Serum gastrin levels in patients with inflammatory bowel disease

The aim of this study was to estimate the levels of serum gastrin in a group of patients with either ulcerative colitis or Crohn's disease and to compare the results with those of a group of normal controls. In 108 consecutive patients with IBD (66 with ulcerative colitis, 32 with Crohn's disease and 10 with indetermined colitis) serum levels of gastrin were measured by radioimmunoassay. One hundred and eight normal people were served as controls. The levels of serum gastrin were significantly elevated in patients with Crohn's disease compared to normal controls (74.4 +/- 43.9 pg/ml vs. 47.5 +/- 32.4 pg/ml, P<0.05), irrespectively of the activity of the disease. On the contrary, patients with ulcerative colitis exhibited no significant differences compared to normal controls. Differences between Crohn's disease and ulcerative colitis patients were statistically significant (P<0.001). The rate of infection by Helicobacter pylori in patients with inflammatory bowel disease was statistically significantly lower as compared with normal controls (31.7% vs. 55.1%, P<0.001). It is concluded that patients with active or inactive Crohn's disease have increased levels of serum gastrin. This may have implications concerning the high incidence of upper GI lesions found in patients with Crohn's disease despite the very low incidence of Helicobacter pylori infection.     

Assessment of the prevalence of infection with Helicobacter pylori in patients with inflammatory bowel disease

OBJECTIVE: To determine the prevalence of Helicobacter pylori in patients with inflammatory bowel disease (IBD) and compare this to the prevalence in a control population with non-organic bowel symptoms, and to investigate the effect of sulphasalazine and other 5-aminosalicylic acid (5-ASA) drugs on the prevalence of H. pylori in IBD patients. DESIGN: Prospective, controlled trial. SETTING: Gastroenterology out-patient department, City General Hospital, North Staffordshire Hospitals NHS Trust, Stoke-on-Trent. PARTICIPANTS: The population comprised 51 patients with ulcerative colitis, 42 patients with Crohn's disease and 40 patients with irritable bowel syndrome as controls. Patients with X-ray- and/or biopsy-proven disease were eligible to be entered into the study. INTERVENTIONS: Subjects filled in a detailed questionnaire, were assessed for seropositivity of H. pylori and underwent a C13 urea breath test (UBT). MAIN OUTCOME MEASURES: Seropositivity for H. pylori and a positive C13 UBT result. RESULTS: A quarter of the irritable bowel syndrome controls were seropositive for H. pylori. Of the ulcerative colitis patients, 21.6% were currently H. pylori-positive on C13 UBT; 17.6% of the ulcerative colitis patients who had been previously treated with sulphasalazine were positive while 23.1% of the ulcerative colitis patients who had been treated with a non-sulphasalazine 5-ASA drug were positive. Of the Crohn's patients, 11.9% were currently H. pylori-positive; 3.6% of the Crohn's patients who had been previously treated with sulphasalazine were positive while 12.5% of the Crohn's patients who had been treated with a non-sulphasalazine 5-ASA drug were positive. CONCLUSIONS: Patients with IBD and Crohn's disease in particular were less likely to be H. pylori-positive than controls. Sulphasalazine treatment further decreased the prevalence of H. pylori, although the reduced prevalence of H. pylori in IBD patients could not be accounted for by this alone.     

Helicobacter pylori and nonspecific intestinal inflammation

In 50 subjects with non-specific inflammations of the gut the total prevalence of Helicobacter pylori positive antibodies was 28%, while in the control group of blood donors its was 54% Patients with ulcerative colitis had lower antibodies--18%, in Crohn's disease the serum positivity was 33%. The lowest value of antibodies was found in patients taking Sulfasalazine--11%. The serum positivity was substantially higher in inactive ulcerative colitis and Crohn's disease--35% than in patients with signs of high activity--13%. In 28 patients with non-specific inflammations of the gut endoscopy was performed, in 60% with a pathological outcome. Histologically confirmed gastritis was in the majority Helicobacter pylori negative. It may be stated that in patients with non-specific inflammations of the gut there is a lower incidence of Helicobacter pylori than in the general population, in particular those subjects who were or are treated with Sulfasalazine. The explanation of this fact is however only speculative.     

