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L'eterogeneità della pancreatite cronica - Gastrolearning®

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Gastrolearning VI lezione
L'eterogeneità della pancreatite cronica - Prof. I. Vantini Università di Verona
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  • And the main but now old concepts were that cronic pancreatitis is (leggi)
  • And the main but now old concepts were that cronic pancreatitis is (leggi)
  • Pathologists told has that there is a particular type of pancreatitis arise from the duodenal wall. In duodenal wall there are islet of pancreas normally. In patients who drank a lot, this islet became inflammed inside the duodenal wall and later may grow and extend toward
  • cresci
  • Pathologists, first of all prof. Kloppel, teach us that in autoimmune pancreatitis the histologic findings are typical for the disease. We can see inflammatory infiltration in to the pancreas, mainly around the ducts, with rupture of the basal membrane and secondary destruction of pancreatic ducts.
  • … . like in this case, presents an enlargement of the pancreatic head, but without any sign of vascular or soft tissue infiltration. This was the first control. Once the diagnosis is suspected, the second examination, ..
  • Felicetti
  • Transcript

    • 1. Università di Verona AOUI di Verona Dipartimento di Istituto del Pancreas Medicina L’eterogeneità della pancreatite cronica Italo Vantini
    • 2. Conoscere una malattia - 1• La conoscenza delle connotazioni di una malattia consente di fornire: – una descrizione utile per l’inquadramento classificativo (nosologico) (che cosa è) • Etiopatogenetica • Clinica • Anatomopatologica • Fisiopatologica – un “nome”’per la sua identificazione nosologica (condivisione di come si chiama)
    • 3. Conoscere una malattia - 2• Una diagnosi – Matching, illness script, exemplars – Percorsi probabilistici – Criteri, strumenti, percorsi, processi• La diagnosi non è “tanto” l’inserimento del paziente in una “casella nosologica, ma un giudizio basato su dati e criteri utili per assumere decisioni operative ai fini della: • Prognosi • Terapia
    • 4. In principio…Sarles H, Sarles JC, Camatte R, Muratore R, Gaini M, Guien C, Pastor J, Le Roy FObservations on 205 confirmed cases of acute Gut 1965; 6: 545-59.
    • 5. Chronic pancreatitisChronic process characterized by inflammatory and fibrotic changes of the pancreas.Irreversible nature of structural changes and progressive functional impairment
    • 6. Chronic pancreatitis  Fibrosis of the pancreas  Damage to the acinar tissuemorphologically  Changes in ductal system • Calcifications
    • 7. Chronic pancreatitis: progressive parenchymal changes Normal pancreas Moderate changes more or less scattered troughout the pancreas Advanced changes (fibrosis)
    • 8. Chronic pancreatitis: pancreatic duct
    • 9. Pancreatic calcification
    • 10. Chronic pancreatitisclinically • Recurrent or persistent pancreatic pain
    • 11. Pain in chronic pancreatitis Clinical pictures Type 1pain recurrent with lasting pain-free intervals Type 2 pain : frequent, persisting, disabling pain PATHOPHYSIOLOGY • Acute inflammation • Ischemia• Increased intraductal and parenchymal pressure • Mechanical compression (e.g. pseudocyst) Pancreatic neural remodelling and neuropathy
    • 12. Chronic pancreatitis • Recurrent or persistent clinically pancreatic pain Changes in ductal system • Fibrosis of the pancreasmorphologically • calcification • Deterioration in functionally pancreatic function (exocrine and endocrine)
    • 13. Frequency of painful relapses/year in 199 patients with chronic pancreatitis (non-operated upon) followed up to 20 years Prevention and treatment percentiles Treatment of 25° early treatment of advanced relapsing exocrine failure late of painful relapses or persisting pain and secondary 50° 5 and complications diabetes 75° 4N. painful relapses in time 3 on sfuncti and dy 2 n 1 Calcificatio 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 25° years since clinical onset Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501. Ammann RW et al. Gastroenterology 1984, 86: 820-8..
