Article Search
검색
검색 팝업 닫기

Metrics

Help

  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

  • 2. Editorial Board

    Editor-in-Chief + MORE

    Editor-in-Chief
    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
  • 3. Editorial Office
  • 4. Articles
  • 5. Instructions for Authors
  • 6. File Download (PDF version)
  • 7. Ethical Standards
  • 8. Peer Review

    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
    The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.

    The final responsibility for the decision to accept or reject lies with the editors. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.

Search

Search

Year

to

Article Type

Online first

Split Viewer

Online first

Current Diagnosis and Treatment of Acute Pancreatitis in Korea: A Nationwide Survey

Eui Joo Kim1,2 , Sang Hyub Lee3 , Min Kyu Jung4 , Dong Kee Jang5 , Jung Hyun Jo6 , Jae Min Lee7 , Jung Wan Choe8 , Sung Yong Han9 , Young Hoon Choi10 , Seong-Hun Kim11 , Jin Myung Park12 , Kyu-Hyun Paik13

1Department of Internal Medicine, Gil Medical Center, Gachon University College of Medicine, Incheon, Korea; 2Department of Medicine, Inha University Graduate School, Incheon, Korea; 3Department of Internal Medicine and Liver Research Institute, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea; 4Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, Korea; 5Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea; 6Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea; 7Department of Internal Medicine, Gyeongsang National University Changwon Hospital, Gyeongsang National University College of Medicine, Changwon, Korea; 8Department of Internal Medicine, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea; 9Department of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital and Pusan National University School of Medicine Busan, Korea; 10Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea; 11Department of Internal Medicine, Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju, Korea; 12Department of Internal Medicine, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea; 13Department of Internal Medicine, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Korea

Correspondence to: Sang Hyub Lee
ORCID https://orcid.org/0000-0003-2174-9726
E-mail gidoctor@snu.ac.kr

Min Kyu Jung
ORCID https://orcid.org/0000-0001-8749-408X
E-mail minky1973@knu.ac.kr

Received: November 2, 2023; Revised: January 20, 2024; Accepted: January 22, 2024

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gut Liver.

Published online May 7, 2024

Copyright © Gut and Liver.

Background/Aims: Acute pancreatitis (AP) is a leading cause of emergency hospitalization. We present the current diagnostic and therapeutic status of AP as revealed by analysis of a large multicenter dataset.
Methods: The medical records of patients diagnosed with AP between 2018 and 2019 in 12 tertiary medical centers in Korea were retrospectively reviewed.
Results: In total, 676 patients were included; of these, were 388 (57.4%) males, and the mean age of all patients was 58.6 years. There were 355 (52.5%), 301 (44.5%), and 20 (3.0%) patients with mild, moderate, and severe AP, respectively, as assessed by the revised Atlanta classification. The most common etiologies of AP were biliary issues (41.6%) and alcohol consumption (24.6%), followed by hypertriglyceridemia (6.8%). The etiology was not identified in 111 (16.4%) patients at the time of initial admission. The overall mortality rate was 3.3%, increasing up to 45.0% among patients with severe AP. Notably, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome had received <4 L per day during the initial 24 hours of admission. Only 23.8% (67/281) of acute biliary pancreatitis patients underwent cholecystectomy during their initial admission. In total, 17.8% of patients experienced recurrent attacks during follow-up. However, none of the patients with acute biliary pancreatitis experienced recurrent attacks if they had undergone cholecystectomy during their initial admission.
Conclusions: This study provides insights into the current status of AP in Korea, including its etiology, severity, and management.
Results reveal disparities between clinical guidelines and their practical implementation for AP treatment.

Keywords: Pancreatitis, Epidemiology, Diagnosis, Therapeutics

Acute pancreatitis (AP) is associated with significant mortality and requires emergency hospitalization.1 Furthermore, the global incidence of AP is increasing.2 In Korea, it has been documented that the annual incidence of admissions for AP reached 9,162 in 2000.3 Nevertheless, the precise count of newly diagnosed cases within this cohort remains undetermined. If organ failure persists for >48 hours during initial treatment in the acute phase, the mortality rate is about 20%.4 Therefore, appropriate treatment in the acute phase is very important. Treatment in the convalescent phase prevents relapse, exocrine and endocrine dysfunction, and progression to chronic pancreatitis (CP), and thus greatly impacts prognosis and quality of life.5,6 To ensure appropriate early and convalescent treatment, it is essential to identify the cause of AP. By addressing the cause, future acute exacerbation, recurrence, and progression to CP can be prevented. However, 16% to 30% of patients have idiopathic AP (IAP); i.e., pancreatitis without an identifiable cause.7,8 Recently, high-resolution imaging techniques including endoscopic ultrasound (EUS) and magnetic resonance imaging have been used to identify the etiology of AP and may affect the incidence of IAP and distribution of AP etiologies.9,10 From a clinical perspective, determining both the cause and severity of AP is widely regarded as crucial for guiding future treatment decisions. Notably, however, the evidence supporting this viewpoint is insufficient.

Based on recent evidence, clinical guidelines have been developed in Korea and many other countries by various organizations but have not been validated through analysis of multicenter data.11 In this study, the current status of the etiology and treatment of AP in Korea is investigated in patients diagnosed with AP for the first time, and ways to improve clinical care are discussed.

1. Patients

From 1 January 2018 to 31 December 2019, we retrospectively analyzed the medical records of adult patients (aged ≥18 years) diagnosed with AP of any cause for the first time and hospitalized at 12 tertiary medical institutions in Korea (Fig. 1). Patients with a history of AP or CP, as well as those currently receiving treatment for these conditions, were excluded. This study was conducted in accordance with the ethical guidelines of the Declaration of Helsinki as revised in 2013 and approved by the Institutional Review Board of each participating institution (IRB number: 2106-073-1226). The informed consent was waived.

Figure 1.Map showing the locations of the 12 Korean institutions participating in this retrospective multicenter study.

2. Data collection

We retrospectively collected the following data from 12 tertiary referral centers in Korea: patient characteristics at admission, including age, sex, body weight, height, comorbidities, smoking history, history of AP or CP, presence of organ failure, presence of systemic inflammatory response syndrome, presence of local complications, bedside index for severity in AP score, severity according to the revised Atlanta classification, and laboratory findings (including hemoglobin, hematocrit, white blood cell count, C-reactive protein, procalcitonin, amylase, lipase, liver function tests, serum blood urea nitrogen, serum creatinine, serum triglyceride, serum glucose, and serum calcium); etiology of AP during admission, including imaging used during the admission and etiology of AP at discharge; treatments received during admission, including the crystalloid fluid infusion volume during the initial 24 hours of admission, use of antibiotics, use of proton pump inhibitors, cholecystectomy during initial admission, reason for not performing cholecystectomy during initial admission, fasting duration, type of refeeding, and route of refeeding; and prognosis, including mortality at initial admission, development of recurrent AP during follow-up, and etiology of recurrence.

3. Definitions

The diagnosis of AP is based on abdominal pain, serum amylase and/or lipase levels >3-fold the upper normal limits, and radiographic findings consistent with AP. A diagnosis of AP is made when at least two of these three criteria are fulfilled. Acute biliary pancreatitis (ABP) was defined as gallstones or microliths in the common bile duct evident on transabdominal ultrasound, computed tomography, EUS, magnetic resonance cholangiopancreatography, or endoscopic retrograde cholangiography and fulfilment of the AP criteria. Hypertriglyceridemia-induced AP (HTG-AP) was defined as a serum triglyceride level ≥1,000 mg/dL at the time of admission. Acute alcoholic pancreatitis was diagnosed in cases of alcohol abuse or a chronic drinking history with no other identifiable cause of AP. Presumptive IAP was diagnosed when no cause was found at initial admission. The definition of severity was based on the revised Atlanta classification.12 We defined mild AP as AP without organ failure or local or systemic complications, severe AP as organ failure lasting >48 hours, and moderately severe AP as AP with transient organ failure (<48 hours) or local complications.

4. Statistical analysis

Continuous variables are presented as means±standard deviations and categorical variables as percentages (%) or number of cases. When comparing two independent groups, the t-test was performed if the data were normally distributed; otherwise, the Mann-Whitney U test was used. One-way analysis of variance was used to compare three or more groups, and Welch test was employed when equal variance could not be assumed. Categorical variables were analyzed using the chi-square test and the Fisher exact test. All p-values <0.05 were considered statistically significant. All statistical analyses were performed using SPSS software (version 19.0; IBM Corp., Armonk, NY, USA).

1. Baseline characteristics

During the study period, 676 patients admitted to 12 tertiary hospitals were diagnosed with AP for the first time and received treatment (Table 1). There were 388 males (57.4%) and the mean age of all patients was 58.6 years (Fig. 2). According to the revised Atlanta classification, 355 cases (52.5%) were mild, 301 (44.5%) were moderate, and 20 (3.0%) were severe. Among all patients, the mortality rate during the first hospitalization was 3.3% (22/676). However, the mortality rate of patients with severe AP was 45.0% (9/20), which was significantly higher than that of patients with moderate (3.0%, 9/301) and mild AP (1.1%, 4/351) (p<0.001). The mean hospitalization period was 6.6±4.7, 10.4±11.7, and 13.7±13.6 days for those with mild, moderate, and severe AP, respectively (p<0.001). Serum levels of the pancreatic enzymes amylase and lipase did not differ significantly according to AP severity at the time of admission (p=0.697 and p=0.933, respectively). On admission, the mean white blood cell count was 10.8±4.6, 12.8±5.5, and 14.2±6.3 ×103/µL in the mild, moderate, and severe AP patients, respectively (p<0.001). The mean blood urea nitrogen levels were 16.3±9.2, 17.7±13.5, and 40.1±23.8 mg/dL, respectively, and were significantly higher in severe than mild and moderate cases (p<0.001). There was no significant difference in body mass index (BMI) according to AP severity (p=0.716). However, after excluding 33 patients without BMI data, the rate of obesity (BMI >30 kg/m2) was significantly higher among patients with severe AP (27.8%, 5/18) compared to mild and moderate AP (9.4%, 59/625) (p=0.026) (Table 2).

