Chronic Pancreatitis — Pain, Ducts and Decisions: ESWL First-Line, DPPHR Doctrine, Bone and Cancer Watch

Definition and framing — a fibro-inflammatory syndrome with a pain-first doctrine

Chronic pancreatitis is a pathological fibro-inflammatory syndrome of the pancreas arising in people with genetic, environmental or other risk factors who mount persistent pathological responses to parenchymal injury — toxic, metabolic, idiopathic, genetic, autoimmune or obstructive triggers converging on acinar injury, duct dysfunction, persistent inflammation and neuro-immune crosstalk.^[1] The damage is progressive and irreversible: ongoing inflammation replaces endocrine and exocrine parenchyma with atrophy and fibrosis, leaving the functional triad of recurrent or constant abdominal pain, diabetes mellitus and maldigestion.^[1] Pain is the commonest symptom and carries the major quality-of-life burden — which is why chronic pain is also the most frequent indication for surgery, and why every drainage, endoscopic and resection step below exists to relieve obstructed-duct pain or a named complication rather than to reverse fibrosis.^[43][44] The single reference spine is the United European Gastroenterology evidence-based guideline, whose GRADEd recommendations span aetiology, imaging diagnosis, exocrine-insufficiency diagnosis, surgical, medical and endoscopic therapy, pseudocysts, pain, nutrition and malnutrition, diabetes, natural course and quality of life.^[16]

Epidemiology — Japan counts, American beds, and a malignancy tail

Japan's 2021 nationwide survey counted 73,590 definite or probable cases — prevalence 58.6 per 100,000, up 30% since 2016 — with 17,490 new diagnoses each year (13.9 per 100,000).^[2] The population is older (mean 64.4 years, diagnosis at 58.7), overwhelmingly male (4.15 to 1), alcohol-led (69.6% with idiopathic disease next at 24.3%), and functionally failed: diabetes in 45.8% and exocrine insufficiency in 36.6% — with malignancy already identified in 18.0%, including 89 pancreatic cancers.^[2] The American inpatient picture concurs on burden: 15,732 chronic-pancreatitis hospitalizations across 2016-2022 (mean age 49.9, 52.8% male), each averaging 4.5 days and $48,068 in charges, even as adjusted hospitalization odds fell about 8% per year.^[3] Board-ready inference: the examiner's long-term population is aging, alcohol-driven, diabetic, exocrine-failed — and carries a one-in-five malignancy tail that justifies both metabolic follow-up and cancer vigilance.^[2]

Aetiology and progression — the AP-to-CP ladder and the cessation lever

A third of acute pancreatitis recurs and one in seven marches to chronic disease: across 501 patients followed 60 months, 32.7% developed recurrent acute pancreatitis and 14.2% progressed to chronic pancreatitis.^[4] Recurrence is driven by smoking (HR 4.09) and organ failure persisting beyond 48 hours (HR 3.52); progression to chronic disease is driven by alcohol (HR 8.79), age over 60 (HR 5.29), smoking (HR 2.50), CT severity index (HR 1.22) and above all recurrence itself (HR 70.69) — with three or more recurrences in alcohol-related disease carrying HR 4.18.^[4] Cessation is the examinable intervention: in 870 patients, former drinkers set against lifetime-history drinkers showed exocrine insufficiency 29% against 59%, pseudocysts 33% against 49%, relapse-free status 37% against 5%, and less abdominal pain — with no dose-response between alcohol quantity and severity, so the advice is abstinence not moderation.^[5] Nicotine matters independently: 29 pack-years is the threshold for early chronic pancreatitis, cumulative smoking tracks severity and pseudocysts, and both alcohol and nicotine abuse raise the need for surgery (OR 1.8 each) — even though the measurable benefit of nicotine cessation alone is less pronounced than that of alcohol cessation.^[5]

