铝碳酸镁和西沙必利对胆汁反流性胃炎的疗效及胃内胆汁的影响

目的 探讨铝碳酸镁对胆汁反流性胃炎疗效及胃内２４小时胆汁的影响。方法 ３０例胆汁反流性胃炎,经胃内２４小时胆汁监测证实,并随机分为３组。一组服用西沙必利５ｍｇ,３次／ｄ;一组服用铝碳酸镁１．０ｇ,３次／ｄ;一组同时服用西沙必利和铝碳酸镁。治疗４周后观察腹痛,腹胀,呕吐胆汁等症状变化,并复查胃内２４小时胆汁监测。结果 治疗后３组患者症状减轻（Ｐ〈０．０１）,有效率分别为９０％、１００％和１００％。２     

铝碳酸镁对胆汁反流性胃炎疗效及胃内24小时胆汁的影响

目的探讨铝碳酸镁对胆汁反流性胃炎疗效及胃内２４小时胆汁的影响。方法１０例胆汁反流性胃炎，均经２４小时胃内胆汁监测证实，其中５例为胃大部切除术后毕氏Ⅱ式吻合患者。铝碳酸镁１０ｇ，每日４次，治疗１周后观察腹痛、反酸、恶心、呕吐胆汁等症状变化，并复查２４小时胃内胆汁监测。结果治疗后患者上述症状均明显减轻（Ｐ值＜００１），总有效率为９／１０。２４小时胃内胆汁反流总时间百分比由治疗前２０７６％±１３３２％降至４９３％±４５９％（Ｐ值＜００１），反流次数由７３６±４３６降至３４５±１５２（Ｐ值＜００５）。结论铝碳酸镁可结合胃内胆汁，为治疗胆汁反流性胃炎的有效药物。     

多潘立酮及铝碳酸镁治疗胆汁反流性胃炎多中心临床观察

目的　探讨多潘立酮对胆汁反流性胃炎的疗效及胃内 2 4h胆汁的影响。方法　 5 5例经胃内 2 4h胆汁监测证实的胆汁反流性胃炎患者随机分为 3组。A组 2 0例 ,予以多潘立酮 10mg ,3次 /d治疗 4周 ;B组 15例 ,予以铝碳酸镁 1.0 g ,3次 /d治疗 4周 ;C组 2 0例 ,予以多潘立酮 10mg ,3次 /d及铝碳酸镁 1.0 g ,3次 /d治疗 4周。分别于治疗前及治疗 4周后观察 3组患者腹胀、上腹痛、恶心及呕吐症状变化 ,并于治疗后复查胃内 2 4h胆汁监测。结果　治疗后 3组患者症状均明显减轻 (P <0 .0 5 ) ,多潘立酮对患者腹胀、上腹痛、恶心及呕吐的总有效率分别为 85 .0 % ,6 6 .7% ,84 .6 %及 87.5 % ;铝碳酸镁组分别为 6 0 .0 % ,80 .0 % ,83.3%及 10 0 .0 % ;多潘立酮联合铝碳酸镁组分别为 88.9% ,82 .4 % ,83.3%及 10 0 .0 %。但各组间症状有效率的比较差异无显著性。 3组患者治疗后胃内 2 4h胆汁反流总时间百分比均显著下降 (P <0 .0 5 ) ,但下降幅度各组间比较差异无显著性 (P >0 .0 5 )。结论　多潘立酮可减少胃内胆汁反流 ,铝碳酸镁可结合胆酸 ,均为治疗胆汁反流性胃炎的有效药物。     

