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。     

吗丁啉和铝碳酸镁合用对胆汁反流性胃炎疗效及胃内胆汁的影响

目的:探讨促动力药吗丁啉和胆盐结合药铝碳酸镁对胆汁反流性胃炎的疗效及胃内２４小时胆汁的影响。方法:２５例胆汁反流性胃炎患者,经胃内２４小时胆汁监测证实,记录上腹痛、饱胀、恶心、呕吐症状的积分后,予以口服吗丁啉１０ｍｇ,每日餐前１５分钟服用,３次/ｄ,铝碳酸镁０．５ｇ,每日餐后６０分钟服用,３次/ｄ。治疗４周后观察上述症状积分的变化,并复查胃内２４小时胆汁反流情况。结果:治疗２周后４种症状积分较治疗前显著降低(Ｐ＜０．０５)。４周后腹痛、饱胀症状进一步改善,２４小时胃内胆汁反流总时间百分比由治疗前的３０．４±２０．２%降至１５．６±６．６%(Ｐ＜０．０１),反流次数由治疗前的１０４．９±５７．６次降至５０．８±１９．６次。结论:吗丁啉与铝碳酸镁合用能有效缓解胆汁反流性胃炎的症状,降低胃内胆汁反流指标,是治疗胆汁反流性胃炎的有效方案。     

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     

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.     

食管pH和胆汁监测用于十二指肠胃食管反流的诊断及对治疗的评价

目的探讨十二指肠胃食管反流(DGER)的诊断方法和胆汁反流在胃食管反流病(GERD)中的临床意义.方法用便携式pH监测仪及胆红素监测仪(Bilitec 2000)对20例健康人及52例有烧心、反酸等症状的患者行24 h食管腔内pH和胆红素同步监测,以光吸收值≥0.14作为发生胆汁反流的阈值,计算24 h反流总时间%等指标.并对15例酸和胆汁混合反流者用铝碳酸镁加西沙必利治疗4周,然后复查两项监测.结果20例健康人中未发现病理性酸反流,52例患者中有47例(包括食管炎12例)存在病理性酸反流,诊为GERD.胆汁反流总时间%在健康人组及反流症状组分别为(0.47±0.71)%及(2.67±3.23)%(P＜0.05),在食管炎及非食管炎者分别为(5.41±4.93)%及(1.68±1.76)%(P＜0.05).47例GERD中15例(32%)为酸及胆汁混合反流,另32例为单纯酸反流,前者有食管炎8例而后者仅为4例(P＜0.05).15例混合反流经治疗后酸和胆汁反流总时间%均明显降低,8例食管炎中有7例炎症消退,1例减轻.结论Bilitec 2000是评价DGER的有用工具,32%的GERD存在酸和胆汁混合反流;胆汁反流在GERD食管黏膜损害中起重要作用.     

马来酸曲美布汀联合铝碳酸镁治疗胆汁反流性胃炎的疗效研究

目的 探讨马来酸曲美布汀联合铝碳酸镁对胆汁反流性胃炎(bile-reflux gastritis; BRG)的疗效.方法 经胃镜及病理证实的胆汁反流性胃炎94例,并随机分为Ⅰ、Ⅱ组.Ⅰ组44例,口服马来酸曲美布汀片200 mg,tid;Ⅱ组50例,口服盐酸伊托必利50 mg,tid,两组同时嚼服铝碳酸镁片1000mg,tid.观察治疗4周前后上腹痛、腹胀、嗳气、烧心或胸骨后痛、恶心或呕吐等症状以及发作频度、胃镜和组织学积分的变化.结果 治疗4周后两组患者症状除Ⅰ组中恶心或呕吐症状评分在治疗前后经比较无统计学意义外(P＞0.05),发作频度、胃镜和组织学评分均有明显降低,各组间治疗前后均有统计学意义(P＜0.05).结论 马来酸曲美布汀联合胃黏膜保护剂铝碳酸镁,能有效减轻BRG的症状及胃黏膜损害程度,可能为治疗BRG的捉供了一种新选择.     

