Epidemiology, Pa Tho Genesis, And Classification of Biliary Stones

Published on May 2018 | Categories: Documents | Downloads: 10 | Comments: 0 | Views: 203
of 9
Download PDF   Embed   Report

Comments

Content

Best Practice & Research Clinical Gastroenterology Vol. 20, No. 6, pp. 1075 e1083, 2006 doi:10.1016/j.bpg.2006.05.009 available online at http://www.sciencedirect.com

7 Epidemiology, pathogenesis, and classification of biliary stones (common bile duct and intrahepatic) Susumu Tazuma*

MD

Professor and Chairman Department of General Medicine and Clinical Pharmacotherapeutics, Hiroshima University Hospital and  Graduate School of Biomedical Sciences, 1-2-3, Kasumi, Minami-ku, Hiroshima 734-8551, Japan

Gallstones are common in Western countries and Japan. Most gallstones are found in the gallbladder, but they sometimes pass through the cystic duct into extrahepatic and/or intrahepatic bile ducts to become bile-duct stones, causing conditions known as choledocholithiasis and hepatolithiasis. Some 10 e15% of gallstone patients concomitantly suffer from bile-duct stones. Bileduct stones can also be formed in the absence of gallbladder stones, and such primary bile-duct stones are more common in East Asian countries than in the Western world. Thus pathogenesis of primary and secondary bile-duct stones is unlikely to be similar. Furthermore, the gallbladder stones are primarily cholesterol or black-pigment stones, whereas most bile-duct stones are brown-pigment stones (calcium bilirubin stones). Thus, epidemiology, pathogenesis and classification of biliary stones are very likely to differ according to stone location (intrahepatic and/or extrahepatic bile duct). Key words: choledocholithiasis; hepatolithiasis; cholesterol gallstone; pigment gallstone; bile infection; infection; bile stasis. stasis.

COMMON-BILE-DUCT STONES Incidence and distribution

Gallstones are extremely common in Western societies and also in Japan. Approximately l5% of the American population is found foun d to have gallstones, and over 0.7 million cholecystectomies are performed every year. 1 Of these, 10e15% cases are found to have concomitant common-bile-duct (CBD) stones, but in the Western world few * Tel./Fax: þ81 82 257 5461. E-mail address: [email protected] 1521-6918/$ - see front matter

ª

2006 Elsevier Ltd. All rights reserved.

1076 1076 S. Taz Tazum umaa

cases are reported with CBD stones in the absence of gallbladder stones. In contrast, contras t, in Japan the overall incidence of gallstones is approximately 10% of the population. 2 Among these, the incidence of bile-duct stones increases with age to become approximately 20% of all gallstones. The gallbladder stones are concomitantly found in 67% of  CBD-stone cases, whereas the prevalence of CBD stones in gallbladder-stone cases is 15% (Table (Table 1). 1). Thus, the gallstone incidence in Japan is epidemiologically similar to that in the Western estern wor world. ld. In additio addition, n, the preval prevalenc ence e of asympt asymptoma omatic tic CBD stones stones,, 3 coincidently detected at cholecystectomy, is 6% in Western countries. Coexisting gallbl gallbladd adder er and CBD stones stones are cor correl relate ated d with with increa increasing sing age, age, chroni chronicc bile-d bile-duct uct inflammation, Asian descent, and possibly hypothyroidism. Primary bile-duct stones which are not associated with gallbladder stones occur frequ frequent ently ly in Asia. Asia. This This is associa associated ted with with the high high incide incidence nce of intrah intrahepa epatic tic bilebileduct stone stones see seen n primar primarily ily in Southe Southeast ast Asian Asian countri countries, es, Taiwan, aiwan, Hong Hong Kong, ong, and 4 Singapore. The relative prevalence of intrahepatic bile-duct stones in all gallstone case casess in Taiwa aiwan n is ex extr trem emel elyy high high (>50%), 50%), and coe coexis xistin tingg intraintra- and extrah extrahepa epatic tic bile-duct stones are found in approximately 70% of these. Primary bile-duct stones are composed predominantly of bilirubin, regardless of the concomitant presence of  intrahepatic bile-duct stones, whereas those secondary to gallbladder stones are composed mainly of cholesterol. Thus, the pathogenesis of the two types of bile-duct stones probably differs. The ratio of women to men with CBD stones is 0.89:1,2 although the prevalence of  gallbladder stones is higher in women than in men (1.22:1). The incidence of gallstones increases with increasing parity, and biliary sludge is i s f ormed ormed in approximately 30% of  5,6 pregn pregnant ant women; women; 1e3% of these form gallstones. The mean age of CBD-stone patients is 67 years, which is older than that of gallbladder-stone patients (56 years). Similarly, gallbladder diseases are found in 5e8% of young women but in 25 e30% of  women over 50 years of age. 7 Thus, risk factors for gallsto gallstones include biological factors such as increasing age, female gender, and pregnancy. 8 Origin e secondary to gallbladder or primitive from the bile duct?