Figure 2.Age distribution of the patients.

Table 1. Baseline Patient Characteristics

CharacteristicAcute pancreatitis (n=676)
Male sex388 (57.4)
Age, yr58.6±17.7
Height, cm164.0±9.8
Weight, kg66.8±27.4
Body mass index, kg/m224.7±8.8
Current smoker123 (18.2)
History
Diabetes mellitus159 (23.5)
Dyslipidemia101 (14.9)
Acute pancreatitis0
Chronic pancreatitis0
Systemic inflammatory response197 (29.1)
Severity, Atlanta classification
Mild355 (52.5)
Moderate301 (44.5)
Severe20 (3.0)
Initial laboratory findings
Hemoglobin, g/dL13.7±2.2
Hematocrit, %40.3±6.1
White blood cell, ×103/μL11.8±5.2
Amylase, U/L866.3±938.8
Lipase, U/L2,024±2,489
Hospitalization, day8.5±9.1
Death22 (3.3)

Data are presented as number (%) or mean±SD.



Table 2. Characteristics of Non-Severe and Severe AP Patients

CharacteristicSevere APNon-severe APp-value
Male sex13 (65.0)375 (57.2)0.505
Age, yr64.6±17.458.4±17.70.123
Height, cm164.1±10.5164.0±9.80.972
Weight, kg68.6±15.166.8±27.70.783
BMI, kg/m225.5±5.124.6±8.90.671
BMI >30 kg/m25 (27.8)59 (9.4)0.026
Current smoker5 (26.3)67 (11.1)0.106
History
Diabetes mellitus6 (30.0)153 (23.3)0.592
Dyslipidemia2 (10.0)99 (15.1)0.753
Systemic inflammatory response16 (80.0)181 (27.6)<0.001
Initial laboratory findings
Hemoglobin, g/dL12.7±2.013.7±2.20.044
Hematocrit, %37.7±6.740.3±6.10.059
White blood cell, ×103/μL14.2±6.311.7±5.10.031
Amylase, U/L984.7±908.6862.7±940.10.284
Lipase, U/L2,088±1,5642,022±2,5130.908
BUN, mg/dL40.1±23.817.0±11.4<0.001
Creatinine, mg/dL3.3±2.81.0±1.10.002
Etiology
Alcohol7 (35.0)159 (24.2)0.293
Biliary8 (40.0)273 (41.6)>0.999
HTG046 (7.0)0.388
Death9 (45.0)13 (2.0)<0.001

Data are presented as number (%) or mean±SD.

AP, acute pancreatitis; BMI, body mass index; BUN, blood urea nitrogen; HTG hypertriglyceridemia.



2. Etiology

Imaging was performed at the discretion of the clinicians. During initial admission, computed tomography, EUS, and magnetic resonance imaging were performed on 95.4% (645/676), 26.3% (178/676), and 17.5% (118/676) of all patients, respectively. The most common etiologies of AP identified during the first hospitalization were cholelithiasis (41.6%, 281/676), alcohol (24.6%, 166/676), and HTG (6.8%, 46/676). Other causes included malignant disease, mucinous cysts, and drug-induced AP in 2.7% (18/676), 2.1% (14/676), and 1.8% (12/676) of patients, respectively. During the first hospitalization, 16.4% (111/676) of patients were discharged with unexplained AP (presumptive IAP). ABP was more prevalent in older age groups, while HTG-AP was more prevalent in younger age groups (Fig. 3).

Figure 3.Age distribution of the patients according to the etiology of acute pancreatitis.

The etiology of AP varied between males and females. In males and females, alcohol and gallstones were the most frequent causes (37.6% [146/388] and 54.2% [156/288], respectively). The severity of AP also differed by sex. In males, the frequencies of mild, moderate, and severe AP were 46.6% (181/388), 50.0% (194/388), and 3.4% (13/388), respectively; the rates for females were 60.4% (174/288), 37.2% (107/288), and 2.4% (7/288), respectively; and the proportion of females with mild AP was higher than that of males (p=0.002). However, when analyzing severity according to etiology, the proportion of severe AP cases was higher among acute alcoholic pancreatitis patients compared to those with AP of other etiologies (4.2% vs 2.5%, p<0.001), and the proportion of mild AP was higher among ABP patients compared to those with AP of other etiologies (59.4% vs 47.6%, p=0.009). Considering that the identified disparity is exclusively derived from univariate analysis, and multivariate analysis has not been undertaken, the potential association between gender and severity remains ambiguous.

3. Initial treatments

After excluding 26 patients for whom the volume of crystalloid fluid administered during the first 24 hours was not recorded, 86.8% (564/650) of the remaining patients received 2 to 4 L of fluid during the first 24 hours of hospitalization and 13.2% (86/650) received ≥4 L. The mortality rate was significantly higher in patients who received ≥4 L of fluid (9.3% vs 2.1%, p=0.002), even when patients with severe AP were excluded (1.3% vs 5.0%, p=0.040). However, deriving a precise conclusion from this dataset poses a challenge because the incidence of severe AP was significantly higher among patients who received ≥4 L of fluid than among those who received <4 L (7.0% vs 2.5%, respectively; p=0.037). Interestingly, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome had received <4 L per day during the initial 24 hours of admission (Table 3).

Table 3. Characteristics of Patients: Initial Aggressive Hydration (>4 L/day) versus Non-Aggressive Hydration (<4 L/day)

CharacteristicAggressive (>4 L/day)Non-aggressive (<4 L/day)p-value
Male sex57 (66.3)315 (55.9)0.079
Age, yr57.7±16.858.7±17.90.644
Height, cm165.1±9.8163.9±9.90.275
Weight, kg67.3±14.666.8±28.90.864
BMI, kg/m224.6±4.524.6±9.30.968
BMI >30 kg/m29 (11.3)53 (9.9)0.842
Current smoker12 (15.6)58 (11.2)0.195
History
Diabetes mellitus28 (32.6)125 (22.2)0.041
Dyslipidemia12 (14.0)87 (15.4)0.752
Systemic inflammatory response35 (40.7)154 (27.3)0.015
Severe AP6 (7.0)14 (2.5)0.037
Initial laboratory findings
Hemoglobin, g/dL13.7±2.213.7±2.20.934
Hematocrit, %40.2±5.840.3±6.10.820
White blood cell, ×103/μL12.8±5.811.6±5.10.056
Amylase, U/L910.4±888.7859.1±947.10.637
Lipase, U/L2,343±2,6951,977±2,4570.208
BUN, mg/dL20.8±14.917.2±12.10.012
Creatinine, mg/dL1.1±0.61.1±1.30.899
Etiology
Alcohol27 (31.4)134 (23.8)0.140
Biliary28 (32.6)243 (43.1)0.078
HTG8 (9.3)36 (6.4)0.353
Death8 (9.3)12 (2.1)0.002

Data are presented as number (%) or mean±SD.

BMI, body mass index; AP, acute pancreatitis; BUN, blood urea nitrogen; HTG hypertriglyceridemia.



Empirical antibiotics were started within 48 hours of hospitalization in 72.9% (493/676) of all patients. Among the patients who did not receive antibiotics within the first 48 hours, 59.8% (110/184), 39.7% (73/184), and 0.5% (1/184) had mild, moderate, and severe AP, respectively. Among patients on antibiotics, 49.8% (245/492), 46.3% (228/492), and 3.9% (19/492) had mild, moderate, and severe AP, respectively. Antibiotics were prescribed mainly to treat cholecystitis and cholangitis (33.3%, 164/493). However, they were also prescribed for shock (4.3%, 21/493), fever (39.6%, 195/493), infected necrosis (0.2%, 1/493), other types of infection (1.6%, 8/493), and other reasons including prophylaxis (21.0%, 104/493).

4. Convalescent treatment

Nutrition was resumed after a mean fasting duration of 2.9±2.7 days, and 94.2% of patients (637/676) were started on an oral diet. Nutrients were delivered via a nasogastric tube in 0.7% of patients (5/676); no nasojejunal tube was employed. In 48.1% of patients (325/676), nutrition was gradually increased starting with sips of water, while in 3.1% the initial dietary recommencement (21/676) was solid food.

During hospitalization, proton pump inhibitors were prescribed for 57.1% of the patients (386/676), including 5.6% (23/386) because of bleeding after endoscopy, 4.9% (19/386) because of gastrointestinal ulcers, 2.6% (10/386) because of gastroesophageal reflux disease, and 84.7% (327/386) for no recorded reason.