Genetics — four genes, earlier failure, PRSS1 hereditary disease

Sequence the early-onset and idiopathic case: targeted sequencing of 1,061 Han Chinese patients against 1,196 controls found rare pathogenic SPINK1, PRSS1, CTRC or CFTR genotypes in 50.42% of chronic pancreatitis against 5.94% of controls (OR 16.12) — with mutation-positive patients reaching disease onset, stones, diabetes and steatorrhea significantly earlier, and positivity running 57.1% in idiopathic, 39.8% in alcoholic and 32.1% in smoking-associated disease.^[6] The hereditary extreme is PRSS1 disease: across 68 studies, over 70% of PRSS1-associated cases present before age 18, with R122H and N29I the commonest pathogenic variants and adult diabetes running 14-26%.^[7] Note the examined restraint in that same review — pancreatic cancer was rarely documented despite the elevated lifetime risk — so genetics explains early onset and predicts earlier functional failure, and earns testing and counselling, never an operation on a gene and never a quoted cancer count.^[7]

Presentation — three painful roads, one painless trap, and the groove mimic

Most chronic pancreatitis announces itself through acute attacks or pain, but not all: across 548 definite cases, 55.8% had acute pancreatitis preceding the diagnosis, 17.5% concurrent with it, 18.2% presented with pain but no acute attack, and 8.4% were primarily painless — with years of lag from index attack (median 4.67 years) or pain onset (median 5.0 months) to diagnosis.^[8] The painless patient is a profile, not a mystery: older (mean 70.0 years), more often male (66.7%), more often idiopathic (50.0%) — so painless disease in an older man still earns the full chronic-pancreatitis workup rather than reassurance.^[8] The structured mimic is groove (paraduodenal) pancreatitis: across 208 multicentre patients, 90.6% abused alcohol and 90.7% smoked, diagnosis came at median 50.5 years after an 18-month symptomatic run-up, 17.9% were already diabetic — and 3% declared pancreatic cancer a mean 10.3 months later, which is why groove disease gets surveillance even when conservative care (successful in 54.5%, against surgery 27.5% and endoscopy 18%) settles the pain.^[9]

Imaging chain — CT opens, MRI maps, secretin unmasks, EUS sees early

CT is often the most appropriate initial modality — it depicts most morphological change and excludes mimics — but it cannot exclude chronic pancreatitis and cannot diagnose early or mild disease on its own.^[10] When CT is blank, MRI with MRCP is superior and specifically indicated; secretin-stimulated MRCP beats standard MRCP for subtle ductal change and additionally reports exocrine function and ductal compliance; and EUS captures parenchymal and ductal change at the early stage.^[10] The American Gastroenterological Association concurs on sequence: after an unrevealing initial evaluation, EUS is the preferred test for unexplained acute and recurrent pancreatitis, with contrast-MRI and cholangiopancreatography as the complementary or alternative test by local expertise and availability.^[11] State the scoring gap plainly in the viva: no validated radiological severity system exists — a modified Cambridge classification has been borrowed for MRCP, and a validated score built on volume loss, ductal change, calcification and fibrosis remains an unmet need.^[10]

EUS criteria — Rosemont majors and minors with the 5/2 rule

Read EUS in Rosemont language: major criteria are shadowing hyperechoic foci with main-duct calculi, and honeycomb lobularity; minor criteria are cysts, ducts 3.5 mm or wider, irregular duct contour, side branches 1 mm or wider, hyperechoic duct wall, strands, nonshadowing foci, and noncontiguous lobules — settled by 32 endosonographers at greater-than-two-thirds consensus.^[12] Apply the international rule of thumb: five or more criteria strongly suggests chronic pancreatitis, two or fewer strongly refutes it — while admitting the ideal threshold is not firmly established, Rosemont standardizes reporting without proven accuracy gain over conventional scoring, and specificity, observer variability and pre-test probability all limit early-disease reliability.^[13] Add function to morphology when baseline imaging is nondiagnostic: in 90 such patients followed 7 years, 21% evolved to overt disease, and abnormal secretin endoscopic function testing (peak bicarbonate under 80) predicted progression with HR 4.7 — EUS impression plus exocrine testing beats either alone.^[14]

Classification — Cambridge images, M-ANNHEIM manages

Keep two systems straight: Cambridge is the established image-based classification of chronic pancreatitis, while clinical assessment runs on ABC and M-ANNHEIM, which score the leading symptoms — pain, exocrine and endocrine insufficiency.^[15] (The modified Atlanta, determinant-based, Marshall and SOFA systems in that same overview belong to acute pancreatitis — importing them into a chronic-pancreatitis answer is a category error.)^[15]

