Microscopic colitis： A retrospective study of clinical presentation in 53 patients

AIM: To evaluate the relationship between symptoms and microscopic colitis (MC) subtypes: to test whether collagenous colitis (CC) and/or lymphocytic colitis (LC) might be related to both constipation and diarrhea. METHODS: A cohort of patients with independently confirmed typical histopathological changes was investigated. Fifty-three patients with histologically proved MC (46 with CC, 7 with LC) were included. The existence of diarrhea or constipation and the co-existence of autoimmune diseases were also investigated and all data were retrospectively analyzed. RESULTS: Twenty-three (43.39%) of MC patients had chronic constipation (20 in CC, 3 in LC patients). Twenty-four (45.28%) of MC patients had autoimmune disease and the diagnosis of autoimmune disease was always prior to MC. Sjogren's syndrome was associated only with the constipation subgroup. CONCLUSION: The Janus face of MC resembles the subgroups of irritable bowel syndrome. The co-existence of autoimmune diseases and MC is confirmed in both the constipation and diarrhea subgroups.     

Clinical characteristics of collagenous and lymphocytic colitis

Background: Microscopic colitides (MC), collagenous colitis (CC) and lymphocytic colitis (LC) share clinical features, but their mutual relationship is unclear, and clinical comparative studies are rare. We aimed to examine the clinical features in CC and LC by focusing on concomitant diseases. Methods: Patients with MC (30 with CC, 54 with LC) were identified in the pathology databases and by reviewing biopsies. Controls included 84 age‐ and sex‐matched persons. The clinical data collected from patient records were prospectively completed by interviews. Results: The female:male ratio was 2:1 in CC and 5.75:1 in LC. Mean age at diagnosis was 53 in CC and 55.4 years in LC. There were no differences in the pattern of symptoms. Concomitant autoimmune diseases were more common in CC (53.3%) than in LC (25.9%; P?=?0.017). Celiac disease was common in both CC (20%) and LC (14.8%). Bronchial asthma was associated with LC (25.9%), but not with CC (6.7%; P?=?0.042). Colon diverticulosis was rare in MC (16%) compared with the controls (39%; P?=?0.001). Hypolactasia was common in MC (45%; 76% in CC, 54% in LC) compared to its prevalence in the Finnish general population (17%). Conclusions: CC and LC are largely similar clinically, but the differences in the occurrence of autoimmune conditions and bronchial asthma suggest that they differ in immunopathogenesis. MC is associated with reduced lactose tolerance and shows a negative association with diverticular disease, possibly related to the small intestinal pathology and abnormal stool consistency.     

Elevated fecal levels of eosinophil granule proteins predict collagenous colitis in patients referred to colonoscopy due to chronic non-bloody diarrhea

Objective: Colonoscopy with biopsy sampling is often performed to detect collagenous colitis (CC) and lymphocytic colitis (LC) in patients with chronic non-bloody diarrhea. However, the diagnostic yield is low and incurs high costs. Fecal calprotectin (FC) and myeloperoxidase (MPO) indicate intestinal inflammation in ulcerative colitis (UC) and Crohn’s disease (CD). In CC, elevated fecal levels of eosinophil protein X (EPX) and eosinophil cationic protein (ECP) have been reported. We aimed to evaluate if F-EPX, F-ECP, FC, and F-MPO could predict the diagnostic outcome in patients with chronic non-bloody diarrhea referred to colonoscopy. We also evaluated serum (S) EPX and ECP in this regard.

Methods: Of 67 included patients, 63 (94%) underwent colonoscopy with biopsy sampling. Fecal EPX, F-ECP, FC, F-MPO, S-EPX, and S-ECP were analyzed.

Results: Diagnostic outcome: normal: n?=?46 (73%), CC: n?=?9 (14%), LC: n?=?4 (6%), UC: n?=?2 (3%), CD: n?=?2 (3%). Higher levels of F-EPX and F-ECP were found in CC compared to a normal diagnostic outcome (p?=?0.01). No change was noted in any of the fecal markers in LC. When all of the fecal markers were normal the probability of a normal diagnostic outcome was 92%. We found no differences in S-EPX and S-ECP between the groups.