Of the 281 patients diagnosed with ABP, 23.8% (67/281) underwent cholecystectomy during their initial hospitalization. Among patients with ABP, 59.4% (167/281) had mild AP, 37.7% (106/281) had moderately severe AP, and 2.8% (8/281) had severe AP. Specifically, only 21.6% (36/167) of those with mild ABP underwent cholecystectomy during their initial hospitalization. Among the 214 patients diagnosed with ABP who did not undergo surgery, 61.2% (131/214) presented with mild AP. Reasons for not undergoing surgery included patient refusal in 37.4% (80/214), severe AP or local complications in 10.3% (22/214), advanced age and/or high-risk comorbidities in 17.8% (38/214), and non-medical reasons such as the surgeon’s opinion or a delay in surgical scheduling in 19.6% (42/214). In total, 21.0% of all patients (142/676) were lost to outpatient follow-up. During follow-up, AP recurrence was confirmed in 17.8% of patients (95/534). Of the patients who developed relapse, 44.2% (42/95) had acute alcoholic pancreatitis and 17.9% (17/95) had ABP. Of the initial 131 patients with mild ABP who did not undergo cholecystectomy, 30 patients were lost to follow-up and 9.9% of the remaining patients (10/101) developed recurrent ABP. None of the patients with recurrent ABP had undergone cholecystectomy at the time of the initial admission, and they subsequently developed recurrent AP within a mean duration of 686 days (range, 55 to 1,235 days).

We investigated the current AP diagnosis and treatment status in Korea by analyzing the largest multicenter dataset available. We have reported the distribution of AP etiologies in the era of high-resolution medical imaging techniques, such as EUS and magnetic resonance cholangiopancreatography. The incidence and mortality rates were reported according to AP severity, and the data suggested a possible relationship between obesity and AP severity. In addition, we tried to bridge the gap between clinical guidelines and real-world practice by identifying real-world treatment trends and reasons for not following guidelines.

The incidence of severe AP in this study (3.0%) is lower than that reported in prior studies. However, in a study based on Korean multicenter data, Lee et al.13 reported the distribution of severity based on the revised Atlanta classification. They found a 3.7% incidence of severe AP, which aligns closely with our own findings. The etiological factors contributing to AP exhibit variations based on global geographical regions. The most frequent causes of AP are gallstones and alcohol abuse in developed countries, and our data are in accordance with this. Retrospective studies conducted in Western countries revealed an equivalent prevalence of alcohol-induced and gallstone-related pancreatitis, with each causative factor contributing to a range of 23% to 36% of cases.14 In another study, dominance of gallstone-related pancreatitis was noted in southern European countries.15 Baig et al.16 identified alcoholism as the predominant cause of AP, followed by biliary stones, and Wang et al.17 similarly found that biliary stones (38%) and alcohol abuse (36%) were the foremost etiological factors in AP. Conversely, Alkareemy et al.18 reported gallstones and idiopathic causes as the most prevalent etiologies. These discrepancies seem to be attributed to regional disparities in alcohol consumption.

In our study, HTG was the third most common cause of AP. Generally, serum triglyceride levels of 500 mg/dL (5.6 mmol/L) are suspected to cause AP, and patients with levels ≥1,000 mg/dL (11.3 mmol/L) are diagnosed with AP.19 However, a major practical difficulty when aiming to identify the etiology of AP is that it is not easy to determine whether HTG simply reflects excessive alcohol consumption or is the cause of AP. Given the retrospective nature of this study, it is possible that the reported HTG frequency was lower than the actual frequency because alcohol may be identified as the cause of AP when clinicians encounter patients who consume it to excess; clinicians may not test for HTG. Some experimental and clinical studies found that HTG-AP was more severe than AP of other etiologies.20,21 However, in the present study, among 46 HTG-AP patients, none had severe AP (mild, n=23; moderate, n=23). Thus, we did not identify a relationship between HTG-AP and AP severity.

Together with HTG, obesity has been suggested to increase AP severity. Obesity is known to exacerbate the systemic inflammatory response and increase mortality.22-25 We found that the proportion of obese patients (BMI >30 kg/m2) was significantly higher among the severe than the mild and moderate AP groups. As the number of obese subjects in Korea is increasing, it is possible that obesity will emerge as a clinically important predictor of AP severity.26 However, according to the 2012 revised Atlanta classification, 20 patients included in this study were classified as having severe AP, and multivariate analysis of risk factors for predicting severe AP was not possible.

Previous studies found that IAP accounted for 16% to 30% of all AP cases.7,8 In this study, the cause of AP during initial admission could not be found in 16.4% of patients. This is lower than the proportions in previous reports, possibly reflecting the use of more recent imaging techniques. EUS sensitively detects ABP, including microlithiasis, and magnetic resonance cholangiopancreatography is comparable to EUS.9,27,28 However, there is no definitive evidence or guidelines supporting the use of any particular imaging modality during the acute phase of AP. Efforts to reduce the frequency of IAP and identify all of the etiologies are still needed because AP can recur and is a risk factor for the development of CP.29

Traditionally, fluid therapy is used to maintain an effective circulating blood volume in patients with AP; rapid fluid therapy has been recommended. It is crucial to achieve an appropriate intravascular blood volume while also avoiding overloading the patient with crystalloid fluid. In this study, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome received <4 L per day during the initial 24 hours of admission. Considering that severity assessment can only be reliably conducted after 48 hours of admission, these findings underscore the challenges of estimating severity within the first 24 hours in current clinical practice. However, recent evidence suggests that excessive fluid administration should be avoided. Several randomized controlled trials have revealed an association between excessive fluid administration and multiple organ failure as well as an increased severity of AP.30-33 Practical severity estimation protocols that can be implemented early in the admission process, ideally at the initial presentation, are required to identify patients who require aggressive fluid therapy as a tailored approach.

Because infection is the leading cause of death 1 month after an initial AP attack, empirical prophylactic antibiotics are widely prescribed. In this study, the prescription rate within the first 48 hours was high (72.8%) considering the frequency of ABP and AP infectious complications requiring antibiotics.34 Antibiotics were prescribed within 48 hours of admission mainly to treat cholecystitis and cholangitis, but they were also administered for shock (4.3%), fever (39.6%), infected necrosis (0.2%), other types of infection (1.6%), and other reasons including prophylaxis (21.0%). However, because this study was multicenter in nature, the observed trend is not indicative of an issue attributed to a single medical center; instead, it underscores the necessity for consensus among experts.

Cholecystectomy at the time of initial admission for ABP is recommended by clinical guidelines because it reduces the frequency of recurrent attacks and is economically advantageous.33,35 However, we found that only 23.8% of ABP patients underwent cholecystectomy during the initial admission. This rate is low given the incidence of mild ABP. Notably, 57.4% of ABP patients did not undergo cholecystectomy because of refusal or non-medical reasons. Because 17.9% of patients who experienced AP recurrence during follow-up were ABP patients who did not undergo cholecystectomy at the time of the first attack, practical efforts such as proper patient education are needed to emphasize that cholecystectomy reduces the incidence of recurrent AP. Additionally, this study involved patients who had visited tertiary hospitals in Korea. The burden of major surgeries for malignancies other than cholecystectomy tends to be higher in tertiary hospitals. Consequently, the rate of patients who were unable to undergo surgery at the time of admission because of surgical scheduling reached 19.6% in this study. To reduce this rate, changes in the domestic healthcare system are warranted.

This study was performed to evaluate the current clinical status of AP in Korea and thus support development of Korean AP guidelines. However, despite utilizing the largest multicenter dataset in Korea to date, the retrospective nature of the study introduced the possibility of selection bias. A multivariate analysis of risk factors for severe AP or mortality was not performed because of the risk of overfitting in the multivariate calibration process. The study collected limited data, thereby impeding assessment of causality in the relationship between treatment interventions and clinical outcomes.

In conclusion, our study constitutes a comprehensive report on the current status of AP in Korea, including the distribution of the etiologies and the severity, mortality, and management, based on detailed clinical information obtained via a retrospective multicenter survey. Our study revealed notable differences in AP severity depending on the etiology, with obesity (BMI >30 kg/m2) serving as a potential risk and predictive factor for severe AP. Nevertheless, the cause of AP was unknown in 16.4% of patients, highlighting the need for long-term prospective studies and practical measures to reduce the incidence of IAP. Moreover, it is critical to address the discrepancies between clinical guidelines and actual clinical practices employed for managing AP.

This research was supported by a 2020 grant from the Korean Pancreatobiliary Association (KPBA).

No potential conflict of interest relevant to this article was reported.

Study concept and design: E.J.K., S.H.L., M.K.J. Data acquisition: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Data analysis and interpretation: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Drafting of the manuscript: E.J.K. Critical revision of the manuscript for important intellectual content: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Statistical analysis: E.J.K. Obtained funding: E.J.K. Study supervision: S.H.L., M.K.J. Approval of final manuscript: all authors.

