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Epidemiology andEtiology ofAlcohol- Induced Pancreatitis

Downloaded from https://onlinelibrary.wiley.com/doi/ by Universität Bern, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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97 te Morsche RH, Drenth JP, Truninger K etal.

UGT1A7 polymorphisms in chronic pancreatitis: an example of genotyping pitfalls. Pharmacogenomics J 2008;8(1):34–41.

98 Frenzer A, Butler WJ, Norton ID etal. Polymorphism in

alcoholSalcohol-

metabolizing enzymes, glutathione

transferases and apolipoprotein E and susceptibility to

induced cirrhosis and chronic pancreatitis.

JGastroenterol Hepatol 2002;17(2):177–182.

99 Muddana V, Lamb J, Greer JB etal. Association between

calcium sensing receptor gene polymorphisms and chronic pancreatitis in a US population: role of serine protease inhibitor Kazal 1type and alcohol. World JGastroenterol 2008;14(28):4486–4491.

100 Takats A, Berke G, Szentesi A etal. Common calcium-

sensing receptor (CASR) gene variants do not modify risk for chronic pancreatitis in a Hungarian cohort. Pancreatology 2021;21(7):1305–1310.

101 Weiss FU, Schurmann C, Guenther A etal.

Fucosyltransferase 2 (FUT2) non-

secretor status and blood group B are associated with elevated serum lipase activity in asymptomatic subjects, and an increased risk for chronic pancreatitis: a genetic association study. Gut 2015;64(4):646–656.

102 Nakamura Y, Ishikawa A, Sekiguchi S, Kuroda M,

Imazeki H, Higuchi S. Spirits and gastrectomy increase risk for chronic pancreatitis in Japanese male alcoholics. Pancreas 2003;26(2):e27–31.

103 Lowenfels AB, Zwemer FL, Jhangiani S, Pitchumoni CS.

Pancreatitis in a native American Indian population. Pancreas 1987;2(6):694–697.

104 Haber PS, Wilson JS, Pirola RC. Smoking and alcoholic

pancreatitis. Pancreas 1993;8(5):568–572.

105 Norton ID, Apte MV, Dixson H, Trent RJ, Pirola RC,

Wilson JS. Cystic fibrosis genotypes and alcoholic pancreatitis. J Gastroenterol Hepatol 1998;13:496–500.

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Epidemiology andEtiology ofBiliary Acute Pancreatitis

Ippei Ikoma, Ko Tomishima, and Hiroyuki Isayama

Department of Gastroenterology, Graduate School of Medicine, Juntendo University, Tokyo, Japan

119

Introduction

Acute biliary pancreatitis (ABP) is caused by a primary common bile duct stone (CBDS) or a CBDS that has moved from the gallbladder. Common channel, duodenal reflux, and ductal hypertension hypotheses for the etiology of ABP are posited. CBDS passage or impaction at the common channel can cause ABP. The treatment strategies for ABP differ from those of other types of acute pancreatitis (AP).

Endoscopic biliary drainage may improve the outcome, and differential diagnosis is important for patients with AP. Abdominal ultrasound, CT, MRI/MRCP, and endoscopic ultrasound (EUS) can be used to diagnose CBDS. EUS has the highest detectability among these modalities but requires an expert endoscopist and is relatively invasive. The standard of care of ABP is treatment of AP with/without endoscopic treatment following cholecystectomy when gallstones are detected. The timing of endoscopic and surgical treatment of ABP is controversial. Here, we summarize recent advancements in the etiology, epidemiology, clinical features, diagnosis, and treatment strategies (including endotherapy and cholecystectomy) of ABP.

Etiology

Biliary pancreatitis is caused by stone passage from the common bile duct to the duodenum through the papilla, including the sphincter of Oddi and common channel. Acosta and Ledesma analyzed the feces of patients with gallstones and pancreatitis and found gallstone in the feces of 94%. By contrast, only 8% of

patients with simple gallstone attacks without pancreatitis had gallstones in their feces[1]. Passage of a CBDS through the papilla may cause gallstone pancreatitis; however, the underlying mechanism is unclear. There are three hypotheses as to the mechanism by which gallstones cause acute pancreatitis: (i) common channel, (ii) duodenal reflux, and (iii) ductal hypertension.

