Hereditary chronic pancreatitis

Teich, Niels; Mössner, Joachim

doi:10.1016/j.bpg.2007.10.019

Cited by 46 publications

(17 citation statements)

References 80 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This chapter describes how chronic pancreatitis is suspected, based on signs, symptoms, and laboratory results, and how the diagnosis is developed. The CQ are very detailed and consist of 12 items, including history taking, physical examination, determination methods for pancreatic enzymes in the blood and urine [5,6], significance of various imaging methods [chest and abdominal radiography, abdominal ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI), endoscopic ultrasound, and pancreatography] in the diagnosis of chronic pancreatitis [7][8][9][10][11][12][13][14][15], exocrine pancreatic function testing, pathological diagnosis, differential diagnosis from pancreatic cancer and intraductal papillary mucinous neoplasm (IPMN), and genetic testing [16][17][18][19][20].…”

Section: Diagnosismentioning

confidence: 99%

Evidence-based clinical practice guidelines for chronic pancreatitis 2015

et al. 2016

View full text Add to dashboard Cite

Chronic pancreatitis is considered to be an irreversible progressive chronic inflammatory disease. The etiology and pathology of chronic pancreatitis are complex; therefore, it is important to correctly understand the stage and pathology and provide appropriate treatment accordingly. The newly revised Clinical Practice Guidelines of Chronic Pancreatitis 2015 consist of four chapters, i.e., diagnosis, staging, treatment, and prognosis, and includes a total of 65 clinical questions. These guidelines have aimed at providing certain directions and clinically practical contents for the management of chronic pancreatitis, preferentially adopting clinically useful articles. These revised guidelines also refer to early chronic pancreatitis based on the Criteria for the Diagnosis of Chronic Pancreatitis 2009. They include such items as health insurance coverage of high-titer lipase preparations and extracorporeal shock wave lithotripsy, new antidiabetic drugs, and the definition of and treatment approach to pancreatic pseudocyst. The accuracy of these guidelines has been improved by examining and adopting new evidence obtained after the publication of the first edition.

show abstract

Section: Diagnosismentioning

confidence: 99%

Evidence-based clinical practice guidelines for chronic pancreatitis 2015

et al. 2016

View full text Add to dashboard Cite

show abstract

“…This is associated with a high risk of developing chronic pancreatitis at a young age and can develop pancreatic cancer. 20 Mutations in the SPINK1 gene, which blocks the active binding site of trypsin, rendering it inactive, is associated with acute and chronic pancreatitis. 21 …”

Section: Hereditary Pancreatitismentioning

confidence: 99%

A clinical study of risk factors of acute pancreatitis in a tertiary care centre in north India

et al. 2017

View full text Add to dashboard Cite

INTRODUCTIONAccording to Atlanta Symposium, acute pancreatitis (AP) was defined as an acute inflammatory process of the pancreas that may also involve peri-pancreatic tissues and/or remote organ systems. 1 The aetiology and pathogenesis of acute pancreatitis have been intensively investigated for centuries worldwide. Most descriptive studies attribute various etiological factors, which vary across populations. It can aetiological initiated by several factors, including gallstones, alcohol, trauma, infections and hereditary factors. Gallstone/ biliary stone are the leading cause in most study followed by alcohol; these two constitute 75% cases.2 Incidence in men is usually more compared to women. In children, abdominal blunt trauma and systemic diseases are the most common causes.The clinical definition of acute pancreatitis requires two of the following three features.• Abdominal pain strongly suggestive of acute pancreatitis ABSTRACT Background: According to Atlanta Symposium, acute pancreatitis (AP) was defined as an acute inflammatory process of the pancreas that may also involve peri-pancreatic tissues and/or remote organ systems. The objective of this study was to know the risk factors of acute pancreatitis in patients admitted in a tertiary care centre in north India Methods: A prospective study was performed with admitted cases of patients with acute pancreatitis over 2 years period. Total 104 patients were selected for study. All data concerning aetiology were recorded and analysed in all patients forming study groups. Results: Among 104 patients with acute pancreatitis 68 (65%) were females and 36 (35%) were males. Mean age of our study group was 40.9 years and maximum incidence was seen in 36-45 years. Most common cause was biliary pancreatitis (63%) followed by alcohol (27%), idiopathic (6%), trauma (3%), infections (1%). In females, most common aetiology was gall stone (88%), in males most commonly by alcohol (78%). As per Atlanta classification 81 patients (77.8%) had acute mild pancreatitis and 23 patients (22.2%) had acute severe pancreatitis. Majority females (66.7%) were admitted in mild acute pancreatitis. The mean age of patients in mild acute pancreatitis was 39.6 years and in severe group was 45.4 years. Gall stone were the leading cause in both mild and severe acute pancreatitis. Conclusions: Females were more commonly affected than men by acute pancreatitis. The most common aetiology was gall stone followed by alcohol which was leading cause in the males.