    • 14. alcool
    • 15. Alcohol and chronic pancreatitis - relative risk - 16 14 12 10 chronic pancreatitisOR 8 6 cancer without CP 4 2 0 0-40 41-80 81- 240 grams of alcohol/day Durbec J, Sarles H: Digestion 1973 Talamini G. et al Dig Dis Sci 1999
    • 16. painfunction
    • 17. Chronic Pancreatitis (“old concepts”) - 1 a single and distinct entity a well defined epidemiological and clinical pattern  Male/female 4:1; age onset 47 year oldalcoholic in origin (in Western Countries) Differs from Acute Pancreatitis(etiology, clinical outcome,prognosis)  Acute and chronic pancreatitis are two distinct entities
    • 18. Pancreatologia felix
    • 19. Chronic Pancreatitis Alcohol abuse in more recent studies 100 90 80% of patients 70 60 50 40 30 20 10 0 Italy 2009° India 2008* USA 2008^ China 2009" 893 pts 1033 pts 540 pts 2008 pts ° Frulloni L et al, PanCroInfAISP, Dig Liv Dis 2009; 41: 311-317 * Balakrishnan V et al, J Pancreas, 2008; 9: 593-600 ^ Withcomb DC et al, NAPS2, Pancreatol, 2008; 8: 520-531 ” Whang LW et al, Chinese CPSG, Pancreas, 2008; 38:248-54.
    • 20. Smoking and chronic pancreatitis: a meta-analysisAndriulli A, Botteri E, Almasio PL, Vantini I, Uomo G, Maisonneuve P: Smoking as acofactor for causation of chronic pancreatitis. Pancreas 2010; 39: 1205- 1210
    • 21. Smoking and pancreatic calcification Giving-up smoking within 5 years since onset of CP reduces the risk of developing pancreatic calcifications Talamini G et al Pancreas. 2007 ;35:320-6.Talamini G, Bassi C, Falconi M, Sartori N, Vaona B, Bovo P, Benini L, Cavallini G, Pederzoli P, Vantini ISmoking cessation at the clinical onset of chronic pancreatitis and risk of pancreatic calcification.
    • 22. Pancreatic acinar cell damage in response to cigarette smoke components : sensitization to acinar cell injury, that can be worsened by alcohol consumption similar Trypsinogen to but not PSTI experimental acute pancreatitis Cytoplasmicoxidative swellingstress andlipidperossidation Alexander M et al Pancreatology; 2011: 11: 469-74
    • 23. Chronic Pancreatitis (“concepts”) -2 a single and distinct entityalcohol and smoke interact as riskfactorsincreased risk of pancreatic cancer  a single clinical pattern, though evolving in time
    • 24. Epidemiological and clinical features of chronic pancreatitis: the identikit• Males (80%)• 45 year old at the clinical onset• Alcohol abusers (40-60%)• Smokers in (> 80%)• Pancreatic calcification (20% at onset)• Dilation/changes of pancreatic duct system• Painful relapses• Progressive pancreatic failure (exocrine and endocrine)
    • 25. Chronic pancreatis principles of therapy-2• Prevention of relapses – Alcohol withdrawal in an early stage• Reduction in the risk of pancreatic calcifications and of the progression of the disease – Smoking withdrawal• Reduction in the risk of pancreatic cancer (?) – Smoking withdrawal• Treatment of relapses – Treatment of acute flares (starvation, IV fluids, analgesic drugs)• Treatment of disabling and severe pain and/or of complications – Surgery (drainage or resection) (not “untimed”) associated with alcohol withdrawal• Treatment of exocrine failure
    • 26. Pancreatologia triumphans
    • 27. a “new” pancreatitis ? men heavy alcohol drinkers heavy smokers calcification (90%) dilation of the pancreatic duct (80%) aggressive painful pancreatitis, often disabling (> 50%) vomiting, jaundice
    • 28. - pathology: cystic and solid types - Cystic Type (75%) Solid Type (25%)
    • 29. EUS findings Normal cyst Duodenal Wall Thickenedduodenal wall cyst
    • 30. Cystic dystrophy of the duodenal wall The “groove” area Groove C Groove C BD D W PD = duodenum P = papilla of VaterBD = common bile duct W = Wirsung’s ductC = cyst
