Brief Reports
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 21, 2005; 11(35): 5535-5539
Published online Sep 21, 2005. doi: 10.3748/wjg.v11.i35.5535
Mechanism of diarrhea in microscopic colitis
Marijana Protic, Njegica Jojic, Daniela Bojic, Svetlana Milutinovic, Dusanka Necic, Bozidar Bojic, Petar Svorcan, Miodrag Krstic, Obren Popovic
Marijana Protic, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Njegica Jojic, Daniela Bojic, Metabolic Department, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Svetlana Milutinovic, Institute for Pathology, Zvezdara University Clinical Center, Belgrade
Dusanka Necic, Metabolic Laboratory, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Bozidar Bojic, Endoscopic Unit, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Petar Svorcan, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Miodrag Krstic, Center for Gastroenterology and Hepatology, Clinical Center of Serbia, Belgrade
Obren Popovic, Center for Gastroenterology and Hepatology, Zvezdara University Clinical Center, Belgrade
Author contributions: All authors contributed equally to the work.
Correspondence to: Marijana Protic, MD, Assistant Professor, Center for Gastroenterology and Hepatology, Zvezdara Clinical Center, 161 Dimitrija Tucovica, Belgrade 11 000, Serbia and Montenegro. marijanaprotic@beotel.yu
Telephone: +381-63-345985 Fax: +381-11-3806340
Received: January 19, 2005
Revised: February 23, 2005
Accepted: February 28, 2005
Published online: September 21, 2005
Abstract

AIM: To search the pathophysiological mechanism of diarrhea based on daily stool weights, fecal electrolytes, osmotic gap and pH.

METHODS: Seventy-six patients were included: 51 with microscopic colitis (MC) [40 with lymphocytic colitis (LC); 11 with collagenous colitis (CC)]; 7 with MC without diarrhea and 18 as a control group (CG). They collected stool for 3 d. Sodium and potassium concentration were determined by flame photometry and chloride concentration by titration method of Schales. Fecal osmotic gap was calculated from the difference of osmolarity of fecal fluid and double sum of sodium and potassium concentration.

RESULTS: Fecal fluid sodium concentration was significantly increased in LC 58.11±5.38 mmol/L (P<0.01) and CC 54.14±8.42 mmol/L (P<0.05) than in CG 34.28±2.98 mmol/L. Potassium concentration in LC 74.65±5.29 mmol/L (P<0.01) and CC 75.53±8.78 mmol/L (P<0.05) was significantly less compared to CG 92.67±2.99 mmol/L. Chloride concentration in CC 36.07±7.29 mmol/L was significantly higher than in CG 24.11±2.05 mmol/L (P<0.05). Forty-four (86.7%) patients had a secretory diarrhea compared to fecal osmotic gap. Seven (13.3%) patients had osmotic diarrhea.

CONCLUSION: Diarrhea in MC mostly belongs to the secretory type. The major pathophysiological mechanism in LC could be explained by a decrease of active sodium absorption. In CC, decreased Cl/HCO3 exchange rate and increased chloride secretion are coexistent pathways.

Keywords: Lymphocytic colitis; Collagenous colitis; Secretory diarrhea