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Background: Microscopic colitis, including collagenous colitis and lymphocytic colitis, mainly affects middle aged and older subjects, with a female predominance in collogenous colitis. The diseases hove previously been regarded as rare. We present an epidemiological study of microscopic colitis in a well defined Swedish population. Methods: Patients were retrospectively searched for in colonoscopy reports of those who had a colonoscopy in the period 1993-1998 for non-bloody diarrhoea. All colonic mucosal biopsies were reassessed using strict diagnostic criteria. Results: Biopsies from 1018 patients were reassessed. Fifty one (45 female) collagenous colitis patients and 46 (31 female) lymphocytic colitis patients were diagnosed. Median age at diagnosis was 64 years in collagenous colitis and 59 years in lymphocytic colitis. The mean annual incidence of collagenous colitis was 4.9/105 inhabitants (95% confidence interval (CI) 3.6-6.2/105) and of lymphocytic colitis 4.4/105 inhabitants (95% CI 3.1-5.7/105). The annual incidence of collagenous colitis increased from 3.7/105 in 1993-1995 to 6.1/105 in 1996-1998 (difference 2.4/105 (95% CI -0.3-5.1/105)) whereas the incidence of lymphocytic colitis increased from 3.1/105 to 5.7/105 (difference 2.6/105 (95% CI 0.1-5.2/105)). Conclusions: The annual incidences of collagenous colitis and lymphocytic colitis are higher than considered previously and are now equal to the incidence of Crohn's disease in Sweden, and combined rates approach the incidence of ulcerative colitis. Microscopic colitis was diagnosed in 10% of all patients with non-bloody diarrhoea referred for colonoscopy and in almost 20% of those older than 70 years. [ABSTRACT FROM AUTHOR]

Background: The Inflammatory Bowel Disease Questionnaire (IBDQ) is a disease-specific health-related quality of life (HRQOL) questionnaire including four dimensions and a sum score. The aim of this study was to assess the internal and external validity, reliability, and sensitivity of a Swedish version of the IBDQ. Methods: Three hundred consecutive patients with ulcerative colitis completed the IBDQ and three other health-related quality of life questionnaires (the Rating Form of IBD Patient Concerns (RFIPC), the Short Form-36 (SF-36) and the Psychological General Well-Being (PGWB) index). Disease activity was evaluated using a 1-week symptom diary, blood tests and rigid sigmoidoscopy. One hundred and fourteen patients filled in the questionnaire a second time, of whom 75 had been in stable remission for over 6 months and 39 had a significant clinical change in disease activity. Results: Factor analysis of the 32 IBDQ items did not support the four dimensional scores. The dimensional scores had sufficient convergent validity, but low discriminative validity and homogeneity. The homogeneity was also low for the sum score. The inter-dimensional correlations were high. The concurrent validity was supported by correlations between the dimensional scores and other measures of disease activity and HRQOL. Patients in relapse scored significantly less on the sum score and the four dimensions compared to patients in remission. The test-retest correlations for the dimensional scores were 0.40-0.76. Patients with a change in disease activity during the 6-month follow-up period had a significant change in IBDQ scores not found in those who remained in remission. Conclusions: The Swedish version of the IBDQ had external validity and was shown to be a reliable and sensitive measure of HRQOL in ulcerative colitis, though there are some concerns regarding the internal validity. The use of a sum score was not supported and the questionnaire may benefit from a redivision of items into dimensions with better homogeneity and discriminative validity. [ABSTRACT FROM AUTHOR]

Correlates the circulating insulin-like growth factor I (IGF-I) and bone mineral density (BMD) in adults with celiac disease. Significance of a gluten-free diet on BMD; Effect of parathyroid hormone on IGF-I; Stimulation of the growth of bone cells.