国产铝碳酸镁治疗胆汁反流性胃炎和24小时胆汁监测

目的　评估国产铝碳酸镁 (威地美 )和进口同类产品 (达喜 )治疗胆汁反流性胃炎的疗效及安全性。方法　 30例伴有腹痛、反酸、恶心、呕吐胆汁患者由胃镜诊断为胆汁反流性胃炎 ,并经胃内 2 4h胆汁监测证实。患者分为两组 ,试验组 15例 ,给予国产铝碳酸镁 1.0 g ,每天 3次 ;对照组 15例 ,给予进口产品 1.0 g ,每天 3次 ,疗程均为 4周。治疗前、后均采用Bilitec测定胃内胆汁酸。观察治疗前后临床症状积分、临床症状消失时间、胃内胆汁酸变化以及药物不良反应。结果　试验组治疗 2、4周后烧心、上腹痛、上腹胀、嗳气、反酸、呕吐胆汁样物等症状均明显减轻 (P <0 .0 5 ) ,总有效率为 10 0 %。与对照组相比疗效相当。两组在治疗过程中 ,烧心、上腹痛、上腹胀、嗳气、反酸、呕吐胆汁样物等症状的消失时间也相当。试验组腹痛完全消失时间为 (7.2± 3.1)d ,对照组为 (6 .9± 4 .8)d。Bilitec监测结果显示 :试验组 2 4h胃内胆汁反流总时间百分比由治疗前的 (17.0± 16 .3) %降至 (4.9± 4 .5 ) % (P <0 .0 5 ) ,对照组由治疗前的 (16 .8± 6 .9) %降至 (3.2± 2 .3) % (P <0 .0 5 )。两组均未见明显的不良反应。结论　国产铝碳酸镁可结合胃内胆汁 ,有效缓解胆汁反流性胃炎症状 ,是治疗胆汁反流性胃炎安全、有效的药     

慢性胃炎患者胃内24小时胆汁监测

目的　胆汁反流是导致胃黏膜炎症的重要因素 ,该文研究不同类型慢性胃炎患者胃内胆汁反流情况。方法　分别对 45例慢性胃炎患者 (慢性浅表性胃炎 17例 ,慢性糜烂性胃炎 2 1例 ,慢性萎缩性胃炎 7例 )行胃内 2 4h胆汁监测 ,获得胆汁反流指标。分析胆汁反流总时间百分比、胆汁反流次数、胆汁反流 >5min次数和最长反流持续时间。结果　不同类型慢性胃炎组之间各项胆汁监测指标相差显著。胆汁反流总时间百分比在慢性萎缩性胃炎组 (16 .2± 18.0 )和慢性糜烂性胃炎组 (14.2± 12 .1)明显高于慢性浅表性胃炎组 (5 .3± 14.1,P <0 .0 1)。结论　胆汁反流与慢性糜烂性胃炎、慢性萎缩性胃炎的发生有关     

调胃降逆胶囊治疗胆汁反流性胃炎70例

目的：观察调胃降逆胶囊对胆汁反流性胃炎的疗效。方法：按《中药新药临床研究指导原则》设立治疗组和对照组,治疗组７０例,药用调胃降逆胶囊,每次６粒,每日３次,药用吗丁啉,每次１０ｍｇ,每日３次,均饭前服,疗程１个月。结果：治疗组总有效率为９２．９％,对照组为７６．７％。经统计学处理,两组疗程有显著性差异。结论;调胃降逆胶囊治疗胆汁反流性胃炎疗效优于吗丁啉。     