Conclusion: Elevated F-EPX and F-ECP could predict CC. None of the fecal markers predicted LC. Serum-EPX and S-ECP are not useful for the diagnosis of CC, LC, UC, or CD. With normal levels in all of the analyzed fecal markers, there is a low probability of a pathologic diagnostic outcome.     

Microscopic Colitis in Routine Colonoscopies

Lymphocytic colitis (LC) and collagenous colitis (CC), both known as microscopic colitis (MC), are uncommon entities with increasing incidence as more clinicians take biopsies from macroscopically normal colons and as pathologists use more rigorous diagnostic criteria to be confident of the diagnosis. Information on the incidence of this type of colitis is limited and based on reported cases. The purpose of this work is to estimate the incidence of LC and CC in reviewed routine colonoscopies. We reviewed 2815 colonoscopies performed at a tertiary referral center with an open-access service using restricted histological criteria in order to establish the frequency rate of LC and CC in routine colonoscopic biopsy material. Cases suspicious for MC were stained with Masson's trichrome or Congo red stain and immunohistochemically for lymphocytes, where appropriate. Review of routine colonoscopic biopsies showed that MC is underreported in our colonoscopic material. Incidence rates of LC and CC (0.9 and 0.4, respectively) were based on morphological assessment of colonoscopic biopsies using stringent criteria together with clinical data and after differentiation with other lesions which can mimic MC. The 10.2% rate of this type of colitis in patients with chronic watery diarrhea indicates the necessity to consider these lesions in older individuals with diarrhea and normal endoscopical colonic mucosa.     

Short-chain fatty acids in pouch contents from patients with and without pouchitis after ileal pouch-anal anastomosis.

Fecal concentrations of short-chain fatty acids were markedly reduced in 6 patients with pouchitis (mean +/- SE, 56.2 +/- 13.3 mmol/L) compared with 28 patients without pouchitis (139.0 +/- 8.5 mmol/L; P less than 10(-3)). The ratios of acetate to propionate to butyrate were not changed (pouchitis, 75:12:11%; normal pouches, 76:12:11%), i.e., all acids were equally reduced. The 24-hour production of total short-chain fatty acids in 16.6% fecal homogenates from patients with pouchitis was decreased (17.5 +/- 5.3 mmol/L) compared with patients without pouchitis (33.3 +/- 3.4 mmol/L; P less than 0.05), which could be overcome by the addition of saccharides to the homogenates. Pouch excretions of saccharides were similar in the two groups, but dilution occurred during pouchitis because of the increased outputs. Concentrations and productions of short-chain fatty acids correlated with pouch concentrations and excretions of sodium and saccharides. L-Lactate was elevated in pouchitis outputs, but differences in stool culture counts, mucosal histology, fecal concentration, assimilation or production of ammonia, nitrogen excretion, pH, and osmolality were not found. Pouchitis is characterized by decreased fecal concentrations and productions of short-chain fatty acids possibly caused by low pouch concentrations of fermentable saccharides.     

Fecal lactoferrin is a sensitive and specific marker in identifying intestinal inflammation

OBJECTIVE: Lactoferrin is a glycoprotein expressed by activated neutrophils. The aim of this study was to determine the sensitivity and specificity of fecal lactoferrin concentrations for inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) versus healthy controls. METHODS: Fresh stool samples were collected from outpatients with ulcerative colitis (UC), Crohn's disease (CD), or IBS. Clinical disease activity for IBD was assessed using a modified Harvey-Bradshaw Activity Index. Fecal lactoferrin concentrations were determined using a polyclonal antibody-based enzyme linked immunoassay. Mean fecal lactoferrin concentrations for each group and sensitivity and specificity of the assay were determined. RESULTS: One hundred-four CD patients, 80 UC patients, 31 IBS patients, and 56 healthy controls were recruited. The mean +/- SE fecal lactoferrin concentration (microg/g fecal weight) was 440 +/- 128 for CD patients, 1125 +/- 498 for UC patients, 1.27 +/- 0.29 for IBS patients, and 1.45 +/- 0.4 for healthy controls. Fecal lactoferrin was 90% specific for identifying inflammation in patients with active IBD. Elevated fecal lactoferrin was 100% specific in ruling out IBS. CONCLUSIONS: Fecal lactoferrin is sensitive and specific for detecting inflammation in chronic IBD. This noninvasive test may prove useful in screening for inflammation in patients presenting with abdominal pain and diarrhea.     

