗,30 d 后因发热、皮疹、抽搐、行走障碍入院.骨穿刺结果提示红细胞形态呈巨幼化,予氯雷他定（10 mg,qd,po）及复方甘草酸苷（60 mg,qd,ivgtt）,停用拉莫三嗪,改用口服丙戊酸钠（早上750 mg,下午500 mg）抗癫痫,12 d后患者病情好转出院,继续服用丙戊酸钠抗癫痫.2 d 后患者皮疹及发热再次加重入院,予甲泼尼龙（40 mg,bid,ivgtt）、氯雷他定（10 mg,qd,po）及复方甘草酸苷（60 mg,qd,ivgtt）,停用丙戊酸钠改用苯巴比妥钠（100 mg,bid,im）抗癫痫治疗,20 d 后改为苯巴比妥钠（30 mg,bid,po）,期间患者发热及皮疹消退、肝功能恢复,于第22 天出院.