原发性胆汁反流性胃炎诊断的探讨

目的　探讨原发性胆汁反流性胃炎的诊断方法及十二指肠胃反流 (DGR)的临床意义。方法　用便携式胆红素监测仪 (Bilitec2 0 0 0 )对 2 0例健康人及 42例有腹痛、腹胀、恶心及呕吐胆汁等症状的非溃疡性消化不良患者进行 2 4h胃内胆红素监测、临床症状评分、胃镜检查及组织活检。分析DGR的严重度与症状、内镜所见和组织学改变之间的关系。结果　 2 4h胆汁反流总时间百分率在健康组和有症状组中分别为 (2 92± 2 39) %及 (1 7 68± 1 7 89) % (P <0 0 1 ) ,病理性DGR的检出率为55 %。内镜下黏液湖胆染、胃窦黏膜糜烂、胆染伴胃窦黏膜糜烂、胆染伴中度以上的充血者中病理性DGR的检出率分别为 86 %、88%、8/8、85 %。内镜检查发现黏液湖胆染和胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DGR的胆汁反流性胃炎 (BRG)者共有 1 1例。幽门螺杆菌(Hp)阴性的BRG者 ,组织学上活动性炎症比生理性DGR组Hp阴性者严重 (P <0 0 5)。各项临床症状的发生率在各组间差异无显著性 (P值均 >0 0 5) ,但BRG组腹胀、恶心及呕吐胆汁等症状的严重程度显著重于生理性DGR组 (P值均 <0 0 5)。结论　完整胃内镜检查发现黏液湖胆染同时伴胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DG     

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。     

铝碳酸镁治疗胃食管反流样症状疗效报告

胃食管反流样症状是临床上较常见的表现,上海市人群发生率在7%以上,其剑突下或上腹痛、反酸、烧心、恶心等症状的发生除了胃酸的作用外,还与胆汁的反流有关。铝碳酸镁能中和胃酸,又可在酸性环境中结合胆酸,对缓解症状有较好疗效。我们应用铝碳酸镁治疗胃食管反流样症状患者60例,特报告如下。1　材料与方法1.1　病例选择　符合以下条件者入选:(1)有剑突下或上腹痛、反酸、烧心、恶心等症状持续4周以上;(2)内镜检查未发现食管糜烂、溃疡,胃十二指肠溃疡和胃癌等器质性疾病;(3)Ｂ超等检查排除肝、胆、胰疾病;(4)无严重心、肝、肾疾病和腹部手术…     

Excretion of metroindazole in human bile. Investigations of hepatic bile, common duct bile, and gallbladder bile

Excretion of metronidazole (MNZ) in the normal and in the diseased biliary tract was investigated in 58 patients after oral or intravenous administration of MNZ. After oral administration MNZ appeared rapidly in hepatic bile, and throughout the period of absorption and elimination almost identical concentrations of MNZ were found in serum and hepatic bile. After intravenous administration no significant differences were found between concentrations of MNZ in common duct bile and serum in the non-obstructed common duct; in common duct obstruction, concentrations of MNZ in common duct bile were 56--99 per cent of corresponding concentrations in serum. MNZ was concentrated in normal gallbladders. In patients with gallbladder stones and preserved function of the gallbladder and in patients with no function of the gallbladder but a patent cystic duct, no significant differences were found between concentrations of MNZ in gallbladder bile, common duct bile, and serum. In most gallbladders with the cystic duct blocked by a stone, no MNZ was found in gallbladder bile.     

