头孢吡肟致老年肾功能不全患者精神异常

1例75岁女性患者,因间质性肺炎合并感染给予头孢西丁、二羟丙茶碱、乙酰半胱氨酸及托拉塞米治疗。用药前外周血白细胞计数9.8×109/ L,中性粒细胞0.76,白蛋白27.6 g/ L,尿素氮7.99 mmol/ L,肌酐130μmol/ L,尿酸388μmol/ L。入院第6天因抗感染治疗效果不佳,停用头孢西丁,换用头孢吡肟2.0 g、2次/ d 静脉滴注,余治疗不变。入院第9天患者出现躁狂,未予特殊处理。入院第10天患者出现躁动不安、言语混乱、谵妄,当日停用头孢吡肟、二羟丙茶碱、乙酰半胱氨酸,分2次肌内注射地西泮共10 mg。入院第12天患者精神症状消失,恢复二羟丙茶碱和乙酰半胱氨酸治疗。此后未再出现上述精神症状。     

乙酰半胱氨酸联用还原型谷胱甘肽致迟发型过敏反应一例

1例65岁男性患者因食管癌术后出现肝功能异常,使用乙酰半胱氨酸注射液8 g qd及还原型谷胱甘肽1.8 g qd。第4日静脉滴注还原型谷胱甘肽过程中,患者突然出现心累,气促,全身大汗,血氧饱和度71%,停用还原型谷胱甘肽,给予吸氧,症状持续7 h后缓解,第5日静脉滴注乙酰半胱氨酸注射液过程中,再次出现类似症状,立即停药,持续3 h后症状缓解,停用该药后,患者未再发生类似症状。     

乙酰半胱氨酸注射液预防对比剂肾病的临床研究

目的探讨乙酰半胱氨酸注射液是否可预防对比剂肾病。方法冠状动脉造影和冠状动脉介入治疗的患者143例,行冠状动脉CT检查的患者共14例,随机分为治疗组和对照组。治疗组第1至3天使用乙酰半胱氨酸注射液4.0 g加入到5%葡萄糖注射液250 mL中静脉滴注,对照组不使用乙酰半胱氨酸注射液,于使用对比剂前、52～72 h后再次检测血清肌酐水平。结果治疗组与对照组相比,在使用对比剂前后血肌酐水平用量少于60 mL及60～130 mL者无显著性差异,用量在超过130 mL时对照组较治疗组血肌酐水平升高,具有显著性差异。结论乙酰半胱氨酸注射液可以预防对比剂肾病。     

盐酸布桂嗪依赖1例报告

1临床资料 患者,男,52岁,因注射盐酸布桂嗪致依赖13年余入院,否认既往使用过其它精神活性物质。 患者自诉于2001年3月间因放鞭炮致左下肢外伤,在当地医院行左下肢截肢术,术后疼痛发作时曾给予肌肉注射盐酸布桂嗪注射液50mg及对症治疗,症状明显缓解。出院后感疼痛时自行肌注盐酸布桂嗪注射液。     

鲑鱼降钙素致腹部绞痛与心律失常2例

2名老年女性患者给予鲑鱼降钙素注射液治疗时出现腹部绞痛、腹泻、心律失常等不良反应。第1例为67岁女性,因腰椎间盘退行性病变、骨质疏松入院,给予葡萄糖酸钙1g,2次/d口服,并在皮肤试验呈阴性后给予肌内注射鲑鱼降钙素50IU,1次/d。注射后30min出现腹部绞痛,排黄色糊状便1次;2h出现心悸,心电图检查示:心律不齐、阵发性室性心动过速、偶发房性期前收缩,持续约1h后症状消失。连续注射3d,症状加重并出现双眼睑水肿,遂改为每周注射1次,注射2周后仍有上述症状,即停药,5d后症状缓解,再行心电图检查正常。第2例为65岁女性,以"腰椎间盘脱出、双膝关节退行性变"入院。实验室检查:血钙2.02mmol/L。于皮试阴性后,给予肌内注射鲑鱼降钙素50IU。注射后2h出现腹部绞痛、尿频、尿急、腹泻。心电图示:窦性心动过速。6h后症状自行缓解,未进行第2次注射。     

