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2019 | 75 | 01 |

Tytuł artykułu

Rola wybranych parametrów biochemicznych w przewidywaniu zmian histopatologicznych w 24. i 48. godzinie od wystąpienia ostrego zapalenia trzustki

Warianty tytułu

EN
Role of biochemical parameters in predicting histopathological changes at 24 and 48 hours from acute pancreatitis induction

Języki publikacji

PL

Abstrakty

EN
The aim of the study was to assess the relationships between the degree of changes in concentrations of the biochemical indicators in serum such as: creatinine, uric acid, total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), lipase, amylase, glucose, iron and magnesium, and histopathological lesions occurring in the pancreas within 24 and 48 hours from the induction of acute pancreatitis (AP). An attempt was made to assess the relation between the changes in concentrations of biochemical indicators and the enhancement of histological lesions in the pancreas based on Spormann score. In the experimental model, the laboratory and histological changes in the 24th hour from administration of taurocholan correspond to the seventh day of the disease in humans. Experiments were conducted on 55 male Wistar rats weighing from 250 g to 300 g. The animals were divided into three groups: Z – a group serving to establish the ranges of studied factors and histological structure; K – a group of animals operated on which were injected with 0.9% NaCl into the biliary-pancreatic duct; E – a group of animals operated on in which acute pancreatitis was induced by an injection of 5% sodium taurocholate into the biliary-pancreatic duct. The material for biochemical and histological examinations was collected after 24 and 48 hours from the induction of AP. Whole pancreases were dissected for histological examinations and the samples were dyed with hematoxylin and saturated alcoholic eosin solution. The degree of pancreatic lesions was assessed according to the Spormann score. Quantitative variables were characterised by arithmetic mean, standard deviation, median, minimum and maximum value and 95% CI. After administration of 0.9% NaCl in the K group, foci of purulent inflammation in the fatty tissue of the pancreas and minor foci of Balser’s necrosis appeared. In the E group, after injection of 5% sodium taurocholate into the biliary-pancreatic duct, more intense lesions were observed: foci of fatty tissue necrosis, hemorrhagic necrosis, multifocal fatty tissue necrosis and inflammatory infiltration. The model was developed in order to assess histological lesions, indicating the character of AP, taking into account edema, inflammatory infiltration, fatty tissue necrosis, glandular necrosis, and ecchymoses. In the period of 24 hours, statistically significant differences between the K group and E group were observed for creatinine, total bilirubin, ALT, lipase, amylase, iron and magnesium, while in the period of 48 hours, statistically significant differences were observed for total bilirubin and ALT. In the group E, in the period of 24 hours concentrations of creatinine, total bilirubin, ALT, lipase, amylase and magnesium were significantly higher than in the group K, but concentrations of iron were significantly lower. In the period of 48 hours, in the E group total bilirubin was significantly lower and ALT was significantly higher than in the K group. In the E group, the intensity of pancreatitis increased together with an increase in ALT concentration in the period of 24 hours; in the period of 48 hours, the intensity of pancreatitis increased together with a decrease in ALT in the E group. In the K group, in the period of 48 hours, intensity of fatty tissue necrosis increased together with a decrease in ALT level. In the period of 48 hours, in the E group intensity of glandular necrosis increased together with a decrease in total bilirubin and AST concentration. In the E group, in the period of 24 hours intensity of edema increased together with an increase in magnesium level. In the period of 48 hours, in the E group intensity of glandular necrosis increased together with a decrease in magnesium or AST level, and the intensity of lesions in the form of ecchymoses increased together with an increase in glucose level. Histopathological lesions occurred prior to changes in laboratory test results, whereas significant correlations with the Spormann score concerned changes in: total bilirubin, AST, ALT, glucose and magnesium. The use of regression analysis with the Spormann score shows statistically significant differences for most of the biochemical parameters in the period of 24 hours correspond to the seventh day of the disease in humans. The presented study results confirm the fact that diagnostics of acute pancreatitis is very difficult and requires monitoring of many laboratory parameters. A search is still going on for an ideal marker of AP which would enable an early prognosis of the progress of the disease and the confirmation of its etiology. A discovery of a simple marker which is cheap to use may turn out to be useful if it is confirmed in prospective studies. The current state of knowledge based on scientific and clinical findings makes it possible to apply interdisciplinary clinical procedures based on matching appropriate laboratory and radiological tests, and on implementing therapeutic procedures.

Wydawca

-

Rocznik

Tom

75

Numer

01

Opis fizyczny

s.41-49,tab.,fot.,bibliogr.

