药源性牙龈增生

目的 探讨药源性牙龈增生的致病机制及其防治方法，为临床合理用药提供参考。方法 检索国内外有关文献，进行文献综述。结果 引起药源性牙龈增生的药物主要有钙拮抗剂、抗癫痫药物和免疫抑制剂环孢素A等。致病机制多种多样，但主要与降低牙龈成纤维细胞表面α2β1整合素与胶原的亲和力、降低胶原的吞噬作用，从而导致Ⅰ型胶原的堆积有关。合理选药和保持口腔卫生是预防牙龈增生的有效方法，牙龈切除仍然是治疗严重牙龈增生的主要方法。结论 药源性牙龈增生可影响咀嚼、语言、刷牙和美容，但一般无严重的临床后果，医务工作者和患者对药源性牙龈增生都应有所认识。     

药物引起的牙龈增生

牙龈增生是牙龈的一种特发性炎症反应，其临床主要表现为：病损主要累及牙间乳头和缘龈，只有少数严重病例波及附着牙；增生牙龈呈桑葚状，或有小的分叶，质地坚实，呈淡粉红色，一般不出血，不痛；病损可累及全口牙龈，但上下前牙区较重。其临床诊断主要为：牙龈纤维瘤与药物性牙龈增生。     

药物引起的牙龈增生

牙龈增生是牙龈的一种特发性炎症反应,其临床主要表现为:病损主要累及牙间乳头和缘龈,只有少数严重病例波及附着牙;增生牙龈呈桑葚状,或有小的分叶,质地坚实,呈淡粉红色,一般不出血,不痛;病损可累及全口牙龈,但上下前牙区较重.其临床诊断主要为:牙龈纤维瘤与药物性牙龈增生.     

药源性血小板减少症及其防治

目的介绍药源性血小板减少症的有关知识,为临床合理用药提供参考。方法检索国内外有关数据库,下载有关药物致血小板减少症的文献,然后进行文献综述。结果药源性血小板减少症的发生率约十万分之一,但不同药物之间的发生率差别很大。致病药物以抗菌药物、解热镇痛药物及血液系统药物多见。致病机制包括血小板破坏增加、生成减少和消耗增加,其中又以免疫介导的血小板减少多见。药源性血小板减少症一般是可逆的,停药后7～10d可望恢复,产生严重后果者少见。结论药源性血小板减少症是一种常见的药源性血液系统疾病,临床医务人员应予以注意。     

硝苯吡啶所致小鼠牙龈增生的组织病理学和细胞凋亡实验研究

目的:通过动物实验来研究硝苯吡啶造成小鼠牙龈增生的发病机制和预防办法,降低临床应用硝苯吡啶的副作用.方法:采用纯系昆明种雄性小鼠为研究对象,灌喂硝苯吡啶不同时间来观察:①牙龈增生与牙龈上皮厚度及胶原纤维的变化;②细胞凋亡指数;③药物作用时间对上述指标的影响;④撤药后增生牙龈的恢复情况.结果:小鼠牙龈上皮厚度明显增加,胶原纤维致密性加大,牙龈凋亡细胞数目减少(P＜0.05),硝苯吡啶撤退后一段时间,增生的牙龈恢复正常.结论:硝苯吡啶可导致小鼠牙龈增生,服药55d细胞凋亡数减少,此损害是可逆的.     

重视药源性哮喘 促进合理用药

目的探讨药源性哮喘的发病机制与特点,临床上如何预防。方法以药源性哮喘为关键词搜索国内期刊数据库,并对文献进行整合分析。结果引起药源性哮喘的药物主要集中于抗菌药物、中药制剂、心血管药物和非甾体抗炎药。结论医疗机构有针对性地开展药物不良反应知识的教育,医患共同提高防范意识,合理用药以减少和避免药源性哮喘的发生。     

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。     

药源性高血糖

药源性高血糖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,出现血糖升高超过正常血糖范围。引起高血糖的药物种类很多,而且不同的药物具有不同的致高血糖的作用机制。本文就引起药源性高血糖的主要药物及其致病机制和防治进行介绍。     

药物所致肾损害96例临床分析

目的 通过研究不同药物肾损害的机制及相关因素分析,进一步提高药源性肾损害的诊治水平.方法 回顾性分析96例药源性肾损害的致病药物,并进行归类统计和分析评价.结果 96例患者中,引起肾损害的药物主要有:抗生素及抗病毒类,非甾体类抗炎药,脱水药类等;其中静脉给药63例,口服给药23例,其他途径10例.结论 合理用药可预防药源性肾损害的发生.     

