银杏达莫注射液致过敏性皮疹2例

目的银杏达莫注射液致过敏性皮疹2例病情及诊治分析,为临床合理用药提供参考。方法通过对1例脑供血不足患者,1例神经性耳聋患者进行银杏达莫注射液静滴,进行回顾性分析。结果银杏达莫注射液不良反应表现以发生过敏性皮疹为主,在注射过程中出现。结论应加强银杏达莫注射液不良反应监测,掌握其相关因素及临床表现,促进合理用药。     

藤黄健骨胶囊致不良反应2例报告及分析

目的分析藤黄健骨胶囊导致不良反应发生的基本情况,为临床安全使用提供理论依据。方法分析2例藤黄健骨胶囊所导致的不良反应报告,对其发生情况进行分析。结果藤黄健骨胶囊导致的不良反应主要表现为消化道反应、皮肤及附件损害。结论医师应做好用药宣教,药师应配合医师工作,加强用药监护及教育,预防不良反应的发生。     

老年感音神经性耳聋血流变检测观察

老年感音神经性耳聋患者在耳鼻喉科临床为一种常见病,其发病机制甚多,如内耳微循环障碍,其中包括神经调节、血液循环动力学、内分泌学的改变、感染、解剖发育异常等。然而,本病的病因尚不明确,近年来有人提出可能和血流变学机制改变有关,由于血管的管径、血黏的改变导致血流的变化而引起本病。我们从1996年7月至2005年10月对300例老年感音神经性耳聋患者的血流变进行了检测,现报告如下。1对象与方法1.1对象的选择:300例老年感音神经性耳聋患者及300例健康老年人,均无心脑血管疾病。耳聋组300例,均选择60岁以上,原因不明的感音神经性耳聋患者…     

鼻咽癌患者放射治疗后感音神经性耳聋的发生率及影响因素分析

目的 观察鼻咽癌患者放射治疗后感音神经性耳聋的发生情况,并探讨诱发的相关因素.方法 选取2013年6月至2014年6月收治的30例(60只耳)鼻咽癌患者,全部患者均接受放射治疗,对患者进行纯音听阈和声阻抗-导纳测试,探讨感音神经性耳聋的发生情况及诱发因素.结果 本组30例患者(60只耳)中,高频段感音神经性耳聋16只耳(26.67％),明显多于低频段感音神经性耳聋5只耳(8.33％);确诊时年龄、随访时间是影响高频段感音神经性耳聋发生的主要因素(P＜0.05).结论 鼻咽癌患者放射治疗后低频段感音神经性耳聋发生率显著低于高频段,诱发高频段感音神经性耳聋发生的因素较多,主要包括患者年龄及随访时间,临床需积极采取相关措施,尽可能降低放射治疗后感音神经性耳聋发生率,提高患者生活质量,改善预后.     

分泌性中耳炎误诊原因分析

目的 分析分泌性中耳炎误诊的相关因素,拟减少误诊率,提高诊治水平.方法 对2002年1月～2004年12月资料完整的365例(405耳)分泌性中耳炎病人中曾发生误诊、漏诊的36例(40耳)进行回顾性分析.结果 误诊为感音神经性耳聋22例,突发性耳聋6例,漏诊8例.主要原因:①纯音测听表现为骨导听力损失误诊为感音神经性耳聋;②声阻抗表现为C型曲线而引起漏诊;③症状不典型、问病史不详细、检查鼓膜不仔细而引起.结论 分泌性中耳炎可引起内耳功能的紊乱,导致骨导听阈改变,应根据年龄、病史、结合听力图及声阻抗进行综合分析,减少误诊率.     