雷贝拉唑和铝碳酸镁治疗胆囊切除术后伴胆汁反流的胃炎作用比较

目的 观察雷贝拉唑、铝碳酸镁及两药联合对胆囊切除后伴有胆汁反流的胃炎的疗效.方法 胆囊切除后,经24 h胃内胆红索监测证实伴有胆汁反流的胃炎患者随机分为4组:空白对照组(n=30)、雷贝拉唑组(n=30,雷贝拉唑20 mg,1次/d)、铝碳酸镁组(n=29,铝碳酸镁1.0 g,3次/d)及联合用药组(n=31,雷贝拉唑+铝碳酸镁,用法同上),疗程8周.观察各组患者腹痛、腹胀、烧心、口苦等症状改善情况,并于治疗结束后2周复查胃镜及组织学检查并再次进行24 h胃内胆红素监测,进行胃镜下黏膜炎性反应程度(充血、水肿),组织学炎性反应程度(炎性反应、活动性)量化评分以及24 h胆红索吸收值(ABS)>0.14总时间百分比、十二指肠内容物反流次数、长反流次数(>5 min)的变化比较.结果 治疗后三组治疗组患者症状均有所改善,联合用药组内镜下水肿程度(2.11±0.77比1.50±0.67,P<0.05)及HE染色组织学活动性评分(2.87±0.72比1.97±0.78,P<0.05)均明显改善,长时间十二指肠内容物反流次数明显减少(18.26±1.80比9.70±1.20,P<0.05),雷贝拉唑组和铝碳酸镁组上述指标治疗前后差异无统计学意义;三组治疗组患者ABS>0.14的时间治疗前后差异均有统计学意义(P<0.05).结论 雷贝拉唑和铝碳酸镁联用可有效治疗伴有胆汁反流的胃炎.     

潘托拉唑和雷尼替丁治疗胃食管反流病的疗效

目的：观察铝碳酸镁治疗胃食管反流（GCR）及反流性食管炎（RE）的疗效及其安全性。方法：西安市3家医院合作,自1999年5月－2000年12月,应用铝碳酸镁治疗胃食管反流40例,并与22例硫糖铝治疗病例进行对照。62例入选者治疗前均经电子内镜检查,如为RE则于治疗4周后复查胃镜。采用症状积分和24h食管pH和胆汁监测进行疗效评估。结论：治疗组中12例内镜检查无食管炎为症状性反流（SGER）,对照组7例为SGER。治疗组给药后2周,胸骨后烧灼感,反酸等症状指数均明显下降（P＜0．01）。胸痛在治疗后4周也有改善。治疗组40例,内镜下有食管炎者28例,总有效率为91．66％。对照组22例,内镜下有食管炎者15例,总有效率66．66％。铝碳酸镁治疗4周食管酸及胆汁反流明显改善者8例（61．53％）;单纯胆汁反流者4例全部好转。对照组7例存在酸或胆汁反流,治疗4周后复查转阴3例（42．8％）。结论：铝碳酸镁具有中和胃酸,胆汁保护粘莫膜作用,是治疗胃食管反流及反流性食管炎的理想药物。     

泮托拉唑联合铝碳酸镁治疗胆囊切除术后胆汁反流性胃炎的研究

目的观察泮托拉唑联合铝碳酸镁治疗胆囊切除术后继发性胆汁反流性胃炎的疗效。方法胃镜确诊胆囊切除术后患有胆汁反流性胃炎的病人120例,随机分为安慰剂组（A组）;单用铝碳酸镁组（B组）;单用泮托拉唑组（C组）;泮托拉唑联合铝碳酸镁组（D组）。疗程4周,治疗结束后,所有病人复查胃镜。评估腹痛、腹胀、烧心、口苦等消化不良症状、胃镜和组织病理的效果。结果临床症状在B组、C组和D组均有缓解,D组病人临床症状缓解程度有显著差异。治疗前后各组间的胃镜充血程度和组织学炎症无显著差异。D组胃镜下水肿程度和组织学活动度有显著差异。结论泮托拉唑联合铝碳酸镁是胆囊切除术继发性胆汁反流性胃炎有效治疗选择。     

多潘立酮与铝碳酸镁治疗胆汁反流性胃炎的疗效分析

目的分析评价多潘立酮与铝碳酸镁治疗胆汁反流性胃炎的疗效。方法选取2015年3月~2016年3月来我院治疗胆汁反流性胃炎的患者128例为研究对象,并在其知情的情况下将其分成观察组和对照组,各64例。对照组给予多潘立酮治疗,观察组给予多潘立酮联合铝碳酸镁治疗,治疗后将两组患者的胆汁反流情况、临床治疗总有效率进行分析对比。结果治疗后观察组胆汁反流情况、临床治疗总有效率均优于对照组,差异有统计学意义(P0.05)。结论对胆汁反流性胃炎患者采用多潘立酮联合铝碳酸镁治疗具有显著的疗效,值得在临床治疗中选用。     

