101份胆右成分分析初步研究

本文对101份胆石行化学定量分析及金属元素测定,并与剖面分类作对比,胆固醇类结石占63.4%,胆红素类结石占35.6%;11种金属元素除铬外,胆红素类结石均高于胆固醇类结石,胆管胆红素类结石中蛔虫残体检出率为35%,表明蛔虫感染的发病学意义。胆石剖面分类能反映胆石的成分特点,值得临床推广,     

胆固醇结石的成份与扫描结构(以胆固醇混合结石为主)

一般认为,胆固醇结石是欧美的主要胆石,在东方则以胆色素结石为多见。近年来发现,胆固醇结石在日本的发生率渐见增多。根据我们最近的粗略统计,我国有些地区胆固醇结石的比例也相当高。考虑到胆结石的性状具有明显的地区特点;有关胆固醇结石的组成情况较为复杂,至少有十来种不同的组合;加上关于胆固醇混合结石性状的论述较少。为此,我们利用红外吸收光谱、原子发射光谱及扫描电镜对这类胆石进行了初步的分析研究。结果发现胆固醇混合结石较之纯胆固醇结石,无论在胆固醇的含量、金属元素的组成和含量、或在扫描结构上均有相     

载脂蛋白A1、免疫球蛋白与胆囊胆固醇结石形成的关系

目的 探讨抑成核因子载脂蛋白A1（apoA1)。促成核因子免疫球蛋白IgA,IgM,IgG与胆囊胆固醇结石形成的关系。方法 收集40例胆囊结石患者血清，胆石和20例对照组血清，测定血清apoA1,IgA,IgM,IgG，胆固醇（TC）和甘油三脂（TG）含量。胆石用快速化学定性法分类。结果 胆囊结石3组中apoA1均增高，CS组中TC，TG，IgA及IgM增高，apoA1与IgA呈正相关。与IgG及IgM不相关。结论 在胆囊胆固醇结石的形成过程中IgA,IgM的成石作用可能比IgG更为重要，apoA1与IgA在胆囊胆固醇结石形成过程中可能有相互影响。     

性激素类药物诱发胆囊结石的实验研究

目的 探索性激素类药物诱发胆囊结石的关系。方法 用大白兔60只,分6组,给予雌二醇、孕酮、睾酮、绒毛膜促性腺激(HCG),ip,设生理盐水和精茶油对照组。实验时间6周,处死检测血液、胆汁、胆囊、胆管、肝脏及胆石。结果 雌二醇组90％成石;HCG组内雌性兔100％成石,雄性兔无结石形成;孕酮组无结石,睾酮组仅1例胆囊结石,两对照组均无结石。成石为胆固醇性结石。结论 性激素类药物中,雌二醇、HCG与胆囊胆固醇结石的形成有关。     

老年静止性胆囊结石

从表1可看出静止性胆囊结石的比率随年龄老化而增长。血胆固醇与胆囊结石的关系。根据红外光谱分析可以将胆石分成:(1)纯胆固醇性结石。(2)纯胆色素结石。(3)混合性结石[由胆固醇、胆色素与钙盐组成]目前已知胆固醇在胆汁中呈过饱和状态是形成结石的重要因素,此种过饱和的胆汁常称为“致石性胆汁”。曾有报道老年人胆汁数量减少,而胆固醇的含量与浓度增高,无机物较少,更因老年人活动较少,使胆固醇易于析出形成结石。     

性激素类药物诱发胆囊结石的实验研究

目的 探索性激素类药物诱发胆囊结石的关系。方法 用大白兔60只，分6组；给予午雌二醇、孕酮、辜酮、绒毛膜促性腺激(HCG)，ip，设生理盐水和精茶油对照组。实验时间6周，处死检测血液、胆汁、胆囊、胆管、肝脏及胆石。结果 雌二醇组90％成石；HCG组内雌性兔100％成石．雄性兔无结石形成：孕酮组无结石，辜酮组仅1例胆囊结石，两对照组均无给石：成石为胆固醇性结石。结论 性激素类药物中，雌二醇、HCG与胆囊胆固醇结石的形成有关。     

胆石核心的细菌学分析

胆石形成的病因较复杂,文献报导胆道异物、寄生虫、寄生虫卵、细菌、脱落细胞、粘液、钙盐未结合胆酸、色素、胆固醇小球等皆可为核心,促使胆石形成。为了探讨胆系细菌感染与胆石形成的关系,我们将1979年10月至1980年2月天津南开医院经手术所获38例结石标本做了胆石核心的细菌学分离及分析,以期对结石形成的病因及预防提高认识。     

超声探讨胆石形成与胃排空运动的关系

目的探讨胆石形成与胃排空运动的关系。方法运用超声观察156例胆石形成各阶段中的胃排空运动和胆道声像。结果胆石形成伴胃排空运动异常,结石前征象占77.3%～97.0%,结石形成后占72.7%。结论胆石形成与胃排空运动有关。     

