Clinical Diagnosis Of Chronic Pancreatitis Research Articles

Adenosquamous Carcinoma of Head of the Pancreas: A Case Report

Adenosquamous carcinoma is a rare variant of exocrine pancreatic neoplasm which is characterized by both squamous and adenomatous components. It has aggressive behavior with poor prognosis. We report a case of adenosquamous carcinoma of pancreas in a 39-year-male presenting with pain in epigastric and hypochondrium region. Clinical diagnosis of chronic pancreatitis with calculi in the main pancreatic duct was made which on histopathological diagnosis revealed a lesion in pancreas with morphological features of adenosquamous carcinoma. Keywords: Pancreas, Adenosquamous carcinoma, Aggressive tumor

Clinical Profile and Management of Chronic Pancreatitis in Tertiary Care Centre

Background Constant inflammation and irreversible pancreatic tissue destruction are hallmarks of the disease of chronic pancreatitis (CP), which results in the decrease of both exocrine and endocrine function over time. It is a multifactorial disease, with a wide range of symptoms and geographic variation. Aim Aim of this study is to study clinical profile and management of CP with respect to demography, clinical findings, lab parameters, imaging investigations and management modalities. Methods A cross-sectional observational study was conducted which included the patients admitted to the tertiary care center presenting with the clinical diagnosis of CP. The study was conducted over a period of 2-years from November 2019 to October 2021. A total sample size of 71 patients was included. Results In the study, it was observed that the majority of patients were in the age group of 51-60-years (47.89%) followed by 41-50-years (21.12%) mean age ranges from 56.54±12.63-years. The majority of patients were male (76.06%) and females were 23.94%. The distribution of patients according to aetiology showed that the majority of patients had aetiology of alcoholism (43.66%) followed by idiopathic (29.57%) Gall/Biliary stones (21.12%) and post-operative (5.63%). Majority of patients presented with pain in the abdomen (85.92%). The distribution of patients according to ultrasound sonography test (USG) findings showed that majority of patients shows pancreatic calcification (54.93%) followed by pancreatic pseudocyst (32.39%) and gall stones (19.72%). The distribution of patients according to computed tomography (CT) findings showed that majority of patients shows pancreatic calcification (70.42%). In the present study, it was observed that majority of patients were managed conservatively (43.66%) followed by cystogastrostomy (18.31%) and cystojejunostomy (8.45%). Endoscopic retrograde cholangiopancreatography (ERCP) was done among 14 (19.72%) patients. Lateral pancreaticojejunostomy was done in 6 (8.45%) patients and pancreaticoduodenectomy (Classical Whipple’s) was done in 4 patients (5.63%). The distribution of patients according to pain relief by various management showed that majority of getting relief from pain by surgery (69.23%) followed by ERCP (35.71%) and the least by conservative/analgesics (6.45%). Conclusion Chronic pancreatitis is progressive inflammatory disease. Alcoholic pancreatitis being most common etiology. Pain is most common presenting symptom. CT scan abdomen most useful in confirming diagnosis in our set up. Pseudocyst being common complication seen. Surgery gives relief of pain in most of the cases. The key to a better outcome is making the right decisions in terms of diagnosis, patient selection for surgery, and surgical type.

Clinical profile and management of chronic pancreatitis in tertiary care centre

Background: Chronic pancreatitis is a multifactorial disease, with a wide range of symptoms and geographic variation. Aim of this study is to study clinical profile and management of chronic pancreatitis with respect to demography, clinical findings, lab parameters, imaging investigations and management modalities.Methods: A cross sectional observational study was conducted which included the patients admitted in tertiary care centre presenting with clinical diagnosis of chronic pancreatitis. The study was conducted over period of 2 years from November 2019 to October 2021. A total sample size of 71 patients were included.Results: In the study, it was observed that majority of patients in age group of 51-60 years which were male (76.06%). Alcoholism (43.66%) was most common etiology and presented with pain in abdomen (85.92%). In the present study, majority of patients were managed conservatively (43.66%).The distribution of patients according to pain relief by various management showed that majority of get relief of pain by surgery (69.23%).Conclusions: Chronic pancreatitis is progressive inflammatory disease. Alcoholic pancreatitis being most common etiology. Pain is most common presenting symptom. CT-SCAN abdomen most useful in confirming diagnosis in our set up. Pseudocyst being common complication seen. Surgery gives relief of pain in most of the cases.