CBD stones are classified according to origin: (1) primary bile-duct stones, forming initially in the bile ducts; (2) secondary to gallbladder stones, originating in the gallbladder and passing into the bile ducts; and (3) secondary to or coexisting with intrahepatic bile-duct stones. Primary bile-duct stones which do not involve the gallbladder are also composed predominant predominantly ly of bilirubin, and this is presumably associated with biliary stasis and 9,10 infection. The incidence of primary CBD stones is low in Western societies, where stones are most commonly found in the gallbladder. Gallstones can pass through the Table 1. Incidence of common bile-duct stones in Japan.

All gallstone cases Gallbladder stone Common bile-duct stone With gallbladder stone Without gallbladder stone Intrahepatic duct stone

1989e1995

1996 e1997

140,884 117,920 (83.7%) 20,006 (14.2%)

6814 5335 (78.3%) 1384 (20.3%) 934/1384 (67.5%) 450/1384 (32.5%) 95 (1.4%)

e e 2959 (2.1%)

Epidemiol Epidemiology ogy,, pathogenesi pathogenesis, s, and classificatio classification n of biliary stones 1077

cystic duct into extrahepatic and/or intrahepatic bile duct to become bile-duct stones secondary to gallbladder stones. In this regard, bile-duct stones coexisting with gallbladder stones are presumably formed secondarily to gallbladder stones. In such cases, the bile-duct stone composition composition is biochemicall biochemicallyy identical identical or extremely extremely similar to that of gallbladder stones, which are composed predominantly of cholesterol. In addition, CBD st s tones are concomitantly found in approximately 70% of intrahepatic bile-duct stones.4 These stones are identical identical or extremely extremely similar to intrahepati intrahepaticc bile-duct stones in biochemical composition. Most of intrahepatic bile-duct stones are brown-pigment stones, relatively rich in cholesterol. Thus, the pathogenesis of primary bile-duct stones probably differs from that of secondary bile-duct stones. Congenital and acquired risk factors

Risk factors for gallstones include congenital, biological, and behavioural factors. Bile stasis stasis and infect infection ion are importa important nt factor factorss for primary primary CBD-st CBD-stone one format formation. ion. On this basis, an anatomical abnorma abnorm ality causing bile stasis is one of the major risk factors, in association with bile infection. 9 In contrast, the dilatation dilatation of the common bile duct is frequently associated with bile-duct stones after cholecystectomy, and a cystic duct dilatation in the aged gallbladder-stone population is directly associated with passage of gallbladder stones into bile ducts to form secondary bile-duct stones. Thus, such an acquired risk in anatomy is also important in both primary and secondary bileduct stone formation. Genetic factors are believed to account for the ethnic difference in the risk of gallstone formation. formation. The prevalence prevalence of cholesterol cholesterol gallstones is higher in Native Native Americans, Chileans, and Hispanics than in age-matched white control su s ubjects, whereas African Americans have a lower prevalence of gallstones than whites, 11 and concomitant CBD stones stones are found in 10 e15% of these populations. Primary bile-duct stones, composed mainly of bilirubin, are much more common in Asians than in Europeans. Another geneti geneticc facto factorr, gall gallston stone e form format ation ion-a -asso ssocia ciate ted d gene geness Lith Lith1 1 and and Lith Lith2, 2, have have be been en 12 recognized in mice, but no human genes definitely linked to gallstones have been identified to date. Furthermore, polymorphisms in the apolip apo lipoprotein oprotein E gene, which 13 are associated with gallstone formation, have been identified. However, However, these genetic factors are not specific for primary bile-duct gallstone formation. Acquired risk factors for gallstone formation include not only biological factors such as age, gender, and lipid metabolism, but also behavioural factors such as nutrition, obesity, rapid weight gain and loss, and exercise. In addition to these factors, cholecystectomy at young ages leading to CBD dilatation is another acquired risk factor for CBD stones.14 Furthermore, chronic inflammatory conditions e such as hypofunction of Oddi, primary sclerosing cholangitis, acquired immunodeficiency syndrome, and parasites e can lead to bile-duct stone formation. Ce C ertain drugs are secreted into bile and may precipitate with calcium to form stones. 15 Classification based on biochemical structure