Background: Perinuclear antineutrophil cytoplasmic antibodies (P-ANCA) are found in 48%-83% of serum samples from patients with ulcerative colitis (UC). Their pathogenic role and initiating stimuli are unknown. In contrast to patients with vasculitides and ANCA reactivities, the antibodies in UC patients do not react with myeloperoxidase (MPO) or proteinase 3 (PR3). The aim of the present study was to investigate whether bacterial species of the intestinal tract and other sources could interfere with P-ANCA in sera from patients with UC. Methods: Seventeen P-ANCA-positive and anti-MPO-negative serum samples from patients with UC were tested with Escherichia coli 014 and Staphylococcus aureus Wood 46. Six of these serum samples with different P-ANCA titres were selected to test further the influence of 15 different gram-negative or gram-positive bacterial strains. Six anti-MPO positive P-ANCA, 5 anti-PR3 positive C-ANCA, and 10 antinuclear antibody (ANA)-positive serum samples were used as controls. The antineutrophil cytoplasmic antibodies (ANCAs) were analysed by an indirect immunofluorescence method (IIF) on ethanol-fixed neutrophils, and the ANAs were tested by IIF on HEp-2 cells or rat liver tissues. The bacteria used in the experiments were either live or killed by formalin or glutaraldehyde fixation or heated at 80°C for 30 min. The test was first performed as a bacterial absorption test with sedimented organisms and then at various temperatures with the supernatant from suspension of live bacteria. Results: Both MPO-positive and MPO-negative P-ANCA reactivity was abolished by absorption of patient sera with live E. coli and Proteus mirabilis but not with bacteria representing members of 10 other species, suggesting that antibody reactivity was absorbed away. However, continued experiments indicated that the inhibition of P-ANCA was not due to classic antigen-antibody interactions but rather to decomposition of the antigenic substrate of the neutrophils by factors present in the supernatants of live E. coli and P. mirabilis. The activity of the supernatant was temperature-dependent, with strong activity at room temperature and 37°C, no activity at 0°C, and abolished by mild heat treatment (56° or 60°C). No activity was shown in the supernatants from bacteria treated with formaldehyde or glutaraldehyde. Conclusions: Soluble material from live E. coli and P. mirabilis has the capacity to decompose the antigenic substrate of neutrophils responsible for both MPO-positive and MPO-negative P-ANCA, most probably brought about through enzymatic activity. Anti PR3-positive C-ANCA were not affected, which suggests substrate specificity of the proposed enzymatic activity. [ABSTRACT FROM AUTHOR]

Nine patients wih Crohn's disease and six healthy individuals were given 400 mg metronidazole twice daily and the concentration was measured in plasma and faeces 6 to 8 h after intake. Quantitative and qualitative bacteriological examinations were performed before and during treatment. The concentrations of metronidazole in plasma varied between 5 and 30 mg/l as measured by liquid chromatography (LC) and between 3 and 20 mg/l as measured by a bioassay (BA) method. There was no significant differences between the results of the two methods in patients but compared with BA the LC values were regularly lower in the healthy subjects. Metronidazole was detected in the faeces of most patients. These findings coincided with a significant reduction of Bacteroides spp in their faeces which was not apparent in healthy individuals in whom metronidazole was not detected in the faeces. Higher faecal metronidazole concentrations were found in patients with active disease and a total colon involvement as compared with the patients with a more quiescent disease and involvement of ileum and ascending colon only. [ABSTRACT FROM PUBLISHER]

BACKGROUND: Data on collagenous colitis have been based on a limited number of patients. AIMS: To obtain more information on this disease from a register set up at Orebro Medical Center Hospital. PATIENTS AND METHODS: Twenty five Swedish hospitals have contributed to this patient register, which comprises 163 histopathologically verified cases. Clinical data were retrospectively analysed. RESULTS: Collagenous colitis followed a chronic intermittent course in most cases (85%) with a sudden onset in 42%. Symptoms were chronic watery diarrhoea, often nocturnal (27%), abdominal pain (41%), and weight loss (42%). Sixty six patients (40%) had one or more associated diseases. Routine laboratory data were mostly normal. The median age at diagnosis was 55 (range 16-86) years, but 25% of the patients were younger than 45 years. Seven patients died of unrelated diseases. The response rate for sulphasalazine was 59%, and 50% and 40% for mesalazine and olsalazine. Prednisolone was most effective with a response rate of 82%, but the required dose was often high and the effect was not sustained after withdrawal. Antibiotics were efficient in 63%. Cholestyramine and loperamide had response rates of 59% and 71% respectively. CONCLUSIONS: Collagenous colitis follows a chronic continuous course. Symptoms can be socially disabling, but the disease does not seem to have a malignant potential. A plan for the treatment of a newly diagnosed patient with collagenous colitis is proposed. [ABSTRACT FROM PUBLISHER]

