Johan Bohr

Collagenous colitis: a retrospective study of clinical presentation and treatment in 163 patients.

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.

Microscopic colitis: a common diarrhoeal disease. An epidemiological study in Örebro, Sweden, 1993–1998

Background: Microscopic colitis, including collagenous colitis and lymphocytic colitis, mainly affects middle aged and older subjects, with a female predominance in collagenous colitis. The diseases have 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.

Collagenous colitis and fecal stream diversion.

BACKGROUND & AIMS The cause of collagenous colitis is unknown. Data on treatment are sparse, and surgical therapy has not been reported. This study reports results of surgical therapy for collagenous colitis. METHODS Nine women with unresponsive collagenous colitis underwent surgery. An ileostomy was performed as the first procedure in 8 patients, and a sigmoidostomy using the Hartmann procedure was performed in 1 patient. RESULTS Preoperatively, all patients had severe diarrhea, and the median thickness of the subepithelial collagenous layer was 20 microns (range, 10-40 microns). Postoperatively, diarrhea ceased in all patients, and the collagen layer was reduced to 2 microns (range, 0-10 microns). Clinical symptoms and the abnormal collagen layer recurred after restoration of intestinal continuity. After the Hartmann procedure, the collagen layer remained abnormally thickened up to 30 microns in the proximal colon but was normalized in the excluded rectosigmoid colon. One year later, the sigmoidostomy was replaced by a split ileostomy; at follow-up, the collagen layer was normal in the whole colon. CONCLUSIONS Fecal stream diversion induced clinical and histopathologic remission in collagenous colitis. After closure of the ostomy, clinical symptoms and the abnormal collagen layer recurred. The findings strongly indicate that a noxious luminal factor is of pathogenetic importance. In older patients with medically resistant disease, a split ileostomy may be the therapeutic procedure of choice.

Lymphocytic colitis: a retrospective clinical study of 199 Swedish patients

Background: Lymphocytic colitis is characterised by chronic diarrhoea and specific microscopic changes in a macroscopically normal colonic mucosa. We report clinical features and treatment outcome in a large patient cohort. Methods: Patients were searched for in 24 Swedish gastroenterology clinics. The biopsy material was reassessed using strict histopathological criteria. Clinical data were obtained from medical notes. Results: Lymphocytic colitis was diagnosed in 199 cases. The female:male ratio was 2.4:1. Median age at diagnosis was 59 (48–70) years. The most frequent symptoms were diarrhoea (96%), abdominal pain (47%), and weight loss (41%). The course was chronic intermittent in 30% of patients, chronic continuous in 7%, and a single attack in 63%, and in these cases the disease duration was 6 (4–11) months. Seventy nine (40%) patients reported associated diseases, of which thyroid disorders, coeliac disease, and diabetes mellitus were the most common. In 34 first or second degree relatives of 24 (12%) patients, a family history of ulcerative colitis, Crohn’s disease, collagenous colitis, or coeliac disease was reported. Drug induced disease was suspected in 19 (10%) patients. A non-significant peak of disease onset was seen in December-January. More than 80% of treated patients improved on corticosteroids, including budesonide. Conclusions: A family history of other bowel disorders is a new finding. The sudden onset and single attack of limited duration may support a possible infectious cause in some cases. Drugs may cause lymphocytic colitis.

Collagenous colitis in Orebro, Sweden, an epidemiological study 1984-1993.

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.

Systematic review : microscopic colitis.

Collagenous and lymphocytic colitis are fairly common causes of chronic non‐bloody diarrhoea, especially in elderly female.

Autoantibodies and immunoglobulins in collagenous colitis.

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.

Familial occurrence of microscopic colitis: a report on five families.

BACKGROUND The etiology and pathogenesis of microscopic colitis is unknown. Whether genetic predisposition is of importance, as in many other gastrointestinal diseases, is unknown. Familial occurrence of collagenous colitis has earlier been reported only in two families. METHODS Familial occurrence of microscopic colitis was searched for in a Swedish national microscopic colitis register. RESULTS Familial occurrence of microscopic colitis was identified in five families. In all families a sister-sister relationship was found. Two sisters with collagenous colitis had been living apart in different Nordic countries for many years before developing the disease. In one pair, the smoking sister had collagenous colitis and the never smoking sister had lymphocytic colitis. CONCLUSIONS Considering the relative rarity of microscopic colitis, these findings indicate that a genetic predisposition may be of importance.Background: The etiology and pathogenesis of microscopic colitis is unknown. Whether genetic predisposition is of importance, as in many other gastrointestinal diseases, is unknown. Familial occurrence of collagenous colitis has earlier been reported only in two families. Methods: Familial occurrence of microscopic colitis was searched for in a Swedish national microscopic colitis register. Results: Familial occurrence of microscopic colitis was identified in five families. In all families a sister- sister relationship was found. Two sisters with collagenous colitis had been living apart in different Nordic countries for many years before developing the disease. In one pair, the smoking sister had collagenous colitis and the never smoking sister had lymphocytic colitis. Conclusions: Considering the relative rarity of microscopic colitis, these findings indicate that a genetic predisposition may be of importance.

Colonic mucosal tears in collagenous colitis

In general, the colonic mucosa is macroscopically normal in collagenous colitis, although minor, non-specific abnormalities may be found. Significant endoscopic abnormalities, “mucosal tears” representing longitudinal mucosal lacerations, have been reported in a few patients with collagenous colitis. We report the cases of three women with collagenous colitis and mucosal tears detected at the index colonoscopy in order to illustrate the endoscopic characteristics and review the literature. Including the present cases, a total of 12 patients with mucosal tears and collagenous colitis have been reported. In 10 patients, the mucosal lacerations involved the ascending or the transverse colon. Three of the 12 patients had a colonic perforation immediately after the colonoscopy. The colonoscopist should be aware that the risk of perforation is likely to be increased when mucosal tears are present.

Yersinia Species in Collagenous Colitis: A Serologic Study

Background: The etiology of collagenous colitis is unknown. An infectious cause seems a possibility, and in a recent report three out of six patients with collagenous colitis were shown to have had an infection with Yersinia enterocolitica. The aim was to investigate the occurrence of Yersinia antibodies in collagenous colitis. Methods: Sera from 32 collagenous colitis patients and 17 healthy controls were analysed for antibodies against Yersinia virulence proteins. Results: Collagenous colitis patients had Yersinia antibodies more often than the controls, 9 having a positive and 4 an intermediate antibody score of the 32 patients. In comparison, 1 out of 17 controls had a positive and 2 an intermediate antibody score, which represents a strong, although not significant, trend ( P = 0.078). Conclusion: The data showed that Yersinia antibodies are more common in collagenous colitis patients than in healthy controls. In some cases, Yersinia might have been the triggering event in the development of collagenous colitis.