CBD stones are composed predominantly of bilirubin, whereas cholesterol is a major component in gallbladder stones (Table ( Table 2). 2). Thus, primary bile-duct stones tend to be higher in bilirubin content and lower in cholesterol content than secondary stones. The pathogenesis of primary bile-duct stones probably differs from that of secondary bile-duct stones.

1078 1078 S. Taz Tazum umaa

Table 2. Classificati Classification on of gallstones gallstones based on biochemical biochemical structure.

Cholesterol stone (%) Bilirubin stone Black-pigment stone (%) Brown-pigment stone (%) Others (%)

Gallbladder stones

Common bile-duct stones

58.3

31.1

23.7 15.9 2.1

11.8 54.3 2.8

Pigment gallstones are divided into two categories: black-pigment stones composed primarily of bilirubin polymers, and brown-pigment stones composed predominantly of calciu calcium m biliru bilirubin binate. ate. Brown Brown-pig -pigmen mentt stone stone is freque frequentl ntlyy found found in primary primary CBD stones, and this contains more cholesterol than black-pigmented stones. In the process of the formation of brown-pigment stone, bacterial infection and biliary stasis are important important factors. factors.9 Thus, bacteria are frequently f ound ound in brown-pigment stones, and bile infection appears to precede stone formation. 10 Parasitic infection is also associated sociated with primary primary duct stones as well as intrahepati intrahepaticc bile-duct bile-duct stones, particularly particularly in Asia. The pathogenesis of these stones is complex, and seemingly involves not only bile infection and stasis but also malnutrition and/or dietary factors. Hydrolysis of bilirubin by bacterial bacterial b-glucuron -glucuronidase idase leads to formation formation of unconjugate unconjugated d bilirubin bilirubin which can precipitate as calcium bilirubinate. Recent investigations clarify the presence of  bacteria not only in brown-pigment stones but also in cholesterol stones, indicating that bacterial infection commonly plays a pathogenic role in cholesterol stone formation.16 Thus, after brown-pigment stone core formation is initiated by bacterial infection and subsequent bilirubin deconjugation, bile composition may change eventually to form brown-pigment stone or cholesterol stones. Similarly, such precipitates and/ or microcalculi can act as foreign bodies to induce bacterial colonization, eventually enhancing precipitation of calcium bilirubinate or modifying original cores. In contrast, contrast, bilirubin bilirubin polymerizat polymerization ion is based upon non-enzymat non-enzymatic ic deconjugati deconjugation on of  biliru bilirubin bin,, and theref therefore ore blackblack-pigm pigment ented ed stone stone format formation ion in the gallbla gallbladde dderr is not associated with bile infection, but rather from chronic haemolysis caused by genetic disorders and/or artificial organs, leading to overproduction of bilirubin. Mucin originating from the biliary tree, bile duct and gallbladder traps precipitates of calcium bilirubinate and bilirubin polymers to form brown- and black-pigment stones. Natural history

