Seroprevalence of Helicobacter pylori infection in inflammatory bowel disease: is Helicobacter pylori infection a protective factor?

BACKGROUND: The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection. METHODS: We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC). 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview. RESULTS: The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years: P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age. CONCLUSIONS: Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.

Smoking is a risk factor for osteoporosis in women with inflammatory bowel disease.

BACKGROUND: Some patients with inflammatory bowel disease have reduced bone mineral density, but the risk factors for osteoporosis in these patients are unclear. METHODS: To evaluate the effect of smoking and other lifestyle factors on bone mineral density in patients with inflammatory bowel disease, we studied 67 patients with ulcerative colitis, 78 with Crohn's disease, 7 with indeterminate colitis, and 73 healthy control subjects. Bone mineral density of the lumbar spine and the proximal femur was measured, using dual-energy X-ray absorptiometry. Measures of smoking and other lifestyle factors were assessed in an interview. RESULTS: The female ex- or current smokers with inflammatory bowel disease (n = 38) had lower age- and sex-adjusted Z-scores of bone mineral density than the female patients who had never smoked (n = 34) (Z-scores in the lumbar spine, -0.277 (1.283) (mean (standard deviation)) and 0.487 (1.056), respectively; p = 0.008; and in the femoral neck, -0.626 (1.055) and -0.013 (1.019); p = 0.015). These differences were not explained by the type or treatment of the disease, the menstrual history, or the use of estrogen preparations. In male patients no differences in bone mineral density were found between ex- or current smokers and non-smokers. Coffee drinking and alcohol consumption were not associated with bone mineral density in these patients. CONCLUSIONS: Smoking is associated with low bone mineral density in women with inflammatory bowel disease. This association is not related to the body mass index, the medical treatment, or the type of disease.

A controlled study of bone mineral density in patients with inflammatory bowel disease.

To assess the prevalence of and risk factors for low bone mineral density in inflammatory bowel disease (IBD), 152 IBD patients and 73 healthy controls were studied. Sixty seven patients had ulcerative colitis, 78 had Crohn's disease (52 of them (66.7%) had ileal disease), and seven had indeterminate colitis. Bone mineral density values (g/cm2) measured by dual energy x ray absorbtiometry at the spine (L2-L4), the femoral neck, Ward's triangle, and the trochanter were 1.177, 0.948, 0.850, and 0.838 in the patients and 1.228 (p = 0.034), 1.001 (p = 0.009), 0.889 (NS), and 0.888 (p = 0.012) in the control group, respectively. The type or extent of the disease or previous small bowel resection did not have any significant effect on the bone mineral density values. There was a weak, but statistically significant negative correlation between bone mineral density and the total lifetime corticosteroid dose (in the lumbar spine r = -0.164, p = 0.04, the femoral neck r = -0.185, p = 0.02, Ward's triangle r = -0.167, p = 0.04, and the trochanter r = -0.237, p = 0.003). The patients whose lifetime corticosteroid dose (prednisone/prednisolone) was more than 10 g had especially low bone mineral density (p < 0.05 compared with the groups with no or less than 5 g of corticosteroid). The patients who had never taken peroral corticosteroids did not have decreased bone mineral density. In conclusion, IBD patients have significantly lower bone mineral density values than healthy controls, but the difference is not so great as has been reported previously. Low bone mineral density values in these patients are related to high lifetime corticosteroid doses.