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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic secretion is involved in circadian regulation of the whole organism. This observation was obtained in animals and humans with pancreatic fistulas. We report on three patients in whom the pancreas was removed totally or subtotally because of chronic pancreatitis with severe pain. A segment of the removed gland was transplanted into the thigh in order to preserve endocrine function. The pancreatic duct was drained by a polyethylene tube until pancreatic duct occlusion. Postoperatively juice volume increased within 3 days and remained constant afterwards with 300 ml in 24 hours. Secretin, cholecystokinin and food intake are able to stimulate the transplanted segment in a typical manner. The secretion showed circadian changes. In all patients the pancreatic juice content of protein, amylase, trypsinogen, calcium, and zink decreased till 11 p.m. After 11 p.m. the content of all substances increased and reached maximal values at 6 a.m. Flow rates and therefore output per minute decreased greatly till 6 a.m. The large juice volume of 300 ml in 24 hours is perhaps the consequence of a break down of the feedback mechanism between intraduodenal trypsin activity and CCK-release. The changes during the night may be of pathogenetic relevance. In the early morning pancreatic juice is highly concentrated and the flow rate is very low. High protein concentrations, high calcium concentrations, and reduced flow rates may lead to protein and calcium carbonate precipitates. This mechanism is under discussion in the pathogenesis of chronic pancreatitis.
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PMID:[Exocrine function of a heterotopically transplanted pancreas segment in humans]. 195 40

By means of consecutive pancreatic stimulation, we have investigated the presence of changes of pancreatic function in alcoholic patients, with and without alcoholic liver disease, in order to detect functional alterations and possible association of hepatic and pancreatic disease. The patients were 49 chronic alcoholics (8 patients without liver disease, 11 hepatic steatosis, 9 alcoholic hepatitis and 21 alcoholic cirrhosis) and 15 non alcoholic subjects (8 normal controls and 7 cases of non alcoholic cirrhosis). In all the cases two consecutive stimulations were carried out: first with secretin and cholecystokinin (CCK) and second with CCK alone. The total volume and concentration as well as the output of bicarbonate, trypsin, amylase and total proteins were measured in the duodenal juice. Patients with alcoholic cirrhosis had larger volumes of duodenal juice and lower concentrations of bicarbonate, enzymes and proteins. There was also a tendency to larger volume and lower bicarbonate concentration as the hepatic lesion was more severe. Bicarbonate output was significatively higher in patients with alcoholic cirrhosis but for the remaining parameters the outputs were similar in all the groups. In conclusion, the alterations in pancreatic function parallel the severity of the liver disease. None of the patients had changes consistent with chronic pancreatitis.
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PMID:[Changes in pancreatic secretion in alcoholic liver disease]. 237 59

There are two different forms of chronic pancreatitis: one is obstructive pancreatitis which results from a pre-existing obstacle (usually a tumour or a scar) and the other, much more frequent, is chronic calcifying pancreatitis which seems to begin with the formation of precipitates in acini and ducts, later transformed into stones and calcifications made up of calcium carbonate, and therefore is a pancreatic lithiasis. Since the pancreatic juice is supersaturated in calcium carbonate, the presence of an inhibitor of crystallization must be postulated. This has now been identified as a 13500 daltons molecular weight protein: the pancreatic stone protein secreted by the acinar cells. This protein is decreased in chronic calcifying pancreatitis irrespective of its origin (alcoholic, hereditary, hypercalcaemic, tropical, idiopathic), although its reduction is unrelated to any of these aetiological factors. Chronic alcohol consumption may encourage calcium stone formation possibly by disturbing the cholinergic regulation of pancreatic secretion, with decrease in citrate secretion (citrate is a chelator of calcium) and increase in enzyme secretion. The diagnostic and therapeutic implications of these findings are already obvious.
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PMID:[Chronic calcifying pancreatitis, pancreatic calculi. New data]. 293 79

