白加黑感冒片致急性药物性肝炎

白加黑是感冒病症中比较常见的用药,能对感冒有着较好的治疗和抵抗效果,而且白天和夜晚用药是区分开的,从人体生理学的的角度来讲,更符合人们的生理作息和机能的调息,但是有时候因个体的体质不同,对白加黑药物的服用会产生不同程度的不良反应,严重的甚至会造成急性肝损坏的严重后果,本文在实际用药过程中因服用白加黑引起的急性药物性肝炎进行举例说明,希望能对这类常用抗感冒药的的使用用所帮助。     

萝芙木致药物性肝炎

1例45岁男性患者因咽痛自行服用萝芙木煎剂(250 ml相当25 g),3次/d.服药第4天出现尿黄,第7天出现恶心、呕吐、乏力、纳差、皮肤和巩膜黄染,第9天入院.实验室检查:丙氨酸转氨酶(ALT)1 735 U/L,天冬氨酸转氨酶(AST) 682 U/L.诊断为药物性肝炎.立即停用萝芙木,给予茵栀黄口服颗粒剂和谷胱甘肽、苦参碱、甘草酸二铵静脉滴注治疗.入院第12天复查肝功能:ALT 97 U/L,AST 32 U/L,患者痊愈出院.     

孟鲁司特致药物性肝炎

1例74岁男性患者因过敏性鼻炎、过敏性咽喉炎口服孟鲁司特及氯雷他定治疗。患者既往无药物过敏史及慢性肝病史。连续服药5 d后,患者出现皮肤黄染、恶心、纳差。肝功能:ALT 670 IU.L-1,AST 594 IU.L-1,T-BIL 79.1μmol.L-1,D-BIL 42.06μmol.L-1,TBA 5.8μmol.L-1。入院后行肝穿刺病理检查提示肝小叶内点片状坏死,汇管区嗜酸性粒细胞浸润,符合药物性肝炎的诊断标准。停用可疑药物,给予复方甘草酸苷、还原型谷胱甘肽、维生素C、茵栀黄口服液等治疗,肝功能逐渐恢复。出院2个月后血生化恢复正常。     

何首乌致药物性肝炎两例

患者男，38岁，无饮酒嗜好，平素体质良好。主因头发花白，自行使用偏方，何首乌30g和鸡蛋2个一起煮，喝汤然后吃鸡蛋。第一次服药后有身冷、发热表现，自以为感冒所致，休息一晚后症状消失。一周后，第二次服药，方法同前，药后再次出现身冷、发热表现，休息后恢复正常。第3周再次服药后夜间出现身冷发热，体温最高39．5°，     

氟康唑引起急性药物性肝炎

患者女,68岁,因发热,皮疹,双下肢关节酸痛8d,于2000年11月24日入院.查体:T39.0℃,上胸部可见片状红色斑丘疹,分布不均匀.     

硫普罗宁片致药物性肝炎

患者男,50岁。因脂肪肝,于2004年8月2日遵医嘱服用硫普罗宁片(凯西莱)100mg,3次/d。服药8d后患者出现尿黄、上腹饱胀感、呃逆及食欲减退等症状,自行减服药量至100mg,1次/d后。不见好转,并出现皮肤黄染,2d后停药。停药后,患者饱胀感即消失,食欲恢复正常,但尿液仍呈深黄色,皮肤黄染未消退。8月15日查尿,尿胆原( ),尿胆红素( );8月16日查肝功能:ALT253U/L、AST112U/L、总胆红素35.6μmol/L、直接胆红素18.9μmol/L、碱性磷酸酶147U/L、谷酰转肽酶775U/L、总胆汁酸224.9μmol/L,乙肝五项均为阴性。8月16日于我院就诊,追问病史:患者曾于…     

口服头孢氨苄致少年急性肾小球肾炎1例

头孢氨苄常用于呼吸道感染、尿路感染和软组织感染.我院在应用该药治疗1例少儿患上呼吸道感染时,患儿出现急性肾小球肾炎症状.【病例】男,14a.受凉感冒,发烧、咳嗽、咽痛.门诊查血、尿常规均正常,诊为上呼吸道感染.治疗用溴棕合剂10ml,咳必清12.5mg,tid,po头孢氨苄胶囊(中国广东火星制药厂,批号95O423)0.25g q6h.服药d2后患儿出现双眼睑明显浮肿,无其他症     

氟胞嘧啶引起急性药物性肝炎

患者男,78岁。2003年1月30日因咳嗽咳痰到我院门诊就诊。查体:T36.8℃,扁桃体不大,双肺呼吸音粗,未闻啰音，肝肋下未及，胸片示双肺纹理粗，血?鎃BC6.5×109/L,N0.673;两次痰培养均示白色念珠菌生长。给予口服氟康唑150mg/d,氟胞嘧啶0.5g,3次/d;14d后停用氟康唑,继续口服氟胞嘧啶0.5g,3次/d。3月11日,患者无发热,痰培养显示金黄色葡萄球菌生长,口服中药12剂治疗。4月20日因咳痰增多口服头孢羟氨苄0.25g,3次/d,治疗,1周。6月19日痰多,胸片示双肺纹理紊乱,给予口服罗红霉素0.15g2次/d,治疗5d。因反复多次痰培养均示白色念珠菌生长,对氟康唑…     