CT平扫诊断胆结石症131例分析

胆结石症是胆道系统常见病,发病率为8％以上,其病理基础是在胆汁淤滞和胆道感染等因素的影响下,胆汁中的胆色素、胆固醇、黏液物质和钙盐析出、凝集而成胆结石。发生在胆囊内的称胆囊结石,发生在胆管内的称胆管结石,统称胆石症［1］。按化学成分可将胆石分为3种类型：胆固醇类结石,胆固醇含量占80％以上;胆色素类结石,胆固醇含量少于25％;混合类结石,胆固醇含量占55％～70％［2］。     

胆石术后再发结石42例临床分析

目的研究胆石术后再发结石发病情况及形成原因。方法对2000年～2003年两年中胆石门诊和1310人体检中发现再发结石者进行分析总结。结果胆石门诊中胆石术后就诊者74例12.7%,其中再发结石38例6.5%,体检中胆石手术者26例,再发结石4例15.38%,术前胆囊结石39例含保胆取石3例。胆管结石2例,胆囊并胆管结石1例,再发结石时间术后3月至40年不等,而再发结石的部位主要为胆总管、肝内胆管、胆囊保胆取石术、胆总管并肝内胆管。结论再发结石的可能原因为胆囊切除,保胆取石术后,形成结石的原因并未完全去除;手术造成胆管、胆囊损伤,由于炎症、黏膜粗糙、胆管不畅,易再发结石;有的在胆管留有残余结石基础上使其结石增大,产生症状;可能与术后随着年龄增长而发生结石有关。     

胆囊病变组织中雌激素与孕激素受体表达和成石原因相关研究

目的 探讨胆囊病变组织雌激素受体（ER）与孕激素受体（PR）的表达及其在发病中的作用.方法 采用免疫组化法进行ER、PR的检测.结果 胆囊癌、胆囊炎伴胆石症患者的阳性表达率明显高于胆囊炎伴胆固醇沉着症、胆囊息肉及单纯性胆囊炎患者（P＜0.05）,ER及PR在胆囊癌及胆囊炎伴胆石症中的阳性表达率分别为100%、70%及100%、50%,其阳性表达率在胆囊炎伴胆石症、胆囊癌中呈现由少到多的关系.结论 雌激素通过诱导该受体表达增加了形成胆囊结石并进一步发展为胆囊癌的易感性.     

A practical guide to the nonsurgical treatment of gallstones.

Until recently, cholecystectomy was the only treatment available for symptomatic gallstone disease. During the past 20 years, better understanding of the pathogenesis of cholesterol gallstone disease has led to alternative nonsurgical methods for treating gallstones in selected groups of patients. Use of 2 naturally occurring bile acids, chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA), was reported in 1972 and 1975, respectively, for successful dissolution of cholesterol gallstones in humans. Both these bile acids act by reducing cholesterol secretion in bile, thus enabling it to solubilise more cholesterol from the stone surface. Micellar solubilisation is involved, together with liquid crystal formation in the case of UDCA. Having been extensively studied in clinical trials to assess efficacy and safety, both these compounds are now available for general use. The efficacy of CDCA can be enhanced by single bedtime dose administration and by taking a low cholesterol diet. Bedtime administration also enhances the effect of a suboptimal dose of UDCA. CDCA induces dose-related diarrhoea and hypertransaminaemia, and UDCA can induce calcification of gallstones, thus rendering them resistant to medical dissolution. A combination of the 2 bile acids at half the recommended dose for each has become an accepted practice for reducing adverse effects, and this may also enhance efficacy. One of the main problems of bile acid therapy is that dissolution of gallstones is a very slow process. Use of extracorporeal shockwave lithotripsy (ESWL) to break the stones into smaller fragments, with concurrent use of bile acids, has been shown to speed dissolution rate and to achieve complete gallstone dissolution in 78% of selected cases within 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

Free fatty acids in gallstones in mice fed a diet containing cholic acid

In mice, combined addition of 1% cholesterol and 0.5% cholic acid to a diet induced cholesterol gallstones within 40 days as a result of the supersaturation of cholesterol in the bile, as has been reported. The major component of the gallstone was cholesterol, which was measured by HPLC. In this study, however, single addition of 1% cholic acid to a diet, which did not decrease cholesterol solubilizing capacity in bile, contributed to gallstone formation in mice within 50 days. The gallstones thus formed contained a large amount of palmitic acid. In the hepatic bile of this animal, palmitic acid was also detected; however, no solid material was observed by light and polarized-light microscopes. Free fatty acids such as palmitic acid seem to be dissolved in a complex micelle composed of bile acids and lecithin. This probably causes gallstone formation by reducing cholesterol solubilizing capacity in bile.     