短期应用小剂量阿托伐他汀钙致肌酸激酶升高

摘要1例71岁男性患者因脑梗死急性期、室性早搏、高同型半胱氨酸血症入院,给予疏血通注射液6ml、醒脑静注射液20ml、吡拉西坦注射液250ml静脉滴注,1次／d;阿司匹林0．1g、叶酸5mg、甲钴胺500μg口服,1次／d。因动脉血管超声示双侧颈动脉粥样硬化,故给予阿托伐他汀钙10mg,1次／d口服。入院时患者肌酸激酶（CK）90U／L,服用阿托伐他汀钙第3天升至777U／L,第6天为1332U／L,尿液呈浅棕色,尿潜血（＋）。停服阿托伐他汀钙,其他治疗无改变,第2天CK降至1126U／L,第7天降至129U／L,尿液呈浅黄色,尿潜血（一）。     

血塞通致过敏反应1例

患者 ,女 ,6 4岁。因脑供血不足于 2 0 0 2年 9月 2日入院。入院后给予 0 .9%氯化钠注射液 2 5 0mL加血塞通注射液 5 0 0mgivdqd。输液第 8天患者全身皮肤出现散在红斑、瘙痒 ,即给氯苯那敏 8mg、维生素C0 .2 gpo ,tid。输血塞通第 9天 ,患者皮肤红斑明显增多 ,局部融合成片 ,奇痒 ,考虑为血塞通过敏 ,立即停用血塞通静滴 ,给予 0 .9%氯化钠注射液 10 0mL加地塞米松 10mgivd ,qd ,当日患者瘙痒症状得以控制 ,第 10天皮肤红斑消退 ,继续抗过敏治疗 ,第 11天过敏症状消失 ,未再出现。血塞通致过敏反应1例@姚艳芳$石家庄市白求恩国际和平医院…     

醒脑静注射液致药物热1例

通过1例女性患者因头部外伤,给予酚磺乙胺3 g,醒脑静注射液20 m L,乙酰谷酰胺0.6 g,甘油果糖250 m L,qd,静脉滴注对症治疗;2 d后停用酚磺乙胺;用药至第13天静脉滴注醒脑静注射液后约1 h出现寒战发热(39.4℃);第14天静滴醒脑静注射液后再次出现发热寒战,该患者发热寒战与使用醒脑静注射液存在因果关系,故考虑该发热寒战是醒脑静注射液所致。     

甲硝唑致肌张力障碍5例

1临床资料病例1:患者,女,16岁,体重47kg。因转移性右下腹疼痛7天,慢性阑尾炎急性发作,于2006年7月7日入院进行手术治疗。术后给予甲硝唑注射液及注射用哌拉西林钠抗感染治疗。甲硝唑注射液200mL,每日1次,静脉滴注,连续3天。7月9日下午2时,患者出现颈部后仰固定,两眼上翻,但神志清楚,立即给予苯巴比妥注射液0.1g肌内注射,2小时后症状逐渐消失。在7月10日以后的治疗中停用甲硝唑注射液,继续使用注射用哌拉西林钠,无不良反应发生。病例2:患者,男,12岁,体重32kg。因转移性右下腹疼痛1天,急性阑尾炎发作,于2006年8月15日入院进行手术治疗。术后…     

乙酰半胱氨酸引起QTc延长

1例68岁女性患者,因肺间质纤维化口服乙酰半胱氨酸片0.6 g,tid。用药第3天患者诉心前区疼痛、心慌、胸闷。心电图示短阵房性心动过速、ST-T改变、QT间期延长,QTc 503 ms。心梗三项、电解质、BNP均在正常范围内。遂停用乙酰半胱氨酸片,其余治疗继续,停药第2天患者未再出现心慌等不适症状,复查QTc 446 ms。停药第3天患者病情好转出院。     

Angioedema after intravitreal bevacizumab injection

A 47-year-old male with a history of diabetes mellitus type 2 exhibited with decreased vision in both eyes. The diagnosis of cystoid macular edema (CME) was made and it was decided to administer bilateral intravitreal bevacizumab (Avastin) injections. After intravitreal bevacizumab injection (1.25?mg/0.05 cc) to the right eye the patient had angioedema and conjunctival chemosis in the right eye which resolved in 48?h. One month later the left eye received intravitreal bevacizumab injection under the same conditions. Thirty minutes after the injection angioedema and conjunctival chemosis occurred in the left eye in which the signs and symptoms improved in 48?h. This report is the first one which describes angioedema after intravitreal bevacizumab injection. Care should be taken against the systemic hypersensitivity reactions when planned to receive intravitreal bevacizumab injection.     