  1. Peery AF, Crockett SD, Murphy CC, et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: update 2021. Gastroenterology 2022;162:621-644.
    Pubmed KoreaMed CrossRef
  2. Iannuzzi JP, King JA, Leong JH, et al. Global incidence of acute pancreatitis is increasing over time: a systematic review and meta-analysis. Gastroenterology 2022;162:122-134.
    Pubmed CrossRef
  3. Kim CD. Current status of acute pancreatitis in Korea. Korean J Gastroenterol 2003;42:1-11.
  4. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med 2016;375:1972-1981.
    Pubmed CrossRef
  5. Das SL, Singh PP, Phillips AR, Murphy R, Windsor JA, Petrov MS. Newly diagnosed diabetes mellitus after acute pancreatitis: a systematic review and meta-analysis. Gut 2014;63:818-831.
    Pubmed CrossRef
  6. Hollemans RA, Hallensleben ND, Mager DJ, et al. Pancreatic exocrine insufficiency following acute pancreatitis: systematic review and study level meta-analysis. Pancreatology 2018;18:253-262.
    Pubmed CrossRef
  7. Párniczky A, Kui B, Szentesi A, et al. Prospective, multicentre, nationwide clinical data from 600 cases of acute pancreatitis. PLoS One 2016;11:e0165309.
    Pubmed KoreaMed CrossRef
  8. Fonseca Sepúlveda EV, Guerrero-Lozano R. Acute pancreatitis and recurrent acute pancreatitis: an exploration of clinical and etiologic factors and outcomes. J Pediatr (Rio J) 2019;95:713-719.
    Pubmed CrossRef
  9. Wan J, Ouyang Y, Yu C, Yang X, Xia L, Lu N. Comparison of EUS with MRCP in idiopathic acute pancreatitis: a systematic review and meta-analysis. Gastrointest Endosc 2018;87:1180-1188.
    Pubmed CrossRef
  10. Pereira R, Eslick G, Cox M. Endoscopic ultrasound for routine assessment in idiopathic acute pancreatitis. J Gastrointest Surg 2019;23:1694-1700.
    Pubmed CrossRef
  11. Choe JW, Lee SH, Cheon YK, Lee HS, Choi M. Revised Clinical Practice Guideline of Korean Pancreatobiliary Association for Acute Pancreatitis: purpose and process of guidelines. Korean J Pancreas Biliary Tract 2022;27:1-5.
    CrossRef
  12. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-111.
    Pubmed CrossRef
  13. Lee HC, Kim HH, Han J, et al. Revised Atlanta classification of acute pancreatitis can predict clinical outcome better: a retrospective, multicenter study. Korean J Pancreas Biliary Tract 2015;20:64-70.
    CrossRef
  14. O'Farrell A, Allwright S, Toomey D, Bedford D, Conlon K. Hospital admission for acute pancreatitis in the Irish population, 1997 2004: could the increase be due to an increase in alcohol-related pancreatitis?. J Public Health (Oxf) 2007;29:398-404.
    Pubmed CrossRef
  15. Gullo L, Migliori M, Oláh A, et al. Acute pancreatitis in five European countries: etiology and mortality. Pancreas 2002;24:223-227.
    Pubmed CrossRef
  16. Baig SJ, Rahed A, Sen S. A prospective study of the aetiology, severity and outcome of acute pancreatitis in Eastern India. Trop Gastroenterol 2008;29:20-22.
  17. Wang X, Xu Y, Qiao Y, et al. An evidence-based proposal for predicting organ failure in severe acute pancreatitis. Pancreas 2013;42:1255-1261.
    Pubmed CrossRef
  18. Alkareemy EA, Ahmed LA, El-Masry MA, Habib HA, Mustafa MH. Etiology, clinical characteristics, and outcomes of acute pancreatitis in patients at Assiut University Hospital. Egypt J Intern Med 2020;32:24.
    CrossRef
  19. Scherer J, Singh VP, Pitchumoni CS, Yadav D. Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol 2014;48:195-203.
    Pubmed KoreaMed CrossRef
  20. Baranyai T, Terzin V, Vajda A, Wittmann T, Czakó L. Acute pancreatitis caused by hypertriglyceridemia. Orv Hetil 2010;151:1869-1874.
    Pubmed CrossRef
  21. Kim TI, Jeong HT, Song JE, Kim HG, Han J. Differences in clinical features between hypertriglyceridemia-induced acute pancreatitis and other etiologies of acute pancreatitis. Korean J Pancreas Biliary Tract 2022;27:97-105.
    CrossRef
  22. Premkumar R, Phillips AR, Petrov MS, Windsor JA. The clinical relevance of obesity in acute pancreatitis: targeted systematic reviews. Pancreatology 2015;15:25-33.
    Pubmed CrossRef
  23. Martínez J, Sánchez-Payá J, Palazón JM, Suazo-Barahona J, Robles-Díaz G, Pérez-Mateo M. Is obesity a risk factor in acute pancreatitis? A meta-analysis. Pancreatology 2004;4:42-48.
    Pubmed CrossRef
  24. Porter KA, Banks PA. Obesity as a predictor of severity in acute pancreatitis. Int J Pancreatol 1991;10:247-252.
    Pubmed CrossRef
  25. Khatua B, El-Kurdi B, Singh VP. Obesity and pancreatitis. Curr Opin Gastroenterol 2017;33:374-382.
    Pubmed KoreaMed CrossRef
  26. Yang YS, Han BD, Han K, Jung JH, Son JW; Taskforce Team of the Obesity Fact Sheet of the Korean Society for the Study of Obesity. Obesity fact sheet in Korea, 2021: trends in obesity prevalence and obesity-related comorbidity incidence stratified by age from 2009 to 2019. J Obes Metab Syndr 2022;31:169-177.
    Pubmed KoreaMed CrossRef
  27. Hallensleben ND, Umans DS, Bouwense SA, et al. The diagnostic work-up and outcomes of 'presumed' idiopathic acute pancreatitis: a post-hoc analysis of a multicentre observational cohort. United European Gastroenterol J 2020;8:340-350.
    Pubmed KoreaMed CrossRef
  28. Del Vecchio Blanco G, Gesuale C, Varanese M, Monteleone G, Paoluzi OA. Idiopathic acute pancreatitis: a review on etiology and diagnostic work-up. Clin J Gastroenterol 2019;12:511-524.
    Pubmed CrossRef
  29. Machicado JD, Yadav D. Epidemiology of recurrent acute and chronic pancreatitis: similarities and differences. Dig Dis Sci 2017;62:1683-1691.
    Pubmed KoreaMed CrossRef
  30. de-Madaria E, Soler-Sala G, Sánchez-Payá J, et al. Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort study. Am J Gastroenterol 2011;106:1843-1850.
    Pubmed CrossRef
  31. Mao EQ, Fei J, Peng YB, Huang J, Tang YQ, Zhang SD. Rapid hemodilution is associated with increased sepsis and mortality among patients with severe acute pancreatitis. Chin Med J (Engl) 2010;123:1639-1644.
    Pubmed CrossRef
  32. de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or moderate fluid resuscitation in acute pancreatitis. N Engl J Med 2022;387:989-1000.
    Pubmed CrossRef
  33. Lee SH, Choe JW, Cheon YK, et al. Revised Clinical Practice Guidelines of the Korean Pancreatobiliary Association for Acute Pancreatitis. Gut Liver 2023;17:34-48.
    Pubmed KoreaMed CrossRef
  34. Párniczky A, Lantos T, Tóth EM, et al. Antibiotic therapy in acute pancreatitis: from global overuse to evidence based recommendations. Pancreatology 2019;19:488-499.
    Pubmed CrossRef
  35. da Costa DW, Bouwense SA, Schepers NJ, et al. Same-admission versus interval cholecystectomy for mild gallstone pancreatitis (PONCHO): a multicentre randomised controlled trial. Lancet 2015;386:1261-1268.
    Pubmed CrossRef

Article

ahead

Gut and Liver

Published online May 7, 2024

Copyright © Gut and Liver.

Current Diagnosis and Treatment of Acute Pancreatitis in Korea: A Nationwide Survey

Eui Joo Kim1,2 , Sang Hyub Lee3 , Min Kyu Jung4 , Dong Kee Jang5 , Jung Hyun Jo6 , Jae Min Lee7 , Jung Wan Choe8 , Sung Yong Han9 , Young Hoon Choi10 , Seong-Hun Kim11 , Jin Myung Park12 , Kyu-Hyun Paik13

1Department of Internal Medicine, Gil Medical Center, Gachon University College of Medicine, Incheon, Korea; 2Department of Medicine, Inha University Graduate School, Incheon, Korea; 3Department of Internal Medicine and Liver Research Institute, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea; 4Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, Korea; 5Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea; 6Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea; 7Department of Internal Medicine, Gyeongsang National University Changwon Hospital, Gyeongsang National University College of Medicine, Changwon, Korea; 8Department of Internal Medicine, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea; 9Department of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital and Pusan National University School of Medicine Busan, Korea; 10Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea; 11Department of Internal Medicine, Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju, Korea; 12Department of Internal Medicine, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea; 13Department of Internal Medicine, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Korea

Correspondence to:Sang Hyub Lee
ORCID https://orcid.org/0000-0003-2174-9726
E-mail gidoctor@snu.ac.kr

Min Kyu Jung
ORCID https://orcid.org/0000-0001-8749-408X
E-mail minky1973@knu.ac.kr

Received: November 2, 2023; Revised: January 20, 2024; Accepted: January 22, 2024

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background/Aims: Acute pancreatitis (AP) is a leading cause of emergency hospitalization. We present the current diagnostic and therapeutic status of AP as revealed by analysis of a large multicenter dataset.
Methods: The medical records of patients diagnosed with AP between 2018 and 2019 in 12 tertiary medical centers in Korea were retrospectively reviewed.
Results: In total, 676 patients were included; of these, were 388 (57.4%) males, and the mean age of all patients was 58.6 years. There were 355 (52.5%), 301 (44.5%), and 20 (3.0%) patients with mild, moderate, and severe AP, respectively, as assessed by the revised Atlanta classification. The most common etiologies of AP were biliary issues (41.6%) and alcohol consumption (24.6%), followed by hypertriglyceridemia (6.8%). The etiology was not identified in 111 (16.4%) patients at the time of initial admission. The overall mortality rate was 3.3%, increasing up to 45.0% among patients with severe AP. Notably, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome had received <4 L per day during the initial 24 hours of admission. Only 23.8% (67/281) of acute biliary pancreatitis patients underwent cholecystectomy during their initial admission. In total, 17.8% of patients experienced recurrent attacks during follow-up. However, none of the patients with acute biliary pancreatitis experienced recurrent attacks if they had undergone cholecystectomy during their initial admission.
Conclusions: This study provides insights into the current status of AP in Korea, including its etiology, severity, and management.
Results reveal disparities between clinical guidelines and their practical implementation for AP treatment.