The natural history of CBD stones varies a great deal according to the life-style of the subjects, subjects, especially dietary habits. habits. CBD stones present present with acute cholangitis, cholangitis, pancreatitis, and hepatic abscesses caused by the obstruction of the bile-duct or Ampulla of  Vater, while approximately 10% are asymptomatic. Such complications are frequently accompanied by bacterial sepsis because the bacterial biofilm on stones is activated under under stone stone obstru obstructi ction-i on-indu nduced ced bile bile stasis. stasis. Patient Patientss become become jaundic jaundiced ed with colic colic pain and fever, requiring urgent drainage. In very few cases with malignant bile-duct obstruction without stones does sepsis result. Also, small CBD stones spontaneously pass into the duodenum without any serious complication. Secondary CBD stones are diagnosed incidentally in screening examination of the biliary tree, and thus in most

Epidemiol Epidemiology ogy,, pathogenesi pathogenesis, s, and classificatio classification n of biliary stones 1079

cases are asymptomatic or associated with symptoms and complications similar to those of gallbladder stones. However, chronic bile stasis based upon biliary obstruction by stones can cause secondary biliary cirrhosis and portal hypertension over the course of years, 17 and acute obstructive suppurative cholangitis and acute pancreatitis frequently need urgent and intensive care. Thus once diagnosed, CBD stones should be removed by endoscopic techniques or surgery. INTRAHEPATIC STONES Worldwide epidemiology

Intrahepatic stones are rare in the Western world but frequent frequ ent in Eastern Asia. The prevalence of intrahepatic stones in the West is 0.6 e1.3%,18,19 but extremely high in Asian societies: for example, 47.3% in Taiwan, 38.0% in China, 17.0% in Korea, and 11.7% in Malaysia. 20 In Japan it is 2.1%. 2 Also, a relatively high incidence is found in Latin America (around 2%), especially in Brazil. 21,22 There are two types of intrahepatic stones: (1) primary stones formed in the intrahepatic bile duct, found in East Asian countries, and (2) secondary stones originating from the gallbladder, commonly found in the Western world. The retrospective study in East Asia indicates that the concomitant intrahepatic and extrahepatic stones are foun found d in appr approx oxim imat atel elyy 70% 70% of all all he hepa pato tolit lithi hias asis is case cases, s, and and that that the the left left he hepa pati ticc duct duct invol involve vemen mentt is similar similarly ly predom predomina inant nt in stone stone locati location on and biliary biliary strict stricture uress 23 (70e90%). Half Half of the intrah intrahepa epatic tic stones stones occ occur ur concom concomita itantly ntly with with gallbl gallbladd adder er stones, suggesting secondary stones. The mean age at presentation is the 50s and 60s, with a similar gender distribution.24,25 The aetiology of intrahepatic stones is not completely understood, but the higher incidence in Asian countries and Brazil, compared to that in Western societies, societies , suggests suggests 20,26 poor sanitary and nutritional conditions as key factors in the pathogenesis. Malnutrition and lo low socio-economic class are associated with a high incidence of intrahepatic stones.27 There is a gradual increase in the incidence of gallbladder stones with Westernization of life-style, and this is associated associated with a decrease in intrahepatic stones 28,29 and CBD stones in Taiwan and Japan. Intrahepatic stones used to be common in  Japan during the 1950s when the diet was low in fat and protein, but with economic econom ic development and improvement in the quality of life its prevalence is clearly declining. 20 Pathogenesis

