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.     

抗-E、抗-c先后2次引起迟发性溶血性输血反应1例

1 病例报告 患者,女,63岁.生有4子女后有过2次不明原因流产史.2003年4月份因左股骨干骨折入院,术后查血常规正常.同年12月7日因糖尿病伤口感染再次入院.查:外周血WBC 8.4×109/L,RBC1.74×1012/L,HGB 52g/L,HCT 0.153,PLT 178×109/L.     

双环铂引起全血细胞减少

1例71岁男性患者因右肺癌切除术后化疗,给予双环铂650 mg加入5%葡萄糖注射液1000 mL静脉滴注,4 h内输注完毕。次日,患者出现双下肢无力,恶心。3周后患者行第2次化疗,方案与第1次相同。次日,患者出现恶心、右侧鼻腔出血。实验室检查：WBC 3.04×109/L,N 0.50,L 0.37,Hb 83 g/L,RBC 2.76×1012/L,PLT 35×109/L。立即行鼻腔局部止血等对症治疗。3 d后鼻腔出血消失,血常规逐渐恢复正常,实验室检查：WBC 4.04×109/L,N 0.53,L 0.35,Hb 86 g/L,RBC4.16×1012/L,PLT 87×109/L。     

头孢曲松致发热及溶血

患者男,51岁。因肝硬化(失代偿期)伴急性泌尿系统感染,于2003年10月10日入院。查体:体温37.3℃,B超示:肝硬化,胆囊内胆泥淤积,有腹水形成,脾大并脾功能亢进症,有门脉高压。血常规:WBC4.0×109/L、RBC2.67×1012/L、HGB105g/L、PLT42×109/L;尿常规:WBC( )。诊断:急性泌尿系统感染伴肝硬化失代偿期。治疗:给予保肝、抗感染等治疗。抗感染治疗期间给予头孢曲松钠(丽珠芬)2.0g加入20mL0.9%氯化钠注射液缓慢静脉推注,2次/d。治疗第5天(10月15日),患者于用药0.5h开始出现畏寒、寒战、发热(T39.3℃)。以后每天用药后均出现相同症状,给予…     

ATRA诱导治疗AML-M2缓解1例

患者,女,15岁,主因头晕、乏力5个月,加重1个月入院.患者于5个月前无明显诱因出现头晕、乏力,未引起重视,于1个月前加重,到当地医院就诊,血常规:WBC 42.6×109/L,RBC 1.55×1012/L, HGB 58 g/L,PLT 29×109/L.     

真性红细胞增多症并心肌梗死、高血压一例

1临床资料患者,女,农民,因"阵发性心前区闷痛3天,加重8小时"于2011年6月24日入院。伴肢冷汗出,恶心呕吐。发现高血压病史2月,最高170/120mmHg。入院急诊心电图示Ⅱ、Ⅲ、AVF、V3R、V4R ST段弓背抬高大于0.15mv,ⅠAVL ST段压低大于0.15mv。入院BP85/60mmHg,CK2271IU/L、CK-MB272IU/L WBC19.27×109HGB149g/l RBC5.11×1012PLT461×109。25日复查心电图ⅢQr波,AVF病理性qR波,Ⅰ、AVL、V4-V6ST段压低大于0.05mv。根据症状、心电图、辅助检查考虑:1.冠心     

头孢曲松致自身免疫性溶血性贫血1例

1病例资料患儿女,4岁,15 kg。因发热、咳嗽、声嘶2 d,以"急性喉气管支气管炎"入院。血常规示WBC15.55×109/L、N 65%、RBC 5.58×1012/L、PLT 289×109/L、Hb 117 g/L及CRP 58 mg/L,不能除外细菌感染故于入院后使用头孢曲松(罗塞嗪,深圳九新药业有限公司,批号1205013)1.5 g,同时静脉滴注喜炎平50 mg及布地     

冷球蛋白血症性肾小球肾炎1例

1 病例介绍 患者,男,38岁,因"腹痛、皮疹、少尿、双下肢水肿半月"人院.入院查体:T 37.3℃,P 90次,分,R 20次,分,BP 140/78 mmHg<1 mmHg=0.133 kPa).神清,无贫血貌.颜面水肿,双侧四肢远端可见散在出血性瘀斑,未高出皮面,心肺(-),腹水征(+),双下肢重度水肿.余未见异常体征.辅助检查:血常规示WBC 12.8×109/L,RBC 4.99×1012/L,PLT 121×109/L,HGB160 g/L,HCT0.436.N 0.86,E 0.01.     

全脊髓麻醉2例救治管理

例1.女,49岁,体重57 kg,因转移性右下腹痛1 d入院,检查发现右下腹有压痛.实验室检查WBC 1.68×109/L ,RBC 2.64×1012/L ,HGB 106 g/L,诊断为急性阑尾炎,拟在硬膜外麻醉下行阑尾切除术.     

保泰松和泼尼松引起多脏器功能衰竭和急性造血功能停滞死亡

1名21岁女性患者因腰痛服用保泰松0.2g,3次/d;泼尼松10mg,3次/d。服药约26d后,出现发热、尿黄、水肿、皮疹。3d后停药,但症状继续加重。9d后入院,T38.7℃,P112次/min,皮肤巩膜重度黄染,实验室检查TBil190.9μmol/L,DBil132.2μmol/L,Alb29g/L,Glob31g/L,ALT251U/L,AST64U/L,ALP233U/L,γ-谷氨酰转移酶(γ-GT)251U/L,LDH594U/L,WBC13.5×109/L。腰椎MRI检查示腰3、4椎体结核。给予抗感染治疗、支持治疗、甲泼尼龙冲击治疗及血浆置换等,但患者黄疸逐渐加深,并出现腹胀,尿少,躯干、四肢出现暗红色小片状出血斑。肾功能检查示BUN15.5mmol/L,Cr189μmol/L。B超提示大量腹腔积液。血常规:WBC1.7×109/L,RBC2.04×1012/L,Hb58g/L,PLT19×109/L。骨髓检查显示为急性造血功能停滞。入院后第9天死亡。     

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.