    • 31. CYSTIC DYSTROPHY OF DUODENAL WALL A bud of dorsal pancreas, associated to the Santorinis duct, entrapped within the duodenal wall during organogenesis
    • 32. Paraduodenal pancreatitis (cystic or solid duodenal dystrophy)  almost all men almost all heavy alcohol abusers  almost all smokers  calcification (90%)  disabling painful relapses  vomiting, jaundice (at onset)
    • 33. Main clinical features in different types of chronic pancreatitisAlcoholicHereditaryParaduod.ObstructivePainlessAIP
    • 34. Alcoholic pancreatitis and paraduodenal pancreatitis (PDP)• PDP pancreatitis shares the same risk factors and similar epidemiological and clinical pattern of alcoholic pancreatitis• Morphologically is a distinc form of CP• PDP clinically behaves a severe clinical form of alcoholic pancreatitis• Though alcohol withdrawal can induce some clinical improvement, more than 50% of the patients are eligible for surgery because of invalidating pain and/or duodenal obstruction• It is probable that old series of patients formerly classified as alcoholic pancreatitis were in fact PDP
    • 35. cysts of the duodenal wall and chronic pancreatitis Dilation of Wirsung Head calcifications D Groove ZoneD = duodenal lumenW=Wirsung’s duct
    • 36. Chronic pancreatitis Classification of Marseille-Rome 1990• Alcoholic pancreatitis• Obstructive pancreatitis• Hereditary and familial pancreatitis• Idiopathic pancreatitis – juvenile – senile (may be painless)• Inflammatory pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
    • 37. Obstruction and chronic pancreatitis• Several experimental data on different animal models show that chronic pancreatitis cannot develop, irrespective of the type of the experimental damage, without an obstruction of the duct system• Periductal inflammation can lead, together with stellate cells activation, to periductal fibrosis that can induce changes in the pancreatic duct system
    • 38. Necrosis-fibrosis mechanism in chronic pancreatitis Kloeppel G. et al. Pancreas, 1993; 8: 659-670
    • 39. Following an acute pancreatitis Chronic pancreatitis can be the consequence of a necrosis-Acute pancreatitis 8 months before fibrosis change, leading to obstruction of pancreatic ductsystem, and then to inflammatory and fibrotic changes. Acute necrotizing pancreatitisan acutelead of can attack to chronic pancreatitis before pancreatitis 6 months
    • 40. Acute pancreatitis: frequency of chronicization (19/88=22%) Lankish PG et al., Am J Gastroenterol, 2009; 104: 2796-2805
    • 41. Acute pancreatitis: frequency of relapses following the first episode (alcoholic vs. non-alcoholic pancreatitis) 40% 32% 15% 10% Lankish PG et al. Am J Gastroenterol, 2009; 104: 2796-2805
    • 42. “obstructive” pancreatitis Factors (different from slow-growing tumors) hampering the pancreatic outflow can trigger a process leading to obstructive pancreatitis A “dysfunction” at the Oddi’s sphincter (SOD) can lead to chronic pancreatitis obstructive Oddi’s sphincter inflammation with altered outflow can “trigger” chronic pancreatitisAn obstacle to the pancreatic outflow can be associated with relapsing pancreatitis without evidence of ductal changes
    • 43. Dilatazione duttale e singola calcificazione ostruente dilatazione duttale Ricorrenze dolorose calcificazione ostruente
    • 44. Obstruction is the most frequentassociated factor in women (46%) DLD 1999; 41. 311-17
    • 45. Main clinical features in different types of chronic pancreatitisAlcoholicHereditaryParaduod.ObstructivePainlessAIP
    • 46. Pain in chronic pancreatitis Clinical pictures Type 1pain recurrent with lasting pain-free intervals Type 2 pain : frequent, persisting, disabling pain PATHOPHYSIOLOGY OF PAIN IN “OBSTRUCTIVE PANCREATITIS” Increased intraductal-parenchymalpressure caused by decreased drainage of pancreatic juice into the duodenum •