Pathogenesis of primary intrahepatic stones, seen primarily in East Asian countries, is complicated and probably involve inv olvess a combination of bile stasis, bile inf  i nf ection, ection, malnutri9,10 30 tion, and parasitic parasitic infestation, infestation, namely oriental cholangiohepatitis. Bile stasis associated with biliary stenosis leads to bacterial colonization, mostly by Escherichia coli  and Enterobacter  species (>95%) that pass into the liver through the portal vein secondarily to repeated parasite intestinal mucosal lesions. Biliary parasites are relatively common in East Asian countries, where sanitary conditions are poor in some places. Biliary infestation by Clonorchis Clonorchis sinensis sinensis and Ascaris lumbricoides lumbricoides leads to inflammation of the biliary epithelium, enhancing mucin secretion and providin provid ingg a nidus for stone formation together with fragments of parasites and/or their eggs. 31 Bacter Bacterial ial enzyme enzymes, s, such such as b-glucu -glucuron ronida idase, se, initiat initiate e the hydr hydroly olysis sis of bilirub bilirubin in digl digluc ucur uron onid ides es to form form unco unconju njuga gate ted d bilir bilirubi ubin n whic which h can can prec precip ipit itat ate e as calc calciu ium m

1080 1080 S. Taz Tazum umaa

bilirubinate.32 Also, bacterial phospholipase induces the breakdown of biliary phospholipids to pr produce free fatty acids and lysophospholipids, both of which are quite waterinsoluble.33 This enhances the precipitation of calcium salts of fatty acids, along with the enhancement of mucin secretion from biliary epithelium. Thus, primary intrahepatic stones are brown-pigment stones composed predominantly of calcium bilirubinate with more cholesterol. The pathogenesis of primary intrahepatic cholesterol stones remains unclear. Recent investigations indicate that intrahepatic stone formation is based upon the dual defects defects of up-regulati up-regulation on of cholestero cholesteroll synthesis synthesis and down-regulation down-regulation of bile-acid bile-acid synthesis in the liver, possibly in association with defective secretion secreti on of phospholipid by its canalicular transporter, multidrug resistance protein (MDR3).34 Congenital and acquired risk factors

Intrahepatic stone formation is affected by congenital and acquired risk factors. Congenital factors include: (1) anatomical anomalies such as biliary strictures associated with sclerosing cholangitis, and extrahepatic anomalies caused by choledochal cyst or Caroli’s disease, and (2) genetic diseases such as haemolytic diseases. The prevalence of left hepatic lithiasis is relatively relatively high, and this can be explained explained by the anatomical anatomical difference between the left and right hepatic ducts. The left hepatic duct forms an acute angle at the junction with the comm co mmon on bile duct, and tends to induce bile stasis when 35,36 associated with biliary strictures. Another anatomical anomaly e branching of the right segmental bile ducts from the left hepatic duct e is possibly associated with left intrahepatic stone formation. Congenital choledochal dilatation, including choledochal cyst, cyst, is frequent in the Orient, but its causal relationship relationship to intrahepat intrahepatic ic stones has yet to be established. In contrast, haemolytic diseases lead to bilirubin overproduction; this is associated with pigment stones regardless of stone location e intrahepatic, extrahepatic, common bile duct and/or gallbladder. In contrast, acquired risk factors include postoperative biliary strictures caused after cholecystectomy, partial hepatectomy, and liver transplantation, and to a lesser degree iatrogenic bile-duct strictures as well as benign benign and malig malignan nantt bile-d bile-duct uct stenos stenosis. is. Benign Benign strict stricture uress can also also occ occur ur after after chemo-embolization of hepatic tumours and chronic pancreatitis. In addition, chronic biliary inflammation is associated with acquired immunodeficiency, immunodeficiency, leading to secondary secondar y sclerosing cholangitis and liver cirrhosis/bile stenosis. Furthermore, environ environmental mental rather than ethnic factors are implicated in the cause 23 of intrahepatic stones. The prevalence of intrahepatic stones differs significantly in areas of East Asia, where the majority of the population is of Chinese descent, and behavioural factors are likely to predispose to intrahepatic stone formation. Among such environmental factors, dietary behaviour, bacterial infection, and biliary parasites are to be considered. Socio-economic status is also speculated to be one of the aetiological factors. In Taiwan, the maj m ajority ority of intrahepatic patients have been reported to 27 belong to low-income brackets. Overview of classification (pathogenetic, biochemical, anatomical and others)

Intrahepatic stones are classified pathogenetically into two types: (1) primary stones formed in the intrahepatic bile duct, which result primarily from bile stasis and infection, and (2) secondary stones originating from the gallbladder and passing through the