萘丁美酮治疗类风湿关节炎

目的 :评估萘丁美酮对类风湿关节炎 (RA)的疗效和安全性。方法 :76例RA病人分 2组 ,萘丁美酮组 4 6例 ,男性 14例 ,女性 32例 ,年龄 4 5a±s 11a(2 2～ 68a) ,给萘丁美酮片 1g ,po ,qd× 4wk。双氯芬酸组 30例 ,男性 6例 ,女性 2 4例 ,年龄 4 4a± 10a(2 6～ 64a) ,给双氯芬酸 5 0mg ,po ,qd× 4wk。观察其临床疗效、实验室指标和不良反应。结果 :萘丁美酮组总有效率为 91% ,明显高于双氯芬酸组 (73% ,P <0 .0 5 ) ,2组治疗后临床各指标均有明显改善 (P <0 .0 1) ,萘丁美酮组不良反应为 15 % ,明显低于双氯芬酸组 (37% ,P <0 .0 5 )。结论 :萘丁美酮对RA具有良好疗效和较低的不良反应     

神经性耳聋耳鸣治疗方法探索

神经性耳聋、耳鸣主要指感音神经受损引发的耳聋、耳鸣现象,病变部位集中于耳蜗与耳蜗后端,为耳鼻喉科常见疾病之一,也是引发患者听力障碍的主要原因之一,目前已被列入世界公共卫生问题之中[1]。现分析神经性耳聋耳病发病原因与临床症状,提出7种主要的中西医治疗方法。1神经性耳聋耳鸣病因与临床症状1.1发病原因目前,神经性耳聋、耳鸣的发病机制尚不明     

萘丁美酮和尼美舒利治疗类风湿关节炎疗效和安全性的比较

目的 :比较 2种非甾类消炎药 (NSAIDs)萘丁美酮和尼美舒利治疗类风湿关节炎 (RA)的疗效和安全性。方法 :6 2例活动性RA病人分为 2组 ,萘丁美酮组 (治疗组 ) 30例 ,给予萘丁美酮 5 0 0mg ,po ,bid ;尼美舒利组 (对照组 ) 32例 ,给予尼美舒利10 0mg ,po ,bid。 2组均给药 4wk。受试前后观察临床和实验室指标的变化。结果 :萘丁美酮组总有效率为 87% ,尼美舒利组总有效率为 83% ,P >0 .0 5。与萘丁美酮治疗有关的不良反应包括 :恶心、胃烧灼感、反酸和嗜睡各 1例 ,不良反应率13% ;尼美舒利组不良反应率为 19% ,P >0 .0 5。结论 :萘丁美酮对RA的疗效和不良反应的发生率均与尼美舒利相似 ,是一种较为有效、安全且服用方便的NSAIDs。     

萘丁美酮对关节炎患者生活质量的影响

目的 :评价萘丁美酮治疗对关节炎患者生活质量的影响。方法 :采用分层随机抽样方法获得关节炎患者 1344例 ,根据病情分别给予萘丁美酮 1.0 g或 1.5 g ,口服。在随访前后分别进行生活质量、药物不良反应测量。结果 :关节炎患者服用萘丁美酮后生活质量各领域均得到改善 (P <0 .0 1) ;不良反应发生率 34.4 % ,绝大部分程度较轻 ,仅 2 .6 %的患者需停药处理。月均收入、受教育年数、消化系统不良反应、用药天数、用药方式和单次用药剂量、生理功能基线得分和总体健康感受基线得分是影响总生活质量改善的因素。结论 :萘丁美酮治疗对关节炎患者生活质量各领域均有改善作用 ,不良反应程度轻微。关节炎患者应注意减少其消化系统不良反应的发生 ,以提高患者的生活质量。     

高压氧治疗感音神经性耳聋的临床疗效

目的观察采用高压氧治疗感音神经性耳聋的临床疗效。方法将78例感音性神经性耳聋患者随机分为两组,每组39例,对照组常规使用扩血管药、维生素、激素等,治疗组在对照组的基础上使用高压氧,两组疗程均30d;比较两组患者治疗前后纯音听力变化。结果治疗组痊愈率、总有效率均高于对照组,组间比较差异有统计学意义（P〈0．05）。结论采用高压氧治疗感音神经性耳聋可明显提高治疗效果,可在临床推广使用。     

Non-steroidal anti-inflammatory drug,nabumetone, prevents indometacin-induced gastric damage via inhibition of neutrophil functions