Organic anions and the diarrhea of inflammatory bowel disease

To determine if organic anions contribute to the diarrhea of inflammatory bowel disease, we measured osmolality, electrolytes, short-chain fatty acids, lactic acid, and some Krebs cycle anions in 24-hr fecal collections from 18 patients with chronic ulcerative colitis, 20 with Crohn's disease of the colon, and 16 normals. Mean lactic acid concentration was significantly elevated in ulcerative and Crohn's colitis, but values correlated with fecal weight only in the former syndrome. In ulcerative colitis, concentrations of each short-chain fatty acid, especially butyrate, were decreased compared with those from normals or Crohn's disease. Lactate and short-chain fatty acids accounted for nearly half the variability in fecal weight in ulcerative colitis. Crohn's patients had elevated mean fecal water osmolality and osmotic gap not observed in ulcerative colitis. Increased lactic acid and/or deficient short-chain fatty acids may modulate the diarrhea of ulcerative colitis. This mechanism seems less important in Crohn's colitis where an additional osmotic component may be significant.This work was supported in part by grant 3651 from an endowment of the T.T. Dee and G.F. Moody Fund through Evanston Hospital, Evanston, Illinois.     

Microscopic colitis： A large retrospective analysis from a health maintenance organization experience

AIM： To examine the demographic data on a large multi-ethnic population of patients with microscopic colitis （MC） in Southern California and to determine the association of MC with inflammatory bowel disease （IBD） and colorectal cancer. METHODS： All patients diagnosed with MC by co- Ionic biopsy from 1996-2005 were identified utilizing a pathology database. All biopsies were reviewed by experienced pathologists utilizing standard histologic criteria. Patients＇ medical records were reviewed and data regarding patient age, co-morbidities, sex, ethnic- ity, and medications were analyzed. An age- and sex- matched standard control group was also generated. Chi-square test was used to evaluate the associations of co-morbidities between lymphocytic colitis （LC）, col- lagenous colitis （CC） and the control group. RESULTS： A total of 547 cases of MC were identified, 376 patients with LC and 171 patients with CC. The fe- male/male ratio was 3：1 in CC and 2.7：1 in LC patients. Celiac disease （P 〈 0.001）, irritable bowel syndrome （IBS） （P 〈 0.001）, and thyroid diseases （P 〈 0.001） were found to have a higher occurrence in MC com- pared to the control group. No statistical differences in the occurrence of colorectal cancer, diabetes and IBD were found between the MC group and the control group. CONCLUSION： This is the largest group of patients with MC known to the authors that has been studied to date. Conditions such as celiac disease, IBS, and thyroid diseases were found to be related to MC. Fur- thermore, neither an increased risk of colorectal cancer nor IBD was associated with MC in this study.     

Mesalazine with or without cholestyramine in the treatment of microscopic colitis: randomized controlled trial

BACKGROUND: Collagenous colitis (CC) and lymphocytic colitis (LC) are chronic inflammatory diseases of the colon with a benign and sometimes relapsing course. Frequency among patients with chronic diarrhea and normal looking colonoscopy is around 10-15%. To date, treatment of CC and LC is not well defined. Data about these conditions are mostly derived from retrospective studies. The aim of the present study was to evaluate the response to treatment and the clinical course of CC and LC in a large group of patients prospectively diagnosed. METHODS AND RESULTS: A total of 819 patients underwent a colonoscopy because of chronic watery diarrhea and among them we found 41 patients with LC and 23 with CC. These patients were later randomized and assigned to treatment with mesalazine or mesalazine + cholestyramine for 6 months. Fifty-four patients (84.37%) had resolved diarrhea in less than 2 weeks. After 6 months a colonoscopy with biopsies was repeated. Clinical and histological remission was achieved in 85.36% of patients with LC and in 91.3% with CC, with a better result in patients with CC treated with mesalazine + cholestyramine. During a mean period of 44.9 months, 13% of patients relapsed; four with LC and three with CC. They were retreated for another 6 months. At the end of this period one patient with CC was still symptomatic and persistence of CC was confirmed at histology. CONCLUSIONS: Treatment with mesalazine seems to be an effective therapeutic option for LC to date, while mesalazine + cholestyramine seems to be more useful in the treatment of CC.     