Bile Salt Metabolism:II. Bile Salts and Disease

Bile salt metabolism. II. Bile salts and disease. C. B. Campbell and A. E. Cowen, Aust. N.Z. J. Med., 1977, 7, pp. 587–595. Alterations of bile salt metabolism have been shown in numerous diseases. Liver damage results in elevated serum bile salt concentrations which may be useful as a sensitive index of hepatocellular disease. Changes in the relative proportions of the individual bile salts in serum occur with cholestasis. Urinary excretion of bile salts, largely in the form of sulphates, increases as a compensatory mechanism. Ileal disease or resection causes bile salt ma/absorption. The increase in colonic bile salts produces a watery diarrhoea while the decrease in duodenal levels may cause steatorrhoea. Cholelithiasis may result from alteration in the relative proportions of cholesterol, lecithin and bile salts in bile. The mechanism apparently differs in various conditions predisposing to gallstone formation. A primary alteration of bile salt metabolism has been postulated in several other conditions. Considerable interest centres on the importance of metabolites of bile salts in the pathogenesis of colonic carcinoma. Chenodeoxy-cholic acid is a successful though costly treatment for selected patients with cholesterol gallstones. Bile salt binding agents, such as cholestyramine, are extremely useful especially in the control of pruritus in patients with cholestasis.     

Bile acid malabsorption

Opinion statement Patients with bile acid malabsorption typically present with chronic, watery diarrhea. Bile acids recirculate between the liver and small intestine in the enterohepatic circulation. They are reabsorbed in the distal small intestine, and normally only a small fraction of the bile acid pool is lost to the colon during each cycle. In patients with bile acid malabsorption, a larger amount of bile acids is spilled into the colon, where the acids stimulate electrolyte and water secretion, which results in loose to watery stools. The common causes of bile acid malabsorption are ileal resection and diseases of the terminal ileum (Crohn’s disease and radiation enteritis), which result in a loss of bile acid transporters and, consequently, diminished reabsorption. Bile acid malabsorption also has been documented in a small group of patients with chronic, watery diarrhea who have no demonstrable ileal disease (idiopathic bile acid malabsorption). The amount of bile acid loss to the colon determines the clinical presentation. Patients with mild to moderate bile acid malabsorption present with watery diarrhea and generally respond very well to treatment (with abolishment of diarrhea) with bile acid binders such as cholestyramine. Patients with more severe bile acid malabsorption have both diarrhea and steatorrhea. Treatment with cholestyramine is of no benefit in this group of patients and may, in fact, worsen steatorrhea. These patients are best treated with a low-fat diet supplemented with medium-chain triglycerides.     

Bile duct disorders

Drug-induced bile duct injury related prolonged or chronic cholestasis is recognized as a common side effect of treatment with several drugs. The severity and duration of the clinical symptoms suggest that this increase in number of reports is not only related to clinician and pathologists being increasingly aware of the condition, but also may represent a true increase in incidence likely related to a time-related growing experience with newer drugs. This clinical presentation encompasses a wide variety of features that may be the source of diagnostic difficulties, especially in the cases where cholestasis occurs days or weeks after the completion of therapy. Even more puzzling is the initial picture of hepatocholangitis, which may be silent and ensuing bile duct paucity with chronic anicteric cholestasis may be another source of diagnostic difficulties in the long-term. These diagnostic difficulties suggest that some of the cases of the so-called "idiopathic adulthood ductopenia" may originate from overlooked drug induced vanishing bile duct syndrome. The pathogenesis of the syndrome remains largely unknown and the determinants of prognosis and outcome. From reproducible data obtained in different studies investigating HLA-dependent predisposition, one may assume that genetics plays a major role even if other unknown additive factors are also likely involved. Severity of initial hepatocholangitis is likely to represent another important determinant of severity and prognosis, however to be assessed in larger longitudinal studies. Therapy of large bile duct injury mimics that of primary sclerosing cholangitis. Treatment of small bile duct injury remains disappointing. Corticosteroids are invariably ineffective. Ursodeoxycholic acid as been shown to induce improvement of clinical and biochemical cholestasis in some selected cases, its efficacy being however unpredictable. Preliminary data about the natural history of the vanishing bile duct syndrome suggest that therapy might be more effective when initiated early.     

