头孢美唑钠致白细胞和粒细胞减少

1例17岁女性患者因感染性心内膜炎静脉滴注头孢美唑钠（2 g,3次/d）和阿米卡星（0.4 g,1次/d）。用药6天血常规检查示白细胞计数23.4×109/L,中性粒细胞0.92,中性粒细胞绝对值21.6×109/L。用药第13天血常规检查示白细胞计数6.6×109/L,中性粒细胞0.70,中性粒细胞绝对值4.6×109/L。第14天停用阿米卡星,继续原剂量静脉滴注头孢美唑钠。用药第28天血常规检查示白细胞计数2.6×109/L,中性粒细胞0.37,中性粒细胞绝对值1.0×109/L。停用头孢美唑钠,更换为万古霉素粉针0.5 g,1次/8 h静脉滴注。更换药物后第7天,血白细胞计数6.1×109/L,中性粒细胞0.60,中性粒细胞绝对值3.7×109/L。     

哌拉西林钠他唑巴坦钠致血小板增多症

1例44岁男性2型糖尿病酮症患者因泌尿系统感染给予注射用哌拉西林钠他唑巴坦钠3.375 g静脉滴注、1次/8 h。用药前患者血小板计数（PLT）288×10 9/L。治疗5 d后PLT升至729×10 9/L。诊断为继发性血小板增多症,考虑可能与哌拉西林钠他唑巴坦钠有关。停用该药,改用左氧氟沙星0....     

哌拉西林钠他唑巴坦钠致血细胞减少误诊为消化道出血

1例79岁男性患者因头部外伤合并大肠埃希菌肺炎给予哌拉西林钠他唑巴坦钠4.5 g静脉滴注、1次/8 h治疗。治疗前白细胞计数（WBC）10.20×10 9/L,红细胞计数（RBC）3.58×10 12/L,血红蛋白（Hb）101 g/L,血小板计数（PLT）202×10 9/L。用药第2天...     

哌拉西林钠他唑巴坦钠致重症肝病患者贫血加重及血小板减少3例

3例重症肝病合并感染患者（均为男性,年龄分别为40、68、50岁）接受碳青霉烯类、利奈唑胺及氟康唑联合治疗,期间未出现明显血象变化。因疗效不佳换用哌拉西林钠他唑巴坦钠4.5 g,8 h/次静脉滴注。其中例1于换用哌拉西林钠他唑巴坦钠11 d后出现贫血及血小板计数下降;例2、例3分别于换用哌拉西林钠他唑巴坦钠4、7 d后出现贫血加重及血小板计数下降。3例患者分别在停用哌拉西林钠他唑巴坦钠后31、21、7 d,血红蛋白及血小板计数明显恢复。     

临床药师参与处理1例哌拉西林钠他唑巴坦钠引起的血小板减少症患者的分析

1例63岁的脑外伤患者在接受硬膜外血肿治疗13 d后发生了导管相关性泌尿系统感染,医师先后给予左氧氟沙星和哌拉西林钠他唑巴坦钠治疗,但在加用哌拉西林钠他唑巴坦钠治疗3 d后,患者的血小板计数从127×109/L降至44×109/L.临床药师早期识别了患者血小板减少发生的原因,及时建议改用阿米卡星治疗并为医师采纳.10 d后患者的泌尿系统感染痊愈,且其间未再出现药物不良反应.     

哌拉西林钠舒巴坦钠引起高热、白细胞减少1例

一例21岁产褥期女性患者因颅内静脉血栓形成、肺部感染给予低分子皮下注射抗凝,哌拉西林钠舒巴坦钠静脉滴注抗感染诊疗,2d后体温正常。哌拉西林舒巴坦使用1周后再次出现高热、白细胞降至2.77±215;109/L,停用哌拉西林钠舒巴坦钠,并继续抗凝后体温恢复正常出院。2周后复查血白细胞恢复正常,确定为哌拉西林钠舒巴坦钠所致药物热。     

注射用哌拉西林钠他唑巴坦钠致药物热的临床分析

目的:为临床及时、准确地判断注射用哌拉西林钠他唑巴坦钠引起的药物热和合理用药提供参考。方法:对2013年9月-2014年9月临床药师收集的30例由注射用哌拉西林钠他唑巴坦钠致药物热住院患者的用药情况、临床表现、实验室检查结果、医师处理方式等进行回顾性统计分析。结果:注射用哌拉西林钠他唑巴坦钠致药物热多发生在连续用药7~14 d,单位累积用量多在1.3~2.7 g/kg之间;30例患者中,73.3%在滴注期间开始发热,体温以≥38.5℃高热为主;嗜酸性粒细胞计数升高、血清C反应蛋白(CRP)和血细胞沉降速率(ESR)轻度升高可作为药物热的判断指标,但白细胞计数降低并不适合作为判断指标;停用该药或改用其他抗菌药物后,患者体温均在24~48 h内降至正常。结论:注射用哌拉西林钠他唑巴坦钠致药物热与患者性别、年龄没有关联,也没有特异性的诊断标准,但与用药时间、累积天数、单位累积用量存在一定的相关性,结合一些血液学检查指标可作为判断药物热的依据。临床医师应提高对药物热的认识和重视程度,及时停用可疑药物。     