Pathogenesis of rotavirus-induced diarrhea

The pathogenesis of diarrhea caused by rotavirus infection was studied in miniature swine piglets. The animals were inoculated orally with 2 X 10(7) plaque-forming units of porcine rotavirus (OSU strain). During the height of diarrhea, intestinal function was investigated by in vivo perfusion of a 30-cm segment of proximal jejunum and a 30-cm segment of distal ileum. Absorption of Na+ and water decreased and 3-O-methylglucose transport was markedly reduced, P less than 0.01 compared to control animals. Mucosal lactase and sucrase levels were depressed in both the jejunum and ileum, P less than 0.001. Na+,K+-ATPase activity was significantly depressed only in the ileum, P less than 0.001. These changes were associated with a marked reduction in villous height, suggesting that the diarrhea could be an osmotic diarrhea due to nutrient (carbohydrate) malabsorption. Fresh stool samples were obtained and analyzed immediately for NA+,K+, osmolarity, glucose, and lactose; the osmotic gap was also determined. Stool osmolarity continually increased from 248 +/- 20 mosm/liter prior to inoculation to 348 +/- 20 mosm/liter at 75 +/- 1 hr postinoculation (P less than 0.005); the majority of the fecal osmotic gap could be accounted for by the amount of lactose present in the stools. Stool sodium increased from 34 +/- 6 mM prior to inoculation to a maximum of 65 +/- 4 mM at 53 +/- 1 hr postinoculation, P less than 0.001. There was no significant change in potassium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fecal osmotic gap and pH in experimental diarrhea of various causes.

Although the osmotic gap of fecal fluid is often used to distinguish osmotic diarrhea from secretory diarrhea, there has never been a scientific evaluation of the validity of this concept. Similarly, although a low fecal fluid pH value is used to indicate that diarrhea is mediated by carbohydrate malabsorption, the validity of this method is unproven. Therefore, in the present study, diarrhea was induced in normal subjects by different mechanisms and fecal fluid osmotic gap (using an assumed fecal fluid osmolality of 290 mOsm/kg) and pH were measured. In secretory diarrhea caused by phenolphthalein, the osmotic gap was always less than 50 mOsm/kg, whereas in osmotic diarrhea caused by polyethylene glycol, magnesium hydroxide, lactulose, and sorbitol, the osmotic gap always exceeded 50 mOsm/kg. In osmotic diarrhea caused by sodium sulfate, the fecal fluid osmotic gap was less than 50 mOsm/kg, but phenolphthalein-induced secretory diarrhea could be distinguished from sodium sulfate-induced osmotic diarrhea by the fecal chloride concentration. When diarrhea was caused by carbohydrate malabsorption (lactulose or sorbitol), the fecal fluid pH was always less than 5.6 and usually less than 5.3; by contrast, other causes of diarrhea rarely caused a fecal pH as low as 5.6 and never caused a pH less than 5.3. It is concluded that measurement of fecal fluid osmotic gap and pH can distinguish various mechanisms of experimental diarrhea in normal subjects. The concepts on which these tests are based are therefore verified experimentally.     

