西咪替丁致骨髓增生异常综合征1例

<正> 谭某,男性,49yr,因面黄乏力、低热2mo,于1987年7月15日入院。患者因十二指肠溃疡病,自1986年4月服用西咪替丁200mg(1片)tid,连续用200片后,症状缓解。服该药中断3mo后,病情复发。自9月起又服该药200mg(1片)tid,共服500片,症状又缓解。本次服药2mo,查WBC3.8×10~9/L,Hb130g/L,Pt160×10~9/L,血象无异常变化。随后停药3mo。于1987年1月,溃疡症状     

误服过量硫酸沙丁胺醇致婴幼儿腹泻

1例8月龄男婴因肺炎拟给予硫酸沙丁胺醇0.8 mg(1/3片),3次/d治疗。但由于其家长的误解,一次性给予患儿7.2 mg(3片)。服药后1 h,患儿出现恶心、呕吐、腹泻(6次,稀水样便)。粪常规检查示稀水便,脂肪球(++)。停用硫酸沙丁胺醇。给予头孢哌酮钠-舒巴坦钠、细辛脑、碳酸氢钠,并行灌肠止泻等治疗,患儿病情得到有效控制。     

服用安乃近片致过敏性休克死亡

1例38岁男性患者因感冒自服安乃近3片(0.5 g/片).约30 min后,患者出现头晕、胸闷、乏力,面部、颈部、躯干及四肢出现红色瘀点和瘀斑.3 h后因病情加重入院.查体:T 37.2℃,HR 118次/min,R 32次/min,BP 30/0 mm Hg,烦躁不安,意识障碍,全身湿冷,尿失禁,双侧瞳孔散大.血常规:WBC 12.6×109/L,N 0.80,PLT 136×109/L.心电图示心动过速,窦性心律不齐.给予肾上腺素、地塞米松、异丙嗪、碳酸氢钠治疗,但抢救无效,患者死亡.     

头孢哌酮钠/舒巴坦钠致急性造血停滞

患者女,71岁。因“肝功能异常1年,乏力尿黄1周”,于2004年10月15日入院。诊断为自身免疫性肝病,给予保肝、降酶、退黄、支持治疗,病情好转。入院时检查血象3系均正常:WBC9.30×109/L、N0.566;RBC3.54×1012/L,HGB127g/L;PLT131×109/L。B超示:脾不大。入院后2周(10月27日)发现双下肺炎症,即加用头孢哌酮钠/舒巴坦钠(优普酮)4g,1次/12h抗感染治疗。4d后检测血常规:WBC4.27×109/L,RBC2.36×1012/L,HGB81g/L,PLT32×109/L。1周后复查:WBC3.10×109/L,RBC2.15×1012/L,HGB74g/L,PLT20×109/L。行骨穿检查,骨髓片检查示增生…     

阿司匹林过敏致多脏器损害一例分析

1例23岁女性患者,因体温升高两天内反复服用阿司匹林6片(0.5g/片)后出现上腹部不适,伴有恶心,并出现面部皮疹,入院治疗,患者皮疹进行性加重,发展为全身麻疹样红斑,且出现胸闷气急,查生化示ALT373U/L,AST 230U/L,TP 54.1g/L,ALB 28.9g/L,患者肝功能异常和低蛋白血症,并出现下肢水肿、胸腔和盆腹腔积液,病情急剧恶化,转上级医院治疗。     

马来酸氯苯那敏致过敏反应

患儿，男，12岁，因发热、流鼻涕，自行口服复方朴尔敏感冒片1片(批号020302)，1h后，躯干部、胸部、颈部出现散在性红斑，并伴瘙痒。既往无过敏史，因怀疑为药物过敏所致，随即给予抗过敏药马来酸氯苯那敏片1片，口服(批号981102)。2h后，瘙痒加剧，红斑遍及全身，随即就诊。体检：T36．8℃，：BP105／63mmHg，神志清，心、肺、脾未见异     