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。     

Drug-induced gingival overgrowth--a review

Drug-induced gingival overgrowth is a side effect associated with 3 types of drugs: anticonvulsants (phenytoin), immunosuppressive agents (cyclosporine A), and various calcium channel blockers for cardiovascular diseases. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. Although the mechanisms of these disorders have not been elucidated, recent studies suggest that these disorders seem to be induced by the disruption of homeostasis of collagen synthesis and degradation in gingival connective tissue, predominantly through the inhibition of collagen phagocytosis of gingival fibroblasts. The integrins are a large family of heterodimeric transmembrane receptors for extracellular matrix molecules. alpha2beta1 integrin serves as a specific receptor for type I collagen on fibroblasts, and alpha2 integrin has been shown to play a crucial role in collagen phagocytosis. Actin filaments, which are assembled from monomers and oligomers, are involved in collagen internalization after binding to integrins. Furthermore, the implication of intracellular calcium in the regulation of integrin-mediated binding activity and gelsolin activity, known as a calcium-dependent actin-severing protein, is also described. In this review, we focus on collagen metabolism in drug-induced gingival overgrowth, focusing on the regulation of collagen phagocytosis in fibroblasts.     

临床药师在1例药物性牙龈增生患者诊治中发挥的作用

目的：探讨临床药师在1例药物性牙龈增生患者诊治中发挥的作用,为临床药师开展工作提供参考。方法：临床药师参与临床查房和会诊,通过询问患者病史和用药史,从病理学、药理学角度分析患者出现牙龈增生的异常反应。结果：临床药师经过综合分析后,判断为药物性牙龈增生并建议医生调整治疗方案。结论：临床药师在治疗团队中要充分发挥自己的职业专长,协助医生和护士解决用药的相关问题,保证患者合理用药,实现临床药师的价值。     

Drug-induced fibrosis: interference with the intracellular collagen degradation pathway

Drug-induced fibrosis and overgrowth of the extracellular matrix are high prevalence lesions of the oral mucosa. Drugs, such as dilantin, cyclosporin A and nifedipine can cause the gum tissues to overgrow, thereby preventing normal mastication and promoting infection. The causes of these disorders are poorly understood but recent evidence suggests that a common pathway targeted by these three drugs is the regulation of the intracellular pathway of collagen degradation. In this review, recent data that implicate calcium deregulation of the critical actin-dependent binding step of collagen phagocytosis will be discussed. These new insights highlight the need for a greater choice of medications for the treatment of transplant rejection and epilepsy to reduce the side effect of gingival overgrowth.     

Establishment of rat model of drug-induced gingival overgrowth induced by continuous administration of phenytoin

It is well-known that the anticonvulsant drug, phenytoin (PHT), induces gingival overgrowth as a side effect. The mechanism of PHT-induced gingival overgrowth, however, is not well understood. One reason for this is the lack of an adequate animal model for the PHT-induced gingival overgrowth. The purpose of this study was to establish a rat model of the drug-induced gingival overgrowth. Fourteen-day-old rats were randomly divided into 3 groups (5 rats/group). The control rats received only the vehicle. The rats in the experimental group were injected with 50 mg/kg per day (group L) and 100 mg/kg per day (group H) of PHT. They received a subcutaneous injection of vehicle or PHT twice a day for 42 days. A charge-coupled device (CCD) laser displacement sensor was used for measurement of the severity of gingival overgrowth of the mandibles. There was no significant difference in the growth of rats between the PHT-injected and the control groups. The CCD laser displacement sensor can measure minute changes in the gingival overgrowth in rats, and a significant extension of the buccal gingiva was observed in groups L and H. Using the CCD sensor, it is possible to quantify the change in the gingiva under precise control of the PHT dose.     

