Saudi Journal of Gastroenterology
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Year : 1995  |  Volume : 1  |  Issue : 3  |  Page : 173-179

Department of Medicine, Gastroenterology Division, College of Medicine, King Saud University, Riyadh, Saudi Arabia

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Gallstone prevalence is correlated with geographical and ethnic variations. It is more preva­lent in Western communities. There are evidences for a high prevalence in Saudi Arabia. According to their chemical constitutes, stones are classified into cholesterol, mixed and pig­ment stones. Three main factors, saturation, gallbladder function and nucleation defect are implemented in the pathogenesis of stone formation. Majority of gallstones patients are asymptomatic. Dyspeptic symptoms are not specific. Ultrasonography has become the method of choice for screening and diagnosis of gallstones. Cholecystoscintigraphy is accu­rate in the diagnosis of acute cholecystitis, biliary obstruction and bile leak. Treatment of gallstones will be discussed in the following issue.

How to cite this article:
Al Mofleh IA. Gallstones. Saudi J Gastroenterol 1995;1:173-9

How to cite this URL:
Al Mofleh IA. Gallstones. Saudi J Gastroenterol [serial online] 1995 [cited 2021 Jul 31];1:173-9. Available from:

   Prevalence of Gallstones Top

Little is known about the incidence of gallstones. In contrast, prevalence has been well established in various populations. Gallstones prevalence is linked with geographical and ethnic variations [1]. It is low in rural Africa [2] and India [3]. Gallstones are less prevalent in China, Japan,

Kashmir and Egypt, compared to Western com­munities [4],[5],[6],[7]. In the West, the prevalence, ranges between 9 and 30%, [8],[9],[10],[11] and increases over 70% in Pima-Indian women [12]. In Saudi Arabia, gallstones prevalence is not well defined. However, recent studies indicate high prevalence and incidence [13],[14],[15].

   Types of Gallstones Top

According to their major constitutes, gallstones are classified into: cholesterol, pigment and mixed stones. This classification is important for the choice of treatment, as only patients with choles­terol stones are candidates for dissolution with bile acids and fragmentation with extracorporeal shock waves [16]. Cholesterol gallstones are more common in Occidentals; while Orientals have more pigment gallstones. Two types of pigment stones, brown and black are known. Black stones are found in association with chronic hemolytic disorders; while brown stones, formed intraduc­tally are often due to infection and stasis, which are frequently precipitated by the presence of periampullary diverticula [17],[18]. Duodenal diverticula promote bacterial growth and forma­tion of beta-glucuronidase, which deconjugates bilirubinate glucuronides, with a subsequent pig­ment precipitation and stone formation [19].

Gallstones are differentiated by measuring their cholesterol content either by infrared spec­troscopy [20] or by enzymatic quantification [21]. The latter is reliable, simple and not time-consum­ing compared to infrared spectroscopy [18]. Cholesterol content of stones varies according to stone type. It is less than 20% in pigment, 20-69% in mixed and over 70% in cholesterol stones [22]. Due to their high content of cholesterol, mixed stones may be considered as a variant of choles­terol stones [23]. Besides chemical typing,visual differentiation is also accurate; cholesterol stones are yellow to light tan, crystalline and laminated in cross-section; while pigment stones are black or brown and have an amorphous cross-section [24] Cholesterol stones are also hard and have a smooth surface, while pigment stones are soft and friable [18]. Furthermore, the presence of choles­terol crystals in fresh gallbladder bile and in duodenal bile after cholecystokinin stimulation, is considered to be highly specific and reasonably sensitive for cholesterol stones and helps in asses­sing suitability for litholytic therapy. Moreover, cholesterol is significantly higher in bile surround­ing cholesterol stones compared to pigment stones [24]. A correlation between age and stone type has been established; while pigment stones are frequently found in the elderly, cholesterol stones are more common in younger subjects [18],[25].

   Gallstones Formation Top

Bile composition

Bile is composed mainly of bile acids and phos­pholipids. Bile acids are derived from cholesterol and exist as cholic, deoxycholic chenodeoxycholic and in small amounts as ursodeoxy and lithocholic acids. In man, phospholipids are represented mainly by lecithin [23]. Other components include cholesterol, bilirubin, protein, water and electrolytes.

   Cholesterol Solubility Top

Although cholesterol contributes only to 5% of bile components, it plays the major role in choles­terol gallstones formation. As cholesterol is water-insoluble, it is maintained in an aqueous solution by a physiological proportion of bile acids and lecithin. Synthesis and excretion of choles­terol, bile acids and phospholipids and bile acid pool are important to maintain this equilibrium.