Nabumetone is a non-steroidal anti-inflammatory drug (NSAID). It works as a prodrug and is extensively metabolized to an active metabolite, 6-methoxy-2-naphthylacetic acid (6MNA). It is well known that neutrophil infiltration and activation are critical in the pathogenesis of NSAID-induced gastric injury, and nabumetone shows less incidence of gastrointestinal irritancy. We examined the effects of nabumetone on neutrophil activation and on indometacin-induced gastric damage. In the indometacin-induced gastric mucosal injury, rats were treated with indometacin and then nabumetone or 6MNA was orally administered. Nabumetone prevented gastric damage accompanied by the reduction of neutrophil infiltration into gastric mucosa, but such an effect was not observed with 6MNA. Nabumetone reduced the formyl methionyl leucyl phenylalanine (fMLP)-induced respiratory burst of human neutrophils to 30% of the control level in-vitro, but 6MNA did not. In addition, nabumetone prevented the fMLP-induced migration of neutrophils. Nabumetone did not inhibit O2- generation in the xanthine-xanthine oxidase system. These results suggest that nabumetone prevents gastric damage induced by the active metabolite, 6MNA, via the suppression of neutrophil activation in gastric mucosa.     

萘丁美酮分散片的制备与含量测定

目的 制备萘丁美酮分散片并建立其含量测定方法。方法通过正交试验考察处方中组分的影响因素,以崩解时限为指标对萘丁关酮分散片处方进行优选;用高效液相色谱（HPLC）法测定分散片中萘丁关酮的含量。结果最佳处方为羧甲基淀粉钠6％,十二烷基硫酸钠1％,微晶纤维素10％,聚乙烯吡咯烷酮浓度2％;优选处方的分散片崩解时间小于3min,分散均匀,均通过2目筛;萘丁美酮质量浓度线性范围为20～100μg／mL,r=0．9999（n=5）,平均回收率为99．54％,RSD=0．48％（n=6）。结论用优选处方制备的萘丁关酮分散片崩解快,分散均匀,且含量测定结果符合限度要求。     

Nabumetone: therapeutic use and safety profile in the management of osteoarthritis and rheumatoid arthritis

Nabumetone is a nonsteroidal anti-inflammatory prodrug, which exerts its pharmacological effects via the metabolite 6-methoxy-2-naphthylacetic acid (6-MNA). Nabumetone itself is non-acidic and, following absorption, it undergoes extensive first-pass metabolism to form the main circulating active metabolite (6-MNA) which is a much more potent inhibitor of preferentially cyclo-oxygenase (COX)-2. The three major metabolic pathways of nabumetone are O-demethylation, reduction of the ketone to an alcohol, and an oxidative cleavage of the side-chain occurs to yield acetic acid derivatives. Essentially no unchanged nabumetone and < 1% of the major 6-MNA metabolite are excreted unchanged in the urine from which 80% of the dose can be recovered and another 10% in faeces. Nabumetone is clinically used mainly for the management of patients with osteoarthritis (OA) or rheumatoid arthritis (RA) to reduce pain and inflammation. The clinical efficacy of nabumetone has also been evaluated in patients with ankylosing spondylitis, soft tissue injuries and juvenile RA. The optimum oral dosage of nabumetone for OA patients is 1 g once daily, which is well tolerated. The therapeutic response is superior to placebo and similar to nonselective COX inhibitors. In RA patients, nabumetone 1 g at bedtime is optimal, but an additional 0.5-1 g can be administered in the morning for patients with persistent symptoms. In RA, nabumetone has shown a comparable clinical efficacy to aspirin (acetylsalicylic acid), diclofenac, piroxicam, ibuprofen and naproxen. Clinical trials and a decade of worldwide safety data and long-term postmarketing surveillance studies show that nabumetone is generally well tolerated. The most frequent adverse effects are those commonly seen with COX inhibitors, which include diarrhoea, dyspepsia, headache, abdominal pain and nausea. In common with other COX inhibitors, nabumetone may increase the risk of GI perforations, ulcerations and bleedings (PUBs). However, several studies show a low incidence of PUBs, and on a par with the numbers reported from studies with COX-2 selective inhibitors and considerably lower than for nonselective COX inhibitors. This has been attributed mainly to the non-acidic chemical properties of nabumetone but also to its COX-1/COX-2 inhibitor profile. Through its metabolite 6-MNA, nabumetone has a dose-related effect on platelet aggregation, but no effect on bleeding time in clinical studies. Furthermore, several short-term studies have shown little to no effect on renal function. Compared with COX-2 selective inhibitors, nabumetone exhibits similar anti-inflammatory and analgesic properties in patients with arthritis and there is no evidence of excess GI or other forms of complications to date.     

