药源性骨质疏松的发病原因、致病药物及防治

骨质疏松是骨强度受到损害而致骨折风险增加的骨骼疾病,可严重降低患者的生活质量与健康状况。导致药源性骨质疏松的常见药物包括口服抗凝药、钙调磷酸酶抑制剂、强效利尿药、质子泵抑制剂、噻唑烷二酮类降糖药、芳香酶抑制剂、蛋白酶抑制剂、糖皮质激素和抗癫痫药等。致病机制为药物通过促进骨吸收、抑制骨形成、抑制骨矿化影响正常骨代谢。骨密度测定可用于诊断药源性骨质疏松。防治药源性骨质疏松的有效措施包括合理用药,定期监测骨密度,缩短用药疗程,给予患者钙剂、维生素D制剂、双膦酸盐类药物、降钙素、选择性雌激素受体调节剂等药物治疗。     

药源性疾病5例报道

药源性疾病（drug-induced disease，DID）是指由于药物作为致病因子引起的人体功能或组织结构损害，并具有相应临床经过的疾病，是药物不良反应在一定条件下产生的后果。近年来，随着人们在治疗过程中用药品种和数量不断增加，药源性疾病的发生量也逐渐增多，已日益受到临床医药工作者的重视。现报告我院典型药源性疾病5例报道如下。     

药源性肠梗阻

鉴于引起肠梗阻的药物品种日益增多，而临床对这一少见的消化道急症的缺乏充分认识，本文就药源性肠梗阻的常见致病药物、发病机理、临床特征及治疗问题进行综述。     

药源性支气管哮喘

本文综述了解热镇痛抗炎药，β－受体阻滞剂，Ｈ２－受体阻滞剂，ＡＣＥ抑制剂，抗生素等药物引起支气管哮喘的发病机理，临床特点及防治措施，过敏体质易发生，值得临床用药时注意。     

药源性谵妄

药物引起的谵妄是较常见的药源性疾病,尤其是存在易感因素（如高龄、神经系统疾病、外科手术和危重症等）的患者更为常见。药源性谵妄主要与药物影响神经递质的合成、释放和代谢,导致神经功能紊乱有关。引起谵妄的药物主要为抗胆碱药和抗抑郁药。合理用药可避免药源性谵妄的发生,及早辨识谵妄症状并及时处理尤为重要。     

药源性糖尿病

药源性糖尿病是指某些药物引起胰岛β细胞分泌胰岛素功能异常或靶细胞对胰岛素的敏感性降低．出现血糖升高．达到糖尿病诊断标准。引起糖尿病的药物种类繁多,而且具有多种不同的作用机制。本文主要就引起药源性糖尿病的药物种类、致病机制及防治作一概述。     

浅释药源性疾病

<正>药物既能治疗疾病挽救生命,是治病的重要手段之一,但药物也能导致疾病,是致病的主要危害因素之一,它能对患者造成损害、残疾,甚至死亡。因此,药源性疾病应该引起全社会的重视,尤其是医务工作者更应该高度重视。     

药源性尿潴留及其防治

尿潴留（urinary retention）是由于膀胱排空功能受限导致尿液潴留于膀胱的一种临床病症。尿潴留分为急性和慢性两种。药源性尿潴留（drug—induced urinary retention）是指由于药物的作用引起膀胱内的尿液不能排出,导致膀胱充盈,下腹部胀痛,患者虽然充满尿意,就是无尿排出。药源性尿潴留在临床上很常见,但一般来讲属于急性病症。现对药源性尿潴留进行综述。     

药源性危象

由于个体差异,药物治疗剂量或治疗方案不当,以及骤然停药等,常可发生药源危象此类情况可使病情复杂恶化甚至病人死亡.为了警惕药源性危象的发生,本文就常用药物引起的药源性危象作简单介绍。     

药源性胰腺炎研究进展

药源性胰腺炎（DIP）的发生率文献报道不一。DIP 如不能确诊,将导致急性胰腺炎反复发作,增加患者痛苦及医药费用。目前引起 DIP 的药物尚无统一的分类方法,常用的有根据 DIP 患者例数及激发试验制定的三分类法和依据患者例数、激发试验、潜伏期以及能否排除其他原因制定的四分类法。DIP 发生机制包括药物直接毒性和特异质反应。因不具有特异的临床表现及诊断标志物,DIP 的诊断较困难,排除常见病因考虑为特发性胰腺炎的患者,需详细询问用药史。DIP 的处理与一般急性胰腺炎类似,停用可疑药物是关键。     

Drug-induced Malabsorption

Abstract

1. The history and relevance of drug-induced malabsorption are reviewed.

2. The tests used to assess intestinal structure and function in man are briefly described.

3. Neomycin, the most potent cause of drug-induced malabsorption, is reviewed in detail. It disturbs small bowel histology, impairs the absorption of actively absorbed substances normally measured in function tests and lowers the serum cholesterol.

4. Each test of intestine absorption is considered separately and the drugs which modify them are discussed. Where possible, the mechanisms of action are described.     

