The BSG/ACPGBI guidelines for colonoscopic screening: what are we missing?

INTRODUCTION: Before publication of the British Society of Gastroenterology and Association of Coloproctology of Great Britain and Ireland guidelines in 2002, screening for people with a family history of colorectal cancer was sporadic and largely dependant on unvalidated local guidelines. Since 1990 we have been screening patients with both high and moderate risk family histories of colorectal cancer using local protocols which were more liberal than the new guidelines. In this study, we have analysed the pathology that would have been missed if we had been using the new guidelines in the period 1990-2002. METHOD: A total of 399 consecutive patients with a positive family history of colorectal malignancy underwent screening endoscopy according to local guidelines. Demographic, endoscopic and pathologic data were prospectively collected. Patients were retrospectively divided into those who would have been screened under the new guidelines (group 1) and those who would not (group 2). The recorded pathology was graded as significant or insignificant and the findings compared between the two groups. RESULTS: A total of 399 patients underwent 557 endoscopies of which 278 (50%) were indicated under the new guidelines (group 1) and 279 (50%) were not indicated (group 2). A significant pathology or carcinoma was found in 15.8% of group 1 endoscopies and 10.0% of group 2 endoscopies. This difference was significant. CONCLUSION: If we had been using the new guidelines in the period 1990-2002, we would not have performed 279 (50%) of the 557 procedures, but would not have discovered significant pathology in 10% of the moderate risk endoscopies representing 39% of the significant pathology, which was actually present in this population.

Recordings of mucociliary activity in vivo: benefit of fast Fourier transformation of the photoelectric signal.

Investigations of mucociliary activity in vivo are based on photoelectric recordings of light reflections from the mucosa. The alterations in light intensity produced by the beating cilia are picked up by a photodetector and converted to photoelectric signals. The optimal processing of these signals is not known, but in vitro recordings have been reported to benefit from fast Fourier transformation (FFT) of the signal. The aim of the investigation was to study the effect of FFT for frequency analysis of photoelectric signals originating from an artificial light source simulating mucociliary activity or from sinus or nasal mucosa in vivo, as compared to a conventional method of calculating mucociliary wave frequency, in which each peak in the signal is interpreted as a beat (old method). In the experiments with the artificial light source, the FFT system was superior to the conventional method by a factor of 50 in detecting weak signals. By using FFT signal processing, frequency could be correctly calculated in experiments with a compound signal. In experiments in the rabbit maxillary sinus, the spontaneous variations were greater when signals were processed by FFT. The correlation between the two methods was excellent: r = .92. The increase in mucociliary activity in response to the ciliary stimulant methacholine at a dosage of 0.5 microgram/kg was greater measured with the FFT than with the old method (55.3% +/- 8.3% versus 43.0% +/- 8.2%, p < .05, N = 8), and only with the FFT system could a significant effect of a threshold dose (0.05 microgram/kg) of methacholine be detected. In the human nose, recordings from aluminum foil placed on the nasal dorsum and from the nasal septa mucosa displayed some similarities in the lower frequency spectrum (< 5 Hz) attributable to artifacts. The predominant cause of these artifacts was the pulse beat, whereas in the frequency spectrum above 5 Hz, results differed for the two sources of reflected light, the mean frequency in seven healthy volunteers being 7.8 +/- 1.6 Hz for the human nasal mucosa. It is concluded that the FFT system has greater sensitivity in detecting photoelectric signals derived from the mucociliary system, and that it is also a useful tool for analyzing the contributions of artifacts to the signal.

Mortality from circulatory diseases, especially ischaemic heart disease in sea pilots and boatmen in Sweden 1951-84: a retrospective cohort study.

A cohort of 1455 sea pilots and boatmen employed after 1921 was established. Those identified and alive in 1951 (n = 1323) were linked to the Swedish cause of death register 1951-84. In 21 352 person-years 383 deaths were observed among sea pilots compared with 379.3 expected (SMR = 101;95% CI between 99 and 112) and in 12,127 person-years the observed number of deaths among boatmen was 136, expected 135.9 (SMR = 100) when Swedish men were used as a reference population. For ischaemic heart disease (IHD) (ICD-8: 410-414) the SMR was equal to 96 (obs = 131, exp = 137.2) for sea pilots and 91 (obs = 44, exp = 48.4) for boatmen. No trend over time or geographical differences could be observed. A healthy worker effect could not explain why there was no excess mortality from IHD.

Reductions in lymphocyte subpopulations after repeated exposure to 1.5 ppm nitrogen dioxide.

In this investigation the effects of repeated exposure to 1.5 ppm NO2 on immune competent cells in bronchoalveolar lavage (BAL) fluid was studied. Special attention was focused on effects on lymphocyte subpopulations. Eight healthy subjects were exposed to 1.5 ppm NO2 every second day on six occasions. Bronchoalveolar lavage fluid was collected at least three weeks before the exposure series as reference and 24 hours after the last exposure. The results obtained were analysed using a non-parametric test for paired observations, with each subject as his own control. Significant reductions were found in the total number and percentage of T cytotoxic-suppressor cells in BAL fluid; this caused an increase in the ratio of T helper-inducer: cytotoxic-suppressor cells. The total number of natural killer cells in the BAL fluid was also reduced. The numbers of all other cell types were unchanged after exposure. No reduction of phagocytosis of opsonised yeast particles by alveolar macrophages in vitro was detected. It is concluded that repeated short term exposures to 1.5 ppm NO2, a moderate occupational concentration, induces significant effects on immune competent bronchoalveolar lymphocytes. This indicates that previous findings of changes in the lymphoid immune system induced by NO2 in animals may well be applicable to humans.

Clara cell protein as a biomarker for ozone-induced lung injury in humans.

Exposure to ozone (O3) impairs lung function, induces airway inflammation and alters epithelial permeability. Whilst impaired lung function and neutrophilia have been observed at relatively low concentrations, altered lung epithelial permeability is only seen after high-dose challenges. The appearance of Clara cell protein (CC16) in serum has been proposed as a sensitive marker of lung epithelial injury. Here, the use of CC16 as an injury biomarker was evaluated under a controlled exposure to O3 and the relationship between this marker of lung injury and early lung function decrements was investigated. Subjects (n=22) were exposed on two separate occasions to 0.2 parts per million O3 and filtered air for 2 h. Blood samples were drawn and lung function assessed at 2 h pre-exposure, immediately before and immediately after exposure as well as 2 and 4 h postexposure. O3 increased CC16 serum concentrations at 2 h (12.0+/-4.5 versus 8.4+/-3.1 microg x L(-1)) and 4 h postexposure (11.7+/-5.0 versus 7.9+/-2.6 microg x L(-1)) compared with air concentrations. Archived samples from O3 studies utilising the same design indicated that this increase was sustained for up to 6 h postexposure (9.1+/-2.6 versus 7.1+/-1.7 microg x L(-1)) with concentrations returning to baseline by 18 h (7.7+/-2.9 versus 6.6+/-1.7 microg x L(-1)). In these studies, the increased plasma CC16 concentration was noted in the absence of increases in traditional markers of epithelial permeability. No association was observed between increased CC16 concentrations and lung function changes. To conclude, Clara cell protein represents a sensitive and noninvasive biomarker for ozone-induced lung epithelial damage that may have important uses in assessing the health effects of air pollutants in future epidemiological and field studies.