Keywords: Pancreatitis, Epidemiology, Diagnosis, Therapeutics

INTRODUCTION

Acute pancreatitis (AP) is associated with significant mortality and requires emergency hospitalization.1 Furthermore, the global incidence of AP is increasing.2 In Korea, it has been documented that the annual incidence of admissions for AP reached 9,162 in 2000.3 Nevertheless, the precise count of newly diagnosed cases within this cohort remains undetermined. If organ failure persists for >48 hours during initial treatment in the acute phase, the mortality rate is about 20%.4 Therefore, appropriate treatment in the acute phase is very important. Treatment in the convalescent phase prevents relapse, exocrine and endocrine dysfunction, and progression to chronic pancreatitis (CP), and thus greatly impacts prognosis and quality of life.5,6 To ensure appropriate early and convalescent treatment, it is essential to identify the cause of AP. By addressing the cause, future acute exacerbation, recurrence, and progression to CP can be prevented. However, 16% to 30% of patients have idiopathic AP (IAP); i.e., pancreatitis without an identifiable cause.7,8 Recently, high-resolution imaging techniques including endoscopic ultrasound (EUS) and magnetic resonance imaging have been used to identify the etiology of AP and may affect the incidence of IAP and distribution of AP etiologies.9,10 From a clinical perspective, determining both the cause and severity of AP is widely regarded as crucial for guiding future treatment decisions. Notably, however, the evidence supporting this viewpoint is insufficient.

Based on recent evidence, clinical guidelines have been developed in Korea and many other countries by various organizations but have not been validated through analysis of multicenter data.11 In this study, the current status of the etiology and treatment of AP in Korea is investigated in patients diagnosed with AP for the first time, and ways to improve clinical care are discussed.

MATERIALS AND METHODS

1. Patients

From 1 January 2018 to 31 December 2019, we retrospectively analyzed the medical records of adult patients (aged ≥18 years) diagnosed with AP of any cause for the first time and hospitalized at 12 tertiary medical institutions in Korea (Fig. 1). Patients with a history of AP or CP, as well as those currently receiving treatment for these conditions, were excluded. This study was conducted in accordance with the ethical guidelines of the Declaration of Helsinki as revised in 2013 and approved by the Institutional Review Board of each participating institution (IRB number: 2106-073-1226). The informed consent was waived.

Figure 1. Map showing the locations of the 12 Korean institutions participating in this retrospective multicenter study.

2. Data collection

We retrospectively collected the following data from 12 tertiary referral centers in Korea: patient characteristics at admission, including age, sex, body weight, height, comorbidities, smoking history, history of AP or CP, presence of organ failure, presence of systemic inflammatory response syndrome, presence of local complications, bedside index for severity in AP score, severity according to the revised Atlanta classification, and laboratory findings (including hemoglobin, hematocrit, white blood cell count, C-reactive protein, procalcitonin, amylase, lipase, liver function tests, serum blood urea nitrogen, serum creatinine, serum triglyceride, serum glucose, and serum calcium); etiology of AP during admission, including imaging used during the admission and etiology of AP at discharge; treatments received during admission, including the crystalloid fluid infusion volume during the initial 24 hours of admission, use of antibiotics, use of proton pump inhibitors, cholecystectomy during initial admission, reason for not performing cholecystectomy during initial admission, fasting duration, type of refeeding, and route of refeeding; and prognosis, including mortality at initial admission, development of recurrent AP during follow-up, and etiology of recurrence.

3. Definitions

The diagnosis of AP is based on abdominal pain, serum amylase and/or lipase levels >3-fold the upper normal limits, and radiographic findings consistent with AP. A diagnosis of AP is made when at least two of these three criteria are fulfilled. Acute biliary pancreatitis (ABP) was defined as gallstones or microliths in the common bile duct evident on transabdominal ultrasound, computed tomography, EUS, magnetic resonance cholangiopancreatography, or endoscopic retrograde cholangiography and fulfilment of the AP criteria. Hypertriglyceridemia-induced AP (HTG-AP) was defined as a serum triglyceride level ≥1,000 mg/dL at the time of admission. Acute alcoholic pancreatitis was diagnosed in cases of alcohol abuse or a chronic drinking history with no other identifiable cause of AP. Presumptive IAP was diagnosed when no cause was found at initial admission. The definition of severity was based on the revised Atlanta classification.12 We defined mild AP as AP without organ failure or local or systemic complications, severe AP as organ failure lasting >48 hours, and moderately severe AP as AP with transient organ failure (<48 hours) or local complications.

4. Statistical analysis

Continuous variables are presented as means±standard deviations and categorical variables as percentages (%) or number of cases. When comparing two independent groups, the t-test was performed if the data were normally distributed; otherwise, the Mann-Whitney U test was used. One-way analysis of variance was used to compare three or more groups, and Welch test was employed when equal variance could not be assumed. Categorical variables were analyzed using the chi-square test and the Fisher exact test. All p-values <0.05 were considered statistically significant. All statistical analyses were performed using SPSS software (version 19.0; IBM Corp., Armonk, NY, USA).

RESULTS

1. Baseline characteristics

During the study period, 676 patients admitted to 12 tertiary hospitals were diagnosed with AP for the first time and received treatment (Table 1). There were 388 males (57.4%) and the mean age of all patients was 58.6 years (Fig. 2). According to the revised Atlanta classification, 355 cases (52.5%) were mild, 301 (44.5%) were moderate, and 20 (3.0%) were severe. Among all patients, the mortality rate during the first hospitalization was 3.3% (22/676). However, the mortality rate of patients with severe AP was 45.0% (9/20), which was significantly higher than that of patients with moderate (3.0%, 9/301) and mild AP (1.1%, 4/351) (p<0.001). The mean hospitalization period was 6.6±4.7, 10.4±11.7, and 13.7±13.6 days for those with mild, moderate, and severe AP, respectively (p<0.001). Serum levels of the pancreatic enzymes amylase and lipase did not differ significantly according to AP severity at the time of admission (p=0.697 and p=0.933, respectively). On admission, the mean white blood cell count was 10.8±4.6, 12.8±5.5, and 14.2±6.3 ×103/µL in the mild, moderate, and severe AP patients, respectively (p<0.001). The mean blood urea nitrogen levels were 16.3±9.2, 17.7±13.5, and 40.1±23.8 mg/dL, respectively, and were significantly higher in severe than mild and moderate cases (p<0.001). There was no significant difference in body mass index (BMI) according to AP severity (p=0.716). However, after excluding 33 patients without BMI data, the rate of obesity (BMI >30 kg/m2) was significantly higher among patients with severe AP (27.8%, 5/18) compared to mild and moderate AP (9.4%, 59/625) (p=0.026) (Table 2).

Figure 2. Age distribution of the patients.

Table 1 . Baseline Patient Characteristics.

CharacteristicAcute pancreatitis (n=676)
Male sex388 (57.4)
Age, yr58.6±17.7
Height, cm164.0±9.8
Weight, kg66.8±27.4
Body mass index, kg/m224.7±8.8
Current smoker123 (18.2)
History
Diabetes mellitus159 (23.5)
Dyslipidemia101 (14.9)
Acute pancreatitis0
Chronic pancreatitis0
Systemic inflammatory response197 (29.1)
Severity, Atlanta classification
Mild355 (52.5)
Moderate301 (44.5)
Severe20 (3.0)
Initial laboratory findings
Hemoglobin, g/dL13.7±2.2
Hematocrit, %40.3±6.1
White blood cell, ×103/μL11.8±5.2
Amylase, U/L866.3±938.8
Lipase, U/L2,024±2,489
Hospitalization, day8.5±9.1
Death22 (3.3)

Data are presented as number (%) or mean±SD..



Table 2 . Characteristics of Non-Severe and Severe AP Patients.

CharacteristicSevere APNon-severe APp-value
Male sex13 (65.0)375 (57.2)0.505
Age, yr64.6±17.458.4±17.70.123
Height, cm164.1±10.5164.0±9.80.972
Weight, kg68.6±15.166.8±27.70.783
BMI, kg/m225.5±5.124.6±8.90.671
BMI >30 kg/m25 (27.8)59 (9.4)0.026
Current smoker5 (26.3)67 (11.1)0.106
History
Diabetes mellitus6 (30.0)153 (23.3)0.592
Dyslipidemia2 (10.0)99 (15.1)0.753
Systemic inflammatory response16 (80.0)181 (27.6)<0.001
Initial laboratory findings
Hemoglobin, g/dL12.7±2.013.7±2.20.044
Hematocrit, %37.7±6.740.3±6.10.059
White blood cell, ×103/μL14.2±6.311.7±5.10.031
Amylase, U/L984.7±908.6862.7±940.10.284
Lipase, U/L2,088±1,5642,022±2,5130.908
BUN, mg/dL40.1±23.817.0±11.4<0.001
Creatinine, mg/dL3.3±2.81.0±1.10.002
Etiology
Alcohol7 (35.0)159 (24.2)0.293
Biliary8 (40.0)273 (41.6)>0.999
HTG046 (7.0)0.388
Death9 (45.0)13 (2.0)<0.001

Data are presented as number (%) or mean±SD..