Epidemiol Epidemiology ogy,, pathogenesi pathogenesis, s, and classificatio classification n of biliary stones 1081

cystic duct. As a biochemical classification, primary stones are divided into calcium bilirubinate stones (>90%), cholesterol stones, and mixed stones. Intrahepatic calcium bilirubinate stones are known as brown-pigment stones, which contain relatively large amounts of cholesterol (up to 20%). There is no universal classification of intrahepatic stones, but the anatomical classification is easy to apply clinically and is useful in determining operative treatment. Important parameters are shown in Table 3. 3. In East Asia, incidences are as follows:    

concomitant intrahepatic and extrahepatic stones, 69%; left lobe involved and predominates, 78% (unilateral, 45%); with gallbladder stones, 48%; presence of strictures in intrahepatic bile duct, 76%.

To date, a clinical classification of intrahepatic stones is under consideration by the Hepatolithiasis Research Group organized by the Ministry of Health, Labour, and Welfare of Japan, and will be released shortly. Natural history

Intrahepatic stones lead to the syndrome of recurrent pyogenic cholangitis, 11 presenting with abdominal pain, fever, and jaundice e the typical Charcot’s triad. Jaundice is due to persistent obstruction of the bile duct, but such an obstruction is usually incomplete. A typical attack can last for hours to days, with the biliary colic located in the upper right quadrant. In some cases, the pain is located in the epigastrium. The severe state of this attack, the Raynold’s pentad e defined as the onset of hypotension and mental confusion in addition to Chardot’s triad e predicts a poor outcome. co me. The The recu recurr rren entt pyo yoge geni nicc chol cholan angi gitis tis caus causes es chole cholest stas asis is with with symp sympto toms ms of   jaundice and pruritus, and this leads to liver abscess and/or secondary liver cirrhosis. As a more important complication, complicatio n, cholangiocarcinoma develops in 10% of the intrahepatic stone population in Japan. 37 This occurs even after the complete removal of  intrahepatic stones, because bile stasis and bacterial infection are likely aetiological factors. Thus, the careful screening for malignant lesions is important in the follow-up of this disease, regardless of whether or not the stones are removed. SUMMARY

In this chapter the epidemiology, pathogenesis, and natural history of CBD stones (choledocholithiasis) and intrahepatic stones (hepatolithiasis) have have been reviewed. reviewed. Gallstones are extremely common in Western Western countries, where the prevalence of bile-duct

Table 3. Classification of intrahepatic stones.

Intrahepatic and/or extrahepatic ducts Right and/or left lobe involvement (unilateral or bilateral) With or without gallbladder stones Location of strictures in intrahepatic bile duct Symptomatic or asymptomatic Complications

