卡马西平相关白细胞及血小板减少

1例58岁女性患者因枕大神经痛入院.入院后血常规:WBC 4.90×109/L,PLT 273×109/L.给予患者卡马西平0.1 g,2次/d.次日,卡马西平改为0.1 g,3次/d,并合用氯硝西泮、罗通定及兰索拉唑.2 d后,头痛症状加重,卡马西平加量至0.2 g,3次/d,且加入氨酚双氢可待因片联用.8 d后患者躯干可见散在皮下出血点;复查血常规:WBC 2.87×109/L,PLT4×109/L.停用卡马西平,其他药物继续使用,并给予酚磺乙胺、甲泼尼龙及血小板等治疗.治疗5 d后,血常规恢复正常.     

葛根素注射液致药物热2例

例1男,77岁,因高血压Ⅲ期、冠心病住院.查体示:T 37℃,P 88次@min-1,BP 165/105mmHg,神清,两肺清音,心界向左下扩张,HR 86次@min,律齐,腹部检查未见异常,肝脾肋下未及.血常规:WBC 6.8×109@L,RBC4.38×1012@L-1,Hb 135g@L-1,PLT 145 × 109@L-1,N0.28,L0.18,Glu(+++).入院后给予葛根素0.4g qd静滴,连用16天;当用药至第12天,葛根素输完后5h左右,患者先出现寒战,继而心慌、呼吸急促、发热,T 39℃,予低流量吸氧,柴胡4ml im,2h后,症状消失,体温正常.     

氯吡格雷相关非重型再生障碍性贫血

1例66岁男性患者因心肌梗死入院,并立即行经皮冠状动脉腔内成形术及支架术。术后当日规律口服氯吡格雷75 mg,1次/d;阿司匹林首剂量300 mg,之后100 mg,1次/d;氟伐他汀20 mg,1次/d;福辛普利钠10 mg,1次/d。1个月后,患者出现寒战、高热。血常规检查:白细胞1.1×109/L,中性粒细胞0.034,中性粒细胞绝对值0.037×109/L,红细胞3.6×1012/L,血红蛋白113 g/L,血小板119×109/L。骨髓穿刺及活检示非重型再生障碍性贫血。给予对症治疗,血常规各项水平继续下降。入院第44天血常规检查:白细胞2.6×109/L,中性粒细胞0.367,中性粒细胞绝对值0.954×109/L,红细胞3.6×1012/L,血红蛋白113 g/L,血小板84×109/L。立即停用氯吡格雷及阿司匹林,改用华法林2.5 mg,1次/d口服,西洛他唑100 mg,2次/d口服,其他药物继续服用。随后血常规检查示全血细胞计数下降至最低值后逐渐上升。再行2次骨髓穿刺检查,结果示骨髓象逐渐恢复。入院第102天血常规检查:白细胞5.8×109/L,中性粒细胞0.552,中性粒细胞绝对值3.202×109/L,红细胞4.2×1012/L,血红蛋白140 g/L,血小板170×109/L。再次加用氯吡咯雷50 mg,1次/d;阿司匹林100 mg,1次/d。1周后血常规检查示全血细胞计数明显下降,2周后血常规检查:白细胞3.4×109/L,中性粒细胞0.349,中性粒细胞绝对值1.187×109/L,红细胞4.0×1012/L,血红蛋白133 g/L,血小板176×109/L。随后,仅停用氯吡咯雷,改为西洛他唑100 mg,3次/d口服。1周后血象恢复正常。     

静脉滴注万古霉素致小儿荨麻疹1例

患儿,男,1岁,体重12kg,因发热,咳嗽3 d,加剧伴气促1 d于2004年2月13日入院.查体:T 39.7℃,呼吸稍促,呼吸音粗,双肺底部可闻及中、小水泡音及哮鸣音.血常规:WBC 9.1×109/L,N.0.53,Hb 111g/L,Plt 241×109/L;胸片示:支气管肺炎不能排除.临床诊断:支气管肺炎.因患者对青霉素类、头孢菌素类药物过敏,同时考虑病毒感染可能性大,入院后予静滴红霉素、更昔洛韦抗感染.     