Common Channel Theory

Opie etal. reported that a patient who died of acute pancreatitis had a stone lodged in the major duodenal papilla of the common duct of the bile and pancreatic ducts[2]. He proposed that the reflux of bile acids into the pancreatic duct caused the pancreatitis. Moreover, Opie injected bile acids into the dog pancreatic duct, which caused inflammation in the pancreas; other studies have yielded similar results[3]. It has become apparent, however, that no more than two- thirds of the population have such a common ductal channel [4,5] and, in many cases, this is so short that a stone obstructing the common bile duct would also obstruct the pancreatic duct.

The common duct is more frequently found in cases of acute biliary pancreatitis [6]. Passage of stones can cause stenosis of the major duodenal papilla, which may lead to functional obstruction of the common duct[7]. Because the pancreatic duct pressure is two-

to threefold higher than that of the normal bile duct, pancreatic secretions flow into the bile duct more easily than bile flows back into the duct. The common channel hypothesis is supported largely by the results of the abovementioned studies[8,9].

The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler, RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/beger/thepancreas4e

Epidemiology andEtiology ofBiliary Acute Pancreatitis

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Duodenal Reflux Theory

The second hypothesis is that pancreatitis is caused by the influx of duodenal contents into the pancreatic duct due to the passage of a stone. This mechanism was proposed in an animal study involving obstruction of the duodenum. Because ligation of the pancreatic duct did not cause pancreatitis, reflux of the contents was considered the main cause[10]. This phenomenon is rarely observed in humans and can cause acute pancreatitis due to obstruction after gastrectomy and duodenal or small bowel reconstruction[11,12].

However, the oblique course of the duct, the sphincter of Oddi, and the mucosal folds around the opening suggest that this is not the mechanism of pancreatitis. Although the sphincter may be injured immediately or shortly after the passage of gallstones, leading to reflux of duodenal contents, it is not thought that EST in ERCP (endoscopic retrograde cholangiopancreatography) causes gallstone pancreatitis or the development of pancreatitis due to reflux of duodenal contents[13]. In a study in rats, isotonic saline inflow into the pancreatic duct caused pancreatitis, suggesting that pancreatitis associated with duodenal obstruction may be related not only to reflux of duodenal contents but also to increased intestinal pressure.

Ductal Hypertension Theory

Learch etal., using opossums[14], compared the severity of pancreatitis in three groups: pancreatic duct alone ligated, pancreatic duct and bile duct separately ligated, and common duct ligated. The results showed no difference in disease severity among the groups, suggesting that bile reflux is not essential for the development or exacerbation of pancreatitis. Other studies have shown that continuous stimulation of secretion in the presence of pancreatic duct obstruction worsens pancreatitis[15]. When the obstruction of the pancreatic duct was released, the pancreatitis improved[16].

When pancreatic secretion is stimulated by obstruction of the pancreatic duct, it causes an increase in intraductal pressure. Although rare, increased intraductal pressure can also be caused by, for instance, duodenal papillary tumors, parasitic infections, and ERCP. Injections of various compounds into the pancreatic duct at high pressure can cause pancreatitis, and the injection pressure is more related to the development of pancreatitis than the absence of injected material [3]. The mechanism is thought to be rupture of the branched pancreatic duct and leakage of secretions into the interstitium or inhibition of secretion of pancreatic juice into the ductal lumen.