    • 47. Uncomplicate chronic pancreatitis - Indication for surgery - The rationale of drainage surgery is a decompression within theductal system and reduction in pain in a substantiaòproprtion of patients
    • 48. Large stone in the ductERCP following sphincterotomy, ESW and fragment extraction
    • 49. Surgery (pancreatojejunostomy) vs. endoscopy (sphincterotomy) in chronic pancreatitisDjuna L Cahen et al NEJM 2007; 356: 676-84Djuna L Cahen et al but in 6/7 evaluable patients submitted to rescue surgery, it was uneffective
    • 50. Who are the main clinical and morphological features of the patients with good results ofdrainage surgery and poor after endotherapy ?• Advanced chronic pancreatitis In advanced chronic pancreatitis• with symptoms and distal Distal obstruction• obstruction, drainage surgery Calcifications (> 90% of the cases) is superior to endoscopic• Severe, recurrent pain therapy• Not too enlarged head of the pancreas
    • 51. Who are the patients with chronic pancreatitis in which the endoscopic therapy seems to be more effective ? • single distal obstruction • single distal stone • short duration of the disease • more aggressive, repeated stenting strategy – Pancreatic sphincterotomy – Stricture dilation – Repeated stenting – Stone removalFarnbacher et al Gastrointest Endosc 2002; 56: 501-59Costamagna G et al Endoscopy 2006; 38: 254-59Dumonceau JM et al ESGE guidelines- Endoscopy 2012, 44. 784-96
    • 52. For treating uncomplicated chronic pancreatitis (aimed at relieving pain) ESGE recommends ESW/ERCP at the first-time interval option. The clinical response should be evaluated at 6-8 weeks. If it is unsatisfactory the case should be discussed in a multidisciplinary team. Surgical options should be considered, in particular in patients with a predicted poor outcome after endosopic therapy (RG B)
    • 53. Candidate parameters for selecting patients for appropriate treatment and timing (a multidimensional approach)• Aethiology, natural history• Duration of the disease (stage)• Clinical features (pain type, complications) and QOL scores• Morphological assessment – Main pancreatic duct and secondary branches changes – Distal stenosis (main duct, Santorini) – “Dominant” duct stricture – Single or multiple obstructions-strictures – Upstream dilation (+/-) – Stone (single, distal, multiple) – Ductal scars (necrosi/fibrosis) However, pain can persist also following – Complications effective treatment of stricture,• Technical aspects and aggressive strategy or it can subside also if the stricture is not disappeared
    • 54. Pain treatment: appropriate patient selection• A proper patient selection is of vital importance in the indication and in the outcome of treatment, in particular case of endoscopic and surgical therapy• A more aggressive endoscopic strategy probably will give better results in properly selected patients• Surgery should be timed and tailored to the clinical features and risk assessment, morphological pictures, and the best as possibile assessment about the presumptive origin of pain. Combination surgery should be considered
    • 55. Chronic pancreatitis: ERCP “Small duct” pancreatitis
    • 56. Langenbecjs Arch Surg 2003; 388: 132-9
    • 57. Frequency of painful relapses/year in 199 patients with chronic pancreatitis (non-operated upon) followed up to 20 years Endoscopy-Surgery percentiles 25° early Endotherapy advanced Medical treatment Medical late Medical treatment treatment 50° 5 75° 4N. painful relapses in time 3 on sfuncti and dy 2 n 1 Calcificatio 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 25° years since clinical onset Scuro LA et al , Am J Gastroenterol 1983; 78: 495-501. Ammann RW et al. Gastroenterology 1984, 86: 820-8..