Клініко-патогенетичні аспекти хронічного панкреатиту в поєднанні з вірусним гепатитом С в амбулаторній практиці

Актуальність. Останніми роками зросла увага до інфекційного агента, вплив якого може призвести до розвитку запального процесу в підшлунковій залозі. Значне поширення вірусного гепатиту С серед населення, різноманітність його позапечінкових проявів обумовлюють актуальність проблеми. Недостатність розробки питань первинної й вторинної профілактики хронічного панкреатиту мотивує до глибшого вивчення механізму його розвитку на тлі вірусного гепатиту С. Мета: вивчити клінічний перебіг хронічного панкреатиту у хворих із супутнім вірусним гепатитом С. Матеріали та методи. Обстежено 57 хворих на хронічний панкреатит із супутнім вірусним гепатитом С. Групу порівняння становили 20 осіб, хворих на хронічний панкреатит. Для встановлення клінічного діагнозу хронічного панкреатиту й вірусного гепатиту С усі хворі були обстежені згідно з протоколами, затвердженими наказами МОЗ України № 638 від 10.09.2014 і № 729 від 18.07.2016. Діагноз хронічного панкреатиту й вірусного гепатиту С верифікували на підставі даних анамнезу захворювання, клінічних проявів і результатів досліджень. Загальноклінічні й біохімічні обстеження проводили хворим на хронічний панкреатит у фазі загострення й нестійкої ремісії, хворим із вірусним гепатитом С — у фазі стійкої ремісії. Результати. У клінічному перебігу хронічного панкреатиту із супутнім вірусним гепатитом С провідне місце посідали больовий, диспептичний синдроми й порушення випорожнення, що були більш вираженими, ніж у групі порівняння (вірогідна відмінність від показників II групи, p < 0,05). У хворих на хронічний панкреатит із супутнім вірусним гепатитом С виявили анемію легкого ступеня, зниження рівня загального білка в крові, гіпербілірубінемію, гіперхолестеринемію, підвищення рівня ферментів аланінамінотрансферази й аспартатамінотрансферази, підвищення рівнів амілази крові й діастази сечі (вірогідна відмінність стосовно II групи, p < 0,05). У хворих на хронічний панкреатит із супутнім вірусним гепатитом С показник копрограми становив (5,20 ± 0,82) бала, а у хворих на хронічний панкреатит — (3,10 ± 0,32) бала (виявлено значно гірші показники, більш виражений запальний синдром і дисбактеріоз). У двох досліджуваних групах переважала стеаторея II типу. Глибина структурних змін у підшлунковій залозі за даними ультразвукового дослідження в групі хворих на хронічний панкреатит із супутнім вірусним гепатитом С становила (2,56 ± 1,10) бала, що відповідає процесу середнього ступеня тяжкості. У контрольній групі ступінь ураження становив (1,90 ± 0,60) бала. Висновки. На підставі оцінки даних дослідження встановлено негативний вплив супутнього вірусного гепатиту С на перебіг хронічного панкреатиту.

Analytically validated protein biomarkers of chronic pancreatitis and pancreatic cancer for potential clinical diagnosis with mass spectrometry.

Chronic pancreatitis (CP) is a pancreatic disease with poor prognosis and pancreatic cancer (PC) is one of the most lethal types of cancer that is symptomless in the early stage. Because the clinical and image findings of CP can overlap that of pancreatic cancer (PC) which leads to confusion in the diagnosis and treatment of PC, discovery/verification/validation of more accurate protein biomarkers to diagnose CP and PC is in urgent need. The PubMed, Web of Science, and Google Scholar were searched using the keywords: 'biomarker', 'marker', 'chronic pancreatitis', "pancreatic cancer" or "proteomics" for highly related researches. We focused on the articles published after the year 2005 in this review. We introduce the background to CP and PC and summarize the diagnosis of CP and PC, analytically validated protein biomarkers, and proteomic approaches for discovery/verification/validation. The potential use of mass spectrometry (MS) in clinical diagnosis is also discussed. Continuously improving sensitivity of MS can provide deeper proteome for new marker discovery and high reliability for protein marker verification, validation, and clinical diagnosis. The analytically validated protein markers could be considered as targeted protein biomarkers for developing a MS platform in the clinical validation process or clinical diagnosis of CP and PC.

T1 mapping for diagnosis of mild chronic pancreatitis.