临床药师参与肺炎伴发药物性皮疹治疗1例

患者,女,73岁,以“咳嗽、咯痰4d,加重伴胸闷1d”入院。患者入院时胸部 X 线片示双肺下野支气管感染征象;血 WBC 9.59×109/ L,N 78.6％,PLT 101×109/ L;CRP 25mg/ L;心电图未见异常。查体：患者神志清,精神可,活动自如,T 36.8℃,R 18次/ min,P 70次/ min,BP 140/75mm Hg。听诊双肺呼吸音粗,双下肺可闻及少许湿啰音。     

清开灵注射液致白细胞减少2例

2例精神病患者因上呼吸道感染,静脉滴注清开灵治疗时出现白细胞减少。例1,1名30岁女性因偏执性人格障碍长期服用文拉法辛(150mg/d)及富马酸喹硫平(0.2mg/d)。入院后第3天,患者发生"上呼吸道感染",查WBC 5.7×109/L,给予清开灵注射液40ml加入0.9%氯化钠注射液500ml静脉滴注,1次/d。次日WBC 3.2×109/L,继续滴注清开灵5d后,WBC 2.0×109/L。停用清开灵后第6天,查WBC 4.7×109/L。此后多次复查WBC均正常。例2,1名35岁女性因患"双相情感障碍"入院,2个月后伴发"上呼吸道感染",查WBC 7.8×109/L,给予清开灵注射液30ml 5%葡萄糖注射液500ml静脉滴注,1次/d,维C银翘片2片,3次/d。第5天上呼吸道感染症状消失,体温恢复正常,查WBC 3.1×109/L。停用清开灵,1周后复查WBC 5.8×109/L。随访3个月WBC均正常。     

红花注射液致过敏性休克1例

1临床资料 患者,女,53岁,因食欲不振、恶心、周身乏力7d于2004年3月9日以慢性肾功能不全收入院.体检:神志清,贫血貌,消瘦体质,体温36℃,脉搏92次/min,血压120/80mmHg.血常规示白细胞12.18×109/L,血红蛋白94g/L,血小板316×109/L;尿常规示红细胞( ).入院后遵医嘱给予5%葡萄糖250mL,红花注射液20mL静滴,1次/d.     

阿维A引起白细胞和血小板增多

1例42岁男性患者,因脓疱型银屑病服用阿维A胶囊30 mg/d治疗.治疗前血常规基本正常:RBC 3.65×1012/L,WBC9.5×108/L,PLT 246×109/L.治疗1周后,RBC 3.67×1012/L,WBC 16.5×109/L,PLT412×109/L.病理学检查示:血小板增多,骨髓增生;B超示脾肿大.将阿维A减量至15 mg/d.3周后复查血象:RBC 3.72×1012/L,WBC 14.3×109/L,PLT446×109/L.阿维A继续减量至10 mg/d,2周后复查血象RBC 3.48×1012/L,WBC 10.3×109/L,PLIT 385×109/L;腹部B超检查未见异常.     

甲巯咪唑致严重粒细胞缺乏

患者女,35岁。因“咽痛、发热1d”于2004年5月4日入院。患者确诊为甲状腺功能亢进3个月,给予甲巯咪唑30mg,3次/d口服。入院前1d出现咽部疼痛、发热(体温39.5℃),全身乏力。血常规显示:WBC0.8×109/L,N0.07,L0.78,M0.15,Hb124g/L,PLT90×109/L。中性粒细胞<0.5×109/L,淋巴细胞相对增多。入院后,查体:咽部有黏膜白斑及红肿,悬雍垂出现溃疡,T39.7℃。给予粒细胞集落刺激因子(特尔津)150μg,皮下注射,1次/d。同时给予左氧氟沙星0.4g,1次/d;氯唑西林3.0g,2次/d,静滴。4d后因体温未下降,血培养示阴性,停用氯唑西林换用头孢他啶,但体温仍高…     

静脉用丙种球蛋白致过敏反应

患者女,85岁。主因咳嗽5d,伴发热1d,于2005年1月6日入院。既往有慢性支气管炎、高血压病及冠心病史,对磺胺类药物过敏。查体:T38.3℃,P78次/min,R18次/min,BP120/60mmHg(1mmHg=0.133kPa)。咽部轻度充血,双扁桃体无肿大。桶状胸,双肺叩清,听诊双肺呼吸音低,左下肺可闻少量湿性啰音，心界向左扩大,心律齐,各瓣膜听诊区未闻及病理性杂音。辅助检查:胸片示:两肺纹理略多、紊乱。血常规:WBC6.78×109/L,N0.815,L0.15。CRP51mg/L;血K 3.2mmol/L,Cr103μmol/L;血气分析:PCO236mmHg,PO262mmHg,SO293%,肺泡动脉血氧分压差(AaD pO2)48mm…     

高效液相色谱法测定膦甲酸钠氯化钠注射液中膦甲酸钠的含量

目的建立HPLC法测定膦甲酸钠氯化钠注射液中膦甲酸钠含量的方法.方法采用阴离子交换柱(Waters IC Pak A柱,50 mm× 4.6 mm,5 μm);以0.05 mol·L-1邻苯二甲酸氢钾溶液(取邻苯二甲酸氢钾0.204 g,加水适量,振摇使溶解,加1mol·L-1硝酸溶液5 mL,加水稀释至2 000 mL,摇匀即得)为流动相;流速1.4 mL·min-1,检测波长290nm.结果本方法在0.98～4.90g·L-1浓度范围呈良好线性关系(r=0.999 4),进样重现性RSD为0.71%(n=5),平均回收率为98.93%.结论本法简便、快速、结果准确可靠,可用于膦甲酸钠氯化钠注射液中膦甲酸钠的含量测定.     