Cholesterol is carried in bile in aqueous state, in the form of mixed bile acid-phospholipid micelles and phospholipid vesicles. Simple bile acid-micel­les formation at a certain concentration of bile-salt molecules in water (, 2 mmol/L is influenced by the concentration of bile constitutes, type of bile acid, temperature and bile pH. Bile acids micelles cholesterol-solubilizing activity, at the hydro­phobic micellar center is enhanced by incorpora­tion of lecithin and formation of mixed micelles. Maximal solubility is achieved at a lecithin-bile acid molar ration between 0.2 and 0.3. In super­saturation, when biliary cholesterol concentration exceeds the solubilizing capability of micelles, cholesterol interacts with phospholipids to form unilamellar vesicles, which are more efficient car­riers of cholesterol [26]. Bile saturation, nuclea­tion defect and impaired gallbladder motility are the main factors implemented in the pathogenesis of gallstones formation. These factors are likely interdependent [27].

   Saturation Top

Bile becomes supersaturated (lithogenic)when the cholesterol concentration exceeds the bile acid-phospholipids solubilizing capacity. Although cholesterol saturation is a prerequisite for stone formation, interestingly not all patients with cholesterol supersaturation, form stones [28]. This indicates the importance of other pathogenic factors such as altered gallbladder function and defective nucleation. Lithogenic bile is found in conditions associated with excessive cholesterol secretion, impaired bile acid and phos­pholipid secretion and diminished bile acid pool.

In lithogenic bile unilamellar phospholipid­cholesterol, vesicles may aggregate and form larger, cholesterol-rich multilamellar vesicles with subsequent cholesterol nucleation and stone for­mation. Cholesterol-overloaded vesicles are likely responsible for precipitated cholesterol [29]. Risk factors for cholesterol gallstones are shown in [Table - 1].

In a similar fashion, bile may become saturated with unconjugated bilirubin which precipitates and forms stones. Most of the bilirubin is found in conjugated, water-soluble form in bile. Very little amounts of unconjugated, water-insoluble, biliru­bin exist normally in bile [23]. Bile supersatura­tion with bilirubinate may result from increased secretion of hydrolysis of bilirubin, increased ioni­zation of unconjugated bilirubin and alteration of unconjugated bilirubin-bile acid ratio [30].

   Gallbladder Function Top

The function of the gallbladder is to store and concentrate excreted hepatic bile and release it .into the duodenum in response to ingested food. The gallbladder concentrates hepatic bile by active transport of sodium, chloride and bicarbo­nate and passive absorption of up to 90% of water from the bile. Bile acid, cholesterol and bilirubin concentration may increase up to 10-folds [31]. Also, calcium and potassium concentration increases in the gallbladder lumen. Diseases of the gallbladder wall may affect calcium diffusion, leading to calcium retention and precipitation [32]. Increased intraluminal gallbladder- calcium concentration inhibits biliary cholesterol solubil­ity [33]. Calcium precipitation appears to be the main determinant factor for initiation of stone for­mation [34].

Gallbladder mucosa plays an important role in stone formation by interfering with nucleation­inhibiting and promoting factors. Calcium and prostaglandins stimulate mucus secretion which trap cholesterol crystals from aggregated vesicles and promote sludge and stone formation[35]; while hydrogen release by the gallbladder mucosa causes bile acidification, and thus increases cal­cium solubility [36].

Gallbladder motility and emptying are mediated mainly by cholecystokinin and appa­rently controlled by a complex of hormonal neurological and pharmacological processes [37]. Although gallbladder filling is similar in both gallstones patients and controls, emptying differs due to a prolonged sensitivity to cholecystokinin in some patients with gallstones. Defective gallbladder emptying is independent of the stone size, number or clinical presentation [38]. The effect of gallstones on gallbladder motility is debatable. While some authors have proven this correlation [39], others could not find a relation between the presence of gallstones and physiology of bile on one, and gallbladder contractibility on the other hand [40]. Gallbladder motility is altered in conditions associated with gallstone for­mation such as obesity [42], prolonged parenteral nutrition [43] and pregnancy [44].

   Nucleation Top

Nucleation is the initiation of gallstone forma­tion from supersaturated bile. Cholesterol is transported by micelles and vesicles. Vesicles form after exhausting the solubilizing capacity of micelles and are considered as the important cholesterol vehicle and determinant of nucleation [29]. Cholesterol crystals precipitate from fused vesicles. Nucleation is influenced by a number of promoting and inhibiting factors which are par­tially secreted by the liver and gallbladder mucosa. A nucleation defect with an increased nucleation-promoting and decreased inhibiting activity has been demonstrated in patients with gallstones compared to controls [45].