哌拉西林他唑巴坦钠致肉眼血尿1例

1例46岁男性患者,因“左侧肢体活动不利6月余”入院行康复治疗,入院后出现发热、白细胞、中性粒细胞百分比、C-反应蛋白升高现象,给予注射用哌拉西林他唑巴坦钠（4.5 g,ivdrip,q8 h）抗感染治疗,当日夜间患者出现肉眼血尿。第2d尿常规示：红细胞8493/μL;第3d肉眼血尿加重,尿常规示红细胞16 469·μL-1,考虑哌拉西林他唑巴坦钠致血尿,立即停用,改用左氧氟沙星氯化钠注射液（0.5 g,qd,ivdrip）治疗。2 d后尿常规示：红细胞8 675·μL-1;5 d后尿常规示：红细胞64·μL-1,已无肉眼血尿。至2020.09.21患者未再出现肉眼血尿。     

丙戊酸钠致严重血小板减少

1例87岁女性患者因抽搐和心动过缓给予注射用丙戊酸钠1200mg静脉持续泵入,20ml／h,1次／d。用药前患者血小板计数为214×10^9／L。用药8d后血小板计数降至63×10^9／L,停用注射用丙戊酸钠,改为口服丙戊酸钠缓释片500mg,1次／d。5d后患者血小板计数降至25×10^9／L。停用丙戊酸钠缓释片,输注血小板1U,口服氨肽素1000mg,3次／d。对症治疗8d后血小板计数升至160×10^9／L。     

哌拉西林钠他唑巴坦钠与阿奇霉素联用治疗肺部感染的研究

目的:观察哌拉西林钠他唑巴坦钠联合阿奇霉素治疗肺部感染的临床疗效和安全性。方法:122例中、重度肺部感染的患者随机分为A、B、C组。A组给予哌拉西林钠他唑巴坦钠4.5g,静脉滴注,bid,3h后给予阿奇霉素0.5g,静脉滴注,qd。B组给予哌拉西林钠他唑巴坦钠4.5g,静脉滴注,bid。C组给予阿奇霉素0.5g,静脉滴注,qd。治疗3d后,B、C组联用其它抗菌药。3组总疗程为7～14d。观察比较3组的疗效和细菌清除率,并记录患者不良反应的发生情况。结果:治疗3d后,A组的有效率及细菌清除率明显高于B、C组,且有显著性差异(P<0.05)。而治疗7～14d后,3组的疗效及不良反应发生率比较,差异无统计学意义(P>0.05)。结论:对于中、重度肺部感染的患者,应用哌拉西林钠他唑巴坦钠联合阿奇霉素治疗快速、安全、有效。     

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。     

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.     

Fondaparinux sodium

Fondaparinux (Org-31540 / SR-90107A) is a new drug chemically synthesized for treatment and prophylaxis of thromboembolic disease. Fondaparinux is a selective inhibitor of activated factor X. Its structure is the copy of the heparin pentasaccharide sequence, the shortest chain required for antithrombin inhibition of activated factor X without antithrombin action. Fondaparinux has no effect on coagulation tests and does not bind to platelet factor 4 or promote heparin-induced thrombocytopenia. Fondaparinux inhibits thrombin generation and the growth of thrombi in in vitro and in vivo models. Phase I trials have shown a 100% bioavailability after subcutaneous (s.c.) administration, a rapid onset of action and an approximate half-life of 13.5 h. Fondaparinux is cleared as an active substance by the kidneys. In elderly patients, renal clearance is reduced and the half-life is longer. The phase II Pentathlon trial demonstrated significant dose-dependent reductions in the frequency of venous thromboembolism in total hip-replacement patients and the optimal dose was determined to be 2.5 mg s.c./24 h. Four phase III trials have evaluated fondaparinux starting 6 hours after surgery compared with enoxaparin for prevention of venous thromboembolism following orthopedic surgery in 7,344 patients. The risk of thrombosis was reduced by 50% with fondaparinux and no differences were observed in death or severe bleeding. In a phase II trial, similar efficacy and incidence of major bleeding were seen with fondaparinux s.c. compared with dalteparin s.c. in the treatment of deep venous thrombosis. In patients with acute myocardial infarction, the efficacy of fondaparinux during fibrinolytic therapy was assessed in 326 patients who had acute coronary syndromes of less than a 6 hour duration, showing a slight but statistically not significant advantage for fondaparinux over unfractionated heparin in the coronary angiographies. There is currently no antidote for fondaparinux.