To determine if the T1 relaxation time of the pancreas can detect parenchymal changes in mild chronic pancreatitis (CP). This Institutional Review Board (IRB)-approved, Health Insurance Portability and Accountability Act (HIPAA)-compliant retrospective study analyzed 98 patients with suspected mild CP. Patients were grouped as normal (n = 53) or mild CP (n = 45) based on history, presenting symptomatology, and concordant findings on both the secretin-enhanced magnetic resonance cholangiopancreatography (S-MRCP) and endoscopic retrograde cholangiopancreatography (ERCP). T1 maps were obtained in all patients using the same 3D gradient echo technique on the same 3T scanner. T1 relaxation times, fat signal fraction (FSF), and anterior-posterior (AP) diameter were correlated with the clinical diagnosis of CP. There was a significant difference (P < 0.0001) in the T1 relaxation times between the control (mean = 797 msec, 95% confidence interval [CI]: 730, 865) and mild CP group (mean = 1099 msec, 95% CI: 1032, 1166). A T1 relaxation time threshold value of 900 msec was 80% sensitive (95% CI: 65, 90) and 69% specific (95% CI: 56, 82) for the diagnosis of mild CP (area under the curve [AUC]: 0.81). Multiple regression analysis showed that T1 relaxation time was the only statistically significant variable correlating with the diagnosis of CP (P < 0.0001). T1 relaxation times showed a weak positive correlation with the pancreatic FSF (ρ = 0.33, P = 0.01) in the control group, but not in the mild CP group. The T1 relaxation time of the pancreatic parenchyma was significantly increased in patients with mild CP. Therefore, T1 mapping might be used as a practical quantitative imaging technique for the evaluation of suspected mild CP. 3 J. Magn. Reson. Imaging 2017;45:1171-1176.

Application value of core needle biopsy technique in the pathological diagnosis of locally advanced pancreatic cancer

To explore the application value of core needle biopsy technique in the pathological diagnosis of locally advanced pancreatic cancer patients. During April 2007 to April 2014, retrospective analysis was conducted for 36 patients of locally advanced pancreatic cancer to summarize the clinical data of core needle biopsy technique. And the relevant data included clinical features, pathological findings and puncture-related complications. Regular postoperative follow-ups were conducted. All received pathological examination of core needle biopsy. And the pathological diagnoses were pancreatic cancer (n=29), pancreatic neuroendocrine tumors (n=2) and chronic pancreatitis (n=5). During the follow-ups, liver metastasis was pathologically confirmed postoperatively at Months 4 and 6 months among 5 chronic pancreatitis patients. The remainder was followed up for over 12 months. There was neither change in size nor metastasis. One case was diagnosed at Peking Union Hospital as autoimmune pancreatitis while another 2 cases had a clinical diagnosis of chronic pancreatitis. The accuracy of core needle puncture was 94.4%. There were 2 cases of postoperative pancreatic fistula in class A. Bleeding complication was absent. The application of core needle biopsy technique is both safe and effective in the pathological diagnosis of locally advanced pancreatic cancer.

Pancreatic/Biliary.

Introduction: Chronic pancreatitis (CP) is a complex syndrome characterized by pancreatic fibrosis (PF), chronic inflammation, and progressive loss of glandular exocrine and endocrine function. The lack of a practical “gold standard” in the diagnosis of CP is a challenge, as direct biopsy of the pancreas to evaluate histology may not be feasible. Endoscopic pancreatic functional tests (ePFTs) can be used to predict PF, a key histologic component of CP. To construct a diagnostic tool based on Fagan’s nomogram for calculating post-test probability of pancreatic fibrosis (PF) utilizing the ePFT in subjects with and without known risk factors for CP. Methods: Exhaustive literature was conducted for review of PF data in surgical histology and autopsy studies. Step 1: Prevalence of PF in histopathology studies of subjects with and without major risk factors (smoking, alcohol abuse, neither smoking nor alcohol) was used to determine pre-test probability of PF. No data was available for subjects with both smoking and alcohol use. Step 2: Positive and negative likelihood ratios (LR) for secretin ePFT detection of PF were calculated based on sensitivity and specificity in literature using histopathology as gold standard (Table 1). Step 3: Fagan’s nomogram (Bayesian analysis) was used to determine the post-test probability of PF incorporating pre-test probability (risk factors) and positive/negative LR of ePFT.Table 1: Test Characteristics of ePFTResults: Based on histologic gold standards, a Fagan’s nomogram was constructed to estimate post-test probability of PF based on pre-test risk factors (smokers, alcoholics, and controls) and ePFT results (Table 2).Table 2: Posttest Pprobability of Pancreatic FibrosisConclusion: ePFT can assist in the assessment for PF, which is a key component of chronic pancreatitis. A negative ePFT (even in the setting of known CP risk factors) is a useful tool to rule out PF. On the other hand, a positive ePFT can predict PF, but should be interpreted in combination with other testing modalities (i.e., EUS, MRI) and clinical features (abdominal pain, recurrent pancreatitis) for a definitive diagnosis of chronic pancreatitis. While not all patients with PF will have clinical diagnosis of chronic pancreatitis, the presence of fibrosis in addition to other factors (exocrine insufficiency, abdominal pain, diabetes) can assist in the diagnostic evaluation.