show abstract

“…Additionally, variants of the calcium-sensing receptor (CASR) seem to influence the pathogenesis in SPINK1 p.N34S carriers. Triplication and duplication of the trypsinogen locus represents a completely new disease-causing mechanism that predisposes to chronic pancreatitis by a so-called gene dosage effect [for further literature, see [24]]. Identification of chymotrypsin C (CTRC) by our group in collaboration with Witt and Sahin-Tóth displayed another reasonable candidate gene [25].…”

Section: Some Aspects On the Pathophysiology Of Pancreatic Acinar Celmentioning

confidence: 99%

New Advances in Cell Physiology and Pathophysiology of the Exocrine Pancreas

Mössner

2010

Dig Dis

Self Cite

View full text Add to dashboard Cite

This review provides some aspects on the physiology of stimulation and inhibition of pancreatic digestive enzyme secretion and the pathophysiology of pancreatic acinar cell function leading to pancreatitis. Cholecystokinin (CCK) stimulates both directly via CCK-A receptors on acinar cells and indirectly via CCK-B receptors on nerves, followed by acetylcholine release, pancreatic enzyme secretion. It is still not known whether CCK-A receptors exist in human acinar cells, in contrast to acinar cells of rodents where CCK-A receptors have been well described. CCK has numerous actions both in the periphery and in the central nervous systems. CCK inhibits gastric motility and regulates satiety. Another major function of CCK is stimulation of gallbladder contraction. This function enables that bile acids act simultaneously with pancreatic lipolytic enzymes. Secretin is a major stimulator of bicarbonate secretion. Trypsinogen is activated by the gut mucosal enzyme enterokinase. The other pancreatic proenzymes are activated by trypsin. Termination of enzyme secretion may be regulated by negative feedback mechanisms via destruction of CCK-releasing peptides by trypsin. Furthermore, the ileum may act as a brake by release of inhibitory hormones such as PYY and somatostatin. In the pathophysiology of acute pancreatitis, fusion of zymogen granules with lysosomes leading to intracellular activation of trypsinogen is regarded as an initiation step. This activation of trypsinogen may be caused by the lysosomal enzyme cathepsin B. However, autoactivation of trypsinogen itself may be a possibility in pathogenesis. Autoactivation is enhanced in certain mutations of trypsinogen. Furthermore, an imbalance of protease inhibitors and active proteases may be involved. The role of pancreatic lipolytic enzymes, the role of bicarbonate secretion, and toxic Ca²⁺ signals by excessive liberation from the endoplasmic reticulum have to be discussed in the pathogenesis of acute pancreatitis.

show abstract

Hereditary chronic pancreatitis

Cited by 46 publications

References 80 publications

Evidence-based clinical practice guidelines for chronic pancreatitis 2015

Evidence-based clinical practice guidelines for chronic pancreatitis 2015

A clinical study of risk factors of acute pancreatitis in a tertiary care centre in north India

New Advances in Cell Physiology and Pathophysiology of the Exocrine Pancreas

Contact Info

Product

Resources

About