Diarrhea in tube-fed patients: feeding formula not necessarily the cause

PURPOSE: This study of diarrhea in tube-fed patients was undertaken to determine the proportion of cases in which feeding formula is not responsible for the diarrhea, the causes other than the feeding formula, and the diagnostic approach to diarrhea in tube-fed patients. PATIENTS AND METHODS: Inpatients at the Truman Memorial Veterans Hospital who received nasoenteric feeding during the time period from October 1986 through May 1988 were eligible for this study. Of 123 patients who received nasoenteric feeding, 32 patients had documented diarrhea (greater than 500 mL per day for at least two consecutive days) and were enrolled. Three of these patients received hypertonic feeding formula, whereas the remaining 29 received isotonic feeding formula. Prospective determinations of the causes of diarrhea were performed. Laboratory tests included fecal leukocytes, stool osmolality, stool electrolytes, and Clostridium difficile toxin assay. Diarrhea was considered osmotic if the stool osmotic gap was greater than 100 mmol/L. Clinical management involved reducing or stopping the feeding formula, stopping suspected medications, or administering appropriate antibiotics. RESULTS: There were 32 episodes of diarrhea in tube-fed patients during the study period. A single cause could be specified in 29 cases. The tube feeding formula was responsible for diarrhea in only 21% of these cases. Medications were directly responsible in 61% and C. difficile in 17% of cases. Stool osmotic gap correctly distinguished osmotic from non-osmotic diarrhea in all cases. CONCLUSION: When diarrhea develops in properly tube-fed patients, the feeding formula is usually not responsible for the diarrhea. Patients receiving nasoenteric tube feeding are frequently placed on liquid forms of medications. Many medicinal elixirs contain sorbitol, which is often the cause of diarrhea in tube-fed patients. Review of the medications and determination of the stool osmotic gap are the initial diagnostic steps of highest yield.     

Towards a new paradigm of microscopic colitis: Incomplete and variant forms

Microscopic colitis (MC) is a chronic inflammatory bowel disease that has emerged in the last three decades as a leading cause of chronic watery diarrhoea. MC classically includes two main subtypes: lymphocytic colitis (LC) and collagenous colitis (CC). Other types of histopathological changes in the colonic mucosa have been described in patients with chronic diarrhoea, without fulfilling the conventional histopathological criteria for MC diagnosis. Whereas those unclassified alterations remained orphan for a long time, the use of the term incomplete MC (MCi) is nowadays universally accepted. However, it is still unresolved whether CC, LC and MCi should be considered as one clinical entity or if they represent three related conditions. In contrast to classical MC, the real epidemiological impact of MCi remains unknown, because only few epidemiological studies and case reports have been described. MCi presents clinical characteristics indistinguishable from complete MC with a good response to budesonide and cholestiramine. Although a number of medical treatments have been assayed in MC patients, currently, there is no causal treatment approach for MC and MCi, and only empirical strategies have been performed. Further studies are needed in order to identify their etiopathogenic mechanisms, and to better classify and treat MC.     

Clinical approach to diarrhea

Diarrhea is defined as reduced stool consistency, increased water content and number of evacuations per day. A wide array of causes and pathophysiological mechanisms underlie acute and chronic forms of diarrhea. This review focuses on the major clinical aspects which should aid clinicians to diagnose chronic diarrhea. Clinical history, physical examination and stool evaluation and the predominant stool characteristic, i.e., bloody, watery, and fatty diarrhea, may narrow the differential diagnosis. Although mainly involved in acute diarrhea, many different infectious agents, including bacteria, viruses and protozoa, can be identified in chronic bloody/inflammatory diarrhea by appropriate microbiological tests and colonoscopic biopsy analysis. Osmotic diarrhea can be the result of malabsorption or maldigestion, with a subsequent passage of fat in the stool leading to steatorrhea. Secretory diarrhea is due to an increase of fluid secretion in the small bowel lumen, a mechanism often identified in gastroenteropancreatic neuroendocrine tumors. The evaluation of the fecal osmotic gap may help to characterize whether a chronic diarrhea is osmotic or secretory. Fatty diarrhea (steatorrhea) occurs if fecal fat output exceeds the absorptive/digestive capacity of the intestine. Steatorrhea results from malabsorption or maldigestion states and tests should differentiate between these two conditions. Individualized diagnostic work ups tailored on pathophysiological and clinical features are expected to reduce costs for patients with chronic diarrhea.     