After ligation of the pancreatic duct, changes first occur within the glandular cells rather than in the stroma or around the pancreatic duct. High pressure in

the lumen of the gland causes exocytosis of zymogens and inhibits the release of Ca ions from the gland cell membrane[17]. Disruption of the cell membrane and its transporter channels inhibits the recovery of Ca ion concentration that occurs after stimulation of CCK. An increase in calcium ion concentration in the entire glandular cell leads to intracellular activation of trypsin, which in turn activates various proteases, leading to

digestion by pancreatic enzymes. CCK stimulation

selfcompounds the effect of ductal obstruction [16,18]. Disruption of acinar Ca

signaling is a key early event in the initiation of intra- acinar enzyme activation[19]. Experimentally, pancreatic duct obstruction causes inhibition of calcium ion signaling[20,21].

These three hypotheses are considered to be related in a complex way, as opposed to one being considered most likely. The development of acute pancreatitis may involve a combination of factors, because obstruction alone often causes biliary complications rather than pancreatitis. When gallstone passage occurs in patients with common ducts, pancreatitis is induced. However, once the stones are cleared, the activated pancreatic enzymes are drained and the pancreas recovers. As a result, only mild pancreatitis occurs clinically. Most cases will be mild, but in rare cases the flow of pancreatic juice, which is rich in digestive enzymes, may become obstructed, causing severe pancreatitis. Even if the stone is passed, severe disease typically develops.

Secondary obstruction may be due to edema of the pancreatic head or papillae after the passage of gallstones. Temporary obstruction of the pancreatic duct by multiple small stones has been reported. Large stones falling into the distal bile duct or papillary region can cause obstruction of the pancreatic duct. If this occurs in stages, it suggests that there is a possibility of preventing further obstruction in the early stages and preventing severe pancreatitis.

Epidemiology

Alcohol and gallstones are the two major causes of acute pancreatitis. In a 2016 survey in Japan, alcoholic was the most common cause (42.8%), followed by gallstone (19.8%) and idiopathic (16.2%) pancreatitis in males. In women, cholelithiasis was the most common (37.7%), followed by idiopathic (24.8%) and alcoholic (12.0%) pancreatitis. Alcoholic pancreatitis was more common among those in their 40s, and gallstone pancreatitis was more common among older adults [22]. Regarding the size of the stones, small stones have a higher risk of pancreatitis. Diehl et al. reported a fourfold increase in the incidence of pancreatitis if the stone diameter was less than 5 mm[23].

Diagnosis ofAcute Biliary Pancreatitis 121

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In the Japanese report, about 60% of patients had passed stones and only about 25% had bile duct stones of 6 mm or more in diameter. Elevated serum pancreatic enzymes were common in patients with small stones. Also, about 70% of severe pancreatitis was due to naturally passed stones. These factors suggest that small bile duct stones are more likely to induce pancreatitis. Large stones are more likely to obstruct the bile duct before falling into the anatomically common duct, whereas small stones are more likely to fall into the common duct and cause pancreatic duct obstruction.

Clinical Features

It has been reported that 15% of acute pancreatitis develops into severe acute pancreatitis [24]. Gallstones and alcohol are the most common causes of acute pancreatitis, and there are various reports on the differences in severity and mortality. Gallstone pancreatitis is reportedly associated with more severe disease and mortality[25,26]. By contrast, ABP caused by alcohol is thought to be more severe, and the mortality rate is higher[27– 29]. Some studies found no clear difference in clinical course between the two groups, and no definite conclusion has been reached [30–32]. In severe pancreatitis, intestinal bacteria migrate out of the intestinal tract at an early stage and cause pancreatic and peripancreatic infections. In the clinical course of acute pancreatitis, such complications of infection are thought to worsen the prognosis. Riity etal. reported differences in the bacterial flora of alcoholic and gallstone infections. A higher percentage of microbes is detected in gallstone pancreatitis, with Gram- positive bacteria being more common in alcoholic pancreatitis and gram- negative bacteria in cholecystic pancreatitis (80% vs. 20%) [33]. A case of severe acute biliary pancreatitis that progressed to walled- off necrosis is presented in Fig.12.1 (Fig.12.1a, b, c). This case required endoscopic drainage and necrosectomy because of infection.