Bile salt diarrhea

Alterations in bile acid metabolism and in the enterohepatic circulation are often associated with chronic diarrhea and should be considered when more common causes of chronic diarrhea have been excluded. Bile acid diarrhea most often occurs in disease or resection of the terminal ileum, in which there is increased exposure of the colonic mucosa to bile salts with consequent activation of fluid and electrolyte secretion. Congenital or acquired defects in the enterohepatic circulation of bile acids also may lead to diarrhea. Although multiple diagnostic tests may be considered to confirm abnormal fecal bile acid losses, the most critical elements of the clinical evaluation of suspected bile acid diarrhea are a careful history to exclude more common causes of chronic diarrhea and a diagnostic trial of bile acid-binding resins.     

Bile acid-lipoprotein interactions

Several studies in the hamster model were undertaken to investigate known and recently disclosed metabolic interactions between bile acids and lipoproteins, particularly between ursodiol and low-density-lipoprotein (LDL) receptors. Three groups of animals, receiving a control 0.027% cholesterol diet, supplementation with 0.1% ursodiol, or supplementation with 0.1% chenodeoxycholic acid, were treated for four weeks. Both bile acids suppressed bile acid synthesis. Chenodeoxycholic acid significantly increased serum total cholesterol compared to ursodiol, and high-density-lipoprotein (HDL) cholesterol decreased significantly with chenodeoxycholic acid compared to ursodiol and control. Since the rate of bile acid synthesis is known to influence LDL receptor activity, LDL uptake under these conditions of synthesis suppression was measured. The animals received infusions of hamster LDL and methylated human LDL. Uptake of hamster LDL (occurring by both receptor-dependent and receptor-independent mechanisms) was significantly higher in the ursodiol-treated group than in the others. Human LDL uptake (occurring only by receptor-independent mechanisms) was not significantly affected by either treatment. The mechanisms by which ursodiol apparently directly stimulates the LDL receptor remain speculative but may involve alteration of cell membrane fluidity, change in the rate of LDL receptor cycling, and increase in the number of LDL receptors.     

Bile acid-induced diarrhoea

Three types of bile acid-induced diarrhoea can be distinguished. The best documented and most common entity is represented by type I bile acid malabsorption, which occurs as the result of a pathologically, anatomically defined ileopathy. Type II bile acid malabsorption is found in the setting of a morphologically completely normal ileum. This primary disorder of bile acid transport, which has been described in only a few paediatric and adult patients, appears to be rare. The third variety of bile acid malabsorption is characterized by the history of a previous cholecystectomy and/or by the presence of other gastroenterological conditions. Severe bile acid malabsorption is relatively uncommon in the type III syndrome. Even in the presence of severe bile acid malabsorption, patients with this condition are rarely found to have secretory concentrations of faecal bile acids, and/or rarely respond satisfactorily to cholestyramine. Present data suggest that bile acids play no significant role in the pathogenesis of idiopathic diarrhoea. A careful history, the measurement of stool weight and pH, a therapeutic trial of cholestyramine and the performance of a bile acid test, such as a bile acid breath test, can be used to establish the diagnosis of bile acid diarrhoea. Cholestyramine is the treatment of choice and is virtually always effective in this syndrome.