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Biomedical subjects

C P Caygill

Publications and source records attributed to C P Caygill.

18 recordsLinked to original sources
PubMed1992

Bacterial infection and human cancer: association or causation?

Environmental factors such as diet, industrial pollution, smoking and viruses account for some 80% of cancers and more than one-quarter of all non-accidental deaths. Little attention has been paid to the relationship between bacterial infection and cancer but there is growing evidence to support this link. For some sites, such as stomach and colorectum, the evidence is relatively strong, whereas for others, such as biliary tract and bladder, it is more circumstantial.

Animals↗
PubMed1992

Malignancy following surgery for benign peptic disease: a review.

Since 1986 there have been a number of large studies of cancer risk after surgery for benign disease involving over 20,000 patients followed for at least 20 years. All show that gastric surgery carries an excess risk of gastric cancer after a 15-20 year latency. There is less agreement about the excess risk at other sites. The size of such risks appears to depend on the size of cohort, type of ulcer, type of surgery, length of follow-up and level of analytical detail. Statistically significant excess risks have been reported for cancer of the colon (6/8 studies), biliary tract (4/5), lung (6/6), bladder (3/3), pancreas (4/7) and all sites (2/3). Our own study showed an excess risk of cancer of the gallbladder (14.3 fold), stomach (4.5), breast (4.0), bronchus (3.9), large bowel (1.6), oesophagus (2.3), pancreas (4.0), bladder (2.4) and all sites (3.3).

Gastrectomy↗
PubMed1991

Trends in European breast cancer incidence and possible etiology.

In this study the trends in breast cancer incidence in a number of European countries, over the last 20 years, have been evaluated. There is a wide range in incidence; the risk being highest in north and west Europe (and highest in Switzerland) and lower in south and in east Europe. There was little difference, however, between countries in the incidence of the disease occurring before the menopause, and this incidence has shown little temporal change in the time period 1960-1985. Indeed, in many countries there has been little change in incidence in any age band since 1975. The use of oral contraception has been claimed to be a risk factor in premenopausal breast cancer. In two countries, the data on oral contraceptive usage were available; in neither was there any evidence that the introduction and growth in such usage was related to the risk of breast cancer in any age band that might have been exposed to them. The reasons for this are discussed in the light of recent reports to the contrary.

Adolescent↗
PubMed1991

Increased risk of cancer mortality after vagotomy for peptic ulcer: a preliminary analysis.

Patients (1,643) undergoing vagotomy for peptic ulcer at York District Hospital were traced through the Office of Populations Censuses and Surveys (OPCS) and cause of mortality obtained for the 577 who had died. Expected mortality for the cohort was calculated using a years at risk calculation in 5 year bands. There was an excess risk of mortality from cancer of all sites (1.5-fold), stomach (1.6-fold), colorectum (1.7-fold), biliary tract (4.1-fold) and lung (1.6-fold). There was no excess risk or mortality from cancer of the oesophagus, pancreas and female breast. The numbers of deaths have been too few and length of follow-up too short to investigate latency. The findings are consistent with the production of carcinogens as a result of the hypoacidity following vagotomy.

Biliary Tract Neoplasms↗
PubMed1991

Endogenous N-nitrosation and cancer of the biliary tract.

Evidence is presented that N-nitroso compounds occur in bile from patients who have undergone surgery for gallstones or had gastrectomy and from unoperated persons. It is unlikely, therefore, that local formation of nitrosamines can account for the excess risk for gallbladder cancer in the first two groups. Gastric formation remains the likeliest hypothesis.

Bile↗
PubMed1990

Occupational and socioeconomic factors associated with peptic ulcer and with cancers following consequent gastric surgery.

Over 3000 patients, treated surgically for peptic ulcers, were assigned to a Social Class and Occupation Group using information obtained either from their death certificates or from their hospital notes. An analysis of the relationship of socioeconomic status and occupation with the site of original ulcer and the risk of cancer is reported. The major observations were: (a) an association of gastric ulcer with manual and of duodenal ulcer with non-manual Social Class; (b) an association of gastric cancer with dusty occupation and colorectal cancer with professional and managerial workers; and (c) no association between post-surgery gastric cancer risk and social class. This implies that the early stages of gastric carcinogenesis are related to poor socioeconomic conditions but the progression from the precursor lesion (in this case gastric ulcer) to gastric cancer is not, and is consistent with the multistage hypothesis of gastric carcinogenesis proposed by Correa [Diet and Human Carcinogenesis (Edited by Joosens, J. V., Hill, M. J. and Geboers, J.), pp. 109-115. Excerpta Medica, Amsterdam (1985)].

Colorectal Neoplasms↗
PubMed1988

Mortality from colorectal and breast cancer in gastric-surgery patients.