Inhibition by tranilast of nifedipine-induced proliferation of cultured human gingival fibroblasts

The appropriate method of etiologic therapy for gingival overgrowth is yet unknown. In this study drug-induced proliferation of Gin-1 cells, a normal human gingival fibroblast cell line, was examined by using the reagent water-soluble tetrazolium-1. Tranilast (100 microM) inhibited the nifedipine (10 microM)-induced proliferation of gingival fibroblasts. The level of basic fibroblast growth factor (bFGF) was determined by using an enzyme-linked immunosorbent assay kit. Tranilast inhibited the release of bFGF from the cells. In conclusion, tranilast depresses the nifedipine-induced proliferation of gingival fibroblasts by inhibiting the release of bFGF. Administration of tranilast may thus be clinically effective for the treatment of gingival overgrowth.     

Calcium antagonists and deep gingival pockets in the population-based SHIP study

AIM: Gingival overgrowth is a common undesired side-effect in patients taking calcium channel blockers. Different reports have suggested that the drug-induced gingival hyperplasia may aggravate inflammatory periodontal disease. However, representative epidemiological data are lacking. We investigated the association between the intake of calcium antagonists and periodontitis in a population-based analysis including the most important risk factors of periodontitis. METHODS: In a cross-sectional epidemiological investigation involving 4290 subjects aged 20-80 years, we recorded periodontal risk factors and identified participants using calcium antagonists. Periodontal parameters, attachment loss, probing depth and number of teeth were assessed. In a subgroup analysis with matched pairs, 456 subjects using calcium antagonists and 456 without were compared for periodontal status. RESULTS: Subjects treated with calcium antagonistic drugs had significantly deeper gingival pockets than their drug-free counterparts. This was observed in the total population of 4290 and confirmed by logistic regression analyses (P < 0.001) controlled for the known risk factors of periodontitis (age, sex, smoking, education). In the matched-pair analysis only the probing depth was increased: extent probing depth > or = 4 mm median 23.5 vs. 17.0% (P < 0.001); mean probing depth 3.0 +/- 0.8 vs. 2.7 +/- 0.9 mm (P < 0.001). No differences were found in extent and severity of clinical attachment loss and in the number of teeth. The risk of gingival overgrowth was aggravated in smokers. CONCLUSION: In the general population, treatment with calcium antagonists leads to gingival overgrowth without an aggravation of periodontal disease. Interaction with smoking indicates the multifactorial background of the undesired effect of calcium antagonists.     

药物性肝炎的致病因素及防治

目的了解药物性肝炎的致病因素及防治。方法对国内外近5年公开发表的有关药物性肝炎致病因素及其防治的文献进行分析整理。结果多种药物可引起药物性肝炎，其治疗方法除使用保肝药物外，还可结合中成药或中草药汤剂进行治疗，并应从用药方面注意对药物性肝炎的预防。结论临床医师、临床药师在用药时应重视药物性肝炎的预防和治疗。     

An involvement of granulocyte medullasin in phenytoin-induced gingival overgrowth in rats

To investigate the relationship between histological changes and distributions of medullasin, a neutrophil elastase-like serine proteinase, in phenytoin-induced gingival overgrowth, we established a rat model of gingival overgrowth. Thirty-two, 20-day-old male Fischer 344 rats were fed a diet containing phenytoin and sacrificed at 1, 2, 4 and 8 weeks. Control rats (n = 40) were fed the same diet, but without the drug and killed at the same weeks as experimental rats (n = 32) and 0 week (n = 8). The mandible specimens were resected and sectioned bucco-lingually between the first and second molars. A marked inflammatory-cell infiltration and elongated rete pegs were seen in the phenytoin-treated group. The extent of the overgrowth assessed by computer image analysis and the density of medullasin-positive cells by immunohistochemistry in the approximal gingiva showed a significant increase in the phenytoin-treated group compared to the control group. A marked infiltration of the positive cells in experimental rats was observed as early as 2 weeks when gingival overgrowth was not fully established. Medullasin-positive cells were mostly neutrophils and partly macrophage-like cells. These findings suggest that medullasin may be involved in mainly host defense and secondarily collagen metabolism in the phenytoin-induced rat model of gingival overgrowth.     

Drug-induced pancreatitis: a practical review

Although numerous drugs have been implicated in the etiology of acute pancreatitis, literature on various aspects of drug-induced pancreatitis is sparse and limited mostly to case reports. Accurate diagnosis and management of this rare entity can be a challenge. This review discusses the clinical and epidemiological features of drug-induced pancreatitis, commonly associated drugs and conditions, possible pathogenic mechanisms, and a systematic approach to the diagnosis and management of drug-induced pancreatitis.