Diagnosis ofAcute Biliary Pancreatitis

Blood Tests

Bilirubin, AST, ALT, ALP, and gamma GTP levels should be measured in all patients to differentiate ABP from other- cause acute pancreatitis[34]. If the blood ALT level is more than 150 IU/L (sensitivity 48–93%, specificity 34–96%, positive Eudox ratio 1.4–12.0, negative Eudox ratio 1.8–4.9)[35,36], or if three or more of the five items (bilirubin, ALP, γGTP, ALT, and ALT/ AST ratio) are abnormal (sensitivity 85%, specificity 69%, positive likelihood ratio 2.7, negative likelihood ratio 4.6), ABP is highly suspected. When combined with abdominal ultrasonography, it is possible to identify the cause of acute biliary pancreatitis with a sensitivity of 95–98%, specificity of 100%, positive likelihood ratio of ∞, and negative likelihood ratio of 20.0 to

50.0[37]. Because trypsinogen 1in blood is specifically elevated

in acute biliary pancreatitis, the ratio of trypsin- 2alpha1- antitrypsin complex to trypsinogen 1in blood is reportedly useful for identifying the etiology of ABP[38].

Abdominal Ultrasonography

If combined with blood tests, it is possible to diagnose the etiology of acute pancreatitis with gallstones in most cases. The probability of detecting a CBDS by abdominal ultrasonography varies from 20% to 90%. The absence of biliary stones or bile duct dilatation on abdominal ultrasonography does not rule out ABP[39– 41]. If the initial examination does not reveal biliary stones but gallstone pancreatitis is suspected, it is necessary to perform repeatedly ultrasonography or MRCP.

Computed Tomography

In many cases, biliary stones are not detected by CT (sensitivity 40~53%), and CT is not suitable for the diagnosis of acute biliary pancreatitis[37,41]. Calcium bilirubinate gallstone is the most frequent CBDS, which cannot be detected by CT because of radiolucency. If the etiology is unclear, CT should be performed because pancreatic cancer or intraductal papillary mucinous tumor may be the cause of acute pancreatitis.

MRI/MRCP

Acute pancreatitis is treated differently depending on the etiology. ERCP improves the prognosis of ABP complicated by cholestasis/cholangitis, though ERCP is contraindicated for other types of acute pancreatitis. Therefore, it is important to distinguish ABP from other forms of pancreatitis because of the need for different treatment strategies.

The sensitivity of MRI/MRCP to detect CBDS is 80%, compared with 20% and 40% for abdominal ultrasonography and CT, and MRI/MRCP is recommended to determine the indication for endoscopic papillary procedure (ERCP/EST)[42]. Compared to ERCP, it can be used at an earlier stage of pancreatitis because it is noninvasive and does not require EST/EPBD, thus there is no risk of worsening

Epidemiology andEtiology ofBiliary Acute Pancreatitis

(a) (b)

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122

Figure12.1 A 59- year- old woman presented with severe acute biliary pancreatitis. The inflammatory response remained high. Contrast-

enhanced computed tomography (CT) showed an irregularly shaped fluid collection with a contrast- enhancing film (a, b), and MRI T2 showed a fluid collection with mixed high and low signals (c).

(c)

acute pancreatitis (Fig.12.2). However, if the diameter of the bile duct is large, if there is ascites, or if the patient is not holding their breath well, the image quality may be low, and small stones of less than 5 mm may be missed.

Endoscopic Ultrasonography (EUS)

EUS is superior to abdominal ultrasonography in its ability to detect the common bile duct (Fig.12.3). When the etiology is not clear on abdominal ultrasonography, EUS

can detect common bile duct stones in 59–78% of cases [43–45]. Although ERCP and EUS are considered the gold standards for the examination of biliary stones, there is an RCT, which showed that ERCP sometimes failed to detect CBDS (14%), whereas EUS was able to detect CBDS in all patients[46]. In a prospective study of the simultaneous diagnostic performance of EUS, MRCP, and CT cholangiography for the detection of CBDS, their diagnostic sensitivity was 100%, 88%, and 88%, respectively[47]. ERCP during an attack of acute pancreatitis

Figure12.2 MRCP shows a shade defect in the dilated common

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bile duct that may be a stone.