AP, acute pancreatitis; BMI, body mass index; BUN, blood urea nitrogen; HTG hypertriglyceridemia..



2. Etiology

Imaging was performed at the discretion of the clinicians. During initial admission, computed tomography, EUS, and magnetic resonance imaging were performed on 95.4% (645/676), 26.3% (178/676), and 17.5% (118/676) of all patients, respectively. The most common etiologies of AP identified during the first hospitalization were cholelithiasis (41.6%, 281/676), alcohol (24.6%, 166/676), and HTG (6.8%, 46/676). Other causes included malignant disease, mucinous cysts, and drug-induced AP in 2.7% (18/676), 2.1% (14/676), and 1.8% (12/676) of patients, respectively. During the first hospitalization, 16.4% (111/676) of patients were discharged with unexplained AP (presumptive IAP). ABP was more prevalent in older age groups, while HTG-AP was more prevalent in younger age groups (Fig. 3).

Figure 3. Age distribution of the patients according to the etiology of acute pancreatitis.

The etiology of AP varied between males and females. In males and females, alcohol and gallstones were the most frequent causes (37.6% [146/388] and 54.2% [156/288], respectively). The severity of AP also differed by sex. In males, the frequencies of mild, moderate, and severe AP were 46.6% (181/388), 50.0% (194/388), and 3.4% (13/388), respectively; the rates for females were 60.4% (174/288), 37.2% (107/288), and 2.4% (7/288), respectively; and the proportion of females with mild AP was higher than that of males (p=0.002). However, when analyzing severity according to etiology, the proportion of severe AP cases was higher among acute alcoholic pancreatitis patients compared to those with AP of other etiologies (4.2% vs 2.5%, p<0.001), and the proportion of mild AP was higher among ABP patients compared to those with AP of other etiologies (59.4% vs 47.6%, p=0.009). Considering that the identified disparity is exclusively derived from univariate analysis, and multivariate analysis has not been undertaken, the potential association between gender and severity remains ambiguous.

3. Initial treatments

After excluding 26 patients for whom the volume of crystalloid fluid administered during the first 24 hours was not recorded, 86.8% (564/650) of the remaining patients received 2 to 4 L of fluid during the first 24 hours of hospitalization and 13.2% (86/650) received ≥4 L. The mortality rate was significantly higher in patients who received ≥4 L of fluid (9.3% vs 2.1%, p=0.002), even when patients with severe AP were excluded (1.3% vs 5.0%, p=0.040). However, deriving a precise conclusion from this dataset poses a challenge because the incidence of severe AP was significantly higher among patients who received ≥4 L of fluid than among those who received <4 L (7.0% vs 2.5%, respectively; p=0.037). Interestingly, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome had received <4 L per day during the initial 24 hours of admission (Table 3).

Table 3 . Characteristics of Patients: Initial Aggressive Hydration (>4 L/day) versus Non-Aggressive Hydration (<4 L/day).

CharacteristicAggressive (>4 L/day)Non-aggressive (<4 L/day)p-value
Male sex57 (66.3)315 (55.9)0.079
Age, yr57.7±16.858.7±17.90.644
Height, cm165.1±9.8163.9±9.90.275
Weight, kg67.3±14.666.8±28.90.864
BMI, kg/m224.6±4.524.6±9.30.968
BMI >30 kg/m29 (11.3)53 (9.9)0.842
Current smoker12 (15.6)58 (11.2)0.195
History
Diabetes mellitus28 (32.6)125 (22.2)0.041
Dyslipidemia12 (14.0)87 (15.4)0.752
Systemic inflammatory response35 (40.7)154 (27.3)0.015
Severe AP6 (7.0)14 (2.5)0.037
Initial laboratory findings
Hemoglobin, g/dL13.7±2.213.7±2.20.934
Hematocrit, %40.2±5.840.3±6.10.820
White blood cell, ×103/μL12.8±5.811.6±5.10.056
Amylase, U/L910.4±888.7859.1±947.10.637
Lipase, U/L2,343±2,6951,977±2,4570.208
BUN, mg/dL20.8±14.917.2±12.10.012
Creatinine, mg/dL1.1±0.61.1±1.30.899
Etiology
Alcohol27 (31.4)134 (23.8)0.140
Biliary28 (32.6)243 (43.1)0.078
HTG8 (9.3)36 (6.4)0.353
Death8 (9.3)12 (2.1)0.002

Data are presented as number (%) or mean±SD..

BMI, body mass index; AP, acute pancreatitis; BUN, blood urea nitrogen; HTG hypertriglyceridemia..



Empirical antibiotics were started within 48 hours of hospitalization in 72.9% (493/676) of all patients. Among the patients who did not receive antibiotics within the first 48 hours, 59.8% (110/184), 39.7% (73/184), and 0.5% (1/184) had mild, moderate, and severe AP, respectively. Among patients on antibiotics, 49.8% (245/492), 46.3% (228/492), and 3.9% (19/492) had mild, moderate, and severe AP, respectively. Antibiotics were prescribed mainly to treat cholecystitis and cholangitis (33.3%, 164/493). However, they were also prescribed for shock (4.3%, 21/493), fever (39.6%, 195/493), infected necrosis (0.2%, 1/493), other types of infection (1.6%, 8/493), and other reasons including prophylaxis (21.0%, 104/493).

4. Convalescent treatment

Nutrition was resumed after a mean fasting duration of 2.9±2.7 days, and 94.2% of patients (637/676) were started on an oral diet. Nutrients were delivered via a nasogastric tube in 0.7% of patients (5/676); no nasojejunal tube was employed. In 48.1% of patients (325/676), nutrition was gradually increased starting with sips of water, while in 3.1% the initial dietary recommencement (21/676) was solid food.

During hospitalization, proton pump inhibitors were prescribed for 57.1% of the patients (386/676), including 5.6% (23/386) because of bleeding after endoscopy, 4.9% (19/386) because of gastrointestinal ulcers, 2.6% (10/386) because of gastroesophageal reflux disease, and 84.7% (327/386) for no recorded reason.

Of the 281 patients diagnosed with ABP, 23.8% (67/281) underwent cholecystectomy during their initial hospitalization. Among patients with ABP, 59.4% (167/281) had mild AP, 37.7% (106/281) had moderately severe AP, and 2.8% (8/281) had severe AP. Specifically, only 21.6% (36/167) of those with mild ABP underwent cholecystectomy during their initial hospitalization. Among the 214 patients diagnosed with ABP who did not undergo surgery, 61.2% (131/214) presented with mild AP. Reasons for not undergoing surgery included patient refusal in 37.4% (80/214), severe AP or local complications in 10.3% (22/214), advanced age and/or high-risk comorbidities in 17.8% (38/214), and non-medical reasons such as the surgeon’s opinion or a delay in surgical scheduling in 19.6% (42/214). In total, 21.0% of all patients (142/676) were lost to outpatient follow-up. During follow-up, AP recurrence was confirmed in 17.8% of patients (95/534). Of the patients who developed relapse, 44.2% (42/95) had acute alcoholic pancreatitis and 17.9% (17/95) had ABP. Of the initial 131 patients with mild ABP who did not undergo cholecystectomy, 30 patients were lost to follow-up and 9.9% of the remaining patients (10/101) developed recurrent ABP. None of the patients with recurrent ABP had undergone cholecystectomy at the time of the initial admission, and they subsequently developed recurrent AP within a mean duration of 686 days (range, 55 to 1,235 days).

DISCUSSION

We investigated the current AP diagnosis and treatment status in Korea by analyzing the largest multicenter dataset available. We have reported the distribution of AP etiologies in the era of high-resolution medical imaging techniques, such as EUS and magnetic resonance cholangiopancreatography. The incidence and mortality rates were reported according to AP severity, and the data suggested a possible relationship between obesity and AP severity. In addition, we tried to bridge the gap between clinical guidelines and real-world practice by identifying real-world treatment trends and reasons for not following guidelines.

The incidence of severe AP in this study (3.0%) is lower than that reported in prior studies. However, in a study based on Korean multicenter data, Lee et al.13 reported the distribution of severity based on the revised Atlanta classification. They found a 3.7% incidence of severe AP, which aligns closely with our own findings. The etiological factors contributing to AP exhibit variations based on global geographical regions. The most frequent causes of AP are gallstones and alcohol abuse in developed countries, and our data are in accordance with this. Retrospective studies conducted in Western countries revealed an equivalent prevalence of alcohol-induced and gallstone-related pancreatitis, with each causative factor contributing to a range of 23% to 36% of cases.14 In another study, dominance of gallstone-related pancreatitis was noted in southern European countries.15 Baig et al.16 identified alcoholism as the predominant cause of AP, followed by biliary stones, and Wang et al.17 similarly found that biliary stones (38%) and alcohol abuse (36%) were the foremost etiological factors in AP. Conversely, Alkareemy et al.18 reported gallstones and idiopathic causes as the most prevalent etiologies. These discrepancies seem to be attributed to regional disparities in alcohol consumption.