    • 58. 25 years ago…..• Amman RW et al Gastroenterology 1986 – in chronic pancreatiis early surgery is associated with a poor cinical outcome – the natural history of CP indicates that in almost 2/3 of the patients pain spontaneously subsides in long-term evolution – Commentary (Gastronterology 1986) • “The patient patient and the impatient surgeon”
    • 59. Chronic pancreatitis Classification of Marseille-Rome 1990• Alcoholic pancreatitis• Hereditary and familial pancreatitis• Idiopathic pancreatitis – juvenile – senile (may be painless)• Obstructive pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2• Inflammatory pancreatitis
    • 60. Gene-mutation associated pancreatitis  Cationic Trypsinogen – PRSS14,5  R122H, N29I, A16V, R116C, E79K, R112C, D22G, K23R  Pancreatic Secretory Trypsin Inhibitor (PSTI) – SPINK16,7  N34S, P55S, M1T, L14P, -53C>T, IVS3+2T>C  CFTR gene1-3 F508 (nel 50-70% dei casi), altre mutazioni1 N Engl J Med, 1998: 339; 645-22 N Engl J Med, 1998; 339: 653-83 Eur J Hum Genet, 2003; 11: 543-64 Gut, 2002;50:271-2.5 Gut, 2002; 50:687-926 J Med Genet, 2000; 37:67-97 Gut, 2002; 50:675-81
    • 61. Gene-mutation associated pancreatitis Main features of Hereditary Pancreatitis Hereditary-Familial one or more relatives of the same familial kindred affected, at different or at the same generation,  No other risk factor of pancreatitis (complete work-up) Juvenile onset < 10 years (< 20 years) Recurrent episodes of mild pancreatitis Progression of pancreatic calcifications Slow progression toward pancreatic failure Survival rate comparable to that of the general population
    • 62. Cumulative risk of cancer in patients with Hereditary Pancreatitis (smokers vs. non smokers) smokers non-smokers Lowenfels AB et al JAMA 2001; 286:169-70
    • 63. pancreatite associata a mutazione del CFTR Pancreatite associata a mutazione del gene SPINK 1
    • 64. SPINK1 Chronic pancreatitis associated with gene mutationSPINK1 Bull-eye sign SPINK1 Bull-eye sign non smokersCFTR smokers Graziani R. et al. Abdominal Radiology, 2010; 115: 885-88 Frulloni L, et al. Pancreas. 2008:371-
    • 65. Chronic pancreatitis Classification of Marseille-Rome 1990• Alcoholic pancreatitis• Hereditary and familial pancreatitis• Idiopathic pancreatitis – juvenile – senile (may be painless)• Obstructive pancreatitis• Inflammatory pancreatitis Sarles H, Scand J Gastroenterol, 1989; 24: 641-2
    • 66. CFTR Normale CFTR Normale 86,7% 95,7% CFTR CFTR 1 Mutazione1 Mutazione 5,3% 13,3% Controlli RR = 2,52 RR = 2,52 600 pazienti Pancreatite Cronica Idiopatica 60 pazienti
    • 67. SPINK1 Normale SPINK1 Normale 77% 99,65% SPINK1 Mutato 23% SPINK1 1 Mutazione 0,35%Pancreatite Cronica Controlli 279 pazienti Giovanile 96 pazienti
    • 68. Chronic pancreatitis and gene mutations• Mutation in PRSS1 is present in ¼ of patients with juvenile-type chronic pancreatitis• Up to 30% of idiopathic pancreatitis have a mutation in the CFTR allele vs. 3-5% in the general population, though a single mutation alone cannot trigger pancreatitis• 20-30% of Hereditary Pancreatitis do not have PRSS1 mutation• Mutation in PRSS1 is found in 20% of subjects who do not have any sign of pancreatitis (carriers) Rebours V et al DLD 2012; 44: 8-15