Drug-induced vasculitis

Therapeutic agents from virtually every pharmacological class have been implicated in the development of drug-induced vasculitis. Clinical manifestations range from small vessel hypersensitivity vasculitis and leukocytoclastic vasculitis to clinical syndromes indistinguishable from classical systemic forms of vasculitis such as Wegener’s granulomatosis, polyarteritis nodosa and Churg–Strauss syndrome (CSS). The exact pathogenic mechanisms involved remain to be elucidated; but both cell-mediated and humoral immunity appear to play important roles. Affected individuals may present with cutaneous involvement alone or life-threatening systemic involvement, which may result in severe and sometimes fatal illness. Since clinical presentation as well as serological and pathological parameters is identical to idiopathic forms of vasculitis, a high index of suspicion is necessary to accurately and expeditiously diagnose drug-induced vasculitis. Withdrawal of the offending agent alone is often sufficient to induce prompt resolution of clinical manifestations, obviating the need for systemic corticosteroids or more powerful forms of immunosuppression.     

Drug-induced cholestasis

Drugs may cause several overlapping syndromes of cholestasis, the pathophysiological syndrome resulting from impaired bile flow. These reactions comprise approximately 17% of all hepatic adverse drug reactions (ADRs) and they may be severe. Causes of 'pure' (bland) cholestasis include oestrogens and anabolic steroids; rarer associations are with antimicrobials and NSAIDs. 'Cholestatic hepatitis' is a common drug reaction in which liver injury and inflammation cause significant elevation of serum alanine aminotransferase (ALT) as well as cholestasis. Chlorpromazine and ketoconazole are classic examples, but it is now exemplified by amoxycillin-clavulanate and other oxy-penicillins. Chronic cholestasis results from small bile duct injury leading to the vanishing bile duct syndrome (VBDS), a disorder mimicking primary biliary cirrhosis, or from injury to larger bile ducts causing secondary sclerosing cholangitis. Whilst there is increasing evidence of a genetic predisposition to cholestatic drug reactions, there are currently no pretreatment tests to predict drug safety. Prevention of severe reactions therefore relies on early detection of liver injury and prompt drug withdrawal. Symptomatic management includes relief of pruritus and correction of fat-soluble vitamin deficiency. In small cohort studies, ursodeoxycholic acid (UDCA) arrested progressive cholestasis in two-thirds of cases, but evidence for use of corticosteroids is anecdotal. This review considers diagnosis, pathogenesis, prevention and management of drug-induced cholestasis, with particular reference to frequently- and newly-described causes.     

Drug-induced vasculitis

Therapeutic agents from virtually every pharmacological class have been implicated in the development of drug-induced vasculitis. Clinical manifestations range from small vessel hypersensitivity vasculitis and leukocytoclastic vasculitis to clinical syndromes indistinguishable from classical systemic forms of vasculitis such as Wegener's granulomatosis, polyarteritis nodosa and Churg-Strauss syndrome (CSS). The exact pathogenic mechanisms involved remain to be elucidated; but both cell-mediated and humoral immunity appear to play important roles. Affected individuals may present with cutaneous involvement alone or life-threatening systemic involvement, which may result in severe and sometimes fatal illness. Since clinical presentation as well as serological and pathological parameters is identical to idiopathic forms of vasculitis, a high index of suspicion is necessary to accurately and expeditiously diagnose drug-induced vasculitis. Withdrawal of the offending agent alone is often sufficient to induce prompt resolution of clinical manifestations, obviating the need for systemic corticosteroids or more powerful forms of immunosuppression.     

Drug-induced stuttering

(1) Remember that some drugs can cause stuttering, even if this side effect appears to be rare.     

Drug-induced lupus

Autoantibodies and, less commonly, systemic rheumatic symptoms are associated with treatment with numerous medications and other types of ingested compounds. Distinct syndromes can be distinguished, based on clinical and laboratory features, as well as exposure history. Drug-induced lupus has been reported as a side-effect of long-term therapy with over 40 medications. Its clinical and laboratory features are similar to systemic lupus erythematosus, except that patients fully recover after the offending medication is discontinued. This syndrome differs from typical drug hypersensitivity reactions in that drug-specific T-cells or antibodies are not involved in induction of autoimmunity, it usually requires many months to years of drug exposure, is drug dose-dependent and generally does not result in immune sensitization to the drug. Circumstantial evidence strongly suggests that oxidative metabolites of the parent compound trigger autoimmunity. Several mechanisms for induction of autoimmunity will be discussed, including bystander activation of autoreactive lymphocytes due to drug-specific immunity or to non-specific activation of lymphocytes, direct cytotoxicity with release of autoantigens and disruption of central T-cell tolerance. The latter hypothesis will be supported by a mouse model in which a reactive metabolite of procainamide introduced into the thymus results in lupus-like autoantibody induction. These findings, as well as evidence for thymic function in drug-induced lupus patients, support the concept that abnormalities during T-cell selection in the thymus initiate autoimmunity.     

Drug-induced catatonia

Catatonia is a heterogeneous syndrome that varies in etiology, presentation, course and sequelae. Initially conceptualized as a subtype of schizophrenia, catatonia is now recognized to occur not only with other psychiatric conditions but also with medical conditions and drug-induced and toxic states. While drug-induced catatonia is now a recognized entity, most studies club it with catatonia due to general medical conditions or organic catatonia, thus precluding any meaningful interpretation of such cases. The literature on drug-induced catatonia mostly draws from scattered case reports. This article attempts to review the available literature in this realm and integrate the information in an attempt to explore the epidemiology, etiology, mechanism and treatment of drug-induced catatonia.