Urinary excretion of bile acids in bile duct-ligated rats

Background. In patients with complete bile duct obstruction, the only pathway of bile acid elimination is through the urine. However, the urinary excretion of various bile acid conjugates in the presence of bile duct obstruction has not been clarified. Given this factor, the urinary excretion of various bile acids was compared in rats that were bile duct-ligated for 3 days. Methods. After urinary bladder cannulation, radiolabeled bile acids were intravenously injected, and urine samples were collected every 2 h for 6 h, and radioactivity was counted. Results. Urinary excretion (cumulative percent dose during 6 h) of taurocholate and cholate was similar (19.3% and 16.8%). Urinary excretion of tauroursodeoxycholate, lithocholate, and taurolithocholate-sulfate was less effective (12.7%, 9.8% and 2.1%, respectively). Cholate was mostly conjugated with taurine, and lithocholate was mostly conjugated with taurine and further hydroxylated. Conclusions. These results indicate that unconjugated bile acids were taken up by the liver and excreted into the blood after further biotransformation even under conditions of complete bile duct obstruction. Although bile acid sulfates are the major bile acids in the urine of patients with obstructive jaundice, monohydroxylated bile acids are considered not to be so effectively excreted into the urine, even with conjugation with taurine and sulfate, in rats. Received: October 4, 2002 / Accepted: November 8, 2002 RID="*" ID="*" Reprint requests to: H. Takikawa Acknowledgments. This work was partly supported by a Grant-in-Aid by the Japan Society for the Promotion of Science (C2-14570510).     

Hypercholeresis induced by unconjugated bile acid infusion correlates with recovery in bile of unconjugated bile acids

Using the isolated perfused rat and hamster liver, the relationship between bile flow, bile acid secretion rate and bile acid biotransformation after the injection of a small, bolus dose of radioactive ursodeoxycholate or of its C23 homolog, norursodeoxycholate, was examined. Ursodeoxycholate was promptly secreted into bile mostly as amino acid conjugates; less than 3% was secreted in unchanged form in the rat and less than 2% in the hamster. In contrast, norursodeoxycholate was secreted slowly, and biotransformed into glucuronide conjugates and unconjugated trihydroxy derivatives; it was also secreted in part in unchanged form. In the rat, 7% was secreted in unconjugated trihydroxy derivatives and 3% in unchanged form; in the hamster, 7% was secreted as unconjugated trihydroxy derivatives and 4% in unchanged form. The secreted bile acid species that showed the highest correlation with bile flow by far was always the unconjugated form in both rat and hamster. By multiple regression analysis, the apparent choleretic activity (microliters of induced bile flow per micromoles recovered bile acid molecules) indicated marked hypercholeresis for the unconjugated bile acid marked hypercholeresis for the unconjugated bile acid with values ranging from 100 to 300 microliters/mumol. Bile flow also correlated with total bile acid recovery for ursodeoxycholate in rat and norursodeoxycholate in hamster, but in all studies the apparent choleretic activity was far lower. Other calculations indicated that most bile flow during the first 30 min was induced by secretion of the unconjugated bile acid species in all experiments, the proportion ranging from 50% to 90%. The results indicate that when a bolus of ursodeoxycholate or norursodeoxycholate is presented to the perfused rodent liver, the secretion of the unchanged bile acid appears to be responsible for most of the bile flow, probably by a cholehepatic shunting mechanism.     

Pathways of cholesterol crystallization in model bile and native bile

Hypersecretion of hepatic cholesterol, chronic supersaturation of bile with cholesterol and rapid precipitation of cholesterol crystals in the gallbladder from cholesterol-enriched vesicles represent the primum movens in cholesterol gallstone formation. Physical-chemical factors and pathways leading to cholesterol crystallization can be investigated in artificial model biles and ex vivo in fresh human bile. Depending on modulatory factors (i.e., lipid concentration, bile salt or phospholipid species, humidity, mucins, etc.), cholesterol can precipitate in several forms (i.e., monohydrate, anhydrous) and habits (i.e., plate-like, needle-like, intermediate arcs, filaments, tubules, spirals). Careful analysis of biliary cholesterol crystals includes biochemical analysis of precipitated crystals, polarizing quantitative light microscopy, and turbidimetric methods. In this paper, recent concepts on cholesterol crystallization in artificial model biles as well as in human bile will be reviewed.     

Insulin in bile

Summary Immuno-reactive insulin is found in the hepatic bile of normal rabbits. Less than 1% of an injected dose of bovine insulin reached the bile. When ¹²⁵I-bovine insulin alone or complexed with antibody was given intravenously, only 40% of the radioactivity recovered in the bile was precipitable with trichloracetic acid, and less than 10% reacted with guinea pig anti-insulin serum. Glucose, fructose, galactose, tolbutamide and phenformin all caused an elevation in bile insulin, which reached a maximum 40 to 50 min after the injection. Alloxan attenuated or abolished these responses.