In a preliminary "years at risk" analysis of 5018 patients treated surgically for peptic ulcer at St. James Hospital, Balham, between 1940 and 1960, there was an increase in mortality from colorectal cancer 20 or more years after operation (1.6 fold; p less than 0.05) and an increase in mortality from breast cancer (4.0 fold; p less than 0.001). During the first 20 post-operative years there was an apparent decrease in mortality from both cancers (relative rate = 0.7 (NS) for colorectal and 0.5 (p less than 0.01), for breast cancer). The excess risk of colorectal cancer after a 20 year latency was almost entirely due to the 9.5 fold (p less than 0.001) excess risk in the 381 female gastric ulcer patients treated by Billroth I operation, and the 8.0 fold (p less than 0.05) excess mortality for the small group of 123 female patients who had vagotomy for duodenal ulcer. The apparent decreased risk during the first 20 post-operative years was entirely due to the 5-fold decrease (p less than 0.01) in risk in the 659 male patients treated by Billroth I surgery for gastric ulcer. The ratio of colon: rectal cancers was very much higher in gastric ulcer than in duodenal ulcer patients (5.6 compared to 1.8) and higher in females than in males (6.0 compared to 2.4). The excess risk of breast cancer after a 20 year latency was 4-fold in both gastric ulcer and duodenal ulcer patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Breast Neoplasms↗
PubMed1987

Increased risk of cancer at multiple sites after gastric surgery for peptic ulcer.

Of 5018 patients who had undergone gastric surgery at St James Hospital, Balham, at least 25 years ago, death certificates have been received for 2768, whilst 1746 patients are still alive and are flagged (Office of Populations, Censuses and Surveys (OPCS) will notify us of their death and its cause) and only 504 could not be traced. Mortality from cancers of various organs has been determined using a 'years at risk' calculation in five year bands. There was no increase in mortality risk from any cancers during the first 15 postoperative years, but from 20 years after operation there was a significant excess risk not only of cancer of the stomach (4.5-fold), but also of the large bowel (1.6-fold), bronchus (3.9-fold), pancreas (4.0-fold), biliary tract (9.1-fold), oesophagus (2.3-fold), bladder (2.4-fold), breast (4.0-fold), and cancer of all sites (3.3-fold). These findings are consistent with the production in the operated-upon stomach of circulating carcinogens with a 20 year latency period.

Humans↗
PubMed1986

Mortality from gastric cancer following gastric surgery for peptic ulcer.

When compared with a matched population group, 4466 ulcer patients who had had gastric surgery between 1940 and 1960 showed no difference in the risk of death from gastric cancer in the first 20 years of follow-up but a 4.5-fold increase thereafter. In duodenal ulcer patients there was an initial decrease in risk followed by a 3.7-fold increase after 20 or more years. Since the initial decrease was seen only in the gastrectomy patients and not in those who had truncal vagotomy and drainage, it may have been due to the reduction in mucosal surface. The increased risk 20 years after duodenal ulcer surgery was greater in vagotomy patients than in gastrectomy patients. In gastric ulcer patients a 3.0-fold increase in risk for the first 20 years rose to a 5.5-fold increase thereafter. After 20 years, patients treated with the Bilroth II operation were at higher risk than those treated with Bilroth I, consistent with a role for bile reflux in gastric carcinogenesis. The finding that the risk differs according to original pathology and type of operation may explain the discrepancies between previous studies.

Drainage↗
PubMed1975

The dependence on vitamin E and selenium of drug demethylation in rat liver microsomal fractions.

1. The effects of vitamin E deficiency, and of vitamin E and selenium deficiency, on rat liver microsomal aminopyrine demethylase activity were investigated. It was found that, over a wide range of substrate concentrations, the enzyme activity in preparations from deficient animals was significantly lower than that in controls. 2. Addition of antioxidants in vitro, either to the homogenization or to the assay media, was without significant effect on the depressed enzyme activity. Castration and alteration in dietary protein concentration were also without effect. The rate of oxidation of NADPH was however, lower in preparations from deficient animals. 3. Lineweaver-Burk plots of the reciprocal of enzyme activity and substrate concentration showed a higher Km value in preparations from vitamin E-deficient animals, irrespective of whether selenium was present; the Vmax. was unaffected. These parameters were unchanged when antioxidants were added in vitro. Induction with phenobarbitone and 3-methylcholanthrene showed large changes in Km value which, for preparations from vitamin E-deficient animals, was higher than that for corresponding controls. 4. Examination of the synergism between NADH and NADPH as donors of reducing equivalents for aminopyrine demethylation showed that vitamin E and selenium were only minimally involved in the phenomenon. However, both the initial rate and the extent of demethylation were significantly lower in vitamin E- and selenium-deficient preparations and both nutrients were required for the restoration of full activity. 5. The significance of these results is discussed in the light of our working hypothesis.

Aminopyrine↗
PubMedDate not supplied

Serum selenium and gastric cancer in two regions of Norfolk.

Selenium concentrations were measured in the serum of 244 patients attending the Norfolk and Norwich Hospital, and 246 attending the James Paget Hospital in Gorleston, Norfolk. Both the mean and the median serum selenium concentration was lower in Gorleston than in Norwich, the difference being much greater in women than in men. Whereas the selenium concentrations were normally distributed about the mean for the Norwich area, there was a skewed distribution for the Gorleston area. The results are discussed in relation to the previously observed high risk of intestinal type gastric cancer in the Gorleston area.

England↗