Objective-To test the hypothesis that minor chronic insults such as smoking, chronic bronchitis, and two persistent bacterial infections may be associated with increases in C reactive protein concentration within the normal range and that variations in the C reactive protein concentration in turn may be associated with levels of cardiovascular risk factors and chronic coronary heart disease.Design-Population based cross sectional study. Setting-General practices in Merton, Sutton, andWandsworth.Subjects-A random sample of 388 men aged 50-69 years from general practice registers. 612 men were invited to attend and 413 attended, of whom 25 non-white men were excluded. The first 303 of the remaining 388 men had full risk factor profiles determined.Interventions-Measurements ofserum C reactive protein concentrations by in house enzyme linked inmunosorbent assay (ELISA); other determinations by standard methods. Coronary heart disease was sought by the Rose angina questionnaire and Minnesota coded electrocardiograms.Main outcome measures-Serum C reactive protein concentrations, cardiovascular risk factor levels, and the presence of coronary heart disease.Results-Increasing age, smoking, symptoms of chronic bronchitis, Helicobacter pylori and Chlamrydia pneumoniae infections, and body mass index were all associated with raised concentrations of C reactive protein. C Reactive protein concentration was associated with raised serum fibrinogen, sialic acid, total cholesterol, triglyceride, glucose, and apolipoprotein B values. C Reactive protein concentration was negatively associated with high density lipoprotein cholesterol concentration. There was a weaker positive relation with low density lipoprotein cholesterol concentration and no relation with apolipoprotein A I value. C Reactive protein concentration was also strongly associated with coronary heart disease.

An increased anti-Cp antibody titre may be a predictor for further adverse cardiovascular events in post-MI patients. Taking a short course of azithromycin may lower this risk, possibly by acting against Cp.

Background-There is evidence suggesting that early life experience may influence adult risk of coronary heart disease (CHD). Chronic bacterial infections have been associated with CHD. Objective-To determine whether Helicobacter pylori, a childhood acquired chronic bacterial infection, is associated with an increased risk of coronary heart disease in later life. We used a case-control comparison to investigate whether H pylori infection was associated with adult CHD. We also studied possible associations of Hpylori infection with cardiovascular risk factors in the control population. Patients and methods PATlENTSWe studied men aged 45-65. The controls came from a single general practice screening clinic and the cases from a series of consecutive patients referred to the cardiology clinic of a local teaching hospital with angiographically confirmed CHD (stenosis >70% in one coronary artery). Potential controls were excluded if they had a firm diagnosis of CHD. METHODSAll subjects completed a questionnaire and 10 ml of serum was drawn and stored at -20°C. Blood pressure was measured in the general practice when the patient was seated. One observer used the same mercury sphygmomanometer throughout the study.We measured H pylori specific IgG antibody titres by an in-house enzyme linked immunoadsorbent assay (ELISA) in duplicate, using a partially purified antigen as described previously. Results were analysed by multiple logistic regression using GLIM7 and multiple regression using the GLM proceedure in SAS. In the logistic regression models, age was grouped into four categories (45-49, 50-54, 55-59, 60-65) and current social class was grouped into six categories according to the Registrar-General's 1980 classification.

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The mechanisms by which the lifestyle risk factors obesity, physical inactivity, and low fiber intake predispose to colorectal cancer (CRC) are unclear. Chronic bowel inflammation predisposes to malignancy in cases of inflammatory bowel disease. Many lifestyle risk factors for CRC are associated with evidence of systemic inflammation as indicated by circulating levels of Creactive protein (CRP), but it is unknown how this relates to inflammation at tissue level. Little is known about the degree of bowel inflammation in general population and the factors that affect it. Therefore, we aimed to assess the relation of levels of bowel inflammation in the general population and lifestyle risk factors for CRC, and to additionally assess whether these associations, if present, were attenuated by controlling for evidence of systemic inflammation.Average CRC risk subjects (320) of either sex aged 50 -70 were recruited in South London. A stool sample was provided for calprotectin measurement (a marker of bowel inflammation), serum for CRP, and a detailed dietary and lifestyle questionnaire completed.There was a significant positive relationship between fecal calprotectin and increasing age (P ‫؍‬ 0.002), obesity (P ‫؍‬ 0.04), physical inactivity (P ‫؍‬ 0.01), and an inverse relationship with fiber intake (P ‫؍‬ 0.02) and vegetable consumption (P ‫؍‬ 0.04). The relationship with obesity was attenuated by controlling for serum CRP.Fecal calprotectin levels are associated with lifestyle risk factors for colorectal cancer. Low-level asymptomatic bowel inflammation may be the link between lifestyle and the pathogenesis of CRC, and circulating proinflammatory cytokines may be part of the mechanism for this link.

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The factors that determine which Helicobacter pylorn infected subjects develop duodenal ulcer (DU) are unclear. This study tested the hypothesis that infection density and urease activity are higher in DU than non-DU subjects. Fifty five DU and 55 age and sex matched non-DU subjects were studied. Quantitative methods were used for measuring infection density (viable organism count) and urease activity (Berthelot reaction). DU subjects had a greater antral infection density ( Studies have attempted to explain the outcome of H pylori infection on the basis of differences in strain virulence.6-8 A cytotoxin obtained from some strains of H pylori has been shown to produce vacuolation in cultured cell lines.9 The association between DU and carriage of cytotoxic strains of H pylori is strong, however, such strains also occur in most subjects without DU7 and therefore can only provide part of the explanation for the development of ulceration.H pylori produces large amounts of urease, the ammonia generated by this has been shown to have cytopathic effects on different cultured cell lines in a concentration dependent manner,10 11 and to be toxic to the gastric mucosa of experimental animals.'2 It is possible that strains of H pylori associated with ulceration produce greater amounts of urease.Histological assessment of the distribution and density of H pylori in the stomach has suggested that there may be greater colonisation of the gastric antrum in DU patients than subjects without DU,13 however, one study has produced conflicting results, showing no significant difference between the two groups. 14 The patchy nature of the distribution of the organism and the tendency of H pylori to colonise gastric glands in large clumps renders semi-quantitative histological studies inadequate for the measurement of a potentially immense range of infection densities in vivo. In addition, no assessment of organism viability is possible on histological sections.In this study we aimed to assess by quantitative methods H pylori infection density and urease activity in patients with DU and in those without; and the relation of infection density to factors associated with DU.