Diagnosis ofAcute Biliary Pancreatitis 123

Figure12.3 EUS shows a stone with acoustic shadow in the

common bile duct.

may worsen the inflammation. In cases of suspected ABP, Liu etal. compared whether to perform EUS or diagnostic ERCP for the diagnosis of gallstones and CBDS. Although there were no statistically significant differences in mortality rate, complication rate, hospital stay, or need for intensive care, the complication rate was lower in the EUS group (7.1%) compared with the ERCP group (14.3%)[46]. Therefore, compared with diagnostic ERCP, EUS is safer because it avoids unnecessary ERCP. In addition, in mild- to- moderate acute pancreatitis, the detection rate of gallstones and CBDS does not differ between EUS and MRCP[48]. In terms of invasiveness, MRCP or CT cholangiography (MRCP is more noninvasive in terms of contrast media allergy) should be performed first. If no stone is found on MRCP/CT, confirmation of small stones by EUS may avoid unnecessary ERCP and contribute to a lower incidence of incidental disease.

ERCP

ERCP is not always necessary for diagnosis of ABP but is performed for its treatment. The British Society of

Figure12.4 ERCP shows multiple shade defects in the common

bile duct and common bile duct stones.

Gastroenterology guidelines recommend ERCP in the presence of jaundice, liver damage, dilatation of the common bile duct, and strong suspected presence of CBDS or repeated attacks of acute pancreatitis[49] (Fig.12.4). Early ERCP in gallstone pancreatitis, which is expected to be severe, does not significantly affect the reduction of fatality, but does affect the reduction of complications of acute pancreatitis[50].

Other indications for diagnostic ERCP were aspiration

and analysis of the bile juice to detect sludge/crystal in the bile juice. Biliary sludge/crystal was difficult to detect by other diagnostic imaging modalities including EUS and analysis of bile juice was mandatory. Biliary sludge is almost certainly not a cause of pancreatitis but is a common finding in patients with acute pancreatitis due to reduction in gallbladder motility. As with gallstones, the essential pathophysiologic mechanism is obstruction to the pancreatic duct at the level of the ampulla of Vater. Biliary sludge is a mixture of particulate matter that precipitates from bile, generally consisting of cholesterol monohydrate crystals, calcium bilirubinate, and other calcium salts embedded in mucin [51]. Biliary sludge often coexists with gallstones[52], and it is questionable whether the formation of sludge represents an early stage of gallstone formation. Biliary sludge has been reported as causing acute pancreatitis in 3.1% of cases [53], although whether this is due to sludge per se or to associated microlithiasis is difficult to judge.

Epidemiology andEtiology ofBiliary Acute Pancreatitis

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124

Lee etal. assessed 86 patients diagnosed with idiopathic pancreatitis and found evidence of biliary sludge in the majority (67%). Although the presence of biliary sludge did not have a causal relationship with the pancreatitis, its presence was predictive of recurrent episodes of acute pancreatitis [54]. Bile aspiration by ERCP and microscopic observation may be diagnostically useful.

Treatment Strategy

ERCP is used to treat pancreatitis, prevent exacerbations, and improve cholangitis. The latter two uses are controversial. Therefore, the suitability of ERCP for ABP is determined by the presence or absence of cholangitis or biliary obstruction. However, we experienced marked improvement of ABP after ERCP. In such cases, the stone was impacted at the papilla, which required the precut technique to extract or push the impacted stone into the bile duct using a catheter.

In other words, after the diagnosis of acute biliary pancreatitis by the tests described above, if there is no cholangitis or biliary obstruction, a standby ERCP/EST should be performed after usual treatment for acute pancreatitis. If there is cholangitis or obstruction of the biliary duct, perform emergency ERCP/EST and then treat the acute pancreatitis and subsequently perform cholecystectomy.