Angioedema after intravitreal bevacizumab injection

A 47-year-old male with a history of diabetes mellitus type 2 exhibited with decreased vision in both eyes. The diagnosis of cystoid macular edema (CME) was made and it was decided to administer bilateral intravitreal bevacizumab (Avastin) injections. After intravitreal bevacizumab injection (1.25?mg/0.05 cc) to the right eye the patient had angioedema and conjunctival chemosis in the right eye which resolved in 48?h. One month later the left eye received intravitreal bevacizumab injection under the same conditions. Thirty minutes after the injection angioedema and conjunctival chemosis occurred in the left eye in which the signs and symptoms improved in 48?h. This report is the first one which describes angioedema after intravitreal bevacizumab injection. Care should be taken against the systemic hypersensitivity reactions when planned to receive intravitreal bevacizumab injection.     

苦黄注射液致新的不良反应1例

1例男性患者因慢性活动型乙型病毒性肝炎入院,入院第一时间内医师给予苦黄注射液为其退黄,患者系首次输注该药,用药期间出现双眼肿胀不适,喉咙有异物感及灼热感,考虑为苦黄注射液引起的不良反应,给予对症治疗,患者症状缓解。临床应用苦黄注射液治疗黄疸型肝炎较为普遍,医生和药师应对苦黄注射液引起的不良反应予以高度重视,保证用药安全。     

Angioedema due to angiotensin-converting enzyme inhibitors

Angiotensin-converting enzyme (ACE) inhibitor associated angioedema was detected in 39 subjects (17%) of 231 consecutive patients examined in the last 5 years at our out-patient clinic for symptoms of angioedema without urticaria. In these patients, angioedema was most commonly localized to the face. The duration of ACE-inhibitor treatment at the onset of angioedema ranged from 1 day to 8 years with a median of 6 months. The time elapsed between onset of angioedema and withdrawal of ACE-inhibitor ranged from 1 day to 10 years with a median of 10 months. Delayed diagnosis is explained by the unusual characteristics of this adverse reaction: angioedema may start years after beginning the treatment and then it recurs irregularly. In fact, ACE-inhibitors seem to facilitate angioedema in predisposed subjects, rather than causing it with an allergic or idiosyncratic mechanism. Thus, while Cl-inhibitor levels are usually normal in subjects developing ACE-inhibitor-dependent angioedema, we found that ACE-inhibitors caused angioedema in Cl-inhibitor-deficient patients. Because the main inactivator of bradykinin is kininase II, which is identical with ACE, it is believed that bradykinin mediates ACE-inhibitor-dependent angioedema. We had the possibility to examine the plasma bradykinin levels in one ACE-inhibitor-treated patient during an angioedema attack and we found very high levels, but we did not find an increase of break-down products of high-molecular-weight-kininogen as observed during acute attacks in hereditary angioedema. Bradykinin fell to normal levels during remission after withdrawal of the drug. These observations indicate that in ACE-inhibitor-induced angioedema, contrary to hereditary angioedema, the reduction of bradykinin catabolic rate plays a predominant role.     

Flu-like symptoms associated with fluoxetine overdose: a case report

The serotonin reuptake inhibitor zimelidine may cause flu-like symptoms and Guillain-Barre syndrome. Guillain-Barre syndrome has not been reported with the use of the structurally related serotonin reuptake inhibitor fluoxetine. Flu-like symptoms are described in the manufacturer's literature on fluoxetine but are absent from published studies. We describe a patient who developed flu-like symptoms, urticaria and angioedema 2 days after fluoxetine overdose. There were no neurologic sequelae. This case confirms that fluoxetine may be associated with flu-like symptoms and suggests that, because these symptoms occurred after overdose, they may be dose related. The additional findings in this patient suggestive of allergy, an unusual feature of drug overdose, are discussed.     

Drug-induced angioedema without urticaria.

