Multicenter Pathological Study of Chronic Pancreatitis. Morphological Regional Variations and Differences Between Chronic Calcifying Pancreatitis and Obstructive Pancreatitis

Sahel, J; Cros, R; Durbec, Jean-Pierre; Sarles, H; Bank, Simmy; Marks, I. N.; Bettarello, A; Duarte, I.D.G.; Guarita, Dulce Reis; Machado, Marcel Cerqueira César; Mott, Carlos de Barros; Dani, Renato; Nogueria, C.; Gullo, Lucio; Priori, P

doi:10.1097/00006676-198611000-00001

Cited by 35 publications

(7 citation statements)

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“…Nach pathomorphologischen Kriterien lassen sich 2 (auch ä tiologisch unterschiedliche) Formen der CP unterscheiden [48]. Die seltenere chronisch obstruktive Pankreatitis entsteht auf dem Boden einer Einengung des Ductus pancreaticus (oder grö ßerer Seitenä ste) durch Pankreastumoren, periampuläre Lä sionen (z.…”

Section: Pathomorphologieunclassified

Neue Aspekte in der Pathophysiologie der chronischen Pankreatitis

Foitzik

Buhr

1997

Chirurg

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Despite numerous experimental and clinical investigations there is no consensus on the evolution of chronic pancreatitis (CP). In the 1970s and 1980s, Sarles persistently emphasised the de novo evolution of CP due to pancreatolithiasis. In recent years, however, clinical and morphological studies have provided strong evidence for the initial proposal of acute pancreatitis progressing to chronic pancreatitis. The so-called necrosis-fibrosis-sequence theory is supported by immunohistochemical work suggesting that inflammatory mediators primarily contribute to tissue destruction and that infiltration of pancreatic nerves by immune cells is a pathogenetic factor for the generation of pain in CP. While Sarles postulates that acinar hypersecretion and an imbalance of pancreatic stone promoting and inhibiting factors trigger the evaluation of CP, the necrosis-fibrosis-sequence theory also involves other pathomechanisms (e.g. changes in ductal permeability, ischemia, oxidative stress) which have been shown to cause (acute) pancreatic injury. Despite this unifying template, which also lessens the need to identify independent mechanisms for the pathogenesis of acute and chronic alcoholic pancreatitis, there are still open questions, e.g. on genetic factors that (like in hereditary CP) may explain the different susceptibility of the pancreas to injury and the individual immunological response.

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Section: Pathomorphologieunclassified

Neue Aspekte in der Pathophysiologie der chronischen Pankreatitis

Foitzik

Buhr

1997

Chirurg

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“…Studies based on large populations with chronic pan creatitis have distinguished two main entities: chronic calcifying pancreatitis and obstructive pancreatitis [6][7][8][9], After a variable time, most patients with chronic pancre atitis will develop certain degrees of radiologically visible pancreatic calcification. Most pancreatic calcifications are pancreatic intraductal calculi, principally composed of two amteriais: 95% as calcium carbonate in the form of calcite and the rest, PSP protein [10].…”

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confidence: 99%

Local Resection of the Head of the Pancreas Combined with Longitudinal Pancreaticojejunostomy: Rationale and Results in Patients with Chronic Pancreatitis

Ho¹,

Frey²

1996

Dig Surg

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Local resection of the head of the pancreas combined with longitudinal pancreaticojejunostomy is an effective surgical procedure for patients with chronic pancreatitis. It is simple to perform, and carries low risk. It requires no division of the pancreas or resection of the uncinate process. It completely decompresses all ductal systems and does not result in significant compromise of endocrine and exocrine function of the pancreas. Pain relief was obtained in 88% of patients with chronic pancreatitis after the procedure. Its results compare favorably with other available surgical options for chronic pancreatitis.

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“…This suggests chat a low or abnormal biosynthesis of PSP is responsible for the predisposition. Can J Gastroenterol 1989;3{ l ): [15][16][17][18][19][20] voir page 16) …”

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confidence: 99%

“…It is now possible to distinguish different forms of chronic pancreatitis presenting with different and specific lesions and etiologies (13)(14)(15)(16). Obstructive pancreatitis: Obstructive pancreatitis is due to the occlusion of the main pancreatic duct, or of one of its branches, before the area of pancreatitis, for example, tumours, fibrous scars of necrotic pseudocysts, or congenital anomalies.…”

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“…Though CCP is due to different causes (alcoholism, tropical juvenile form , hereditary, hypercalcemia. idiopathic), its lesions are similar regardless of etiology ( 13,15,16). They are characterized by their patchy distribution: the intensity of the lesions of one lobule or group of lobules (and of the d uct draining them) is different from neighbouring lobules, varying from a completely n~rmal appearance to complete destruction.…”

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Pathogenesis of Chronic Pancreatitis

Sarles

Bernard

1989

Canadian Journal of Gastroenterology

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Studies from the Marseille group allowed differentiation of acute pancreatitis (a group of lesions secondary to either extrapancreatic causes such as gallst6ncs or to pancreatic diseases such as cancer and chronic pancreatitis), from chronic pancreatitis. Two forms of chronic pancreatitis arc easily distinguished: obstructive pancreatitis secondary to pre-existing obstruction on pancreatic ducts (tumours, scars, etc); and the most frequent disease, chronic calcifying pancreatitis, which is a pancreatic lithiasis due to a double phenomenon. This double phenomenon is the precipitation of insoluble calcium salts and the precipitation of degraded fragments of a newly discovered secretory protein known as pancreatic stone protein (PSP). This family of glycoproteins, the amino acid sequence of which has been established, is synthesized by the pancreatic acinar cell and its biosynthesis is decreased in patients presenting with chronic calcifying pancreatitis. The secretory form of PSP prevents the formation of calcium salt crystals in the pancreatic juice which is normally supersaturated in calcium. Though the lesions and the secretory modifications of PSP are common to all forms of chronic calcifying pancreatitis, there are different etiological forms of the disease; alcoholic, tropical, hypercalcemic, hereditary and idiopathic. Alcohol consumption acts on pancreatic secretion by different mechanisms and is responsible for an increased secretion of secretory protein (enzymes) due to cholinergic, vagal reflexes sensitive to ethanol. Alcohol consumption is generally associated with protein rich and either fat rich or fat poor diets, both of which are risk factors. Hypercalcemia also increases the secretion of protein and the viscosity of pancreatic juice. The tropical form is not due, as previously suggested, co cassava (manioc) consumption or kwashiorkor, but it is endemic in populations submitted to fat poor, protein poor diets. These etiological factors are only acting on predisposed patients. This suggests chat a low or abnormal biosynthesis of PSP is responsible for the predisposition. Can J Gastroenterol 1989;3{ l ): [15][16][17][18][19][20] voir page 16)

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Multicenter Pathological Study of Chronic Pancreatitis. Morphological Regional Variations and Differences Between Chronic Calcifying Pancreatitis and Obstructive Pancreatitis

Cited by 35 publications

References 0 publications

Neue Aspekte in der Pathophysiologie der chronischen Pankreatitis

Neue Aspekte in der Pathophysiologie der chronischen Pankreatitis

Local Resection of the Head of the Pancreas Combined with Longitudinal Pancreaticojejunostomy: Rationale and Results in Patients with Chronic Pancreatitis

Pathogenesis of Chronic Pancreatitis

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