Exocrine failure — define it, find it with elastase, treat it with enzymes

Pancreatic exocrine insufficiency is a reduction in exocrine secretion below the level that allows normal digestion of nutrients — with pancreatic disease and pancreatic surgery as its main causes.^[17] Find it with faecal elastase: across 519 diabetic patients at five centres, 20.2% had FE-1 under 200 µg/g indicating insufficiency — prevalence exceeding one in five and independent of diabetes duration, which supports screening diabetics for elastase failure and offering enzyme replacement to those found insufficient.^[18] Treat it with pancreatic enzyme replacement — which does double duty, because replacement is associated with improved bone density and vitamin-D levels against no treatment, making maldigestion correction also osteoporosis therapy.^[39]

Type 3c diabetes — the brittle, maldigestive diabetic

Expect diabetes in more than 30% of adults with chronic pancreatitis — driven by insulin deficiency, insulin resistance, decreased pancreatic polypeptide and, in a small subset, possible beta-cell autoimmunity.^[19] Recognize the type-3c signature: combined endocrine and exocrine failure producing insulin deficiency, glycemic variability and maldigestion together — a diagnostic process that stays complex, shares features with type 2 disease, and has no standardized criteria.^[20] Manage accordingly: oral hypoglycemics have limited efficacy once exocrine failure is present, so the frame is insulin with enzyme replacement and nutritional support, individualized — and every chronic-pancreatitis follow-up checks glucose, because nearly every second patient in the Japan survey was diabetic.^[20][2]

Pain ladder — measure multidimensionally, neuromodulate fenced, block briefly, narcotics last

Assess pain the consensus way: generic instruments are valid but chronic pancreatitis demands multidimensional tools that capture phenotypic variability, central sensitization, treatment side effects and placebo effects — alongside quality of life and psychiatric comorbidity — built from 27 PICO questions through 36-expert Delphi review.^[43] Quote pregabalin inside its fence: the entire Cochrane evidence is one 64-patient Pfizer-funded trial of 150-600 mg daily for three weeks — opiate use down 26 mg and pain scores down 12% from baseline at moderate quality, but adverse events up (RR 1.71), overall quality low-to-moderate, short-term outcomes only, and the clinical implication of the short-term decreases explicitly not known.^[21] Quote antioxidants the same way: twelve small high-dropout trials in 585 patients give a visual-analogue reduction of 0.33 points at moderate quality, no significant difference in becoming pain-free (RR 1.73, low quality), and more adverse events with treatment.^[22] Price the celiac block by its decay curve: pooled efficacy 53% across 729 patients, mean relief 81 days — roughly three months — falling to 19% at 12 weeks and 3% at 26 weeks, with adverse events in 8% and the authors calling for a sham-controlled trial.^[23] The year-in-review rule stands behind all three: try pain-modulation adjuncts before starting narcotics — chronic opioid therapy marks strategy failure, not strategy.^[24]

Endotherapy — ESWL first-line, EHL rescue, ASGE stent rules

Start with shock waves for the obstructed head-or-body duct: ESWL with or without ERCP is recommended first-line therapy for painful uncomplicated disease with main-duct obstruction — and 68.1% of 640 patients achieved greater-than-50% Izbicki relief.^[25] Predict who fails before booking: independent predictors of persistent pain are tobacco (OR 4.09), ductal stricture (OR 8.50), alcohol (OR 1.93), duct size (OR 1.22) and symptom duration (OR 1.02) — the smoking patient with a stricture needs multidisciplinary and surgical thinking early.^[25] Rescue residual stones pancreatoscopically: electrohydraulic lithotripsy cleared stones completely or partially in 70.6% of 34 patients with head-or-neck stones over 5 mm — 80% complete and 20% partial over a median two ERPs plus one EHL session — dropping mean Izbicki scores from 62.3 to 27.5 at six months, at the price of seven mild pancreatitis episodes managed conservatively.^[26] Run the ASGE rulebook for the rest: surgical evaluation before endoscopy whenever surgery is feasible and complete ductal clearance is the question; a single largest-caliber plastic stent first for duct strictures; covered metal over multiple plastics for symptomatic benign biliary strictures; endoscopic over surgical therapy for symptomatic pseudocysts; and EUS-guided over percutaneous celiac block.^[27] The international consensus sets the sequence: endoscopic decompression for immediate relief, then surgery if it fails or needs repeated endoscopy; endoscopic extraction for post-ESWL fragments; a plastic stent placed then replaced at two to three months; endoscopic drainage preferred for portal-splenic thrombosis and fistula; endoscopic first for bile-duct obstruction with surgery on failure; and percutaneous endovascular therapy preferred for hemosuccus pancreaticus.^[28]