The most current form of chronic pancreatitis, i.e. chronic calcifying pancreatitis, is often related to nutritional causes. This disease is characterized by formation within the pancreatic ducts and the lumina of accini of precipitates and calculi composed of calcium carbonate and of a newly discovered protein, the pancreatic stone protein (PSP). The formation of precipitates depends on two mechanisms: (1) a non etiological disorder reducing the secretion of PSP. This small phosphoglycoprotein is a calcium stabilizer which prevents the crystallization of calcium carbonate in a super saturated solution such as pancreatic juice, (2) modifications of the pancreatic juice related to the cause of the disease. In Occidental countries the main etiological factor is alcohol consumption associated with protein-and-fat-rich or fat-poor diets. Like hypercalcaemia, another cause of the disease, a chronic consumption of alcohol increases the pancreatic secretion of secretory proteins (enzymes) via its action on the cholinergic nerves. In some tropical countries, chronic pancreatitis is observed in children and associated to malnutrition. However, according to recent studies neither kwashiorkor nor manioc consumption seem to be responsible for the occurrence of this disease.
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PMID:[Etiopathogenesis of chronic nutritional pancreatitis]. 330 3

Recently, in our laboratory, a protein extracted from human pancreatic stones was characterized and purified and a specific antibody was obtained. This pancreatic stone protein (PSP) was shown to have an inhibitory effect on the CaCO3 crystal growth in vitro. The cellular origin of such a protein and its repartition along the digestive tract were studied by immunolocalization (protein A-colloidal gold method) at the ultrastructural level. Surgical biopsies of pancreata from normal or chronic pancreatitis patients, needle liver biopsies, gastric mucosa, and jejunum and duodenum biopsies were minced and fixed in the Karnovsky medium or in buffered 4% paraformaldehyde. The specimens were washed in buffer, dehydrated through ethanol, and embedded in Epon 812. Ultrathin sections, collected on uncoated nickel grids, were submitted to the following reactives at room temperature: protein A 1 mg/ml, anti-PSP (1:2 to 1:100), and protein A-colloidal gold. The specificity of the localization was checked by substituting buffer or nonimmune rabbit serum to anti-PSP. The stone protein was markedly present in the zymogen granules and condensing vacuoles of the normal pancreatic acinar cells, the label was found in the acinar and ductal lumen. In chronic pancreatitis, the localization of PSP, when it occurred, was extremely weak in the acinar cells. No PSP was specifically characterized in hepatocytes, gastric mucosa, and enterocytes. However, a weak but specific reaction was found in the secretory granules of Paneth cells. These results in pancreas confirm the acinar secretory origin of the PSP and are in good agreement with its possible function in stabilizing pancreatic juice in vivo, which is normally supersaturated in calcium carbonate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunocytochemical localization of pancreatic stone protein in the human digestive tract. 355 Jul 81

The first lesion of chronic calcifying pancreatitis (CCP), the most frequent form of chronic pancreatitis is the formation in the ducts of plugs build up of protein and calcium carbonate which are at the origin of pancreatic calculi. Pancreatic juice is supersaturated in calcium carbonate. A novel protein, the pancreatic stone protein (PSP) has been purified from human pancreatic juice and its amino-acid composition has been determined. It is biosynthesized in the acinar cell as well as enzymes. PSP prevents the formation of calcium carbonate crystals in a supersaturated solution. Its secretion is decreased in patients presenting with CCP. It is proposed that this decrease plays an important part in the pathogenesis of CCP.
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PMID:[Pancreatic lithogenesis]. 396 39

A quantitative correlation between computer-tomographic (CT) findings and exocrine pancreatic function following secretin-ceruletide stimulation was performed in 48 patients with chronic pancreatitis; thereby a significant correlation between the degree of morphological changes in CT and the stage of functional impairment was found (r = 0,7841, p less than 0,001). Bicarbonate secretion/h showed the strongest correlation to CT findings (r = -0,7193, p less than 0,001) within the single functional parameters. CT showed a limited sensitivity (50%) in detecting chronic pancreatitis in cases with a slight functional impairment (stage 1). Morphological signs as calcifications, pancreatic duct ectasia were constantly coupled with a severe degree of functional impairment, whereas enlargement and cysts were found throughout the different functional stages.
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PMID:[Ct-morphology and exocrine function in chronic pancreatitis]. 619 9