Low prevalence of Helicobacter pylori in inflammatory bowel disease: association with sulphasalazine.

The prevalence of IgG antibodies to Helicobacter pylori was examined in 110 patients with inflammatory bowel disease (IBD) (63 ulcerative colitis, 47 Crohn's disease) and compared with 100 age and sex matched control patients. The overall prevalence of H pylori seropositivity in the IBD patients was 22%, which was significantly less than that of 52% in the controls (p < 0.002). There was no difference in prevalence between ulcerative colitis and Crohn's patients. The low seropositivity in the IBD patients resulted from a very low prevalence of 10% in those currently receiving sulphasalazine (n = 40) and similarly low prevalence of 7% in those previously receiving sulphasalazine (n = 30). In those receiving olsalazine or mesalazine and who had never had sulphasalazine, the prevalence of seropositivity was 45%. Further studies using 14C urea breath test and microscopy of antral biopsy specimens confirmed that the negative serology in patients receiving sulphasalazine resulted from absence of the infection rather than absence of humoral immune response to it. In six control patients with H pylori infection, a two week course of sulphasalazine (500 mg four times daily) only caused slight suppression of the 14C urea breath test. In vitro studies failed to show any direct antibacterial effect of sulphasalazine on H pylori. These findings indicate that longterm treatment with sulphasalazine leads to eradication of H pylori infection and that this does not result from a direct antibacterial effect. It may be caused by the drug treating the gastritis and thereby depriving the bacterium of essential nutrients exuded by the inflamed mucosa.     

Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis

OBJECTIVES: Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohn's disease. However, the utility of FEG for distinguishing Crohn's disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohn's disease. METHODS: This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System. RESULTS: FEG was present in 28 of 43 (65.1%) children with Crohn's disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohn's disease and in 12 of 24 (50%) patients with ulcerative colitis. CONCLUSIONS: The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn's disease, it does not reliably differentiate between Crohn's disease and ulcerative colitis.     

Nodular duodenitis involving CD8+ cell infiltration in patients with ulcerative colitis

BACKGROUND/AIMS: Limited efforts have been made to determine changes in the upper gastrointestinal tract in ulcerative colitis. The aim of this study was to analyze gastroduodenal lesions in patients with ulcerative colitis. METHODOLOGY: The endoscopical appearance of lesions in the duodenum and stomach was first examined. Biopsy specimens taken from 25 patients with ulcerative colitis, as well as 21 with Crohn's disease and 16 with nonspecific gastroduodenitis who had no Helicobacter pylori infection, were then evaluated by histology and immunohistochemistry for CD8, CD68 and HLA-DR. In ulcerative colitis patients, the HLA-phenotype was also analyzed by the standard NIH complement-dependent microlymphocyte toxicity assay. RESULTS: Endoscopically evident alteration of nodularity in the descending part of duodenum was prominent in ulcerative colitis and Crohn's disease, but not gastroduodenitis. Histological inflammatory change of the duodenal bulb in ulcerative colitis and Crohn's disease was mild as compared to gastroduodenitis cases. Endoscopic and histological change (redness and deformity of villi) in the duodenum were more prominent in ulcerative colitis patients with pancolitis than those with left-sided/proctitis. CD8+ cells infiltrating both the duodenum and stomach were increased in ulcerative colitis and Crohn's disease as compared to gastroduodenitis whereas focal perifoveolar accumulation of CD68+ cells and enhanced epithelial expression of HLA-DR were characteristic of Crohn's disease. Histopathological alteration in the duodenum was particularly prevalent in ulcerative colitis patients with HLA-DR4 and Cw1. CONCLUSIONS: Nodular, histologically mild duodenitis involving CD8+ cell infiltration, the severity of which positively correlates with the extent of colitis, is characteristic of ulcerative colitis.     