中药汤剂致药物性肝炎病例分析

目的对中药汤剂中可能导致药物性肝炎的药物进行分析。方法根据《急性药物性肝损伤诊治建议》及医学科学国际组织委员会（CIOMS）提出的急性药物性肝损害的评价标准对1例中药汤剂引起的药物性肝炎患者肝损害的程度进行评价,查阅相关文献对处方中的可疑药物进行分析。结果本例患者为中药汤剂导致的药物性肝细胞性肝损伤,汤剂中的白鲜皮导致药物性肝细胞性肝损伤可能性较大。结论临床在选择中药汤剂进行治疗时,应警惕其可能导致的药物性肝损伤。     

Antimicrobial-associated acute hepatitis

Recently, the case history of a 44-year-old woman who experienced acute hepatitis subsequent to therapy for chronic sinusitis was reviewed. The patient sequentially was administered clarithromycin, levofloxacin, amoxicillin-clavulanate, and gatifloxacin. Her adverse events were attributed definitively to gatifloxacin, a surprising conclusion because many other possible causes of hepatitis existed in this case. Not ruled out as potential causes of the clinical and laboratory adverse events were hepatitis other than hepatitis A or B. Other antimicrobials administered were dismissed. In particular, extended treatment with amoxicillin-clavulanate has been clearly linked to hepatotoxic effects that may occur long after therapy begins. Thus, while we agree that physicians must be aware of the potential for antimicrobial hepatotoxicity, we believe that this case study is not a solidly documented case of hepatitis attributable to gatifloxacin and overlooks other possible causes of acute hepatitis of which prescribers should be aware.     

Mefloquine-induced acute hepatitis

Mefloquine is an effective drug for prophylaxis and treatment of malaria caused by Plasmodium falciparum. It is generally well tolerated with few side effects. Minimal elevation of liver function tests has been reported after exposure to mefloquine, especially in susceptible individuals with prior abnormal liver function tests. Our patient, who had had elevated liver function tests attributed to heart failure, experienced an acute elevation of liver transaminases 6 weeks after exposure to mefloquine 250 mg/week. Cessation of the drug caused test results to return to normal. Mefloquine should be prescribed cautiously in patients with liver disease.     

Gatifloxacin-associated acute hepatitis.

Gatifloxacin, a fluoroquinolone with extended gram-positive activity, has become extensively used in both the community and hospital environments. Unfortunately, concerns have been raised about the use of certain fluoroquinolones because of adverse drug reactions. A 44-year-old woman developed acute hepatitis while receiving gatifloxacin for chronic sinusitis. After 5 days of receiving antibiotics, the patient developed nausea, lethargy, and abdominal pain, all of which progressed over the next few days. Liver function tests were elevated, with bilirubin peaking at 9.4 mg/dl. The patient also became jaundiced. A percutaneous liver biopsy showed acute hepatitis with eosinophilic infiltrates consistent with drug-induced hepatitis. All other drugs and disease processes were ruled out as likely causes of the patient's hepatitis. Clinicians should be alerted to the possibility that hepatitis may occur with gatifloxacin administration.     

Treatment of acute hepatitis C

Progression from acute to chronic HCV infection occurs in 50% to 84% of cases. In light of the risk of developing chronic disease and the response rate to treatment once the disease is established, it is important to consider early treatment of acute HCV infection before it progresses to the chronic state. Several studies evaluated the efficacy of either alpha or beta IFN monotherapy in patients with acute hepatitis C, but nearly all trials are small and present great variability regarding timing, schedule, response definition and patient characteristics. To overcome these limits, IFN efficacy has been assessed by meta-analyses demonstrating that antiviral therapy during the acute phase of HCV significantly reduces evolution to chronic hepatitis. Accordingly, treatment of persons with acute hepatitis C is warranted. However, several issues remain to be addressed, such as the optimal regimen and timing. Recent data would indicate that induction with daily IFN is needed to optimize response and pegylated IFN monotherapy could be the best option. Combination therapy with ribavirin does not seem to increase the response rate but could be proposed as a second choice to patients non responding to IFN monotherapy. Delaying treatment by 2-3 months might allow the identification of cases who would spontaneously resolve without compromising efficacy. However, additional data are required to improve the selection of those patients at great risk of progressing to chronic disease, and also to establish the optimal treatment in terms of risk/benefit and cost-effectiveness ratio.     

Clinical presentation of acute viral hepatitis

Acute viral hepatitis may be asymptomatic, symptomatic but anicteric, or a classical icteric hepatitis; rarely it is very severe and may be fatal. Different types of illness may be caused by the various hepatitis viruses. This does not help precise diagnosis, which is based on serological tests. This paper describes hepatitis seen with the A, B, C, D and E viruses, and also some of the unusual complications which have been recognized. Serological tests allow precise diagnosis of acute hepatitis A and B, and should be used more widely, because viral hepatitis is often diagnosed when jaundice is caused by other conditions. They also allow diagnosis when viral hepatitis has an atypical presentation, and is thus not considered as the cause of the liver disease. Negative tests suggest the need for further investigation.     

Cellular immunity and acute hepatitis C infection

Hepatitis C virus (HCV) infects an estimated 170 million people globally and persistent infection within the liver is the usual outcome of infection. The resulting liver disease leads to substantial morbidity and to date no vaccine exists. Furthermore the treatments available are frequently ineffective. A minority of those exposed will however successfully control the virus and the factors that dictate this remain elusive. The events that occur in the immediate and early phase post exposure are thought to play a crucial role in determining the outcome and virus specific T cells have a confirmed role in directing the immune response towards a successful outcome. An understanding of the T cell responses and the strategies, which allow the virus to evade these responses in the majority, is an essential prerequisite both for vaccine design and the development of therapeutic agents. We review here the characteristics of the cellular immune responses in acute infection and how the virus manages to undermine these responses and establish chronicity.