A variety of substances such as mucin, glycop­rotein, calcium bilirubinates and other salts, para­sites, ova, bacteria and detached cells promote nucleation [23]. In conditions associated with bile stasis such as parenteral nutrition and pregnancy, cholesterol crystals and pigment granules are trap­ped by mucus-forming sludge. Sludge is consi­dered as a precursor of gallstone formation [46]. Several factors including oxygen radicals, released during hepatic or gallbladder injuries; increased phospholipase- A concentration in hepatic bile and prostaglandins play a considera­ble role in sludge formation [47]. Prostaglandins alter the gallbladder-concentrating ability through reduction of sodium and water absorp­tion [48]. They also trigger mucus hypersecretion and promote nucleation [49]. Aspirin and nonsteroidal anti-inflammatory drugs inhibit nucleation through inhibition of prostaglandin pathways [50],[51]. Antinucleating effect is pro­vided also by apolipoprotein 1 & 2 and by hydro­gen (H+) release from gallbladder mucosa and acidification of gallbladder content. Acidification improves calcium solubility and prevents stone initiation [36]. Nucleation is classified according to the nature of the nucleating agent into homogeneous and heterogeneous forms. While in homogeneous nucleation, cholesterol forms the nidus; other nucleating agents are forming the nidus in the heterogeneous form [23].

The pathogenesis of pigment stones depends on the type of stone. Black stones form usually in the gallbladder and are found mainly in association with chronic hemolytic disorders, infection and stasis [52]. Dietary factors including carbohyd­rates diet could also contribute to black pigment stones formation [53]. Brown stones on the other hand, form mostly in the bile duct and are related to infection [54]. They are found in approximately 40% of patients in association with juxtapapillary duodenal diverticula [18],[55]. Duodenal diver­ticula promote the growth of beta- glucuronidase­producing bacteria, which deconjugate bilirubin and split fatty acid from lecithin with subsequent precipitation and stone formation [18],19]. Cal­cium bilirubinate and palmitate represent the main constitutes of brown stones [52]. The risk factors and possible mechanisms of pigment stone formation are summarized in [Table - 2].

   Diagnosis of Gallstones Top

Clinical presentation an1d natural course

As there are no specific symptoms for gallstones disease, the presentation depends on the develop­ment of complications such as: acute cholecystitis, cholangitis, biliary pancreatitis and other compli­cations listed in [Table - 3]. Majority of the patients (70-90%), remain asymptomatic until they develop complications [8],[56],[57]. Dyspeptic symptoms are not specific and do not correlate with the presence of gallbladder stones [58]. There has also been no correlation between pain on one, and motility, size and number of stones on the other hand [57]. In a long follow-up period of approximately 30 (median 13.5) years, 30% of patients developed biliary pain. Cystic duct obstruction, acute pancreatitis, and severe cholecystitis have occurred in 18, 5.5 and 4% of patients, respectively [59]. Asymptomatic stones, detected coincidentally by ultrasonography have rarely been associated with clinical significance [56]. Complications that have occurred in 11% over the following five years are in concordance with suggested yearly complication rates of 2-3 [60],[61].

Plain abdominal film

It is not very helpful in the diagnosis of gallstones, as the rate of opaque stones is as low 15% (62). Plain film, however, may help in detect­ing stones which may respond to fragmentation and bile acid dissolution therapy.

Oral cholecystography

It is accurate in detecting stones in the gallblad­der and is rarely false positive. A correct diagnosis is achieved in 90% [63]. Fatty meal-induced gallbladder contraction may enhance the detec­tion of small gallbladder stones. Oral cholecystog­raphy was the method of choice for screening for gallbladder stones before the era of ultrasonog­raphy.


Is a simple method used for clinical and epidemiological survey. It is accurate with a sen­sitivity of 98% [8],[58]. The positive predictive value is 86% [58]. Ultrasonography is inconclu­sive in only a very small proportion, ranging from 1.1-2.8% [8],[64]. Therefore, ultrasonography has become the method of choice for the screening and diagnosis of gallstones [8],[65].

Computed tomography (CT)

It is useful for detection of heavily-calcified stones. However, due to its low sensitivity, CT is inferior to ultrasonography in detecting gallblad­der and common bile duct stones [66],[67].


Is a useful technique in cases with non-function­ing gallbladder due to cystic duct obstruction. Cholecystoscintigraphy is also helpful in the diag­nosis of bile duct obstruction, biliary leak and gallbladder perforation [68].

Retrograde cholangiopancreatography (ERCP)

ERCP provides an accurate image of the biliary tree with the advantage of the therapeutic facilities, and up to 90% successful clearance of bile duct stones [69].

   References Top

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Correspondence Address:
Ibrahim A Al Mofleh
Division of Gastroenterology (59) P.O. Box 2925 Riyadh 11461
Saudi Arabia
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