Appendicectomy, childhood hygiene, Helicobacter pylori status, and risk of inflammatory bowel disease: a case control study

Aims—To examine the relation between inflammatorybowel disease and appendicectomy, childhood domestic hygiene, andHelicobacter pylori infection.
Methods—Case control study involving 213 patientswith ulcerative colitis, 110 with Crohn's disease, and 337 controlshaving elective surgery.
Results—Nine patients with ulcerative colitis(4.5%) reported a previous appendicectomy compared with 57 controls(19%) (odds ratio (OR) 0.20, 95% confidence interval (CI) 0.1-0.4,p<0.0001). The inverse association was unaffected by excludingoperations performed after the age of onset of ulcerative colitis andwas stronger for appendicectomy performed before age 20 (OR 0.14). Noassociation with appendicectomy was found for Crohn's disease and noassociations with tonsillectomy for either disease. The availability ofa fixed hot water supply in early childhood (before age 11) wasassociated with Crohn's disease (OR for hot water not always versusalways available 0.56, 95% CI 0.3-0.9, p=0.02) but not withulcerative colitis. No other aspect of domestic hygiene before or afterage 11 was associated with either Crohn's disease or ulcerativecolitis. Although H pylori seroprevalence was positively associated with overcrowding (p<0.001) and the absence of running hotwater in childhood it was not associated with the presence of eitherCrohn's disease or ulcerative colitis. H pyloriseroprevalence was no lower in patients who had been exposed tosulphasalazine than in controls or those not exposed.
Conclusions—Our findings confirm the stronginverse association between previous appendicectomy and the developmentof ulcerative colitis and suggest that the protective effect is greaterfor appendicectomy performed in childhood.

Keywords:inflammatory bowel disease; appendicectomy; tonsillectomy; childhood hygiene; Helicobacter pylori; sulphasalazine

     

Specific gastroduodenoscopic findings in Crohn''s disease: Comparison with findings in patients with ulcerative colitis and gastroesophageal reflux disease

BACKGROUND: Crohn's disease patients often carry gastroduodenal lesions. However, few reports have addressed specific gastroduodenoscopic findings in Crohn's disease patients. METHODS: The gastroduodenoscopic findings of 63 Crohn's disease patients were examined. Those of 62 ulcerative colitis and 63 age- and gender-matched gastroesophageal reflux disease patients were also reviewed as controls. Findings of bamboo-joint-like appearance, gastric antral erosions, and duodenal lesions were the specific findings that were highlighted. RESULTS: Of 63 Crohn's disease patients, 47 (75%) had at least one of the specific gastroduodenoscopic findings, and the prevalence of these findings was significantly higher in Crohn's disease patients than in ulcerative colitis and gastroesophageal reflux disease patients (ulcerative colitis, 24/62, 39%; gastroesophageal reflux disease, 15/63, 24%, P < 0.0001). In particular, bamboo-joint-like appearance was almost unique to Crohn's disease patients (Crohn's disease, 28/63, 44%; ulcerative colitis, 3/62, 5%; gastroesophageal reflux disease, 0/63, 0%, P < 0.0001). Analysis of the relationship between the Crohn's disease patient's background and gastrodunodenoscopic findings revealed that both patients with disease affecting the ileum and those with previous gut operations were more likely to exhibit the specific gastroduodenoscopic findings (P = 0.030 and P = 0.043, respectively). CONCLUSION: Specific gastroduodenoscopic findings were observed in Crohn's disease patients. In particular, bamboo-joint-like appearance could be a unique marker of Crohn's disease.     