    • 69. Pancreatite associata ad alterazioni geniche Esordio clinico = Pancreatite acuta SI (87%) NO (13%) Età all’esordio p = 0.005 Età all’esordio 28 ± 14 anni 44 ± 18 aaCFTR-S = 30 ± 14 anniCFTR-S = 30 ± 14 anni Clinica all’esordio: Clinica all’esordio:CFTR-D = 20 ± 12 anniCFTR-D = 20 ± 12 anni  Dolore aspecifico (6)  Dolore aspecifico (6)SPINK1 = 24 ± 14 anniSPINK1 = 24 ± 14 anni  Dispepsia (2)  Dispepsia (2) p = 0.027 p = 0.027  Ittero (1)  Ittero (1)  Altra patologia (2)  Altra patologia (2) STORIA NATURALE DELLA PANCREATITE 10 di 11 pazienti 10 di 11 pazienti ASSOCIATA A MUTAZIONI GENICHE = PC all’esordio Giulia De Marchi = PC all’esordio Tesi di Laurea, 2011
    • 70. Long time ago…. “Why should the pancreas be the only human organ not involved by anLudovico Antonio Scuro autoimmune process?” 1924 – 1989
    • 71. Autoimmune pancreatitis• Described by H. Sarles in 1961 yet,• More than 900 papers published (most since ’90s)• Accounts for – 4-6 % of all the patients with chronic pancreatitis referring to a terziary centre and for – about 20-40 % of idiopathic chronic pancreatitis• Its aethiology is still unknown antibodies: CA II, Lactoferrin, SPTI antibodies (against host antigens); genetics: association with haplotype DRB1 0405 DQB1 0401; Polymorfism of Cytotoxic Lymphocyte-associated antigen-4 49A
    • 72. Autoimmune Pancreatitis Main Clinical FeaturesNo drinker and no smoker patientsFrequent association with other autoimmune diseasesAsymptomatic jaundice at onset (particularly in focal type)“Atypical” pancreatitis at onset (particularly in diffuse type)
    • 73. AIP Type 1 (70-85%) AIP Type 2 (15-30%)Pathology Definition Lympho-Plasmacytic Idiopathic Sclerosing Duct-Centric Pancreatitis Pancreatitis (LPSP) (IDCP) IgG4+ (ICH) – GEL– IgG4– (ICH) – GEL+ IgG4 systemic disease Inflammatory Bowel DiseaseClinic Relapses YES Relapses NO Steroids Steroids
    • 74. From Zamboni G et al Type 1Autoimmune Pancreatitis is a chronic pancreatitis LP . periductal inflammation IgG4 positive plasmacells Duct desctruction and narrowing Storiform fibrosis
    • 75. Granulocytic Epithelial Lesion – GEL –Zamboni G et at, Vierchow Arch, 2004; 445: 552-563 Type 2
    • 76. Diffuse AIP Sausage-like Irregular narrowing mild pancreatitisswelling Capsule-like rim
    • 77. Narrowed and irregular duct in autoimmune chronic pancreatitis Associated with a clinical picture
    • 78. Autoimmune pancreatitis Focal and mass forming Early arterial phase FocalMass forming jaundice University of Verona: Dpt. of Radiology
    • 79. Mass forming AIP ry a to d an m The problem is not to confirmhistologically AIP, but to exclude cancer by US or EUS-guided biopsies University of Verona: Dpt. of Radiology
    • 80. Mass-forming AIP: response to steroid therapyCT at admission 15 days after initiation of steroids
    • 81. Pancreatite acuta lieve seguitaReperto da precoce ricorrenza lievedi base e persistenza di moderata elevazione degli enzimi Dopo terapia steroidea01-2009 02-2009
    • 82. ICDC Autoimmune pancreatitis type 1: cardinal diagnostic criteria and levels of reliability Shimosegawa T et al, Pancreas, 2011: 40: 352-358