To test the discriminatory potential of certain indices of pancreatic function we performed duodenal perfusion studies and measured trypsin, bicarbonate, and lactoferrin outputs, and plasma concentrations of pancreatic polypeptide and motilin in the basal state and during continuous intravenous stimulation with 100 ng kg-1h-1 Ceruletide and 1 CU kg-1h-1 secretin. The following groups were studied: 12 normal volunteers (NV), seven patients with chronic pancreatitis with steatorrhea (CPS), and seven without steatorrhea (CP). Stimulated trypsin outputs, after 45 min of stimulation, were the best discriminant among the groups (NV versus CPS, p less than 0.0005; NV versus CP, p less than 0.005; CP versus CPS, p less than 0.05). Basal trypsin outputs showed similar patterns but failed to discriminate between NV and CP. Bicarbonate outputs were less discriminatory than trypsin outputs. Lactoferrin outputs failed to discriminate, but transient high peak outputs occurred in the initial stimulation period in all four patients with calcific chronic pancreatitis, suggesting a washout phenomenon. Basal motilin levels were elevated in both groups of pancreatitis (p less than 0.05). Stimulated pancreatic polypeptide levels were lower in CPS (NV versus CPS, p less than 0.05) but higher in CP (NV versus CP, p less than 0.005). These differences were also apparent in the basal state. We conclude that the best discrimination among the three groups was achieved by measurement of trypsin outputs, after 45 min of stimulation. In addition, the pancreatic polypeptide response may be used as a marker of residual pancreatic function in chronic pancreatitis.
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PMID:Pancreatic exocrine and endocrine responses in chronic pancreatitis. 636 35

The effects of repeated intravenous calcium administration on pancreatic juice secretion were investigated in four Thomas fistula dogs. During stimulation by 1.0 U kg-1h-1 GIH secretin, three Ca doses were administered: 2, 4 and 8 mu mol kg-1 min-1 during 1 h, saline being used in control tests; one dose only was tested per day. It was found that Ca administration induced both acute and long-lasting effects. Acute effects were characterized by an increased response to secretin stimulation. Fluid, HCO3(-), protein and Ca outputs increased significantly in a dose-dependent manner, the increase of protein output being the most dramatic. Long-lasting effects, until now unrecognized, were characterized by a progressive increase of protein secretion during the first hour of secretin stimulation. This increase kept going during the 3 months of repeated calcium injections. Although protein plugs were observed in the juice, sometimes stopping the flow of juice, no pancreatic lesion was found. A second protocol showed that, after discontinuing calcium injections, the long-lasting effects decreased progressively, but protein hypersecretion was still significant 3.5 months later. The importance of these findings regarding chronic pancreatitis due to hyperparathyroidism is discussed.
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PMID:Dose-dependent, and long-lasting, effects of repeated intravenous injections of calcium on the canine secretin-stimulated pancreatic juice secretion. 678 25

Pancreatic calcification is a frequent complication of chronic pancreatitis, and pancreatic stones (95% CaCO3 as calcite) are observed in both humans and cattle, but little is known about the complex equilibriums governing calcium solubility. Using the Ca2+ electrode and equilibrium dialysis of NaHCO3-CaCl2-NaCl solutions (24 +/- 2 degrees C; total ionic strength = 0.153-0.161), studies were made at variable pH and total calcium and carbonate concentrations to determine the formation constants of the three possible calcium complexes: CaHCO3+, CaC03(0), and Ca(HCO3)20. If the first two complexes were present, a plot of ([Ca]/[Ca2+]-1)/[HCO3-] against the ionic ratio [C03(2)-]/[HCO3-] should be linear with intercept of the CaHCO3+ formation constant (K'aB) and slope of the CaC03(0) formation constant (K'aC). This was found to be the case in both dialysands and dialysates, using two different methods ("pH" and "K'sp") for estimation of [CO32-] values. Two other methods of data analysis were also used: simultaneous equations and multiple linear regression by matrix analysis. For all three methods, mean K'aB = 12.48 and mean K'aC = 1,870. There was no evidence for a Ca(HCO3)2(0) complex. We conclude that CaHCO3+ and CaC03(0) complexes may account for a substantial fraction of total soluble calcium is pancreatic juice. These studies provide a necessary step toward the construction of a quantitative physicochemical model of pancreatic calcium solubility.
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PMID:Pancreatic calcification: formation constants of CaHCO3+ and CaC03(0) complexes determined with Ca2+ electrode. 727 Jun 96


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