Accumulation of mast cells and macrophages in focal active gastritis of patients with Crohn's disease

BACKGROUND/AIMS: Recent studies have shown that focal active gastritis seems to be the typical gastric pathology in Crohn's disease. The aim of this study was to compare the incidence of focal active gastritis, Helicobacter pylori infection and distribution of gastric mast cells and macrophages in patients with Crohn's disease, ulcerative colitis and H. pylori gastritis without inflammatory bowel disease. METHODOLOGY: Patients with histologically confirmed Crohn's disease (n = 25) or ulcerative colitis (n = 25) and control patients without inflammatory bowel disease (n = 25) were included in this study. Biopsy specimens were obtained from the antrum and corpus of each patient, and stained with hematoxylin and eosin and immunostained using antibodies to tryptase (AA1) and CD68. The number of mast cells and macrophages located in the lamina propria was determined. RESULTS: Focal active gastritis was detected in 54% of H. pylori-negative patients with Crohn's disease, but it was not found in patients with ulcerative colitis nor in the control group. The density of mast cells and macrophages in the lamina propria of H. pylori-positive patients was significantly higher than in H. pylori-negative patients in all groups. In the Crohn's disease group, the number of mast cells (antrum; 83 +/- 11, body; 89 +/- 11/mm2) and macrophages (antrum; 94 +/- 22, body; 92 +/- 17/mm2) in the lamina propria of H. pylori-negative patients with focal active gastritis was halfway between that in H. pylori-positive and H. pylori-negative patients. In focal active gastritis, mast cells accumulated at the border of focal active gastritis, whereas macrophages accumulated in the center of such lesions. CONCLUSIONS: Our findings indicated that the diagnosis of focal active gastritis, using immunostain for mast cells and macrophages, is the histological hallmark of gastric Crohn's disease. Macrophages might be associated with the formation of focal active gastritis in patients with Crohn's disease.     

Increased prevalence of Helicobacter pylori in patients with diabetes mellitus

BACKGROUND: Whilst upper gastrointestinal disturbances are frequently observed in patients with diabetes mellitus, little is known about the prevalence of Helicobacter pylori infection and peptic disease in these patients. AIM: To evaluate prevalence of Helicobacter pylori infection and peptic disease lesions in diabetics with dyspeptic symptoms. PATIENTS AND METHODS: Study population comprises 74 consecutive diabetes mellitus patients with dyspepsia and 117 consecutive non diabetic dyspeptic patients. Upon enrolment, each patient completed an interview screening questionnaire to obtain information concerning presence and severity of dyspepsia. All patients underwent upper gastrointestinal endoscopy with biopsy specimens being collected from gastric antrum and body Helicobacter pylori was evaluated in each patient by rapid urease test and histology (Giemsa). Gastritis was classified according to the Sydney System. Statistical analysis was performed by chi-square, Fisher exact or t test and logistic regression analysis. A p value <0.05 was considered significant. RESULTS: Prevalence of Helicobacter pylori infection was found to be significantly higher in diabetics than in controls. The prevalence rate of endoscopic lesions was comparable in the two groups, but the association between endoscopic lesions and Helicobacter pylori infection was significantly higher in diabetics. Overall, the presence of chronic gastritis, both non atrophic and atrophic, as well as intestinal metaplasia were comparable in the two groups of patients, whilst the association between chronic gastritis and Helicobacter pylori infection or gastritis activity were significantly higher in diabetics. In neither group, was any correlation found between severity of dyspepsia and presence of endoscopic lesions, chronic gastritis or Helicobacter pylori infection. CONCLUSIONS: These data show a higher prevalence of Helicobacter pylori infection in diabetes mellitus patients with dyspepsia. Helicobacter pylori infection was significantly associated both with the presence of endoscopic lesions and chronic gastritis in diabetic patients, but not in the controls.     