A study of the effects of nabumetone (BRL 14777), a novel anti-inflammatory drug,on cell infiltration into sterile cotton pellets implanted in rats

Nabumetone a new non-steroidal anti-inflammatory drug is active in reducing the DNA content of implanted cotton pellets in rats on various dosing regimens. The effect of nabumetone can be seen during the early and late phases of the cellular reaction to the implant implicating effects upon polymorphonuclear leucocytes and monocytes. The levels of two lysosomal enzymes are reduced in the exudate by the drug treatment.     

Effects of Nimesulide,Acetylsalicylic Acid,Ibuprofen and Nabumetone on Cyclooxygenase‐1‐ and Cyclooxygenase‐2‐Mediated Prostanoid Production in Healthy Volunteers ex vivo

Abstract: The beneficial actions of non‐steroidal anti‐inflammatory drugs (NSAIDs) have been associated with inhibition of cyclooxygenase‐2 (COX‐2), whereas some of their adverse effects are associated mainly with inhibition of COX‐1. Selective COX‐2 inhibitors reduce the risk of gastrointestinal adverse events, but increase the risk of thromboembolic events pointing to importance of optimal COX‐1/COX‐2 inhibition in drug safety. We compared the effects of acetylsalicylic acid, ibuprofen, nabumetone and nimesulide on COX‐1 and COX‐2 pathways in healthy volunteers in an ex vivo set‐up using single oral doses commonly used to treat acute pain. In a randomized, double‐blind four‐phase cross‐over study, 15 healthy volunteers were given orally a single dose of either acetylsalicylic acid 500 mg, ibuprofen 400 mg, nabumetone 1 g or nimesulide 100 mg. Blood samples were drawn before and 1, 3, 6, 24 and 48 hr after the drug for the assessment of COX‐1 and COX‐2 activity. COX‐1 activity was measured as thromboxane₂ production during blood clotting and COX‐2 activity as endotoxin‐induced prostaglandin E₂ synthesis in blood leucocytes. The data show that after a single oral dose these four NSAIDs have different profiles of action on COX‐1 and COX‐2. As expected, acetylsalicylic acid appeared to be COX‐1‐selective and ibuprofen effectively inhibited both COX‐1 and COX‐2. Nabumetone showed only a slight inhibitory effect on COX‐1 and COX‐2. Nimesulide caused almost complete suppression of COX‐2 activity and a partial reduction of COX‐1 activity. This confirms the relative COX‐2 selectivity of nimesulide.     

New insight into NSAID-induced gastropathy

Objective To assess the impact of nabumetone’s pharmacological profile on gastric safety. Methods Direct topical uptake of nabumetone by the gastric mucosa was assessed via autoradiography. The opportunity for nabumetone to cause indirect topical damage to the gastrointestinal tract was determined by examining the ability of 6-methoxy-2-naphthylacetic acid (6-MNA) to be secreted in the bile. The ability for 6-MNA to cause damage to the gastric mucosa via the systemic circulation was assessed via the preferential activity of 6-MNA on cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2). Results Nabumetone was shown not to exhibit direct uptake by the gastric mucosa when administered orally. 6-MNA, the active metabolite of nabumetone, was not found to undergo enterohepatic circulation. 6-MNA was found to act preferentially on COX-2. Conclusions Nabumetone does not cause direct topical damage to the gastric mucosa because it is a non-acidic prodrug that will not concentrate in the gastric mucosa via ‘ion trapping’. 6-MNA, the active metabolite of nabumetone, does not recirculate in the bile, and therefore will not cause damage to the gastric mucosa via secretion into the bile and reflux back into the stomach. Finally, 6-MNA has a low propensity to cause damage to the gastric mucosa via the systemic circulation due to its preferential inhibition of COX-2.     

Safety of the nonselective NSAID nabumetone : focus on gastrointestinal tolerability.