Pancreatic Morphological Changes in Long-Term Follow-Up after Initial Episode of Acute Alcoholic Pancreatitis

ObjectiveThe long-term morphological changes induced by a single episode of alcoholic pancreatitis are not known. Our aim was to study these morphological changes in secretin-stimulated magnetic resonance cholangiopancreatography (S-MRCP) after the first episode of alcohol-associated acute pancreatitis and to evaluate the risk factors and possible protective factors potentially associated with later chronic findings. We have previously reported 2-year follow-up results in pancreatic morphology. This study extends the follow-up to 9 years. Patients and MethodsIn this prospective follow-up study, S-MRCP imaging was performed for 44 (41 M, 3 F; mean age, 46 (25–68) years) patients after their first episode of alcohol-associated pancreatitis. Pancreatic morphology was evaluated at 3 months and at 2, 7, and 9 years after hospitalization. Recurrent attacks of pancreatitis were studied and pancreatic function was monitored by laboratory tests. Patients’ alcohol consumption was evaluated with questionnaires, laboratory markers, and self-estimated alcohol consumption via interview. Smoking and body mass index were annually recorded. ResultsAt 3 months, 32 % of the patients had normal findings in S-MRCP, 52 % had acute, and 16 % had chronic changes. At 7 years, S-MRCP was performed on 36 patients with normal findings in 53 %, the rest (47 %) having chronic findings. Pancreatic cyst was present in 36 %, parenchymal changes in 28 %, and atrophy in 28 % of the cases. There were no new changes in the pancreas in the attending patients between 7 and 9 years (18 patients). Of the patients with only acute findings at 3 months, 60 % resolved to normal in 7 years, but the rest (40 %) showed chronic changes later on. The initial attack was mild in 65 %, moderate in 25 %, and severe in 10 % of the patients. Patients with mild first attack had fewer chronic changes at 7 years compared to patients with moderate or moderate and severe together (p = 0.03, p = 0.01). Of the patients in the seventh year of S-MRCP, 22 % had suffered a recurrent episode of acute pancreatitis (mean, 22 (2–60) months) and 11 % had a clinical diagnosis of chronic pancreatitis. At 7 years, 88 % of the patients with recurrences had chronic findings in S-MRCP versus 36 % with nonrecurrent pancreatitis (p = 0.02). Six (17 %) patients abstained from alcohol throughout follow-up (mean, 8.7 (7–9.1) years), but even one of these developed pancreatic atrophy. Out of the non-abstinent patients who did not suffer recurrences, 4/22 (18 %) had developed new findings during at follow-up S-MRCP (NS). In univariate analysis, heavy smoking showed no correlation with increased chronic changes compared to nonsmoking. ConclusionsMorphological pancreatic changes increase with recurrent episodes of acute pancreatitis. Patients with mild first attack have fewer chronic changes in the pancreas in the long term. However, even a single episode of acute alcoholic pancreatitis may induce chronic morphological changes in long-term follow-up.

Advanced Imaging of Chronic Pancreatitis

Chronic pancreatitis is characterized by continuing inflammation, destruction, and irreversible morphological changes in the pancreatic parenchyma and ductal anatomy. These changes lead to chronic pain and/or loss of function. Although these definitions are simple, the clinical diagnosis of chronic pancreatitis remains difficult to make, especially for early disease. Routine imaging modalities such as transabdominal ultrasound and standard CT scans are insensitive for depicting early disease, and detect only advanced chronic pancreatitis. Advances in imaging modalities including CT, MRI with gadolinium contrast enhancement, MRI with magnetic resonance cholangiopancreatography (MRI/MRCP), MRI/MRCP with secretin-stimulation (S-MRCP), endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasound (EUS) allow earlier diagnosis of chronic pancreatitis. This article reviews the recognized findings, advantages, and disadvantages of the various imaging modalities in the management of chronic pancreatitis, specifically CT, MRI with or without MRCP and/or S-MRCP, ERCP, and EUS.