BACKGROUND: The aetiology and pathogenesis of collagenous colitis are unknown. Autoimmunity has been suggested, but no serological findings have supported such a theory. AIMS AND METHODS: Serum from 38 collagenous colitis patients and 38 matched healthy controls was analysed for autoantibodies--that is, antinuclear antibodies, antineutrophil cytoplasmic antibodies, smooth muscle and mitochondrial antibodies, rheumatoid factor and antibodies to thyroglobulin and microsomal antigen, together with antibodies to endomysium, gliadin, and cardiolipin. The serum values of IgA, IgG, IgM, and IgG-subclasses, and complement factors C3 and C4 were also determined. RESULTS: In patients with collagenous colitis the mean value of IgM was significantly increased 2.5 g/l (95% CI; 1.9, 3.2) compared with 1.4 g/l (95% CI; 1.2, 1.7) in controls (p = 0.002). Antinuclear antibodies occurred in nine of 38 patients compared with three of 38 controls, this difference was not statistically significant (p = 0.11). The results of all other immunoglobulins, complement factors, and specific antibodies showed no statistical difference between patients and controls. CONCLUSIONS: No firm evidence for an autoimmune genesis in collagenous colitis is found in this study, although the findings of a positive ANA-titre in some patients and an increased IgM level might give some support for this hypothesis. [ABSTRACT FROM PUBLISHER]

The incidence and prevalence of collagenous colitis are unknown. An epidemiological study was undertaken between 1984-93. All patients living in the immediate catchment area of Orebro Medical Center Hospital with the diagnosis collagenous colitis were identified. Biopsy specimens classified as unspecific intestinal fibrosis were re-examined to identify cases not correctly diagnosed at first. Medical records were scrutinised and colorectal biopsy specimens re-evaluated. Thirty patients with collagenous colitis were diagnosed during the study period. The female:male ratio was 9:1. The median age at diagnosis was 64 (28-78) years. The prevalence at 31 December 1993, was 15.7/10(5) inhabitants (95% CI; 9.8 to 21.6/10(5)). The mean annual incidence during the period 1984-93 was 1.8/10(5) inhabitants (95% CI; 1.2 to 2.4/10(5)). A peak incidence was found in women 70-79 years old. Collagenous colitis occurs mainly in middle aged women, and the frequency is higher than earlier anticipated. The prevalence and incidence is similar to primary biliary cirrhosis. In women 70-79 years of age, the incidence for collagenous colitis approaches the incidence for ulcerative colitis. [ABSTRACT FROM PUBLISHER]

Perinuclear antineutrophil cytoplasmic antibodies (P-ANCA) have been demonstrated in patients with ulcerative colitis and in a higher frequency than expected in their first degree relatives. A hypothesis was proposed that P-ANCA is genetically determined and may represent a subclinical marker of genetic susceptibility to ulcerative colitis. This study analysed P-ANCA in monozygotic twins with inflammatory bowel disease to evaluate this hypothesis further. P-ANCA was analysed with indirect immunofluorescence technique in 12 monozygotic twin pairs with ulcerative colitis and 14 twin pairs with Crohn's disease. Furthermore, the study included 21 non-twin patients with ulcerative colitis, 18 non-twin patients with Crohn's disease, and 52 healthy controls matched for sex and age. In ulcerative colitis P-ANCA occurred in nine of 14 (64.3%) monozygotic twins and in 13 of 21 (61.9%) non-twin cases, which was significantly different compared with healthy controls who were positive in three of 52 (5.8%) cases (p < 0.0001). P-ANCA was found in two of 10 (20%) healthy twin siblings to twins with ulcerative colitis, which was not significantly different from healthy controls (p = 0.18). The results in Crohn's disease did not differ from healthy controls. Previous findings of P-ANCA occurring in ulcerative colitis but not in Crohn's disease are supported. This study does not support the hypothesis that P-ANCA is a subclinical marker of genetic susceptibility to ulcerative colitis. [ABSTRACT FROM PUBLISHER]

To evaluate the optimum dose of olsalazine for maintaining remission in ulcerative colitis, 198 patients in remission for more than three months were randomly assigned to receive 0.5 g, 1.0 g, or 2.0 g/day for 12 months. A dose-ranging effect was detected in the per protocol analysis, with remission rates of 60% (0.5 g), 70% (1.0 g), and 78% (2.0 g) (p = 0.03, trend in proportions). The higher dose was most effective in patients with proctitis (90% remission on 2 g/day, p = 0.03) or those in remission for less than 12 months before the trial (88% remission on 2 g/day, p = 0.0006). There was little dose-ranging effect in patients with extensive colitis or those in remission for more than 12 months. Diarrhoea necessitated treatment withdrawal in 12%. The optimal dose of olsalazine for maintaining remission in ulcerative colitis is 1 g/day. For patients with proctitis or recent relapse, 2 g/day may be preferable, although the dose seems to be less important in patients with more extensive disease or those in long term remission. [ABSTRACT FROM PUBLISHER]