Angioedema without urticaria is a clinical syndrome characterised by self-limiting local swellings involving the deeper cutaneous and mucosa tissue layers. Most occurrences of angioedema respond to treatment with a histamine H1 receptor blocker (antihistamine) because they are an allergic or parallergic reaction. A small number of cases do not respond to antihistamine treatment. Such cases tend to occur in patients with deficiency or dysfunction of the inhibitor of the first component of the complement (C1-INH), but more rarely can occur in patients with other conditions and as an adverse drug reaction. Angioedema is well documented in patients taking ACE inhibitors. Considering that 35 to 40 million patients are treated worldwide with ACE inhibitors, this drug class could account for several hundred deaths per year from laryngeal oedema. ACE inhibitors certainly do not mediate angioedema through an allergic or idiosyncratic reaction. For this reason the relationship with this drug is often missed and consequently quite underestimated. Rare instances of angioedema have also been reported with angiotensin II receptor antagonists. This adverse effect seems to occur less frequently with angiotensin II receptor antagonists than with ACE inhibitors. However, we do not know whether this adverse effect has the same mechanism with the 2 classes of medications. Some cases of severe angioedema have been recently reported after treatment with fibrinolytic agents. Scattered reports suggest the possibility of angioedema associated with the use of estrogens, antihypertensive drugs other than ACE inhibitors, and psychotropic drugs. Angioedema can also occur with nonsteroidal anti-inflammatory drugs. Prevention of angioedema relies first on the patient history. Estrogen and ACE inhibitors should be avoided in a patient with congenital or acquired C1-INH deficiency. In the case of ACE inhibitors, the appearance of angioedema following long term treatment does not lessen the probability that such an agent could be the cause. The most important action to take in a patient with suspected drug-induced angioedema is to discontinue the pharmacological agent. Epinephrine (adrenaline), diphenydramine and intravenous methylprednisolone have been proposed for the medical management of airway obstruction, but so far no controlled studies have demonstrated their efficacy. If the acute airway obstruction leads to life-threatening respiratory compromise an emergency cricothyroidotomy must be performed.     

Angioedema due to ACE inhibitors: increased risk in patients of African origin

AIMS: To determine patterns in presentation, risk factors, management and outcome of patients with ACE inhibitor associated angioedema in one British teaching hospital. METHODS: Cases of ACE inhibitor associated angioedema in patients presenting to the City Hospital, Birmingham between 1993 and 1999 were collected and entered prospectively onto a computerised register. RESULTS: A total of 20 cases (mean age 60 years, range 42-82 years) of ACE inhibitor associated angioedema were reported (11 female and 9 male) with 65% (n=13) of patients being black/Afro-Caribbean. In 70% of cases (n=14), angioedema occurred within 4 weeks of starting therapy, although three patients presented following long-term treatment (24-48 months). ACE inhibitors were continued in 50% (n=10) patients, despite at least one documented episode of angioedema. Admission to hospital was necessary in 40% (n=8) patients, with three of these admitted to the intensive care unit, and one of these died as a result of severe laryngeal obstruction. CONCLUSIONS: ACE inhibitor related angioedema is a serious and potentially fatal complication which is relatively rare in the general population, but is more common amongst black/Afro-Caribbean patients. ACE inhibitors are frequently continued following an episode of angioedema and it is important that these episodes are minimised by prompt cessation of the drug, careful patient counselling and heightened awareness in all clinicians who prescribe this common group of drugs.     

伏立康唑与奥美拉唑可能的不良相互作用致肌病及肝功能恶化

1例35岁男性患者,因慢性重型乙型肝炎并自发性腹膜炎入院,给予保肝、退黄、利尿、抑酸(奥美拉唑)和抗病毒(阿德福韦酯+拉米夫定)药物治疗,其间发生肺部侵袭性真菌感染。给予卡泊芬净抗真菌治疗10 d,实验室检查结果及临床症状好转。后因经济原因改为口服伏立康唑(首剂量0.4 g,之后0.2 g2,次/d),治疗第3天患者开始出现频繁的恶心、呕吐,对症治疗效果不佳;第10天改为伏立康唑0.2 g、2次/d静脉滴注,仍频繁呕吐;治疗第14天出现四肢肌肉酸痛症状,实验室检查示:AST880 U/L,ALT 166 U/L,CK 22 855 U/L and CK-MB 442 U/L。停用伏立康唑4,d后患者CK和CK-MB水平分别降至5625 U/L和73 U/L,但AST和ALT水平分别升至1226 U/L和396 U/L。该肌病和肝功能恶化考虑可能与伏立康唑和奥美拉唑不良相互作用有关。患者最终肝衰竭,家属主动要求出院。