哌拉西林钠他唑巴坦钠致抽搐

1例26岁男性患者,4年前行肾移植术,近5个月接受血液透析,因肺部感染给予哌拉西林钠他唑巴坦钠4.5 g加入0.9%氯化钠注射液100 ml、1次/d静脉滴注。第2次用药后5 h,患者突发抽搐、意识丧失、双眼上翻、双腿抽动。先后给予地西泮10 mg肌内注射及7 mg静脉注射,上述症状消失。     

Inhaled sodium metabisulphite induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

1. The effects of nedocromil sodium and sodium cromoglycate on bronchoconstriction induced by inhaled sodium metabisulphite have been studied in eight atopic subjects, three of whom had mild asthma. 2. Nedocromil sodium (4 mg, 7.8 X 10(-6) M), sodium cromoglycate (10 mg, 24.1 X 10(-6) M) and matched placebo were administered by identical metered dose inhalers 30 min before a dose-response to sodium metabisulphite (5-100 mg ml-1) was performed. 3. Maximum fall in sGaw after placebo pre-treatment was -43.9 +/- 3.3% baseline (mean +/- s.e. mean). At the same metabisulphite concentration maximum fall in sGaw after sodium cromoglycate was -13.0 +/- 3.6% and after nedocromil sodium was +4.3 +/- 6.8%. Nedocromil sodium prevented any significant fall in sGaw even after higher concentrations of metabisulphite. 4. Both nedocromil sodium, 4 mg, and sodium cromoglycate, 10 mg, inhibited sodium metabisulphite induced bronchoconstriction but nedocromil sodium was significantly more effective. Relative in vivo potency of the two drugs is broadly in line with other in vivo and in vitro studies.     

头孢哌酮钠-舒巴坦钠致血小板减少

1名83岁男性患者因胆道系统感染,静脉给予注射用头孢哌酮钠-舒巴坦钠2.0g,1次/白天;1.0g,1次/晚上。用药6d内血小板进行性下降,由164×109/L下降到68×109/L。停用头孢哌酮钠-舒巴坦钠,改用左氧氟沙星治疗。1周后患者PLT恢复正常。     

哌拉西林钠他唑巴坦钠致白细胞减少

1例46岁女性患者,因术后颅内感染静脉滴注哌拉西林钠他唑巴坦钠4.5 g,1次/8 h。用药第13、15天外周血白细胞计数从用药前的10.61×109/L分别降至1.79×109/L和1.00×109/L。立即换用其他抗菌药物,同时给予重组人粒细胞巨噬细胞集落刺激因子(rhGM-CSF)150μg皮下注射,1次/d。改变治疗后4 d,血白细胞计数升至6.95×109/L。改变治疗后6 d脑脊液白细胞数由首次用药后15 d的8×106/L升至56×106/L,再次给予哌拉西林钠他唑巴坦钠4.5 g静脉滴注,1次/8 h,rhGM-CSF剂量未变。用药6 d颅内感染治愈,遂停用抗菌药物。治疗第2、5天白细胞计数分别为2.67×109/L和1.65×109/L。第8天停用rhGM-CSF后为5.75×109/L,第15天为4.56×109/L。     

Fondaparinux sodium

black triangle Fondaparinux sodium, a selective factor Xa inhibitor, is the first in a new class of antithrombotics. It binds selectively with high affinity to antithrombin III and specifically catalyses the inactivation of factor Xa. The elimination half-life of fondaparinux sodium permits once daily treatment. black triangle A randomised, double-blind, parallel-group, dose-ranging, multicentre phase IIb study in 933 eligible patients established that a subcutaneous dose of between 1.5 and 3mg of fondaparinux sodium has the optimum efficacy and safety profile for prophylaxis of venous thromboembolism in patients undergoing major orthopaedic surgery. black triangle Fondaparinux sodium, given to more than 3600 patients undergoing major orthopaedic surgery who participated in prospective, randomised, double-blind, multicentre phase III clinical trials, significantly reduced the incidence of venous thromboembolism, with an overall risk reduction of 55.2% compared with enoxaparin. black triangle Fondaparinux sodium was well tolerated by patients undergoing major orthopaedic surgery, and at the recommended clinical dose of 2.5mg has a similar tolerability profile, including bleeding events, to standard enoxaparin regimens. Fondaparinux sodium has not been reported to cause antibody-induced thrombocytopenia.     

