The hexosamine concentration and output in human pure pancreatic juice in chronic pancreatitis

Harada, Hideo; Takeda, Masahiko; Yabe, Hideyuki; Hanafusa, Eiji; Hayashi, Tamaki; Kunichika, Keizo; Kochi, Fumiko; Mishima, Kuniki; Kimura, Ikuo; Ubuga, Toshihiko

doi:10.1007/bf02773918

Cited by 20 publications

(3 citation statements)

References 13 publications

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“…They reported that since these patients also showed a significantly high trypsin activity in pancreatic juice, increased protein concentrations in pancreatic juice caused the high viscosity. Harada et al (1980Harada et al ( , 1981 have reported that patients with established or suspected chronic pancreatitis had elevated hexosamine, calcium, and protein levels in pure pancreatic juice, particularly in the washout phase. They concluded that there were close correlations between pancreatic juice viscosity, enzyme protein levels and hexosamine levels.…”

Section: Discussionmentioning

confidence: 99%

Initial pathophysiological changes in chronic pancreatitis induced by pancreatic ductular obstruction model.

Matsuno

Sasaki

Kobari

et al. 1991

Tohoku J. Exp. Med.

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An experimental chronic pancreatitis model was made in five dogs with chronic pancreatic fistula by injection of microspheres into the peripheral pancreatic duct. Sequential changes of pancreatic exocrine and endocrine functions with morphology were studied. Significant decreases in volume, bicarbonate output and amylase output were detected in each sample collected separately on secretin and secretin cerulean stimulation. While the viscosity of pancreatic juice was significantly increased with a concomitant increase in hexosamine concentration, chronic pancreatitis was demonstrated morphologically. These results suggest that concentrated pancreatic juice caused by a decrease in volume and an increase in viscosity of pancreatic juice with a concomitant increase in hexosamine concentration brings about the progression of chronic pancreatitis in this experimental model. experimental chronic pancreatitis ; microsphere ; viscosity of pancreatic juice

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Section: Discussionmentioning

confidence: 99%

Initial pathophysiological changes in chronic pancreatitis induced by pancreatic ductular obstruction model.

Matsuno

Sasaki

Kobari

et al. 1991

Tohoku J. Exp. Med.

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“…A partial loss of CFTR function may reduce ductal fl uid secretion in the vicinity of acini and thus may increase the concentrations of enzymes and other proteins such as PSP/ reg protein. The elevated concentration of Ca 2+ in pancreatic juice in the early stage of chronic pancreatitis, together with that of hexosamine, 22,23 probably promotes the deposition of CaCO 3 within and around the plugs.…”

Section: Ductal Factorsmentioning

confidence: 97%

Is genetic analysis helpful for diagnosing chronic pancreatitis in its early stage?

2007

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Diagnosis of chronic pancreatitis in its early stage is an extremely difficult task. If the genetic predispositions are identified, it may help make possible the earlier diagnosis of chronic pancreatitis or the detection of patients at risk. There are two major hypotheses about the pathogenesis of chronic pancreatitis known as the "necrosis-fibrosis" and "pancreatic stone protein" hypotheses. Recent molecular and genetic evidence suggests that both pathways contribute to the pathogenesis of chronic pancreatitis. Chronic pancreatitis may be caused by either increased proteolytic activity [the cationic trypsinogen (PRSS1) gene] or decreased protease inhibition (the pancreatic secretory trypsin inhibitor (PSTI) gene]. The impaired pancreatic duct function [cystic fibrosis transmembrane conductance regulator (CFTR) gene] may also be involved in the pathogenesis of the disease. Except for PRSS1 mutations, the known genetic risk for chronic pancreatitis is not high. The high individual variability and low incidence of chronic pancreatitis suggest that yet unidentified genetic and environmental factors are important. Further genetic analysis is necessary for understanding the pathogenesis of chronic pancreatitis, which may be helpful for the earlier diagnosis of the juvenile- or young-onset disease.

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“…There are increased levels of immunoglobulins and albu min [10], hexosamines [11] and lactoferrin. Leukocytes and epithelial cells, as well as fibrin and various amor phous substances may be present [12], These changes are consistent with, and understandable as a result of the breaches in the normal barrier of the ducts as has been described above.…”

Section: Changes In Pancreatic Juicementioning

confidence: 99%

Chronic Pancreatitis: Morphology and the Role of Nerves

Bockman¹

1994

Dig Surg

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Chronic pancreatitis is a regressive disease, sometimes progressing to the point of insufficient secretion from both the exocrine and the endocrine pancreas. Functional decline is matched by morphological changes in the parenchyma and stroma. Acinar cells redifferentiate to produce tubular complexes and degenerate, resulting in a larger proportion of ductular cells than normal. The decrease in parenchyma is more than made up for by an increase in stroma. Characteristically, marked fibrosis occurs. Chronic inflammatory cells are prominent, frequently occurring as clusters. The large pancreatic ducts are altered as well. They may be denuded of their epithelium, eliminating the barrier that normally exists. Plasma cells and inflammatory cells in their walls contribute to the extra components that are found in pancreatic juice. Pancreatic stones, consisting of calcium carbonate precipitated in an organic matrix, may form in the ducts. Chronic inflammatory cells cluster around nerves in and around the pancreas, inducing damage to the perineurium and eventually affecting nerve fibers. This direct damage, coupled with abnormal access of foreign substances to the interior of the nerves due to lack of the perineurial barrier, may provide a partial explanation for the chronic pain that is associated with the disease.

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The hexosamine concentration and output in human pure pancreatic juice in chronic pancreatitis

Cited by 20 publications

References 13 publications

Initial pathophysiological changes in chronic pancreatitis induced by pancreatic ductular obstruction model.

Initial pathophysiological changes in chronic pancreatitis induced by pancreatic ductular obstruction model.

Is genetic analysis helpful for diagnosing chronic pancreatitis in its early stage?

Chronic Pancreatitis: Morphology and the Role of Nerves

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