厄贝沙坦胶囊口服致鼻衄1例

患者女,57岁,无任何家族病史,患糖尿病肾病10年,因病情加重,于2009年1月来我院肾病中心住院治疗。2个月后病情好转出院,医生给予抗高血压药:硝苯地平缓释片每次30 mg、每日2次,阿替洛尔片每次12.5 mg、每日2次,硝苯地平片每次10 mg、每日2次,血压仍波动于160～180/90～110 mmHg。2009年3月23日再次来我院门诊就医,测血压180/110 mmHg,加服厄贝沙坦胶囊(珠海润都民彤制药有限公司,批号为20090101105),每次1粒,每天1次。     

拜心同致急性尿潴留1例

患者 ,男 ,6 8岁。因尿毒症于 1999年 2月 13日行肾移植术 ,术后一直口服三联免疫抑制剂 :泼尼松片、环孢素A胶囊、硫唑嘌呤 ,同时联用的药物有抗高血压药硫氮 艹卓 酮缓释片和治疗前列腺炎的保列治片。患者因高血压曾先后服用过硝苯地平片、可乐定片、氨氯地平 (络活喜 )片、贝那普可(洛汀新 )片和哌唑嗪片。曾因服用络活喜片后双踝部水肿而停用。自 2 0 0 1年 3月 ,患者一直联用洛汀新片 10mg/qd ,哌唑嗪片 0 .15mg/qid及可乐定片 0 .75mg/tid降压治疗 ,血压维持在 12 0～ 130 /85～ 90mmHg。 2 0 0 1年 10月 2 0日因血压升高而遵医嘱于…     

琥乙红霉素片与环丙沙星片同服引发急性肾功能不全1例

患者,男,42岁,汉族,既往体健,无肾病史。于2013年11月10日因上呼吸道感染后自服琥乙红霉素片、环丙沙星片（具体剂量不详）后,出现头晕、尿量明显减少、周身轻度浮肿,以眼睑较为明显、食欲不振。故3d 后来市医院就诊,门诊查尿蛋白（PRO）（﹢﹢﹢）,嘱住院治疗,但患者拒绝接受住院治疗。门诊予以口服药物：吲哚美辛肠溶片50mg、复合维生素 B250mg、双氢克尿噻片50mg,每天3次,治疗后,尿量略有增加,1周后自觉全身浮肿加重,以眼睑及双下肢为甚。故再次来院就诊,查尿 PRO（﹢﹢﹢﹢）,以“药源性肾炎”收住院治疗。入院查体：T 36℃,P 64次/ min,R 20次/ min,BP 130/70mm Hg。神志清,精神差,颜面部轻度浮肿,双肺呼吸音粗,心律齐,未闻及病理性杂音。腹软,无压痛,肝脾未及肿大,双肾区叩击痛（﹢）,双下肢凹陷性水肿。化验尿 PRO（﹢﹢﹢﹢）,尿素氮（BUN）16.8mmol/ L。既往有“磺胺类药”过敏史。住院治疗：氢化可的松注射液200mg ﹢10％葡萄糖注射液500ml,每天1次静脉滴注,葡萄糖酸钙注射液10ml ﹢10％葡萄糖注射液20ml,每天1次静脉推注,口服双氢克尿噻片50mg,维生素 C片0.2g,马来酸氟苯那敏（扑尔敏片）8mg,醋酸泼尼松片10mg,多潘立酮（吗丁啉片）10mg,每天3次。并予以对症支持治疗,病情逐日好转,住院1周后,患者病情明显好转,无头晕及全身肿胀感,眼睑及双下肢浮肿减退,尿量正常,于2013年11月27日好转出院,出院后2周,因上述症状重新出现而到上级医院就诊。     