Operative doctrine — early surgery wins pain, DPPHR preserves, MDT selects

Operate earlier than tradition teaches: pooled across three randomized trials and two retrospective studies (602 patients), early surgery beat endoscopy for pain relief (OR 0.46) with 1.66 fewer procedures — and no difference in complications, endocrine or exocrine failure, or length of stay — though the authors still call for larger randomized trials.^[29] When the head is the problem, resect rather than drain: head-mass symptoms make resection superior to pure drainage, both Whipple and duodenum-preserving head resection deliver durable relief in about 80%, and the less invasive preserving operation is the procedure of choice — with Beger, Frey and Berne techniques comparable on pain, quality of life and function, the simpler Berne modification winning on technique.^[44] The long-term numbers bear that out: across 92 duodenum-preserving resections at nearly five years, morbidity ran 30% overall (20% surgical) for Frey against 40% (31%) for Beger, with 62% against 50% completely pain-free — while diabetes (60% against 57%, one-third de novo) and exocrine failure (76% against 74%, one-third de novo) landed identically, a tendency to better Frey pain control with equal function.^[30] Against Whipple, honesty is equipoise: five randomized trials (269 patients, 135 preserving against 134 Whipple) give only a low-quality signal for shorter stay with preservation and no evidence of difference in mortality, adverse events or quality of life — imprecise, with better trials still needed.^[31] So selection is multidisciplinary and individual: surgery is no longer last-resort by default, but the optimal moment remains unknown — anatomy, stricture, smoking status and fitness choose the operation in conference, not the surgeon's habit.^[32][24]

Local complications — bile, duodenum, veins, cysts, blood

Count biliary and duodenal involvement by setting: among hospitalized pancreatitis patients, biliary stricture runs about 6% and duodenal obstruction 1.2% — but among patients reaching operation for chronic pancreatitis, 35% carry a biliary stricture and 12% a duodenal obstruction.^[33] The bedside marker is a twofold alkaline-phosphatase rise flagging possible duct stenosis; the ERCP signature is a long smoothly tapered intrapancreatic stricture; and the stakes are biliary cirrhosis and cholangitis at about 10% each.^[33] Add the vascular list: superior mesenteric, portal and splenic vein thrombosis join pseudocysts, bile-duct stricturing and duodenal narrowing as late structural features — with endoscopic drainage the preferred route for portal-splenic thrombosis and fistula.^[1][28] Drain pseudocysts endoscopically by default: with lumen-apposing metal stents, EUS-guided drainage is the standard approach, and the eight-centre Taiwan cohort reports 100% technical and 96.97% clinical success in 33 patients with one self-limited bleed and no mortality.^[34][35] Mind the disconnected-duct trap: recurrence runs 71.43% with disconnected-duct syndrome against 38.46% without — and exchanging metal for transmural double-pigtail plastic lowers recurrence — while the scoping review admits endoscopic superiority over laparoscopy as the index intervention is unproven and specific pseudocyst recommendations are lacking.^[35][36] The consensus tie-breakers close the section: symptomatic or complicated pseudocysts earn intervention; bile-duct obstruction goes endoscopic first with surgery on failure or repetition; duodenal stenosis goes surgical; hemosuccus pancreaticus goes percutaneous endovascular.^[28]