Twórcy

autor
  • Zakład Anatomii Prawidłowej, Katedra Anatomii Człowieka, Uniwersytet Medyczny w Lublinie, ul.Jaczewskiego 4, 20-090 Lublin
  • Zakład Anatomii Prawidłowej, Katedra Anatomii Człowieka, Uniwersytet Medyczny w Lublinie, ul.Jaczewskiego 4, 20-090 Lublin
  • Oddział Chirurgii Plastycznej, Centralny Szpital Kliniczny MSWiA w Warszawie, ul.Wołoska 137, 02-507 Warszawa
autor
  • Katedra i Klinika Chirurgii Urazowej i Medycyny Ratunkowej, Uniwersytet Medyczny w Lublinie, ul.Staszica 16 (SPSK Nr 1), 20-081 Lublin
  • Instytut Elektroniki i Technik Informacyjnych, Politechnika Lubelska, ul.Nadbystrzycka 38A, 20-618 Lublin
autor
  • II Katedra i Klinika Chirurgii Ogólnej, Gastroenterologicznej i Nowotworów Układu Pokarmowego, Uniwersytet Medyczny w Lublinie, ul.Staszica 16 (SPSK Nr 1), 20-081 Lublin

Bibliografia

  • Aho H. J., Konkensalo M. L., Nevalainen T. L.: Experimental pancreatitis in the rat. Sodium taurocholate induced acute haemorrhagic pancreatitis. Scand. J. Gastroenterol. 1980, 15, 411-416.
  • Aho H. J., Nevalainen T. J.: Experimental pancreatitis in the rat. Ultrastructure of Sodium Taurocholate-induced pancreatic lesions. Scand. J. Gastroenterol. 1980, 15, 417-424.
  • Banks P. A., Freeman M. L.: Practice Guidelines in Acute Pancreatitis. Am. J. Gastroenterol. 2006, 101, 2379-2400.
  • Beaux A. C. de, Palmer K. R., Carter D. C.: Factors influencing morbidity and mortality in acute pancreatitis: an analysis of 279 cases. Gut 1995, 37, 121-126.
  • Blum T., Maisonneuve P., Lowenfels A. B., Lankisch P. G.: Fatal outcome in acute pancreatitis: its occurrence and early prediction. Pancreatology 2001, 1, 237-241.
  • Davidson B. R., Neoptolemos J. P., Leese T., Carr-Locke D. L.: Biochemical prediction of gallstones in acute pancreatitis: a prospective study of three systems. Br. J. Surg. 1988, 75, 213-215.
  • Dholakia K., Pitchumoni C. S., Agarwal N.: How often are liver function tests normal in acute biliary pancreatitis? J. Clin. Gastroenterol. 2004, 38, 81-83.
  • Isenman R., Rau B., Beger H. G.: Bacterial infection and extent of necrosis are determinants of organ failure in patients with acute necrotizing pancreatitis. Brit. J. Surg. 1999, 86, 1020-1024.
  • Lankisch P. G., Burchard Reckert S., Lehnick D.: Underestimation of acute pancreatitis: patients with only a small increase in amylase/lipase levels can also have or develop severe acute pancreatitis. Gut 1999, 44, 542-544.
  • Lankisch P. G., Pflichthofer D., Lehnick D.: No strict correlation between necrosis and organ failure in acute pancreatitis. Pancreas 2000, 20, 319-322.
  • McKay C. J., Imrie C. W.: The continuing challenge of early mortality in acute pancreatitis. Br. J. Surg. 2004, 91, 1243-1244.
  • Muddana V., Whitcomb D. C., Khalid A., Slivka A., Papachristou G. I.: Elevated serum creatinine as a marker of pancreatic necrosis in acute pancreatitis. Am. J. Gastroenterol. 2009, 104, 164-170.
  • Munoz A., Katerndahl D. A.: Diagnosis and management of acute pancreatitis. Am. Fam. Physician. 2000, 62, 164-174.
  • Spormann H., Sokolowski A., Letko G.: Effect of temporary ischemia upon development and histological patterns of acute pancreatitis in the rat. Path. Res. Pract. 1989, 184, 507-513.
  • Spormann H., Sokolowski A., Letko G.: Experimental acute pancreatitis – a quantification of dynamics at enzymic and histomorphologic levels. Pathol. Res. Pract. 1989, 185, 358-362.
  • Steer M. L.: Workshop on experimental pancreatitis – report of workshop. Dig. Dis. Sci. 1985, 30, 575-581.
  • Stimac D., Miletic D., Radic M., Krznaric I., Mazur-Grbac M., Perkovic D., Milic S., Golubovic V.: The role of nonenhanced magnetic resonance imaging in the early assessment of acute pancreatitis. Am. J. Gastroenterol. 2007, 102, 997-1004.
  • Tenner S., Dubner H., Steinberg W.: Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis. Am. J. Gastroenterol. 1994, 89, 1863-1866.
  • Vissers R. J., Abu-Laban R. B., McHugh D. F.: Amylase and lipase in the emergency department evaluation of acute pancreatitis. J. Emerg. Med. 1999, 17, 1027-1037.
  • Yadav D., Agarwal N., Pitchumoni C. S.: A critical evaluation of laboratory tests in acute pancreatitis. Am. J. Gastroenterol. 2002, 97, 1309-1318.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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