1082 1082 S. Taz Tazum umaa

stones is relatively low. In contrast, primary choledocholithiasis and hepatolithiasis appear to be more frequent in East Asian countries than in Western societies, where bile-duct bile-duct stones are mostly secondary to gallbladder gallbladder stones passing through the cystic cystic duct. Primary bile-duct stones are composed predominantly of calcium bilirubinate, namely brown-pigment stones. The pathogenesis of primary bile-duct stones is based upon bile stasis and infection, which are associated with bile-duct strictures, extrahepatic anomalies and biliary parasites. In contrast, secondary stones are considered to originate from gallbladder stones, and are commonly composed of cholesterol. Congenital and acquired risk factors predisposing to bile-duct stones include anatomical anomalies, genetic diseases of bilirubin and cholesterol, bacterial infection, and socioeconomic problems. Bile-duct stones typical present with fever, abdominal pain, and  jaundice (Charcot’s triad), and in severe cases also hypotension and mental confusion (Raynold’s pentad) which predicts a poor clinical outcome. Furthermore, silent cholangiocarcinoma develops in 10% of the intrahepatic stone cases even after the removal of  stones, and therefore the follow-up of these cases is of clinical importance. REFERENCES 1. Everhart Everhart JE, Khare M, Hill M et al. Prevalence Prevalence and ethnic differences differences in gallbladder gallbladder disease in the United States. Gastroenterology  1999; 117: 632e639. *2. Japan gallstone gallstone study group. group. J Jpn Biliary Assoc  1998; 12: 276e293. 3. Johnso Johnson n AG & Hoskin Hoskingg SW. SW. Apprai Appraisal sal of the manage managemen mentt of bile bile duct stones. stones. Br J Surg  1987; 74: 555e560. *4. Kim MH, Sekijima J & Lee SP. SP. Primary intrahepatic intrahepatic stones. Am J Gastroenterol  1995; 90: 540e548. 5. Valdivieso V, V, Covarrubias C, Siegel F et al. Pregnancy and cholelithiasis: pathogenesis and natural course of gallstones diagnosed in early puerperium. Hepatology  1993; 17: 1e4. 6. Maringhini Maringhini A, Ciambra M, Baccelliere Baccelliere P et al. Biliary Biliary sludge and gallstones gallstones in pregnancy: pregnancy: incidence, incidence, risk  factors, and natural history. Ann Intern Med  1993; 119: 116e120. *7. Barbara L, Sama C, Morselli-Labate AM et al. al. A population study on the prevalence prevalence of gallstone disease: the Sirmione study. Hepatology  1987; 7: 913e919. 8. The Rome Group Group for Epidemiology Epidemiology and Preve Preventio ntion n of Cholelithiasis Cholelithiasis (GREPCO). (GREPCO). The epidemiology epidemiology of  gallstone disease in Rome, Italy. Part I. Prevalence data in men. Hepatology  1988; 8: 904e906. *9. Kaufman Kaufman HS, Magnuson Magnuson TH, Lillemoe Lillemoe KD et al. The role of bacteria in gallbladder gallbladder and common duct stone formation. Ann Surg  1989; 209: 584e592. 10. Cetta F. F. Bile infection documented as initial event in the pathogenesis of brown pigment biliary stones. Hepatology  1986; 6: 482e489. 11. Miquel Miquel JF, JF, Covarrubia Covarrubiass C, Villaroel Villaroel L et al. Genetic epidemiology epidemiology of cholestero cholesteroll cholelithia cholelithiasis sis among Chilean Hispanics, Amerindians, and Maoris. Gastroenterology  1998; 115: 937e946. 12. Khanuja Khanuja B, Cheah Y-C, Y-C, Nishina PM et al. Lith1, Lith1, a major gene affecting cholestero cholesteroll gallstone formation formation among inbred strains of mice. Proc Natl Acad Sci U S A 1995; 92: 7729e7733. 13. Bertomeu Bertomeu A, Ros E, Zambon Zambon D et al. Apolipoprotein Apolipoprotein E polymorphism polymorphism and gallstones. gallstones. Gastroenterology  1996; 111: 1603e1610. *14. Caddy GR, Kirby J, Kirk SJ et al. Natural history history of asymptomat asymptomatic ic bile duct stones at time of cholecyscholecystectomy. Ulster Med J 2005; 74: 108e112. 15. Lopez AJ, O’Keefe P, P, Morrissey Morrissey M et al. Ceftriaxone Ceftriaxone induced cholelithiasi cholelithiasis. s. Ann Intern Med  1991; 115: 712e714. 16. Swidsinski Swidsinski A, Ludwig W, W, Pahlig H et al. Molecular Molecular genetic evidence evidence of bacterial bacterial colonizatio colonization n of cholescholesterol gallstones. Gastroenterology  1995; 108: 860e864. 17. Scobie BA & Summerskil Summerskilll WHJ. Hepatic Hepatic cirrhosis secondary secondary to obstruction obstruction of the biliary system. Am  J Dig Dis 1965; 10: 135e146. 18. Lindstro Lindstro¨ m CG. Frequency of gallstone disease in a well defined Swedish population: a prospective necropsy study in Malmo. Gastroenterology  1977; 12: 341e346.