A total of 61 human gastric isolates of Helicobacter pylori were studied for their ability to induce an oxidative burst in human neutrophils measured by luminol enhanced chemiluminescence. About one third of the strains induced strong and rapid chemiluminescence in neutrophils even without serum opsonins and agglutinated these cells on glass slides within two minutes. For other strains complement was required, although even then the reactions remained at a lower level. The activating and agglutinating property was bound to the cells, heat labile, and sensitive to several enzymes but resistant to acid. Strains possessing such activity were more common in patients with peptic ulcer disease than in patients with active chronic gastritis only (p = 0.0261, Fisher's exact test, two tailed). The activity shown might be a new indicator for ulcerogenic strains and could also partly explain the accumulation of neutrophils in the gastric mucosa during H pylori infection. [ABSTRACT FROM PUBLISHER]

Serum samples from 26 monozygotic twin pairs concordant or discordant with regard to inflammatory bowel disease, and rectal biopsies from 42 twins of the same subject group, were examined for IgG subclasses. They were all compared with normal controls. Almost all affected twins were in clinical remission. Paired immunofluorescence staining of the rectal mucosa showed that those with ulcerative colitis had a significantly higher (p < 0.01) proportion of IgG1 producing mucosal immunocytes than normal controls (78.1% v 55.9%). Conversely, the IgG2 cell fraction was significantly reduced (15.9% v 34.6%). Healthy twins from ulcerative colitis pairs tended to show a raised proportion of IgG1 cells and the IgG2 cell fraction was significantly reduced (p < 0.05). In discordant ulcerative colitis twin pairs, no difference appeared in the cellular IgG subclass pattern between healthy and affected twins. Furthermore, the proportion of IgG1 in these healthy and diseased twins showed good correlation (T = 0.867). The results in rectal mucosa of twins with Crohn's disease were widely scattered and affected twins did not differ significantly from normal controls. Healthy twins, however, showed a marginally raised IgG1 cell proportion, but no correlation was seen between the IgG subclass fractions in discordant Crohn's disease twin pairs. The serum concentrations of IgG1 and IgG2 did not differ from normal controls in twins of either category. These results suggested that in ulcerative colitis, the aberrant mucosal production of IgG1 and IgG2 does not depend on active disease, but is apparently at least partially explained by a genetic impact. Conversely, the mucosal IgG subclass pattern in Crohn's disease appears to be determined mainly by exogenous variables. [ABSTRACT FROM PUBLISHER]

To assess whether dietary antigens play a role in inflammatory bowel disease, 26 monozygotic twin pairs with inflammatory bowel disease and 52 healthy controls were investigated for serum antibodies (IgA, IgG, IgM) against ovalbumin, betalactoglobulin, gliadin, whole yeast (Saccharomyces cerevisiae) and yeast cell wall mannan. The twins were made up of five pairs concordant and nine pairs discordant for Crohn's disease, and two pairs concordant and 10 pairs discordant for ulcerative colitis. Two patients with Crohn's disease had a slight increase in disease activity, the others were in clinical remission. Two striking observations were made: first, individuals with ulcerative colitis were indistinguishable from healthy twins, and controls except for the response to gliadin. Both healthy and diseased twins had higher IgA levels to gliadin than controls. Second, twins who had developed Crohn's disease displayed higher antibody titres towards yeast cell wall mannan in particular, but also to whole yeast (Saccharomyces cerevisiae) of all antibody types (IgA, IgG, and IgM). In contrast, the response to gliadin, ovalbumin, and betalactoglobulin did not differ from healthy twins and was even lower than in the controls. The results argue against an increased systemic antigen presentation caused by an impaired mucosal barrier in the inflammatory bowel disease. Rather, they suggest that yeast cell wall material--that is, mannan, or some antigen rich in mannose and cross reacting with mannan, may play an aetiological role in Crohn's disease, but not in ulcerative colitis. The increases in IgA and IgM, as well as IgG suggest that local and systemic immune systems are selectively activated by antigen(s) present in the cell wall of baker's yeast. [ABSTRACT FROM PUBLISHER]