    • 83. ICDC Autoimmune pancreatitis type 2: cardinal diagnostic criteria and levels of reliability Shimosegawa T et al, Pancreas, 2011: 40: 352-358
    • 84. Tipi di pancreatite autoimmune dopo completo work-up (ICDC)92 Pazienti Tsukasa Ikeura et al 2013, submitted
    • 85. Three types of AIP: overlaps among diagnostic features AIP type 2 AIP type 1 AIP NOS
    • 86. Phil A Hart et al: Long-term outcomes of autoimmune pancreatitis:a multicentre, international analysisGut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361 Type 123 institutions 1064 ICDC 978 10 countries patients criteria Type 2 86 * Type 1 31% Relapse rate (> in IgG4 –related sclerosing cholangitis) Type 2 9% * retreatment with steroids was equally effective
    • 87. Phil A Hart et al: Long-term outcomes of autoimmune pancreatitis:a multicentre, international analysis Gut Online First, published on December 11, 2012 as 10.1136/gutjnl-2012-30361
    • 88. Chronic pancreatitis paraduodenal alcoholic AIPgeneti c obstructive idiopatic painless Eterogeneity and ovelap
    • 89. Classificazioni della pancreatite cronica• Etiologia, clinica e morfologia (nosografica) – Marsiglia 1963 – Cambridge, 1983 – Marsiglia 1984 – Marsiglia-Roma 1988• Per stadio di malattia (early, late, advanced) – Chari ST, Singer MV Scand J Gastroenterol 1994; 29: 949-60• Per fattori di rischio – TIGAR-O Etemad B, Whitcomb DC. Gastroenterology. 2001• Per approccio operativo-terapeutico – Cavallini G, 2000 (“classificazione di Verona”)• Per probabilità di diagnosi (clinica, imaging, funzione, istologia) – Zurich 1997 – JAP 1997• Per combinazione di clinica, probabilità di diagnosi, stadiazione, severità + score – M-ANNEHEIM (Schneider A, Lohr JM, Singer MV. J Clin Gastroenterol 2007; 42: 101-119)
    • 90. M-ANNHEIM classification of chronic pancreatits Risk Probabaility of• EZIOLOGICO factors the diagnosis Classification by Clinical Severity features and stageSchneider A, Löhr JM, Singer MV.The M-ANNHEIM classification of chronic pancreatitis: introduction of a unifyingclassification system based on a review of previous classifications of the disease.J Gastroenterol. 2007; 42:101-19.
    • 91. Chronic pancreatitis - classifications and operative needs -• Nosographic classification• Diagnostic matching with illness scripts, exemplars,categories• Operative classification• Operative diagnosis targeted to decisions• Complexity/undefined aspets/variation in time• Diagnosis (disease) reliability : defined, probable, possible, undefined
    • 92. EBM
    • 93. EBM Evidence Level (EL) of the literature information/source of the statements 40 35 30 25 % of the 20statements 15 10 5 0 1 2 3 4 5 According to Oxford Centre for Evidence Based Medicine
    • 94. EBM Recommendation strenght of the statements, and agreement (consensus) rate 40 35 30 25 % of the 20 statements 15 10 5 0 A B C D According to Oxford Centre for Evidence Based Medicine 83% of the statements: agreement rate*> 80%* Agreement rate: “strongly agree or with minor reserve”
    • 95. In principio…Sarles H, Sarles JC, Camatte R, Muratore R, Gaini M, Guien C, Pastor J, Le Roy FObservations on 205 confirmed cases of acute Gut 1965; 6: 545-59.
    • 96. George Wirsung………Wirsung duct 1642
    • 97. Padova: giardino dei semplici (botanic garden )