The epidemiology of microscopic colitis: a 10-year pathology-based nationwide Danish cohort study

Abstract

Objective. Microscopic colitis (MC) includes two main types: collagenous colitis (CC) and lymphocytic colitis (LC). Previous studies have indicated an increasing incidence, but these have mainly been based on regional databases. We found it important to study the epidemiology based on a comprehensive nationwide cohort. Material and methods. We studied the epidemiological data of MC in Denmark from 2002 to 2011. The cohort consisted of all patients with a recorded diagnosis of either CC or LC in the Danish Pathology Register during the study period. Data on all patients with a registered colon biopsy were also included. Results. A total of 7777 patients, 4749 (61%) with CC and 3028 (39%) with LC, were identified. Over the study period, the annual incidence of diagnosed cases of CC increased from 2.9/10⁵ to 14.9/10⁵ and of LC from 1.7/10⁵ to 9.8/10⁵. In 2011, the incidence of MC was 24.7/10⁵ inhabitants. The age-specific incidence showed that the risk of both CC and LC increased with age. The female/male ratio, distribution of the type of colitis and mean age at diagnosis were relatively stable during the study period. The annual number of registered colon biopsies in the pathology register increased from 21.583 in 2002 to 39.733 in 2011, indicating an increased diagnostic activity. Conclusion. In a nationwide cohort study, the incidence of CC and LC continued to increase from 2002 to 2011. An increased diagnostic activity could in part explain the increase in the number of diagnosed cases.     

The effect of oral-administered lactulose on colonic nitrogen metabolism and excretion.

The influence of lactulose on organic acid fermentation, nitrogen metabolism and excretion in the colon associated with its mechanism of action on hepatic encephalopathy was investigated. Orally administered lactulose in increasing amounts (0 to 20 to 40 to 80 to 160 gm/day) to 12 healthy volunteers decreased ammonia production in 16.6% fecal homogenates incubated 6 hr and 24 hr at 37 degrees C (mean +/- S.E.M.: from 7 +/- 1 to 0 +/- 0 and from 13 +/- 2 to 0 +/- 0 mmol/L, respectively). Every dose of lactulose was given for 3 days with intervals of 1 to 2 wk, and 24-hr stools were collected on day 3. Fecal concentrations of ammonia decreased (from 50 +/- 9 to 11 +/- 3 mmol/L), but ammonia excretions increased (from 6 +/- 2 to 17 +/- 4 mmol/24 hr). Total fecal concentrations of nitrogen decreased (from 1,043 +/- 78 to 300 +/- 136 mmol/L), but excretions of nitrogen increased fourfold (from 111 +/- 21 to 457 +/- 113 mmoL/24 hr) because of the increase in stool mass. Fecal pH declined (from 6.9 +/- 0.1 to 4.9 +/- 0.1), but total organic acids (short-chain fatty acids and DL-lactate; range = 105 to 148 mmol/L) and osmolality in feces (417 to 450 mOsm/L) did not change, although the colonic fermentation of lactulose had a major impact on the proportions between the nontoxic acetate (increased from 65% +/- 2% to 89% +/- 3%) and the potentially neurotoxic 3-6-carbon fatty acids (decreased from 35% +/- 2% to 11% +/- 2%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intestinal protein loss in acute and persistent diarrhea of early childhood

GOALS: To determine fecal protein loss in children with acute and persistent diarrhea. BACKGROUND: In children with diarrhea, ongoing losses of endogenous proteins have been suggested as contributing to impairment of nutritional and immunologic status. However, there is a paucity of information and inconclusive data in the literature. STUDY: Fecal protein loss was assessed prospectively in children (<3 years of age) with acute diarrhea (<7 days' duration) or persistent diarrhea (>14 days) and in controls using alpha-1-antitrypsin determination; fecal protein loss then was correlated with age, duration of diarrhea, nutritional status, plasma proteins, and stool pathogens. RESULTS: Children with acute diarrhea (n = 43) and those with persistent diarrhea (n = 41) had significantly higher fecal alpha-1-antitrypsin levels compared with controls (n = 14) (2.26 +/- 1.71 and 2.25 +/- 1.51, respectively, vs. 1.02 +/- 0.73 mg/g stools; p = 0.002). However, there was no significant decrease of plasma albumin, globulin, or immunoglobulins. Fecal protein loss did not differ significantly among stool pathogens (bacterial, viral, and parasitic) and demonstrated no significant correlation with age, duration of diarrhea, or nutritional status (mild malnutrition). CONCLUSIONS: Enhanced fecal protein loss was observed in more than 50% of children with acute and persistent diarrhea caused by various pathogens. This did not correlate with age, duration of diarrhea, or nutritional status and did not result in significant decrease of plasma proteins or immunoglobulins. This protein-losing enteropathy does not appear to have a causal role in perpetuation of diarrheal episodes in children with mild malnutrition.     