Cancer watch, bone watch, and the examined limits

Watch for cancer beyond the pancreas: across 678 Nottingham residents followed a median 7.3 years, standardized incidence ratios ran 12.4 for upper respiratory tract, 10.8 pancreatic, 8.8 liver, 5.6 lung, 4.8 renal tract, 4.8 oesophageal and 2.5 colorectal cancers — chronic pancreatitis as a high-risk malignancy state that hypothesizes, not yet proves, the case for risk-based surveillance.^[37] Watch the skeleton from the first visit: in P-BONE's 211 patients, vitamin D was deficient in 56% and vitamin K in 32%, osteopenia touched 42% and osteoporosis 22% — driven by female sex (OR 2.78), advancing age (OR 1.07 per year) with body mass protective (OR 0.84), and, in men, vitamin-K deficiency alone (OR 4.23).^[38] The screening frame is set: bone disease affects roughly two-thirds of chronic-pancreatitis patients, so screen early, correct maldigestion with enzyme replacement, and supplement fat-soluble vitamins — with ESPEN adding that every patient counts as malnutrition-at-risk and that osteoporosis with fracture risk deserves acknowledged prevention.^[39][40] Add sarcopenia to the nutrition review: prevalence runs 20-70%, including substantial numbers at normal or elevated body mass — so the well-padded patient is not the well-nourished patient.^[41] State the examined limits and stop: no validated radiological severity score exists; type-3c diabetes has no standardized criteria; pancreatic cancer stays rarely documented even in PRSS1 cohorts despite elevated lifetime risk; and this topic makes no claim beyond its kept abstracts.^{[10][20][7][42]}

Revision summary

Chronic pancreatitis is a fibro-inflammatory syndrome whose triad is pain, diabetes and maldigestion — a third of acute cases recur and one in seven becomes chronic, with alcohol (HR 8.79) and smoking driving progression and cessation cutting insufficiency, cysts and relapse.^[1][4][5] Four genes explain early onset (OR 16.12, idiopathic positivity 57.1%) with PRSS1 disease presenting before 18 in over 70%; phenotypes split 55.8% post-attack, 18.2% painful-only and 8.4% painless, with groove disease mimicking cancer closely enough to earn surveillance.^[6][7][8][9] Image CT first but never stop at a clean CT — MRI with secretin-MRCP then EUS, read in Rosemont with the 5-suggests/2-refutes rule, classified Cambridge for pictures and M-ANNHEIM for management.^{[10][12][13][15]} Exocrine failure is FE-1 under 200 (one in five diabetics) treated with enzymes; type-3c diabetes passes 30% and defeats oral agents; pain is measured multidimensionally with pregabalin, antioxidants and celiac block all fenced and narcotics last.^{[18][19][20][21][22][23][24]} ESWL leads for obstructed-duct pain (68.1% relief, smokers with strictures fail most), EHL rescues stones, ASGE sets stent rules; early surgery beats endoscopy for pain (OR 0.46) with duodenum-preserving resection the choice (80% relief, one-third de novo metabolic cost) and Whipple equivalence honestly stated.^{[25][26][27][29][44][30][31]} Biliary stricture (6% admitted, 35% operative) and duodenal obstruction (1.2%, 12%) join vein thrombosis and pseudocysts — drained endoscopically by LAMS standard with the disconnected-duct trap priced — while cancer SIRs peak at 10.8 pancreatic within a multi-organ excess, bone disease touches two-thirds, and cessation plus enzymes plus surveillance carry the long game.^{[33][34][35][37][38][5]}

morbidity 30%/20% Frey vs 40%/31% Beger; pain-free 62% vs 50%; diabetes 60% vs 57% (de novo 34% vs 17%); exocrine failure 76% vs 74% (de novo ~one-third each) — a tendency to better pain control with Frey, identical function (PMID 20033344).^[30]