Trypsinogen Copy Number Mutations in Patients With Idiopathic Chronic Pancreatitis

We have recently reported that the triplication of a approximately 605 kilobase segment containing the PRSS1 (encoding cationic trypsinogen) and PRSS2 (encoding anionic trypsinogen) genes causes hereditary pancreatitis. Here we went further to investigate whether this copy number mutation could account for some unidentified French white patients with idiopathic chronic pancreatitis (ICP) or familial chronic pancreatitis (FCP) as well as Indian patients with tropical calcific pancreatitis (TCP). Patients and controls were screened by means of previously described quantitative fluorescent multiplex polymerase chain reaction and/or genotyping of the microsatellite marker rs3222967. The approximately 605 kilobase triplication and a novel duplication (confirmed by fluorescence in situ hybridization) of the trypsinogen locus were detected in 10 and 2 of 202 ICP patients, respectively (age of disease onset, <or=20 years) but were absent in 282 French controls. In addition, the duplication mutation was found in 2 of 1044 ICP patients whose age of disease onset was >20 years. However, the 2 trypsinogen copy number mutations were observed in neither 103 FCP patients nor 268 Indian TCP patients. Our findings revealed the molecular basis of 6% of the young ICP patients and further demonstrated that chronic pancreatitis is a genomic disorder. Our findings also add to the mounting evidence showing that trypsinogen gene mutations do not appear to play an important role in the pathogenesis of TCP in the Indian population. Finally, a dividend of this study is that we have provided convincing evidence to show that all 5 previously described copy number variations involving PRSS1 or/and PRSS2 are artifacts.

Using faecal elastase-1 to screen for chronic pancreatitis in patients admitted with acute pancreatitis

Background: Patients presenting with acute pancreatitis may have co-existing chronic pancreatitis, the accurate diagnosis of which would potentially guide appropriate management. Gold standard tests are often invasive, costly or time-consuming, but the faecal elastase-1 assay has been shown to be comparatively accurate for moderate and severe exocrine deficiency. This study aimed to evaluate fecal elastase-1 concentration [FE-1] against clinical criteria for chronicity in an acute setting. Patients and methods: [FE-1] was performed on patients admitted with acute onset of epigastric pain and a serum lipase at least three times the upper limit of normal. Clinical diagnosis of chronic pancreatitis was defined by the presence of specific clinical, pathological or radiological criteria. A [FE-1] value of <200 µg/g was similarly considered indicative of chronic exocrine insufficiency. Thus a 2×2 table comparing [FE-1] and clinical diagnosis was constructed. Results: After exclusion of liquid stool specimens, 105 stool specimens from 87 patients were suitable for [FE-1] determination. [FE-1] was evaluated against the clinical diagnosis of chronic pancreatitis, initially for the whole sample, and then after exclusion of cases of moderate and severe acute pancreatitis (Ranson score >2). The latter analysis, based on an exocrine insufficiency threshold of 200 µg/g, yielded a sensitivity of 79.5%, specificity of 98.0%, positive predictive value of 96.9% and negative predictive value of 86.0%. Conclusion: [FE-1] is an accurate screening tool for underlying chronic exocrine insufficiency when taken in the course of a hospital admission for mild acute pancreatitis.

Assessment of Exocrine Pancreatic Dysfunction in Chronic Pancreatitis

The clinical diagnosis of chronic pancreatitis is usually based on imaging studies, pancreatic function tests, and the presence of characteristic clinical features. In Japan, diagnostic criteria for chronic pancreatitis were established in 1995. The secretin test (a duodenal intubation test) and the combination of noninvasive tests, N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA) and fecal chymotrypsin (FCT), have been recommended for evaluating exocrine pancreatic function in patients with chronic pancreatitis. In the present study, the diagnostic value of these two noninvasive tests was compared to the secretin test. Although noninvasive tests are less sensitive and specific for determining exocrine pancreatic dysfunction than the secretin test, greater reliability for diagnosing chronic pancreatitis can be obtained by performing the BT-PABA and FCT simultaneously. Assessment of exocrine pancreatic function is important not only to diagnose chronic pancreatitis but also to decide a treatment method with pancreatic enzyme preparation.