The effects of smoking on the localisation and clinical course of Crohn's disease is evaluated in 231 patients. Heavy smokers (greater than 10 cigarettes/day) had an increased risk of operation at least once--odds ratios for heavy smokers compared with never smokers after five and 10 years were 1.14 and 1.24 respectively (p = 0.03 and p = 0.017). The risk of further operations was even higher and after 10 years the odds ratio was 1.79 (p = 0.015). The accumulated number of fistulae and/or abscesses was higher for smokers than for never smokers (p = 0.046). Patients with a high life time tobacco exposure (greater than 150 cigarette years) and heavy smokers (greater than 10 cigarettes/day) had small bowel disease more often than patients with lower life time exposure (less than or equal to 150 cigarette years) and patients smoking less than or equal to 10 cigarettes/day (p = 0.002 and p = 0.045 respectively). The course of Crohn's disease analysed in different ways was unfavourable for smokers, especially heavy smokers. Patients with Crohn's disease should be dissuaded from smoking. [ABSTRACT FROM PUBLISHER]

By running the Swedish twin registry containing about 25,000 pairs of twins of the same sex together with the central national diagnosis register of hospital inpatients, 80 twin pairs suffering from inflammatory bowel disease were found. In the ulcerative colitis group one of 16 monozygotic pairs was concordant for the disease, but all the other 20 pairs (dizygotic or unknown zygosity) were discordant. In the Crohn's disease group eight of 18 monozygotic pairs and one of 26 dizygotic pairs were concordant. The proband concordance rate among monozygotic twins was 6.3% for ulcerative colitis and 58.3% for Crohn's disease. The calculated heritability of liability based on monozygotic pairs was 0.53 and 1.0 respectively. Thus heredity as an aetiological factor is stronger in Crohn's disease than in ulcerative colitis. Monozygotic twins with Crohn's disease were more likely to be smokers than monozygotic twins with ulcerative colitis. Smoking did not explain the discordance of twin pairs with either ulcerative colitis, or Crohn's disease. The combination of identical heredity and similar smoking habit is not sufficient to cause disease. [ABSTRACT FROM PUBLISHER]

A population case controlled study of smoking habits at the time of diagnosis was done in 260 patients with ulcerative colitis and 144 with Crohn's disease. Smokers had a decreased risk of acquiring ulcerative colitis in comparison with never smokers (relative risk 0.7) which appeared to be dose dependent. In former smokers a rebound effect was seen, especially in former heavy smokers, where the risk was sharply increased (relative risk 4.4). No sex difference was recorded. Smoking doubled the risk of acquiring Crohn's disease without any dose dependent pattern. In former smokers a non-significantly increased risk was observed. This might be caused by a carry over effect after stopping smoking, however, which possibly is reduced by time. No sex difference was seen. [ABSTRACT FROM PUBLISHER]

Sixty two patients with a clinical suspicion of biliary dyskinesia were investigated with endoscopic manometry of the sphincter of Oddi before and after intravenous injection of cholecystokinin or ceruletide. In 52 patients injection was followed by decreased pressure in the sphincter of Oddi; 43 of these had normal prestimulatory values (group I), while the values were raised in the other nine patients (group II). A paradoxical response to intravenous injection was observed in 10 women (group III): increased baseline sphincteric pressure occurred in eight and increase in the amplitude of phasic contractions in four patients. The prestimulatory sphincteric pressure was raised in five and normal in the remaining patients. Eight patients were treated with papillotomy (seven) or balloon dilatation of the sphincter (one). They experienced relief of pain during a follow up period of 11-16 months. Intravenous injection of cholecystokinin or ceruletide may disclose a special type of biliary dyskinesia even in patients with normal prestimulatory manometric findings. Hormone injection increases the diagnostic yield of endoscopic manometry in patients suspected of biliary dyskinesia. [ABSTRACT FROM PUBLISHER]

Azodisal sodium is a highly effective means of oral delivery of 5-amino-salicylic acid to the colonic mucosa. Administration of this drug to patients intolerant of sulphasalazine, however, occasionally results in liquid stools. In preliminary experiments, which comprised 10 healthy volunteers treated with colectomy for ulcerative colitis, ileostomy fluid output increased (p less than 0.001) during oral intake of azodisal sodium (1 g/day). In a double blind, placebo controlled crossover study, comprising eight similar volunteers, ileostomy fluid output increased (p less than 0.05) in a dose related manner during intake of azodisal sodium (1 g/day vs 2 g/day) compared with placebo or sulphasalazine (2 g/day). Concentrations of prostaglandin (PG)F2 alpha in free ileal water determined by equilibrium in vivo dialysis of ileostomy contents decreased (p less than 0.05) during intake of azodisal sodium (2 g/day), whereas concentrations of PGE2 and the output of PGE2, PGF2 alpha, and 'PGE2 + PGF2 alpha' remained unchanged. Thus increased formation of PGs is apparently not the cause of increased ileostomy fluid output associated with azodisalicylate intake. [ABSTRACT FROM PUBLISHER]