Epidemiol Epidemiology ogy,, pathogenesis pathogenesis,, and classificatio classification n of biliary stones 1083 19. Simi M, Loriga P, P, Basoli A et al. Intrahepatic Intrahepatic lithiasis: lithiasis: study of thirty-six thirty-six cases and review of the literature. Am J Surg  1979; 137: 317e322. *20. Nakayama Nakayama F & Koga A. Hepatolithi Hepatolithiasis: asis: present present status. status. World J Surg  1984; 8: 9e14. 21. Bove P, de Ramos Ramos Olivei Oliveira ra Mde & Speran Speranzin zinii M. Intrah Intrahepa epatic tic lithia lithiasis. sis. Gastroenterology  1963; 44: 251e256. 22. Herman P & Machado Machado MCC. Primary intrahepati intrahepaticc lithiasis. Probl Gene Surg  2001; 18: 51e55. *23. Nakayama Nakayama F, F, Soloway Soloway RD, RD, Nakama Nakama T et al. Hepatolithias Hepatolithiasis is in East Asia. Retrospectiv Retrospective e study. study. Dig Dis Sci  1986; 31: 21e26. 24. Fan ST, ST, Choi TK, Lo CM et al. Treat Treatment ment of hepatolith hepatolithiasi iasis: s: improvement improvement of result result by a systematic systematic approach. Surgery  1991; 109: 474e480. 25. Nagase M, Hikasa Y, Y, Soloway RD et al. Gallstones in Western Japan: factors affecting the prevalence of  intrahepatic gallstones. Gastroenterology  1980; 78: 684e690. 26. Chang TM & Passaro Passaro E. Intrahepatic Intrahepatic stones: the Taiwan experience. experience. Am J Surg  1983; 146: 241e244. 27. Wen CC & Lee HC. Intrahepatic Intrahepatic stones: a clinical clinical study. study. Ann Surg  1972; 175: 166e177. 28. Su CH, Lui WY & Peng FK. Relative Relative prevalence prevalence of gallstone gallstone disease in Taiwan Taiwan.. Dig Dis Sci  1992; 37: 764e768. 29. Nakayama Nakayama F, F, Furusawa Furusawa T & Nakama Nakama T. Hepatolithi Hepatolithiasis asis in Japan: present present status. status. Am J Surg  1980; 139: 216e220. 30. Stock FE & Fung JH. Oriental cholangioh cholangiohepatit epatitis. is. Arch Surg  1962; 84: 409e412. 31. Chen HH, Zhang WH, Wang SS et al. Twenty-two Twenty-two year experience with the diagnosis and treatment of  intrahepatic calculi. Surg Gynecol Obstet 1984; 159: 519e524. 32. Leung JW, JW, Sung JY & Costerton Costerton JW. JW. Bacteriolog Bacteriological ical and electron electron microscop microscopyy examinati examination on of brown pigment stones. J Clin Microbiol  1989; 27: 915e921. *33. Kaufman Kaufman HS, Magnuson Magnuson TH, Lillemore Lillemore KD et al. The role of bacteria bacteria in gallbladder gallbladder and common bile duct stone formation. formation. Ann Surg  1989; 209: 584e592. *34. Shoda J, Inada Y & Osuga T. T. Molecular Molecular pathogenesi pathogenesiss of hepatolithi hepatolithiasis. asis. Front Biosci  2006; 11: 669e675. 35. Ong GB. A study of recurrent recurrent pyogenic pyogenic cholangiti cholangitis. s. Arch Surg  1962; 84: 199e225. 36. Simi M, Loriga P, P, Basoli A et al. Intrahepati Intrahepaticc lithiasis. Am J Surg  1979; 137: 317e322. *37. Chijiiwa Chijiiwa K, Ichimiya Ichimiya H, Kuroki Kuroki S et al. Late development development of cholangiocar cholangiocarcinoma cinoma after the treatment treatment of  hepatolithiasis. Surg Gynecol Obstet 1993; 177: 279e282.

Sponsor Documents

Or use your account on DocShare.tips

Hide

Forgot your password?

Or register your new account on DocShare.tips

Hide

Lost your password? Please enter your email address. You will receive a link to create a new password.

Back to log-in

Close