Helicobacter pylori seroprevalence in Crohn's disease: lack of influence by pharmacological treatment

BACKGROUND/AIMS: Helicobacter pylori infection has a low prevalence in Crohn's disease, possibly because of sulphasalazine therapy. We investigated Helicobacter pylori seroprevalence in patients with Crohn's disease never treated with sulphasalazine in order to assess the possible role of antibiotic treatment. METHODOLOGY: Two groups of patients with Crohn's disease (group I: subjects treated with ciprofloxacin, metronidazole or both during the last six months; Group II: subjects who were not given antibiotics during the last six months) and a control group of 30 patients with irritable bowel syndrome were considered. IgG anti-H. pylori levels were measured in all patients. RESULTS: Serology was positive respectively in 16.6%, 13.3% and 36.6% of cases in the three groups. CONCLUSIONS: Our findings confirm the Helicobacter pylori infection is infrequent in Crohn's disease. Neither sulphasalazine nor antibiotics appear to play a role.     

Screening for p53 and K-ras mutations in whole-gut lavage in chronic inflammatory bowel disease

OBJECTIVES: Molecular screening for frequently mutated genes may increase the likelihood of identifying cancer risk groups, such as patients with longstanding inflammatory bowel disease. This study investigated the prevalence and time course of p53 and K-ras mutations in colonic lavage fluid of patients with inflammatory bowel disease. METHODS: Colonic lavage fluid from 190 patients with ulcerative colitis (73), Crohn's disease (58) or controls (49 non-tumour, 10 colorectal cancer) was studied by oligomer-specific hybridization for K-ras mutations and single-strand conformation polymorphism (SSCP) for p53 mutations. Follow-up investigations were carried out after 1-3 years. RESULTS: Mutations were most frequent in carcinomas (5/10, 50%) and rare in non-tumour controls (1/49, 2.0%). They were found in Crohn's colitis in 15.4%, in extensive ulcerative colitis in 18.6%, in left-sided ulcerative colitis in 13.3%, and in distal ulcerative colitis in 6.7% (P > 0.05). There was a positive association with disease duration (> or =11 years, P < 0.05). Follow-up investigations detected the same mutation in four patients and revealed new mutations in three patients. CONCLUSIONS: In our large series of patients with inflammatory bowel disease, K-ras and p53 mutations could be detected with reasonable frequency and confirmed at follow-up in at least some patients. Our data encourage the use of molecular screening for the detection of malignant precursor lesions in at-risk patients.     

Anti-saccharomyces cerevisiae antibodies in patients with inflammatory bowel disease and their first-degree relatives: potential clinical value

Anti-Saccharomyces cerevisiae antibodies (ASCA) have been described as specific markers in Crohn's disease and their healthy first-degree relatives. 171 patients with Crohn's disease, their 105 first-degree relatives, 145 patients with ulcerative colitis and 101 first-degree relatives of patients with ulcerative colitis, 50 patients with infectious enterocolitis and 100 healthy controls were tested for ASCA employing the ELISA technique. When compared with the healthy controls (p < 0.0001) and patients with infectious enterocolitis (p < 0.0001) the prevalence of ASCA was significantly increased in patients with Crohn's disease and their first-degree relatives (p < 0.01). Further significant differences concerning the frequency of ASCA within the different groups of our study population were not observed. In particular, ASCA were not found in increased prevalence in infectious enterocolitis. These observations are compatible with a role of ASCA as a marker of genetic predisposition to Crohn's disease.     

Frequency and clinical evolution of indeterminate colitis: a retrospective multi-centre study in northern Italy. GSMII (Gruppo di Studio per le Malattie Infiammatorie Intestinali).