Intraductal papillary-mucinous tumors of the pancreas: Clinicopathologic features, outcome, and nomenclature. Members of the Pancreas Clinic, and Pancreatic Surgeons of Mayo Clinic

BACKGROUND & AIMS: Intraductal papillary-mucinous tumor (IPMT) of the pancreatic ducts is increasingly recognized. This study investigated if clinical, imaging, or, histological features predicated outcome, formulated a treatment algorithm, and clarified relationships among IPMT, mucinous cystic neoplasms of the pancreas (MCN), and chronic pancreatitis. METHODS: The medical records, radiographs, and pathological specimens of 15 patients with IPMT (dilated main pancreatic duct or branch ducts with mucin overproduction) who were evaluated between October 1983 and January 1994 were reviewed. RESULTS: One patient had hepatic metastases. Fourteen underwent an operation (6 distal pancreatectomy, 4 total pancreatectomy, and 4 pancreaticoduodenectomy); all had dysplastic intraductal epithelium and chronic pancreatitis, whereas 3 had invasive adenocarcinoma. After a median of 25 months, 10 patients were alive; 3 of 4 with malignant and 2 of 11 with benign IPMT died (P < 0.05). Patients with or without carcinoma had similar clinical and radiographic features. A clinical diagnosis of chronic pancreatitis had been made in 9 patients with benign IMPT and in none with malignant IPMT (P < 0.05). CONCLUSIONS: IPMT is a dysplastic and likely precancerous lesion that is frequently diagnosed as chronic pancreatitis and is separate from MCN. Because it is not possible to distinguish noninvasive from invasive IPMT preoperatively, complete surgical excision of the dysplastic process is our treatment of choice whenever appropriate. (Gastroenterology 1996 Jun;110(6):1909-18)

Diagnosis and grading of chronic pancreatitis by morphological criteria derived by ultrasound and pancreatography

The most commonly used modalities in the diagnosis of chronic pancreatitis are ultrasonography, computed tomography (CT) and endoscopic retrograde pancreatography (ERP). Computed tomography scanning is only of value in severe chronic pancreatitis. Both ultrasound and pancreatography are capable of showing ductal changes in mild forms of the disease, but comparison of the two methods has been difficult. A scheme of morphological criteria and descriptive terminology of pancreatitis was applied to 58 out of 85 patients with a firm clinical diagnosis of chronic pancreatitis. Twenty-seven patients were excluded from the study, four with a faulty clinical diagnosis and 23 with non-diagnostic pancreatograms. There was an exact classification into normal, equivocal, mild, moderate or marked chronic pancreatitis in 50 out of 58 patients (86%) and an almost perfect correlation (+ or − one grade) in 54 out of 58 (93%). There were four discrepancies. Ultrasound examination missed focal pancreatitis in the tail, a small cavity in the uncinate process and a variant of chronic pancreatitis. One ultrasound scan was of poor quality. Morphological grading by different techniques is feasible and use of this scheme can reduce diagnosis to a simple and specific set of rules.

A diagnostic approach to inflammatory disease of the pancreas by means of endoscopic retrograde cholangio-pancreatography.

Role of ERCP in the diagnosis of inflammatory lesions of the pancreas was evaluated and following conclusions were obtained. 1) Following criteria were considered to be practical for clinical diagnosis of chronic pancreatitis by ERCP; a) More than moderate irregularity or rigidity of margin, dilatation, or irregularity in caliber of PDS, whether extensive or localized, or b) Cyst formation or c) Obstruction of PDS. These criteria permit to diagnose 100% of pancreatolithiasis, 82% of chronic pancreatitis without pancreatolithiasis and 64% of histologically diagnosed chronic pancreatitis but about 13% of "false positive results" must be taken into consideration. 2) ERCP plays an important role in detecting and locating localized or scattered lesions without noticable abnormalities in P-S test. It is also useful in deciding an indication for surgical intervention. However, it has limitations in detecting minimal to moderate pancreatitis. Some of these cases are often picked up by P-S test. 3) Combined approach with ERCP and P-S test is required for diagnosis of inflammatory lesions of the pancreas and either one is incomplete by itself.

On the Etiology and Clinical Diagnosis of Chronic Pancreatitis

On the Etiology and Clinical Diagnosis of Chronic Pancreatitis

Clinical diagnosis of chronic pancreatitis

Clinical diagnosis of chronic pancreatitis