Physicochemical investigations of dipolar aprotic solvents as potential cholelitholytic agents

A number of dipolar aprotic solvents have been examined as potential co-solvents for gallstone dissolution. The power of these agents to solubilize such gallstone components as cholesterol, calcium carbonate, calcium palmitate and palmitic acid was determined and compared with that of monooctanoin (Capmul), using the synthetic solubility method. The solubilities of cholesterol and palmitic acid were greater in the N-methyl, N-ethyl and N-butylpyrrolidone derivatives than in monooctanoin. In contrast, the solubilities of the calcium salts were very low (less than 0.25% w/w) in all solvents examined. The influence of N-methylpyrrolidone (NMP) on both the in-vitro dissolution of cholesterol from gallstones and the decrease in stone weight with time was determined. NMP proved to be a better solvent than monooctanoin for human stones. NMP, which is miscible with water and monooctanoin, may have potential as a co-solvent in the design of solvent systems for gallstones.     

Lipid lowering drugs and gallstones: a therapeutic option?

Cholelithiasis is a common disease worldwide. The majority of gallstones can occur when the bile is supersaturated with cholesterol. Dyslipidaemia, obesity, insulin resistance are associated with an increased risk for cholesterol gallstone formation as well as with vascular risk. Statins and ezetimibe are used to treat dyslipidaemia and appear to have some effect on bile composition and cholesterol gallstone formation. Statin (e.g. pravastatin, simvastatin, fluvastatin and lovastatin) monotherapy or combined with ursodeoxycholic acid (UDCA) have shown reductions in bile cholesterol saturation, preventing gallstone formation and even dissolving pre-existing stones. However, this effect was not consistently reported in all studies. Statin use has also been associated with a reduced risk for cholecystectomy in 2 large epidemiological studies. Ezetimibe was shown to have a beneficial action against cholelithiasis in animal studies but data in humans - although promising - are very limited. The effect of these drugs on gallstone disease warrants further investigation in large human trials. We also consider the links between cholelithiasis, vascular risk and the use of lipid lowering drugs.     

Stress- and morphine-induced elevations of plasma and tissue cholesterol in mice: reversal by naltrexone

Our earlier studies indicated that stress-induced facilitation of gallstone formation could be prevented by the opiate antagonist naltrexone. In view of the possible link between gallstone formation and atherosclerosis, the present study examined the possibility that endogenous opioids might also mediate stress-induced hypercholesterolemia. A 28-day immobilization stress schedule was used to induce increases in plasma, aortic and liver cholesterol of mice maintained on a high cholesterol diet. These stress-induced increases in plasma, hepatic and aortic cholesterol were reversed by pretreatment with the opiate antagonist, naltrexone (1 mg/kg). Exposure of mice to morphine (0.1% in the drinking water for 28 days) resulted in elevations of plasma, liver, and aortic cholesterol levels, similar to those observed following immobilization. In contrast, chronic exposure to the peripherally restricted opiate agonist, loperamide (0.1% in the drinking water for 28 days), was ineffective. The antagonism by naltrexone and duplication by morphine but not loperamide suggest that stress-induced hypercholesterolemia may require the activation of central endogenous opioid systems.     

Pathobiology of cholesterol gallstone disease: from equilibrium ternary phase diagram to agents preventing cholesterol crystallization and stone formation

The primum movens in cholesterol gallstone formation is hypersecretion of hepatic cholesterol, chronic surpersaturation of bile with cholesterol and rapid precipitation of cholesterol crystals in the gallbladder from cholesterol-enriched vesicles. Associated events include biochemical defects (increased biliary mucin, and increased proportions of hydrophobic bile salts in the intestine and gallbladder), motility defects (gallbladder smooth muscle hypocontractility in vitro and gallbladder stasis in vivo, sluggish intestinal transit), and an abnormal genetic background. The study of physical-chemical factors and pathways leading to cholesterol crystallization in bile has clinical relevance and the task can be carried out in different ways. The lithogenicity of bile is investigated in artificial model biles made by three biliary lipids - cholesterol, bile salts and phospholipids - variably combined in systems plotting within the equilibrium ternary phase diagram; also, crystallization propensity of ex vivo incubated human bile is studied by biochemical analysis of precipitated crystals, polarizing quantitative light microscopy and turbidimetric methods. The present review will focus on the recent advances in the field of pathobiology of cholesterol gallstones, by underscoring the role of early events like water transport, lipid transport, crystallization phenomena - including a genetic background - in gallstone pathogenesis. Agents delaying or preventing precipitation of cholesterol crystals and gallstone formation in bile will also be discussed.     

兔胆囊管不全结扎形成胆囊结石实验研究

根据发现青少年胆囊结石病人有胆囊管解剖异常现象，设计了动物兔胆囊管不全梗阻可形成胆囊结石的假说。取健康家兔２４只，雌雄不限，体重２．５ｋｇ～３．０ｋｇ，在无菌条件下行剖腹术，随机分实验组（胆囊管不全结扎１７只）和对照组（假手术７只）。成石标准以肉眼可见颗粒状或团块状结石或褐色糊状胆泥为准，并经Ｂ超、手术和病理证实。实验组成石率为６４．７％（１１／１７），对照组为１４．３％（１／７），经χ２检验，Ｐ＜０．０２５。实验表明，兔胆囊管不全梗阻与胆囊结石形成间存在着因果关系。