Fecal lactate and ulcerative colitis

Impaired metabolism of short-chain fatty acids, as well as a modified fecal ionogram, have been reported in ulcerative colitis. Fecal water samples from 62 patients with ulcerative colitis were analyzed in the present investigation to evaluate changes in SCFAs and lactic acid in relation to activity and severity of disease. Short-chain fatty acid levels were high in quiescent and mild disease (162.6 +/- 63.6 and 147.8 +/- 63.2 mM/L, respectively), but significantly decreased in the severe form (64.7 +/- 46.9 mM/L). Lactate showed a progressive increase from mild colitis (3.0 +/- 1.8 mM/L) to severe colitis (21.4 +/- 18.6 mM/L). It thus appears that mild colitis displayed a fecal pattern characterized by normal pH and bicarbonate, slightly impaired electrolyte handling, high short-chain fatty acid values, and only moderately increased lactate. Severe colitis, on the other hand, was characterized by low fecal pH, bicarbonate, and potassium, high sodium and chloride, low short-chain fatty acid levels, and very high lactate levels. A critical lowering of intraluminal pH, which shifts bacterial metabolism from short-chain fatty acid to lactate production, may be responsible for the intraluminal pooling of lactate.     

Microscopic colitis in patients with ulcerative colitis or Crohn’s disease: a retrospective observational study and review of the literature

Objectives: Onset of microscopic colitis (MC) in patients with ulcerative colitis (UC) or Crohn’s disease (CD), or vice versa, has been reported occasionally but the subject is not well described. We therefore report a retrospective observational study of such patients and review the literature.

Methods: Forty-six Swedish gastroenterology clinics were contacted about patients with diagnoses of both inflammatory bowel disease (IBD) and MC. Publications were searched on PubMed.

Results: We identified 31 patients with onset of MC after a median (range) of 20 (2–52) years after diagnosis of IBD, or vice versa; 21 UC patients developed collagenous colitis (CC) (n?=?16) or lymphocytic colitis (LC) (n?=?5); nine CD patients developed CC (n?=?5) or LC (n?=?4); one CC patient developed CD. Of the 21 UC patients, 18 had extensive disease, whereas no consistent phenotype occurred in CD. Literature review revealed 27 comprehensive case reports of patients with diagnoses of both IBD and MC. Thirteen MC patients developed IBD, of which four required colectomy. Fourteen IBD patients later developed MC. There were incomplete clinical data in 115 additional reported patients.

Conclusions: Altogether 173 patients with occurrence of both IBD and MC were found. The most common finding in our patients was onset of CC in a patient with UC. Although these are likely random associations of two different disorders, MC should be considered in the patient with UC or CD if there is onset of chronic watery diarrhoea without endoscopic relapse of IBD.     

Distinct colonoscopy findings of microscopic colitis：Not so microscopic after all？

Microscopic colitis(MC) is considered an umbrella term,comprising two subtypes,i.e.,collagenous colitis(CC) and lymphocytic colitis(LC).They are classically associated with normal or unremarkable colonoscopy.In the last few years,reports have been published revealing findings that are thought to be characteristic or pathognomonic of MC,especially CC.A systematic electronic and manual search of PubMed and EMBASE(to December 2010),for publications on distinct endoscopic findings in MC,resulted in 42 relevant ...