B J Ammori1, G R Barclay, Mike Larvin, Michael J McMahon. 1. Division of Surgery, The University of Leeds, and Center for Digestive Diseases, The General Infirmary, Leeds, United Kingdom. Bammori@aol.com
Abstract
INTRODUCTION: Hypocalcemia is not uncommon during acute pancreatitis and is associated with a poor outcome. Whilst the mechanisms responsible for its development remain unclear, there is evidence to implicate endotoxemia in other models of sepsis. AIM: To investigate the potential role of systemic endotoxin exposure in the development of hypocalcemia in patients with acute pancreatitis. METHODOLOGY: Adjusted serum calcium was measured daily, and the lowest value within 72 hours of admission for acute pancreatitis was determined. Serum endotoxin and both IgG and IgM antiendotoxin core antibodies (EndoCAbs) were measured on admission. Attacks were classified as mild (n = 51) or severe (n = 21) according to the criteria of the Atlanta International Symposium of 1992. RESULTS: Hypocalcemia was significantly more frequent (86% versus 39%, p < 0.001) and reached significantly lower levels during severe attacks than during mild attacks (median [interquartile range], 2.06 [1.78-2.17] mmol/L, versus 2.23 [2.15-2.30] mmol/L; p < 0.001). Endotoxemia was present in a significantly greater proportion of patients with severe disease (71% versus 41%; p = 0.037), and serum IgM and IgG EndoCAbs were significantly depleted during severe attacks in comparison with mild attacks (p = 0.007 and p = 0.039, respectively). A negative and significant correlation was observed between endotoxemia and both the admission and lowest serum concentrations of adjusted calcium (r = -0.424 and p = 0.022; r = -0.383 and p = 0.037, respectively), and the latter correlated significantly with serum IgG EndoCAb concentrations (r = 0.251; p = 0.036). CONCLUSION: Systemic endotoxin exposure appears to play a significant role in the development of hypocalcemia in patients with acute pancreatitis.
INTRODUCTION:Hypocalcemia is not uncommon during acute pancreatitis and is associated with a poor outcome. Whilst the mechanisms responsible for its development remain unclear, there is evidence to implicate endotoxemia in other models of sepsis. AIM: To investigate the potential role of systemic endotoxin exposure in the development of hypocalcemia in patients with acute pancreatitis. METHODOLOGY: Adjusted serum calcium was measured daily, and the lowest value within 72 hours of admission for acute pancreatitis was determined. Serum endotoxin and both IgG and IgM antiendotoxin core antibodies (EndoCAbs) were measured on admission. Attacks were classified as mild (n = 51) or severe (n = 21) according to the criteria of the Atlanta International Symposium of 1992. RESULTS:Hypocalcemia was significantly more frequent (86% versus 39%, p < 0.001) and reached significantly lower levels during severe attacks than during mild attacks (median [interquartile range], 2.06 [1.78-2.17] mmol/L, versus 2.23 [2.15-2.30] mmol/L; p < 0.001). Endotoxemia was present in a significantly greater proportion of patients with severe disease (71% versus 41%; p = 0.037), and serum IgM and IgG EndoCAbs were significantly depleted during severe attacks in comparison with mild attacks (p = 0.007 and p = 0.039, respectively). A negative and significant correlation was observed between endotoxemia and both the admission and lowest serum concentrations of adjusted calcium (r = -0.424 and p = 0.022; r = -0.383 and p = 0.037, respectively), and the latter correlated significantly with serum IgG EndoCAb concentrations (r = 0.251; p = 0.036). CONCLUSION: Systemic endotoxin exposure appears to play a significant role in the development of hypocalcemia in patients with acute pancreatitis.