References44ShowHide

1. [1]Kleeff J, Whitcomb DC, Shimosegawa T, et al. Chronic pancreatitis. Nat Rev Dis Primers, 2017.PMID 28880010
2. [2]Masamune A, Matsumoto R, Takikawa T, et al. The evolving landscape of chronic pancreatitis in Japan: findings from a nationwide epidemiological survey in 2021. J Gastroenterol, 2026.PMID 42726107
3. [3]Boateng S, Nguefang G, Mapouka M, et al. Chronic pancreatitis hospitalizations in the United States, 2016-2022: Trends, disparities, and outcomes. Clin Res Hepatol Gastroenterol, 2026.PMID 42178091
4. [4]Park JY, Bang S, Jeon TJ, et al. Risk of and factors influencing the progression from acute to recurrent acute to chronic pancreatitis. Pancreatology, 2025.PMID 40280847
5. [5]Göltl P, Murillo K, Simsek O, et al. Impact of alcohol and smoking cessation on the course of chronic pancreatitis. Alcohol, 2024.PMID 38013125
6. [6]Zou WB, Tang XY, Zhou DZ, et al. SPINK1, PRSS1, CTRC, and CFTR Genotypes Influence Disease Onset and Clinical Outcomes in Chronic Pancreatitis. Clin Transl Gastroenterol, 2018.PMID 30420730
7. [7]Wu D, Radisic G, De Sousa SMC, et al. The Epidemiology of PRSS1 Hereditary Pancreatitis and Its Clinical Implications: A Systematic Review. Pancreas, 2026.PMID 42132515
8. [8]Yousefli Z, Kassir Z, Faghih M, et al. Clinical Characteristics of Chronic Pancreatitis Patients Presenting With Acute Pancreatitis, Abdominal Pain, or Primary Painless Disease. Pancreas, 2026.PMID 41411514
9. [9]Rizzo GEM, Tacelli M, Crinò SF, et al. Clinical features and evolution of paraduodenal (groove) pancreatitis: A multicenter study. Pancreatology, 2026.PMID 41350195
10. [10]Frøkjær JB, Akisik F, Farooq A, et al. Guidelines for the Diagnostic Cross Sectional Imaging and Severity Scoring of Chronic Pancreatitis. Pancreatology, 2018.PMID 30177434
11. [11]Strand DS, Law RJ, Yang D, et al. AGA Clinical Practice Update on the Endoscopic Approach to Recurrent Acute and Chronic Pancreatitis: Expert Review. Gastroenterology, 2022.PMID 36008176
12. [12]Catalano MF, Sahai A, Levy M, et al. EUS-based criteria for the diagnosis of chronic pancreatitis: the Rosemont classification. Gastrointest Endosc, 2009.PMID 19243769
13. [13]Mel Wilcox C, Gress T, Boermeester M, et al. International consensus guidelines on the role of diagnostic endoscopic ultrasound in the management of chronic pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club. Pancreatology, 2020.PMID 32631791
14. [14]Monachese M, Lee PJ, Harris K, et al. EUS and secretin endoscopic pancreatic function test predict evolution to overt structural changes of chronic pancreatitis in patients with nondiagnostic baseline imaging. Endosc Ultrasound, 2021.PMID 33885007
15. [15]Hoß KF, Attenberger UI [Classification of pancreatitis]. Radiologe, 2021.PMID 33988737
16. [16]Dominguez-Munoz JE, Drewes AM, Lindkvist B, et al. Recommendations from the United European Gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis. Pancreatology, 2018.PMID 30344091
17. [17]Vujasinovic M, Iglesia D, Dominguez-Muñoz JE, et al. Recommendations from the European guidelines for the diagnosis and therapy of pancreatic exocrine insufficiency. Pancreatology, 2025.PMID 40097316
18. [18]Kadaj-Lipka R, Wynimko M, Borowska K, et al. The prevalence of exocrine pancreatic insufficiency in diabetes mellitus - a multicentre study. Prz Gastroenterol, 2026.PMID 42483623
19. [19]Parra Villasmil MG, Bellin MD Risk Factors and Mechanisms for Diabetes in Pancreatitis. Gastroenterol Clin North Am, 2025.PMID 39880526
20. [20]Wang D, Jiao Y Pancreatogenic diabetes: Pathophysiology, diagnosis, and management challenges. World J Gastrointest Surg, 2025.PMID 41357647
21. [21]Gurusamy KS, Lusuku C, Davidson BR Pregabalin for decreasing pancreatic pain in chronic pancreatitis. Cochrane Database Syst Rev, 2016.PMID 26836292
22. [22]Ahmed Ali U, Jens S, Busch OR, et al. Antioxidants for pain in chronic pancreatitis. Cochrane Database Syst Rev, 2014.PMID 25144441