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Insulin im Gallensaft. Wirkung von Monosacchariden und blutzuckersenkenden Substanzen

Zusammenfassung Immunoreaktives Insulin wird in der Leber-Galle normaler Kaninchen gefunden. Weniger als 1% einer injizierten Dosis von Rinder-Insulin erreicht die Galle. Wenn man reines oder an Antikörper gebundenes ¹²⁵I-Rinderinsulin intravenös verabreicht, lassen sich mit Hilfe von Trichloressigsäure nur 40% der Radioaktivität ausfällen, die in der Galle gefunden wird, und weniger als 10% reagieren mit Meerschweinchen-Anti-Insulinserum. Glucose, Fructose, Galaktose, Tolbutamide und Phenformin verursachen ein Ansteigen von Insulin in der Galle, welches ein Maximum innerhalb von 40 bis 50 Min. nach der Injektion erreicht. Alloxan vermindert oder hebt diese Effekte auf.

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L'insuline dans la bile. L'effet de monosacharrides et d'agents hypoglycémiants

Résumé On trouve de l'insuline immunoréactive dans la bile hépatique de lapins normaux. Moins de 1% d'une dose injectée d'insuline bovine atteint la bile. Quand de l'insuline bovine ¹²⁵I, seule ou liée à l'anticorps, est administrée par voie intraveineuse, seulement 40% de la radioactivité retrouvée dans la bile est précipitable avec l'acide trichloracétique et moins de 10% réagit avec le sérum anti-insuline de cobaye. Le glucose, le fructose le galactose, le tolbutamide et la phenformine provoquent tous une élévation de l'insuline dans la bile, qui atteint son maximum 40 à 50 min après l'injection. L'alloxane atténue ou abolie ces réponses.

     

Spontaneous formation of pigmentary precipitates in bile salt-depleted rat bile and its prevention by micelle-forming bile salts

During studies on the effect of bile salt-pool depletion in the bile-fistula rat (adult male Sprague-Dawley), the spontaneous formation of an orange-brown precipitate was noted. The nature of this phenomenon and its relationship to BS and calcium concentration was investigated in depth. Bile from 18 animals was collected in the dark into transparent tubes containing sodium azide, ascorbic acid, and glucaro-1,4-lactone. The tubes were flushed with nitrogen, sealed, and incubated at 37 degrees C. The pigmentary precipitate formed in all the bile salt-depleted (less than 3-5 mM) bile samples (i.e., those collected after 5-7 h of external biliary drainage), but not in bile salt-rich biles. It appeared within 30-240 min after collection, both in bile samples collected at room temperature and at 37 degrees C, initially as a pale flocculation and then slowly sedimenting to form, after centrifugation, a solid, dark-orange pellet. There were no pH changes during incubation, and bile cultures were negative. Under polarizing microscopy, the precipitate appeared amorphous, and there was no evidence of birefringence. High-performance liquid chromatography showed that unconjugated bilirubin was the prevalent pigmentary component, but significant amounts of monoconjugated bilirubin also coprecipitated. Lipid chemistry showed the presence of lecithin (80.1% of total lipids), which was rich in palmitoyl and linoleoyl fatty acids, and of fatty acids (predominantly palmitic and oleic). Infrared spectroscopy and x-ray diffraction showed the presence of calcium bilirubinate and palmitate. In-vivo replenishment of the bile salt pool by intravenous infusion of either taurocholate or taurochenodeoxycholate (1 mumol/min) completely prevented the pigmentary precipitation. In vitro experiments showed inhibition of the precipitate formation by the addition of individual bile salt in concentrations approximating their critical micellar concentration. Precipitate formation was hastened by the addition of calcium chloride (4-12 mM), but only in bile salt-depleted biles. As the composition of the precipitate closely resembles that of human brown-pigment stones and sludge, these findings may provide new insights into an understanding of the pathogenesis of pigment gallstone disease.