OBJECTIVE: To evaluate the prevalence and the clinical evolution of patients with an initial diagnosis of indeterminate colitis. DESIGN: Retrospective, observational study. SETTING: Fifteen gastrointestinal units in northern Italy. PARTICIPANTS: Patients with an initial diagnosis of indeterminate colitis seen between 1988 and 1993. INTERVENTIONS: Patients were traced through a common database and centres were requested to update their clinical follow-up. MAIN OUTCOME MEASURES: Frequency of patients with an initial diagnosis of indeterminate colitis among those with IBD; rate of patients who subsequently had a definite diagnosis of either Crohn's disease or ulcerative colitis. RESULTS: Fifty out of 1113 IBD patients (4.6%) had been diagnosed as having indeterminate colitis. During follow-up, 37 patients (72.5%) had a definite diagnosis of either Crohn's disease or ulcerative colitis. The cumulative probability of having a definite diagnosis of either ulcerative colitis or Crohn's disease was 80% 8 years after the first one (i.e. the first diagnosis). The probability of having a diagnosis of Crohn's disease was increased in patients with fever at onset, segmental endoscopic lesions or extra-intestinal complications and in current smokers. The probability of having a diagnosis of ulcerative colitis was increased in patients who had not undergone appendectomy before diagnosis. CONCLUSIONS: In our area, indeterminate colitis accounts for about 5% of initial diagnoses of IBD. In about 80% of patients, a diagnosis of either ulcerative colitis or Crohn's disease is made within 8 years. Several clinical and demographic features can help in identifying those patients more likely to have a subsequent diagnosis of Crohn's disease and those more likely to have a subsequent diagnosis of ulcerative colitis.     

Measles is more prevalent in Crohn's disease patients. A multicentre Israeli study

The question whether there is a transmissible pathogenetic agent as a cause for Crohn's disease, remains unanswered. Measles virus has been the subject of many intensive studies, in the attempt to find a role for it in the pathogenesis of inflammatory bowel disease. Whether an early infection with measles virus may predispose to Crohn's disease in later life is still not clear. We conducted a large scale multicentre study, in order to obtain sufficient data to answer this question. To do so, we compared inflammatory bowel disease patients, with Crohn's disease or ulcerative colitis, with two matched control groups: clinical controls, and community controls. A total of 531 patients, 271 with ulcerative colitis and 260 with Crohn's disease were interviewed, as well as 903 matched controls. Blood from 104 inflammatory bowel disease patients and 50 controls was tested for antibodies to measles virus. We did not find any differences related to measles vaccination, either in Crohn's disease or in ulcerative colitis. Exposure to measles in childhood was more frequent in Crohn's disease patients than in their controls, the difference being statistically significant (p < 0.05) in relation to community controls. The presence of IgG antibodies to measles virus was higher in patients with Crohn's disease than in patients with ulcerative colitis or controls (p = 0.084). Another observation of interest was the finding that Crohn's disease patients who had measles in childhood, more frequently had large bowel disease than those who had not had measles. These data lead us to postulate that there may be a role for measles infection in Crohn's disease, even if, at present, this role remains unclear.     

Antibodies to Saccharomyces cerevisiae: are they useful in clinical practice?

BACKGROUND/AIMS: Antibodies to Saccharomyces cerevisiae are associated with Crohn's disease. The aim of this study was to assess the sensitivity and specificity of antibodies to Saccharomyces cerevisiae for Crohn's disease in an Italian population and to evaluate their clinical role. METHODOLOGY: Antibodies to Saccharomyces cerevisiae serum levels were assessed in 72 inflammatory bowel disease patients (30 Crohn's disease; 42 ulcerative colitis) and 35 age-matched controls. Patients were divided into subgroups on the basis of disease behavior and clinical feature were evaluated. RESULTS: Antibodies to Saccharomyces cerevisiae sensitivity and specificity for Crohn's disease patients were 50% (31-68) and 91% (77-98), for IgG and 56% (37-64) and 94% (80-99), respectively, for IgA. No correlation was observed between the presence of antibodies to Saccharomyces cerevisiae and clinical features. Antibodies to Saccharomyces cerevisiae were more prevalent in Crohn's disease than in ulcerative colitis patients (IgA: 57% vs. 26%; IgG: 50% vs. 17%; p < 0.05). Interestingly, in Crohn's disease patients, the prevalence of antibodies to Saccharomyces cerevisiae was higher in patients with small bowel involvement than in patients with pure colonic disease (IgA: 66% vs. 17%; IgG: 58% vs. 17%). No difference in antibodies to Saccharomyces cerevisiae prevalence was observed between ulcerative colitis and pure colonic Crohn's disease patients. CONCLUSIONS: Our data show an association between Crohn's disease and antibodies to Saccharomyces cerevisiae. However, it does not seem useful in discriminating between ulcerative colitis and colic Crohn's disease.     