In our study, HTG was the third most common cause of AP. Generally, serum triglyceride levels of 500 mg/dL (5.6 mmol/L) are suspected to cause AP, and patients with levels ≥1,000 mg/dL (11.3 mmol/L) are diagnosed with AP.19 However, a major practical difficulty when aiming to identify the etiology of AP is that it is not easy to determine whether HTG simply reflects excessive alcohol consumption or is the cause of AP. Given the retrospective nature of this study, it is possible that the reported HTG frequency was lower than the actual frequency because alcohol may be identified as the cause of AP when clinicians encounter patients who consume it to excess; clinicians may not test for HTG. Some experimental and clinical studies found that HTG-AP was more severe than AP of other etiologies.20,21 However, in the present study, among 46 HTG-AP patients, none had severe AP (mild, n=23; moderate, n=23). Thus, we did not identify a relationship between HTG-AP and AP severity.

Together with HTG, obesity has been suggested to increase AP severity. Obesity is known to exacerbate the systemic inflammatory response and increase mortality.22-25 We found that the proportion of obese patients (BMI >30 kg/m2) was significantly higher among the severe than the mild and moderate AP groups. As the number of obese subjects in Korea is increasing, it is possible that obesity will emerge as a clinically important predictor of AP severity.26 However, according to the 2012 revised Atlanta classification, 20 patients included in this study were classified as having severe AP, and multivariate analysis of risk factors for predicting severe AP was not possible.

Previous studies found that IAP accounted for 16% to 30% of all AP cases.7,8 In this study, the cause of AP during initial admission could not be found in 16.4% of patients. This is lower than the proportions in previous reports, possibly reflecting the use of more recent imaging techniques. EUS sensitively detects ABP, including microlithiasis, and magnetic resonance cholangiopancreatography is comparable to EUS.9,27,28 However, there is no definitive evidence or guidelines supporting the use of any particular imaging modality during the acute phase of AP. Efforts to reduce the frequency of IAP and identify all of the etiologies are still needed because AP can recur and is a risk factor for the development of CP.29

Traditionally, fluid therapy is used to maintain an effective circulating blood volume in patients with AP; rapid fluid therapy has been recommended. It is crucial to achieve an appropriate intravascular blood volume while also avoiding overloading the patient with crystalloid fluid. In this study, 70.0% (14/20) of patients with severe AP and 81.5% (154/189) of patients with systemic inflammatory response syndrome received <4 L per day during the initial 24 hours of admission. Considering that severity assessment can only be reliably conducted after 48 hours of admission, these findings underscore the challenges of estimating severity within the first 24 hours in current clinical practice. However, recent evidence suggests that excessive fluid administration should be avoided. Several randomized controlled trials have revealed an association between excessive fluid administration and multiple organ failure as well as an increased severity of AP.30-33 Practical severity estimation protocols that can be implemented early in the admission process, ideally at the initial presentation, are required to identify patients who require aggressive fluid therapy as a tailored approach.

Because infection is the leading cause of death 1 month after an initial AP attack, empirical prophylactic antibiotics are widely prescribed. In this study, the prescription rate within the first 48 hours was high (72.8%) considering the frequency of ABP and AP infectious complications requiring antibiotics.34 Antibiotics were prescribed within 48 hours of admission mainly to treat cholecystitis and cholangitis, but they were also administered for shock (4.3%), fever (39.6%), infected necrosis (0.2%), other types of infection (1.6%), and other reasons including prophylaxis (21.0%). However, because this study was multicenter in nature, the observed trend is not indicative of an issue attributed to a single medical center; instead, it underscores the necessity for consensus among experts.

Cholecystectomy at the time of initial admission for ABP is recommended by clinical guidelines because it reduces the frequency of recurrent attacks and is economically advantageous.33,35 However, we found that only 23.8% of ABP patients underwent cholecystectomy during the initial admission. This rate is low given the incidence of mild ABP. Notably, 57.4% of ABP patients did not undergo cholecystectomy because of refusal or non-medical reasons. Because 17.9% of patients who experienced AP recurrence during follow-up were ABP patients who did not undergo cholecystectomy at the time of the first attack, practical efforts such as proper patient education are needed to emphasize that cholecystectomy reduces the incidence of recurrent AP. Additionally, this study involved patients who had visited tertiary hospitals in Korea. The burden of major surgeries for malignancies other than cholecystectomy tends to be higher in tertiary hospitals. Consequently, the rate of patients who were unable to undergo surgery at the time of admission because of surgical scheduling reached 19.6% in this study. To reduce this rate, changes in the domestic healthcare system are warranted.

This study was performed to evaluate the current clinical status of AP in Korea and thus support development of Korean AP guidelines. However, despite utilizing the largest multicenter dataset in Korea to date, the retrospective nature of the study introduced the possibility of selection bias. A multivariate analysis of risk factors for severe AP or mortality was not performed because of the risk of overfitting in the multivariate calibration process. The study collected limited data, thereby impeding assessment of causality in the relationship between treatment interventions and clinical outcomes.

In conclusion, our study constitutes a comprehensive report on the current status of AP in Korea, including the distribution of the etiologies and the severity, mortality, and management, based on detailed clinical information obtained via a retrospective multicenter survey. Our study revealed notable differences in AP severity depending on the etiology, with obesity (BMI >30 kg/m2) serving as a potential risk and predictive factor for severe AP. Nevertheless, the cause of AP was unknown in 16.4% of patients, highlighting the need for long-term prospective studies and practical measures to reduce the incidence of IAP. Moreover, it is critical to address the discrepancies between clinical guidelines and actual clinical practices employed for managing AP.

ACKNOWLEDGEMENTS

This research was supported by a 2020 grant from the Korean Pancreatobiliary Association (KPBA).

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

AUTHOR CONTRIBUTIONS

Study concept and design: E.J.K., S.H.L., M.K.J. Data acquisition: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Data analysis and interpretation: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Drafting of the manuscript: E.J.K. Critical revision of the manuscript for important intellectual content: D.K.J., J.H.J., J.M.L., J.W.C., S.Y.H., Y.H.C., S.H.K., J.M.P., K.H.P. Statistical analysis: E.J.K. Obtained funding: E.J.K. Study supervision: S.H.L., M.K.J. Approval of final manuscript: all authors.

Fig 1.

Figure 1.Map showing the locations of the 12 Korean institutions participating in this retrospective multicenter study.
Gut and Liver 2024; :

Fig 2.

Figure 2.Age distribution of the patients.
Gut and Liver 2024; :

Fig 3.

Figure 3.Age distribution of the patients according to the etiology of acute pancreatitis.
Gut and Liver 2024; :

Table 1 Baseline Patient Characteristics

CharacteristicAcute pancreatitis (n=676)
Male sex388 (57.4)
Age, yr58.6±17.7
Height, cm164.0±9.8
Weight, kg66.8±27.4
Body mass index, kg/m224.7±8.8
Current smoker123 (18.2)
History
Diabetes mellitus159 (23.5)
Dyslipidemia101 (14.9)
Acute pancreatitis0
Chronic pancreatitis0
Systemic inflammatory response197 (29.1)
Severity, Atlanta classification
Mild355 (52.5)
Moderate301 (44.5)
Severe20 (3.0)
Initial laboratory findings
Hemoglobin, g/dL13.7±2.2
Hematocrit, %40.3±6.1
White blood cell, ×103/μL11.8±5.2
Amylase, U/L866.3±938.8
Lipase, U/L2,024±2,489
Hospitalization, day8.5±9.1
Death22 (3.3)

Data are presented as number (%) or mean±SD.


Table 2 Characteristics of Non-Severe and Severe AP Patients

CharacteristicSevere APNon-severe APp-value
Male sex13 (65.0)375 (57.2)0.505
Age, yr64.6±17.458.4±17.70.123
Height, cm164.1±10.5164.0±9.80.972
Weight, kg68.6±15.166.8±27.70.783
BMI, kg/m225.5±5.124.6±8.90.671
BMI >30 kg/m25 (27.8)59 (9.4)0.026
Current smoker5 (26.3)67 (11.1)0.106
History
Diabetes mellitus6 (30.0)153 (23.3)0.592
Dyslipidemia2 (10.0)99 (15.1)0.753
Systemic inflammatory response16 (80.0)181 (27.6)<0.001
Initial laboratory findings
Hemoglobin, g/dL12.7±2.013.7±2.20.044
Hematocrit, %37.7±6.740.3±6.10.059
White blood cell, ×103/μL14.2±6.311.7±5.10.031
Amylase, U/L984.7±908.6862.7±940.10.284
Lipase, U/L2,088±1,5642,022±2,5130.908
BUN, mg/dL40.1±23.817.0±11.4<0.001
Creatinine, mg/dL3.3±2.81.0±1.10.002
Etiology
Alcohol7 (35.0)159 (24.2)0.293
Biliary8 (40.0)273 (41.6)>0.999
HTG046 (7.0)0.388
Death9 (45.0)13 (2.0)<0.001

Data are presented as number (%) or mean±SD.

AP, acute pancreatitis; BMI, body mass index; BUN, blood urea nitrogen; HTG hypertriglyceridemia.