ERCP

Gallstone pancreatitis is caused by bile duct stones or bile sludge in the common papillary duct, resulting in pancreatic duct obstruction and papillary edema. Pancreatitis severity was more than 80% in cases where pancreatic duct obstruction due to insufficiency persisted for more than 48 hours [55]. Therefore, early ERCP/EST may relieve pancreatic duct obstruction and papillary edema and prevent worsening of pancreatitis and cholangitis by pancreatic duct decompression and bile duct drainage. However, performing ERCP/EST at the extreme stage of acute pancreatitis may cause additional stress to, and thus worsen, the pancreatitis.

Several metaservative treatment for acute biliary pancreatitis[56–60]. Excluding cases of complications of cholangitis, all reports showed no significant difference in mortality and complication rates between early ERCP and conservative treatment for cholelithiasis, irrespective of the degree of pancreatitis. In 2012, Tse etal. reported [59] that early ERCP significantly reduced the risk of mortality (RR 0.20, 95% CI 0.06~0.68), and local (RR 0.45, 95% CI 0.20~0.99) and systemic complications (RR 0.37, 95% CI 0.18~0.78). However, in RCTs only, excluding patients with cholangitis,

analyses compare early ERCP with con-

early ERCP tended to increase mortality (RR 1.91, 95% CI

0.85~4.30) and the incidence of local (RR 1.15, 95% CI 0.69~1.92) and systemic complications (RR 1.02, 95% CI

0.44~2.36). In 2020, Nicolien etal. reported[61] an RCT of early ERCP vs. conservative treatment in severe cholelithiasis without cholangitis and found no significant difference in the risk of complications or mortality. Based on these results, routine early ERCP is not recommended for all ABP cases. Early ERCP is recommended for patients with or suspected of having acute cholangitis. For patients with uncomplicated acute cholangitis, priority should be given to treatment of acute pancreatitis.

Timing ofCholecystectomy following Acute Biliary Pancreatitis

Recurrent pancreatitis with gallbladder stones may cause ABP as a result of recurrent stone passage from the gallbladder to the duodenum. Cholecystectomy was performed even though CBDS were not detected by various diagnostic modalities.

To prevent its recurrence, cholecystectomy was performed after improvement of ABP. In a study using a Canadian database, the 6- and 12- month cumulative readmission rates for the cholecystectomy and non- extraction groups were 4.9%, 5.6%, 12.4%, and 14.0%. In a study using the Kaiser Permanente database (USA), the incidence of recurrent acute pancreatitis in the ERCP/EST group without cholecystectomy and the no- treatment group was

8.2% and 17.1%, respectively. By contrast, the recurrence rate in the cholecystectomy group was 5.4%. In cases of acute pancreatitis with gallbladder stones, cholecystectomy should be the first choice to prevent recurrence; however, the timing is controversial.

There are claims that early surgery is associated with a risk of perioperative complications[62]. By contrast, there are reports that surgery can be safely performed within 48 hours irrespective of abdominal symptoms and blood test findings, leading to shorter hospital stays [63,64]. The PONCHO trial, an RCT reported in the Lancet in 2015, compared a group who underwent cholecystectomy in the same hospital with a group who underwent standby cholecystectomy[65]. The mortality, gallstone-

related complication, and rehospitalization due to recurrent pancreatitis rates were lower in the former group than in the latter. However, there was no difference in the rate of transition from laparoscopy to laparotomy. AGA recommend cholecystectomy in the same hospitalization.

There is a report of nine trials comparing early (within 48 hours) and late (after 48 hours) cholecystectomy in mild acute cholecystic pancreatitis [66]. Early surgery reportedly leads to shorter hospital stays without increasing the complication or mortality rate, and early surgical intervention

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is desirable if the condition permits. By contrast, in the 2004 cohort, there were more infectious complications and more postoperative complications in surgeries performed within 5days of severe acute cholangitis onset or during hospitalization for acute pancreatitis. In AGA, cholecystectomy is recommended in severe pancreatitis with fluid retention around the pancreas after the fluid retention has improved or after 6weeks if a pseudocyst has formed.

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