P-ANCA in monozygotic twins with inflammatory bowel disease.

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.     

Studies of Isolated Parietal and Enterochromaffin-Like Cells from the Rat

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.     

Prevalence and family risk of ulcerative colitis and Crohn's disease: an epidemiological study among Europeans and south Asians in Leicestershire.

The family history of patients identified during incidence studies in Leicestershire were investigated and the prevalence and comparative risks calculated; 1254 patients aged 15 to 80 years were sent a questionnaire about their family history. All cases with a positive family history were reviewed and confirmed cases included in the study. In Europeans the standardised prevalence of Crohn's disease was 75.8/10(5) and that of ulcerative colitis 90.8/10(5). The prevalence of Crohn's disease among South Asians was 33.2/10(5) and that of ulcerative colitis 135/10(5). The prevalence of Crohn's disease in Europeans was significantly greater than that in Hindus (chi 2 = 16, p < 0.001), while the prevalence of ulcerative colitis was significantly lower in Europeans than Hindus (chi 2 = 27, p < 0.001) and Sikhs (chi 2 = 4.4, p < 0.05). The comparative risk of developing ulcerative colitis in first degree relatives of Europeans patients with ulcerative colitis was increased by approximately 15, but the risk of Crohn's disease was not increased. The comparative risk of developing Crohn's disease among first degree relatives of patients with Crohn's disease was increased by up to 35, the comparative risk of ulcerative colitis was approximately 3. The risk among relatives of South Asian patients with Crohn's disease was not increased, but the risk of ulcerative colitis to relatives of patients with ulcerative colitis was. This study supports the view that Crohn's disease and ulcerative colitis arise in people with a genetic predisposition and exposed to some, as yet unknown, environmental factor.     

Increased levels of lipoprotein (a) in Crohn's disease: a relation to thrombosis?

OBJECTIVE: Lipoprotein (a) is recognized as a risk factor for arterial and venous thrombosis, a property that might be related to its structural similarity to plasminogen. Since patients with inflammatory bowel disease frequently suffer from thromboembolic events, we studied the role of lipoprotein (a) in conjunction with lipids and apolipoproteins in Greek patients with ulcerative colitis and Crohn's disease. METHODS: Lipoprotein (a), total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, apolipoprotein A-1 and apolipoprotein B-100 were determined in sera from 129 consecutive fasting Greek patients with inflammatory bowel disease (66 with ulcerative colitis and 63 with Crohn's disease) and from 66 matched healthy controls. RESULTS: In Crohn's disease patients, the mean serum lipoprotein (a) level was significantly higher than in control patients (41.2 mg/dl vs 22.9 mg/dl; P = 0.005). Mean apolipoprotein A-1 and apolipoprotein B-100 levels were significantly lower in Crohn's disease patients than in the controls. In ulcerative colitis patients the mean levels of lipoprotein (a) and apolipoprotein A-1 were not significantly different to the controls, but the levels of apolipoprotein B-100 were significantly lower. Raised levels of lipoprotein (a) of > 30 mg/dl were found in 29 Crohn's disease patients (46%), 15 ulcerative colitis patients (23%) and 11 control patients (17%). Patients with active Crohn's disease had significantly higher mean lipoprotein (a) and lower apolipoprotein A-1 than patients with non-active disease. CONCLUSIONS: Our results suggest that Crohn's disease patients have different lipoprotein (a) and apolipoprotein patterns compared to ulcerative colitis patients and healthy controls. These changes in Crohn's disease patients may possibly expose them to a higher risk of thrombosis.