23. [23]Machicado JD, Tanner S, Adoor D, et al. Endoscopic ultrasound-guided celiac plexus block for painful chronic pancreatitis: A systematic review and meta-analysis. Pancreatology, 2025.PMID 40813224
24. [24]Gupte AR, Forsmark CE Chronic pancreatitis. Curr Opin Gastroenterol, 2014.PMID 25032948
25. [25]Gurav N, Jagtap N, Koppoju V, et al. Predictors of persistent pain after extracorporeal shockwave lithotripsy for painful chronic calcific pancreatitis. Endoscopy, 2024.PMID 38267001
26. [26]van der Wiel SE, Stassen PMC, Poley JW, et al. Pancreatoscopy-guided electrohydraulic lithotripsy for the treatment of obstructive pancreatic duct stones: a prospective consecutive case series. Gastrointest Endosc, 2022.PMID 34906545
27. [27]Sheth SG, Machicado JD, Chalhoub JM, et al. American Society for Gastrointestinal Endoscopy guideline on the role of endoscopy in the management of chronic pancreatitis: summary and recommendations. Gastrointest Endosc, 2024.PMID 39115496
28. [28]Kitano M, Gress TM, Garg PK, et al. International consensus guidelines on interventional endoscopy in chronic pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club. Pancreatology, 2020.PMID 32792253
29. [29]Boregowda U, Echavarria J, Umapathy C, et al. Endoscopy versus early surgery for the management of chronic pancreatitis: a systematic review and meta-analysis. Surg Endosc, 2022.PMID 35922602
30. [30]Keck T, Wellner UF, Riediger H, et al. Long-term outcome after 92 duodenum-preserving pancreatic head resections for chronic pancreatitis: comparison of Beger and Frey procedures. J Gastrointest Surg, 2010.PMID 20033344
31. [31]Gurusamy KS, Lusuku C, Halkias C, et al. Duodenum-preserving pancreatic resection versus pancreaticoduodenectomy for chronic pancreatitis. Cochrane Database Syst Rev, 2016.PMID 26837472
32. [32]Udd M, Kylänpää L, Kokkola A The Role of Endoscopic and Surgical Treatment in Chronic Pancreatitis. Scand J Surg, 2020.PMID 32192421
33. [33]Vijungco JD, Prinz RA Management of biliary and duodenal complications of chronic pancreatitis. World J Surg, 2003.PMID 14534824
34. [34]Capurso G, Rizzo GEM, Coluccio C, et al. The i-EUS consensus on the management of pancreatic fluid collections - Part 1. Dig Liver Dis, 2024.PMID 39048418
35. [35]Chung CS, Kuo YT, Chiu YC, et al. Multicenter study of the efficacy and safety of electrocautery-enhanced lumen-apposing metal stents for the internal drainage of pancreatic fluid collections. Sci Rep, 2024.PMID 38443387
36. [36]Thakur M, Dhiman AK Laparoscopic vs Endoscopic Management of Pancreatic Pseudocysts: A Scoping Review. Cureus, 2023.PMID 36909096
37. [37]Quammie S, Rashid A, Munyal R, et al. The expanding cancer landscape in chronic pancreatitis. Cancer Epidemiol, 2026.PMID 41849829
38. [38]Stigliano S, Waldthaler A, Martinez-Moneo E, et al. Vitamins D and K as Factors Associated with Osteopathy in Chronic Pancreatitis: A Prospective Multicentre Study (P-BONE Study). Clin Transl Gastroenterol, 2018.PMID 30323223
39. [39]Barkin JA, Barkin JS Chronic Pancreatitis and Bone Disease. J Clin Densitom, 2020.PMID 31558406
40. [40]Arvanitakis M, Ockenga J, Bezmarevic M, et al. ESPEN practical guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr, 2024.PMID 38169174
41. [41]Bonsdorff A, Oyon D, Klatte D, et al. Sarcopenia and body composition abnormalities in chronic pancreatitis: Pathophysiology, assessment, and clinical impact. Clin Nutr, 2026.PMID 42275988
42. [42]Ramsey ML, Conwell DL, Hart PA Complications of Chronic Pancreatitis. Dig Dis Sci, 2017.PMID 28281169
43. [43]Drewes AM, van Veldhuisen CL, Bellin MD, et al. Assessment of pain associated with chronic pancreatitis: An international consensus guideline. Pancreatology, 2021.PMID 34391675
44. [44]Strobel O, Büchler MW, Werner J [Duodenum-preserving pancreatic head resection: technique according to Beger, technique according to Frey and Berne modifications]. Chirurg, 2009.PMID 18820883