复方鳖甲软肝片联合替比夫定治疗慢性乙型肝炎肝硬化疗效分析

目的 探讨复方鳖甲软肝片联合替比夫定治疗慢性乙型肝炎肝硬化的疗效.方法 选择病情、病程相近且满足入选标准的40例患者,采用分层随机(随机分配表)、单盲法分为治疗和对照组,治疗组给予口服替比夫定0.6g/次,1次/d,复方鳖甲软肝片4片/次,3次/d;对照组仅口服替比夫定0.6g/次,1次/d.治疗48周后统计疗效.观测指标为治疗前后临床症状和肝功能、血清纤维化指标、腹部肝脾超声检查.使用SPSS 13.0统计软件进行分析,计量资料用t检验,计数资料用,检验.结果 治疗2两组临床症状均有明显改善,但比较差异无统计学意义(P＞0.05);2组治疗后肝功能ALT、白蛋白、白/球比值、血清TBil均明显好转,但治疗组优于对照组,2组比较差异有统计学意义(P＜0.05);2组治疗后肝纤维化指标比较,对照组透明质酸酶、层粘连蛋白、Ⅲ型前胶原分别为(142±26)、(131±31)、(103±50) μg/L,治疗组分别为(93±21)、(85±28)、(90±52) μg/L,治疗组优于对照组,2组比较差异有统计学意义(P＜0.05);治疗后治疗组肝脾超声检查结果优于对照组,2组比较差异有统计学意义(P＜0.05).结论 复方鳖甲软肝片联合替比夫定治疗慢性乙型肝炎肝硬化优于单用替比夫定,两者联合有协同作用.肝硬化治疗是长期过程,寻找多途径、多靶点药物联合,可能比单一用药效果更好.     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.     

2-(Acetoxyphenyl)-(Z)-styryl sulfides as cyclooxygenase inhibitors

2-(Acetoxyphenyl)-(Z)-styryl sulfides are described as selective cyclooxygenase-2 (COX-2) inhibitors, useful for treating inflammation and COX-2-mediated disorders including neoplasia. 2-(Acetoxyphenyl)-(Z)-styryl sulfide is claimed to be the most potent COX inhibitor in the series with a COX-2 selectivity ratio of 33. This compound is also claimed to be superior to celecoxib (Celebrex^®, Pfizer) in inhibiting cell growth of colorectal carcinoma cells. In this evaluation, the COX inhibitory activity of this compound is compared to that previously disclosed for diarylheterocycles and 2-(acetoxyphenyl)alkyl sulfides. The validity of the DLD-1 cell line in the growth inhibition studies is questioned based on recent literature reports indicating the lack of COX-2 expression in this cell line.     

Sleep-disordered breathing with chronic opioid use

Chronic opioid use for pain relief or as substitution therapy for illicit drug abuse is prevalent in our societies. In the US, retail distribution of methadone and oxycodone has increased by 824 and 660%, respectively, between 1997 and 2003. μ-Opioids depress respiration and deaths related to illicit and non illicit chronic opioid use are not uncommon. Since 2001 there has been an emerging literature that suggests that chronic opioid use is related to central sleep apnoea of both periodic and non-periodic breathing types, and occurs in ～ 30% of these subjects. The clinical significance of these sleep-related abnormalities are unknown. This review addresses the present knowledge of control of ventilation mechanisms during wakefulness and sleep, the effects of opioids on ventilatory control mechanisms, the sleep-disordered breathing found with chronic opioid use and a discussion regarding the future research directions in this area.     

Drug targets for cognitive enhancement in neuropsychiatric disorders

The investigation of novel drug targets for treating cognitive impairments associated with neurological and psychiatric disorders remains a primary focus of study in central nervous system (CNS) research. Many promising new therapies are progressing through preclinical and clinical development, and offer the potential of improved treatment options for neurodegenerative diseases such as Alzheimer's disease (AD) as well as other disorders that have not been particularly well treated to date like the cognitive impairments associated with schizophrenia (CIAS). Among targets under investigation, cholinergic receptors have received much attention with several nicotinic agonists (α7 and α4β2) actively in clinical trials for the treatment of AD, CIAS and attention deficit hyperactivity disorder (ADHD). Both glutamatergic and serotonergic (5-HT) agonists and antagonists have profound effects on neurotransmission and improve cognitive function in preclinical experiments with animals; some of these compounds are now in proof-of-concept studies in humans. Several histamine H3 receptor antagonists are in clinical development not only for cognitive enhancement, but also for the treatment of narcolepsy and cognitive deficits due to sleep deprivation because of their expression in brain sleep centers. Compounds that dampen inhibitory tone (e.g., GABA_A α5 inverse agonists) or elevate excitatory tone (e.g., glycine transporter inhibitors) offer novel approaches for treating diseases such as schizophrenia, AD and Down syndrome. In addition to cell surface receptors, intracellular drug targets such as the phosphodiesterases (PDEs) are known to impact signaling pathways that affect long-term memory formation and working memory. Overall, there is a genuine need to treat cognitive deficits associated with many neuropsychiatric conditions as well as an increasingly aging population.