RESUMEN
BACKGROUND: Previous studies on gastrin levels in chronic pancreatitis (CP) patients have given conflicting results. These studies did not take into consideration the influence of Helicobacter pylori (H. pylori) infection on gastrin release. Also, there is no previous study that compared alcoholic CP patients to patients with idiopathic pancreatitis. Our aim was to measure basal and postprandial plasma gastrin levels in all CP patients, including subgroups of alcoholic, idiopathic, severe and mild CP patients, and compare them with healthy subjects after the eradication of H. pylori infection. PATIENTS AND METHODS: Basal and postprandial gastrin levels were measured in 30 patients with CP (10 patients with alcoholic and 20 patients with idiopathic CP) and in 25 healthy subjects. RESULTS: A significant increase in basal gastrin levels was found only in a subgroup of alcoholic CP (P<0.05) in comparison to healthy subjects. A significant increase in postprandial plasma gastrin levels (P<0.01) was found in all chronic pancreatitis compared to healthy subjects. CONCLUSION: In the absence of H. pylori infection, plasma gastrin levels were significantly higher in chronic pancreatitis patients than in healthy subjects. Chronic alcoholism, however, does not appear to be the only factor responsible for the increased plasma gastrin levels in these patients.
RESUMEN
BACKGROUND/AIMS: The existence of a negative-feedback mechanism between pancreatic enzyme secretion and intraduodenal proteases and the role of cholecystokinin in its mediation in humans is debatable. The presence of such a feedback mechanism in chronic pancreatitis patients with exocrine enzyme deficiency possibly leads to an increase in cholecystokinin plasma levels. Somatostatin has been used in many studies in the therapy of pain in chronic pancreatitis and plays a role in the regulation of cholecystokinin levels, however data on its plasma levels are still lacking. METHODOLOGY: Basal and the postprandial cholecystokinin and somatostatin levels in 30 patients with chronic pancreatitis (11 with severe chronic pancreatitis and 19 with mild chronic pancreatitis) were measured 14 days after discontinuation of enzymatic substitution therapy and then were compared with the levels taken from 25 healthy subjects. RESULTS: The cholecystokinin postprandial plasma levels were significantly higher in patients with chronic pancreatitis when compared with those of healthy individuals (P < 0.01). Basal, somatostatin, cholecystokinin and postprandial somatostatin levels were not significantly higher than those in healthy subjects. There was no correlation between basal and postprandial levels of cholecystokinin and somatostatin in our study. CONCLUSIONS: The cholecystokinin postprandial plasma levels were significantly higher in all patients with chronic pancreatitis when compared with healthy individuals, which suggests the role of cholecystokinin in the feedback control of pancreatic secretion.
Asunto(s)
Colecistoquinina/sangre , Pancreatitis/sangre , Somatostatina/sangre , Adulto , Colecistoquinina/fisiología , Enfermedad Crónica , Femenino , Humanos , Masculino , Persona de Mediana Edad , Periodo PosprandialRESUMEN
The mortality rate in acute pancreatitis (AP) is significantly lower in patients hospitalized directly at the intensive care unit than in patients admitted to hospital in 2 weeks after the assessment of diagnosis, prophylactic administration of low-molecular protease inhibitor reduces the occurrence of post ERCP pancreatitis a well a coincident complications. Despite rational considerations concerning the significance of pryphylactic administration of antibodies (ATB) in severe AP, there still not enough convincing data which could be recommended a standard therapy. One of the concepts of causal therapy of AP. Suggest that inhibition of exocrine pancreatic enzymatic secretion reduces autodigestion of the gland (setting the gland at rest). The reports on success of secretin-inhibiting substances a glucagon, calcitonin, atropine and somatostatin require confirmation in randomized or accurately defined comparable groups. The initial studies on the therapeutic significance of lexipanphate-antagonist of platelet activating factor (PAF) in acute pancreatitis is promising. A long-term lavage had reduced the mortality.
Asunto(s)
Pancreatitis/terapia , Enfermedad Aguda , HumanosRESUMEN
The theory of pancreatic gland autodigestion by pancreatic enzymes assumed by Chiari 1886 as the crucial moment in the pathogenesis of acute pancreatitis (AP) remains accepted so far. The appearance of mutations of cationic trypsinogen gene on the 7th chromosome in several families with hereditary AP, supports the significance of trypsin in the initiation of AP. The generally recognized etiologic factors of AP include the biliary tract disease and alcohol. Opie in his "Common Channel theory" assumed that the impacted gallstone in the ampulla of Vater could cause a permanent obstruction and subsequently AP. Later clinical studies have confirmed that a short-term block of the common pancreatic duct caused by migrating gallstones is associated with onset of AP. Chronic consumption of alcohol evokes subclinical pancreatic disturbances already prior to the onset of AP. PAP (pancreatic associated protein) being the marker of pancreatic inflammation was significantly increased in chronic alcoholism without signs of AP. Many pathophysiological concepts and effective therapeutic procedures which were successful in the animal studies have not turned out to be appropriate in man. The destruction of both cellular structure and cellular connections is an early event in the development of experimental AP. There is much evidence that free oxygen radicals and the disturbances of microcirculation determine the severeness of AP. The roles of NO (nitric oxide) and kinins remain to be clarified cytokins a interleukin 2 (IL2) and interleukin 10 (IL10) had a protective effect in experimental AP. In humans the antagonist of PAF (platelet activating factor) had reduced the occurrence of organ failure. There is hope, that this knowledge, will lead to new therapeutic possibilities.