Table 3 Characteristics of Patients: Initial Aggressive Hydration (>4 L/day) versus Non-Aggressive Hydration (<4 L/day)

CharacteristicAggressive (>4 L/day)Non-aggressive (<4 L/day)p-value
Male sex57 (66.3)315 (55.9)0.079
Age, yr57.7±16.858.7±17.90.644
Height, cm165.1±9.8163.9±9.90.275
Weight, kg67.3±14.666.8±28.90.864
BMI, kg/m224.6±4.524.6±9.30.968
BMI >30 kg/m29 (11.3)53 (9.9)0.842
Current smoker12 (15.6)58 (11.2)0.195
History
Diabetes mellitus28 (32.6)125 (22.2)0.041
Dyslipidemia12 (14.0)87 (15.4)0.752
Systemic inflammatory response35 (40.7)154 (27.3)0.015
Severe AP6 (7.0)14 (2.5)0.037
Initial laboratory findings
Hemoglobin, g/dL13.7±2.213.7±2.20.934
Hematocrit, %40.2±5.840.3±6.10.820
White blood cell, ×103/μL12.8±5.811.6±5.10.056
Amylase, U/L910.4±888.7859.1±947.10.637
Lipase, U/L2,343±2,6951,977±2,4570.208
BUN, mg/dL20.8±14.917.2±12.10.012
Creatinine, mg/dL1.1±0.61.1±1.30.899
Etiology
Alcohol27 (31.4)134 (23.8)0.140
Biliary28 (32.6)243 (43.1)0.078
HTG8 (9.3)36 (6.4)0.353
Death8 (9.3)12 (2.1)0.002

Data are presented as number (%) or mean±SD.

BMI, body mass index; AP, acute pancreatitis; BUN, blood urea nitrogen; HTG hypertriglyceridemia.


References

  1. Peery AF, Crockett SD, Murphy CC, et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: update 2021. Gastroenterology 2022;162:621-644.
    Pubmed KoreaMed CrossRef
  2. Iannuzzi JP, King JA, Leong JH, et al. Global incidence of acute pancreatitis is increasing over time: a systematic review and meta-analysis. Gastroenterology 2022;162:122-134.
    Pubmed CrossRef
  3. Kim CD. Current status of acute pancreatitis in Korea. Korean J Gastroenterol 2003;42:1-11.
  4. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med 2016;375:1972-1981.
    Pubmed CrossRef
  5. Das SL, Singh PP, Phillips AR, Murphy R, Windsor JA, Petrov MS. Newly diagnosed diabetes mellitus after acute pancreatitis: a systematic review and meta-analysis. Gut 2014;63:818-831.
    Pubmed CrossRef
  6. Hollemans RA, Hallensleben ND, Mager DJ, et al. Pancreatic exocrine insufficiency following acute pancreatitis: systematic review and study level meta-analysis. Pancreatology 2018;18:253-262.
    Pubmed CrossRef
  7. Párniczky A, Kui B, Szentesi A, et al. Prospective, multicentre, nationwide clinical data from 600 cases of acute pancreatitis. PLoS One 2016;11:e0165309.
    Pubmed KoreaMed CrossRef
  8. Fonseca Sepúlveda EV, Guerrero-Lozano R. Acute pancreatitis and recurrent acute pancreatitis: an exploration of clinical and etiologic factors and outcomes. J Pediatr (Rio J) 2019;95:713-719.
    Pubmed CrossRef
  9. Wan J, Ouyang Y, Yu C, Yang X, Xia L, Lu N. Comparison of EUS with MRCP in idiopathic acute pancreatitis: a systematic review and meta-analysis. Gastrointest Endosc 2018;87:1180-1188.
    Pubmed CrossRef
  10. Pereira R, Eslick G, Cox M. Endoscopic ultrasound for routine assessment in idiopathic acute pancreatitis. J Gastrointest Surg 2019;23:1694-1700.
    Pubmed CrossRef
  11. Choe JW, Lee SH, Cheon YK, Lee HS, Choi M. Revised Clinical Practice Guideline of Korean Pancreatobiliary Association for Acute Pancreatitis: purpose and process of guidelines. Korean J Pancreas Biliary Tract 2022;27:1-5.
    CrossRef
  12. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-111.
    Pubmed CrossRef
  13. Lee HC, Kim HH, Han J, et al. Revised Atlanta classification of acute pancreatitis can predict clinical outcome better: a retrospective, multicenter study. Korean J Pancreas Biliary Tract 2015;20:64-70.
    CrossRef
  14. O'Farrell A, Allwright S, Toomey D, Bedford D, Conlon K. Hospital admission for acute pancreatitis in the Irish population, 1997 2004: could the increase be due to an increase in alcohol-related pancreatitis?. J Public Health (Oxf) 2007;29:398-404.
    Pubmed CrossRef
  15. Gullo L, Migliori M, Oláh A, et al. Acute pancreatitis in five European countries: etiology and mortality. Pancreas 2002;24:223-227.
    Pubmed CrossRef
  16. Baig SJ, Rahed A, Sen S. A prospective study of the aetiology, severity and outcome of acute pancreatitis in Eastern India. Trop Gastroenterol 2008;29:20-22.
  17. Wang X, Xu Y, Qiao Y, et al. An evidence-based proposal for predicting organ failure in severe acute pancreatitis. Pancreas 2013;42:1255-1261.
    Pubmed CrossRef
  18. Alkareemy EA, Ahmed LA, El-Masry MA, Habib HA, Mustafa MH. Etiology, clinical characteristics, and outcomes of acute pancreatitis in patients at Assiut University Hospital. Egypt J Intern Med 2020;32:24.
    CrossRef
  19. Scherer J, Singh VP, Pitchumoni CS, Yadav D. Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol 2014;48:195-203.
    Pubmed KoreaMed CrossRef
  20. Baranyai T, Terzin V, Vajda A, Wittmann T, Czakó L. Acute pancreatitis caused by hypertriglyceridemia. Orv Hetil 2010;151:1869-1874.
    Pubmed CrossRef
  21. Kim TI, Jeong HT, Song JE, Kim HG, Han J. Differences in clinical features between hypertriglyceridemia-induced acute pancreatitis and other etiologies of acute pancreatitis. Korean J Pancreas Biliary Tract 2022;27:97-105.
    CrossRef
  22. Premkumar R, Phillips AR, Petrov MS, Windsor JA. The clinical relevance of obesity in acute pancreatitis: targeted systematic reviews. Pancreatology 2015;15:25-33.
    Pubmed CrossRef
  23. Martínez J, Sánchez-Payá J, Palazón JM, Suazo-Barahona J, Robles-Díaz G, Pérez-Mateo M. Is obesity a risk factor in acute pancreatitis? A meta-analysis. Pancreatology 2004;4:42-48.
    Pubmed CrossRef
  24. Porter KA, Banks PA. Obesity as a predictor of severity in acute pancreatitis. Int J Pancreatol 1991;10:247-252.
    Pubmed CrossRef
  25. Khatua B, El-Kurdi B, Singh VP. Obesity and pancreatitis. Curr Opin Gastroenterol 2017;33:374-382.
    Pubmed KoreaMed CrossRef
  26. Yang YS, Han BD, Han K, Jung JH, Son JW; Taskforce Team of the Obesity Fact Sheet of the Korean Society for the Study of Obesity. Obesity fact sheet in Korea, 2021: trends in obesity prevalence and obesity-related comorbidity incidence stratified by age from 2009 to 2019. J Obes Metab Syndr 2022;31:169-177.
    Pubmed KoreaMed CrossRef
  27. Hallensleben ND, Umans DS, Bouwense SA, et al. The diagnostic work-up and outcomes of 'presumed' idiopathic acute pancreatitis: a post-hoc analysis of a multicentre observational cohort. United European Gastroenterol J 2020;8:340-350.
    Pubmed KoreaMed CrossRef
  28. Del Vecchio Blanco G, Gesuale C, Varanese M, Monteleone G, Paoluzi OA. Idiopathic acute pancreatitis: a review on etiology and diagnostic work-up. Clin J Gastroenterol 2019;12:511-524.
    Pubmed CrossRef
  29. Machicado JD, Yadav D. Epidemiology of recurrent acute and chronic pancreatitis: similarities and differences. Dig Dis Sci 2017;62:1683-1691.
    Pubmed KoreaMed CrossRef
  30. de-Madaria E, Soler-Sala G, Sánchez-Payá J, et al. Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort study. Am J Gastroenterol 2011;106:1843-1850.
    Pubmed CrossRef
  31. Mao EQ, Fei J, Peng YB, Huang J, Tang YQ, Zhang SD. Rapid hemodilution is associated with increased sepsis and mortality among patients with severe acute pancreatitis. Chin Med J (Engl) 2010;123:1639-1644.
    Pubmed CrossRef
  32. de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or moderate fluid resuscitation in acute pancreatitis. N Engl J Med 2022;387:989-1000.
    Pubmed CrossRef
  33. Lee SH, Choe JW, Cheon YK, et al. Revised Clinical Practice Guidelines of the Korean Pancreatobiliary Association for Acute Pancreatitis. Gut Liver 2023;17:34-48.
    Pubmed KoreaMed CrossRef
  34. Párniczky A, Lantos T, Tóth EM, et al. Antibiotic therapy in acute pancreatitis: from global overuse to evidence based recommendations. Pancreatology 2019;19:488-499.
    Pubmed CrossRef
  35. da Costa DW, Bouwense SA, Schepers NJ, et al. Same-admission versus interval cholecystectomy for mild gallstone pancreatitis (PONCHO): a multicentre randomised controlled trial. Lancet 2015;386:1261-1268.
    Pubmed CrossRef
Gut and Liver

Vol.18 No.3
May, 2024

pISSN 1976-2283
eISSN 2005-1212

qrcode
qrcode

Share this article on :

  • line

Popular Keywords

Gut and LiverQR code Download
qr-code

Editorial Office