Talaporfin sodium

Importance of the field: Despite therapeutic advances, cancer remains the cause of an estimated 23% of deaths in the USA. New treatments for malignancy are greatly needed.

Areas covered in this review: Talaporfin sodium is a light-activated drug that causes tissue death through induction of apoptosis. Systemic antitumor effects mediated by CD8⁺ T cells have been demonstrated in preclinical studies, providing a mechanism for distant response of tumors noted in clinical trials. Talaporfin sodium is approved in Japan for early-stage endobronchial cancer. Phase I and II studies in solid tumors have shown tumor regression in patients refractory to other therapies. Phase III pivotal studies against hepatocellular carcinoma as monotherapy and liver-metastatic colorectal cancer in combination with chemotherapy are ongoing. Talaporfin sodium is also in studies in men with symptomatic benign prostatic hyperplasia. Substantial safety data from clinical trials so far indicate that the drug is well tolerated.

What the reader will gain: Talaporfin sodium has a broad safety profile and a mode of action that could affect growth in treated and untreated tumors.

Take home message: Clinical and preclinical studies indicate that talaporfin sodium treatment may offer a powerful option to synergize current therapies, as well as an alternative monotherapy in treating cancer.     

Danaparoid sodium

Danaparoid sodium (Orgaran, Organon) is a heparinoid glycosamino-glycuronan antithrombotic agent approved for the prophylaxis of post-operative deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE) in patients undergoing elective hip replacement surgery. Danaparoid is a low molecular weight heparinoid consisting of a mixture of heparan sulphate (84%), dermatan sulphate (12%) and small amounts of chondroitin sulphate (4%), whose antithrombotic activity has been well established. Its pharmacological effect is exerted primarily by inhibiting Factors Xa (FXa) and IIa (FIIa) at a ratio greater than heparin, with a minimal effect on platelet function. Danaparoid exhibits low cross-reactivity with heparin-induced antibodies when compared with heparin or low molecular weight heparins (LMWH), thereby making it an excellent choice for the management of heparin-induced thrombocytopenia (HIT). It has excellent bioavailability following s.c. injection. Danaparoid has little effect on routine coagulation tests (activated partial thromboplastin time [aPTT], prothrombin time [PT], and thrombin time [TT]). Patients with elevated serum creatinine should be monitored carefully. For its FDA approved indication (DVT prophylaxis during hip replacement surgery), its cost per day is approximately eight times more than LMWH. Even though monitoring is not routinely necessary according to the manufacturer for its approved indication, monitoring is frequently necessary when it is used in other clinical scenarios. Its higher cost than comparable therapies for DVT prophylaxis and the low availability of the FXa assay in most non-tertiary care hospitals has limited the widespread use of danaparoid. Danaparoid has been found to be effective in the treatment of HIT although this is an off label use, despite being the most frequent reason why danaparoid is used.     

Diclofenac sodium

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of diclofenac sodium are reviewed. Diclofenac, the first nonsteroidal anti-inflammatory agent (NSAID) to be approved that is a phenylacetic acid derivative, competes with arachidonic acid for binding to cyclo-oxygenase, resulting in decreased formation of prostaglandins. The drug has both analgesic and antipyretic activities. Diclofenac is efficiently absorbed from the gastrointestinal tract; peak plasma concentrations occur 1.5 to 2.0 hours after ingestion in fasting subjects. Even though diclofenac has a relatively short elimination half-life in plasma (1.5 hours), it persists in synovial fluid. The drug is metabolized in the liver and is eliminated by urinary and biliary excretion. In clinical trials, diclofenac was as effective as aspirin, diflunisal, indomethacin, sulindac, ibuprofen, ketoprofen, and naproxen in improving function and reducing pain in patients with rheumatoid arthritis. For treatment of osteoarthritis, diclofenac was equivalent in efficacy to aspirin, diflunisal, indomethacin, sulindac, ibuprofen, ketoprofen, naproxen, flurbiprofen, mefenamic acid, and piroxicam. Diclofenac was as effective as indomethacin or sulindac in treating ankylosing spondylitis. The most frequent adverse effects reported for diclofenac were gastrointestinal, but these effects were fewer and less serious than occurred with aspirin or indomethacin; in addition, diclofenac caused fewer central nervous system reactions than indomethacin. Diclofenac is administered in divided doses with meals. The recommended total daily dosage is 100 to 150 mg (osteoarthritis and ankylosing spondylitis) or 150 to 200 mg (rheumatoid arthritis). Diclofenac is effective, but no more so than other NSAIDs. It is structurally distinct and offers another choice in the treatment of rheumatological conditions.