Although effective in the treatment of pain associated with rheumatic conditions such as osteoarthritis and rheumatoid arthritis, long-term use of NSAIDs is primarily limited by their association with upper gastrointestinal (GI) toxicity. Adverse effects range from dyspepsia and abdominal pain to ulceration and bleeding. GI damage elicited by NSAIDs arises as the result of biochemically induced topical irritant effects and by topical and systemic pharmacological suppression of gastroprotective prostaglandins. Variation in the physicochemical properties and pharmacological profiles among the individual NSAIDs translate into inter-agent differences regarding propensity to cause adverse GI effects. Nabumetone is a nonselective NSAID that offers distinct advantages over other agents in this class with regard to GI tolerability. Its non-acidic nature and pro-drug formulation, together with the lack of biliary secretion of its active metabolite, 6-methoxy-2-naphthylacetic acid, are thought to contribute to the improved GI tolerability of this drug. In head-to-head trials with other NSAIDs, nabumetone has demonstrated significant benefits regarding the incidence of GI events and more serious perforations, ulcers and bleeds (PUBs). Pooled data from eight postmarketing, randomized, controlled trials demonstrated a lower cumulative frequency of PUBs with nabumetone (0.03%; 95% CI 0.0, 0.08) versus comparator NSAIDs (1.4%; 95% CI 0.5, 2.4). Large-scale database studies also indicate that risk of serious GI complications is lower with nabumetone than comparator NSAIDs. Limited comparative data suggest that nabumetone offers a GI tolerability profile similar to that of cyclo-oxygenase-2 selective NSAIDs (coxibs). Although adverse cardiovascular outcomes appear to be a class effect of the coxibs, conventional NSAIDs may also have the potential for causing atherothrombotic complications. However, based on available data, nabumetone does not appear to be associated with increased cardiovascular risk. Finally, there is no particular concern about the nephrotoxic and hepatotoxic potential of nabumetone. Nonetheless, the potential for adverse drug reactions remains, and hence nabumetone, as with any NSAID, should be used at the lowest dose, which is effective for each patient, and for the shortest time necessary to control symptoms.     

Nabumetone: new preparation. Just another NSAID

(1) Nabumetone is a nonsteroidal antiinflammatory drug recently marketed in France. It has been available in other countries for about 15 years. Its licensed indications cover chronic inflammatory rheumatism and osteoarthritis. (2) The clinical file is bulky, but available trials in chronic inflammatory rheumatism involve only rheumatoid arthritis. (3) In rheumatoid arthritis (4 trials) and osteoarthritis (11 trials), nabumetone was no more effective than other nonsteroidal antiinflammatory drugs with which it was compared. (4) Clinical trial data, pharmacovigilance surveys and epidemiological studies suggest that nabumetone is among the antiinflammatory drugs with the least gastrointestinal adverse effects, but it has not yet been shown that they are less frequent than those of diclofenac, etodolac, ibuprofen or sulindac.     

Effect of nabumetone treatment on vascular responses of the thoracic aorta in rat experimental arthritis

Nabumetone is a nonsteroidal anti-inflammatory (NSAI) drug which is known to cause less gastrointestinal damage than other NSAI drugs. This study was performed to evaluate whether nabumetone treatment might alter the vascular aberrations related to inflammation in a rat model of adjuvant-induced arthritis. Nabumetone treatment (120 or 240 mg x kg(-1) x day(-1), orally) was initiated on the 15th day of adjuvant inoculation and continued for 14 days. Arthritic lesions, vascular contractile and relaxant responses and gastroduodenal histopathological preparations were evaluated 29 days after adjuvant inoculation. The contractile responses of aortic rings to phenylephrine and KCl were increased in grade 2 arthritic rats. In grade 3 arthritis only the phenylephrine contractility was decreased. The relaxant responses to acetylcholine and sodium nitroprusside were decreased in grades 2 and 3. In healthy rats, nabumetone did not change the vascular responses. After treatment of arthritic rats with nabumetone, both the contractile and relaxant response of the aortic rings returned to normal, and arthritic score and paw swelling were reduced. Gastroduodenal histopathology did not show erosions or ulcers in any of the groups. In conclusion, nabumetone improved the systemic signs and vascular alterations in experimental arthritis without showing any gastrointestinal side effects.