Serum beta-glucuronidase activity in human diabetes mellitus, granuloma annulare and necrobiosis lipoidica.
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Biomedical subjects
Publications and source records attributed to C Chilvers.
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Site-specific cancer mortality data for 20 United States cities have been abstracted from United States Government publications to explore further the hypothesis that fluoridation of water supplies causes cancer. Changes in mortality (standardised for age, sex, and ethnic group) between 1958-62 and 1968-72 in 10 fluoridated and 10 non-fluoridated United States cities have been examined. Of the seven sites (or groups of sites) examined, for only one is there a statistically significant difference between the fluoridated and non-fluoridated cities with respect to average change in mortality. This difference, for cancers of the genital organs, favours the fluoridated cities. These data do not provide evidence of a positive association between fluoridation of water supplies and cancer of any of the sites considered.
This study was designed to investigate whether exposure to nitrate-containing dust during fertiliser manufacture was associated with an excess of deaths from cancer in general or specifically from cancers of the digestive tract, liver, lung, and bladder. It was based on data extracted from census schedules by the Office of Population Censuses and Surveys, occupational characteristics recorded by fertiliser workers at the 1961 and 1971 censuses of England and Wales being related to subsequent mortality ascertained through the National Health Service Central Register. The 1961 cohort, followed up until 1978, showed a "healthy worker effect" and no evidence of excess mortality from cancer at any site. The 1971 cohort also showed below average mortality during 1971-7 for all causes of death and for circulatory diseases, but there were more deaths from cancer than expected, due mainly to an excess of cancers of the lung and digestive tract. The excess of cancer was more pronounced, but not statistically significant, when compared with other employed men. Though the numbers for comparison were small, there was weak evidence of an association between cancer mortality and frequency of exposure to nitrate-containing dust in this cohort. It is difficult to reconcile the excess cancer mortality in the 1971 cohort with the more favorable level in the earlier cohort, since industrial hygiene has improved and the cohorts showed a similar distribution by region and social class. To examine further these conflicting results the 1971 cohort will be followed for a longer period and re-examined when more deaths have accrued.
A group of 122 postmenopausal patients with histologically proven node-positive primary breast cancer have been randomized to receive aminoglutethimide-hydrocortisone or placebo aminoglutethimide-placebo hydrocortisone for 2 years. Median follow-up is 17 months. In general, treatment was well tolerated, but 15 patients required a reduction in the dose of aminoglutethimide, and of these four patients were unable to continue therapy due to side effects. Primary staging, incidence of extensive node involvement, and estrogen receptor were similar in the treatment and control arms. Dehydroepiandrosterone sulfate (DHA-S) and estrone were measured in a subgroup of patients, and significant suppression of DHA-S levels throughout the duration of the treatment period as seen in patients receiving the active drug. No significant suppression of either DHA-S or estrone levels was seen in the controls. Patients were monitored for metastases by serial liver function tests, carcinoembryonic antigen, and chest X-rays, and of 26 relapsing patients only three patients were not detected by this screen. We conclude that adjuvant aminoglutethimide is moderately well tolerated. It is capable of suppressing DHA-S throughout 2 years of treatment. A further 280 patients will be entered into the study to assess the survival benefit for those taking aminoglutethimide-hydrocortisone.
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Nineteen patients with chronic airflow obstruction measured their morning and evening peak expiratory flow (PEF) daily for 28 days. A placebo was taken for the first week and prednisolone 20 mg twice daily was taken for the last three weeks. The mean PEF in 13 patients who responded to prednisolone reached a maximum after eight days' treatment. The majority of the 19 patients had asthma and were thought to represent a typical cross section of patients who would be considered for a trial of oral corticosteroids. Most responsive patients will achieve a maximum response within eight days.
Nitrites, derived mainly from ingested nitrates, may react in vivo with secondary nitrogen compounds occurring naturally in certain foods to form N-nitroso compounds, which are potent carcinogens in laboratory animals. This paper reviews the mechanism of their formation and the evidence from epidemiological studies that high nitrate ingestion is involved in the aetiology of human cancer.
Until recently the basic geographical unit in England and Wales for the compilation of population and mortality data has been the local authority administrative district. Epidemiologists have made little use of the mortality data available from 1950 for small administrative districts: municipal boroughs, urban and rural districts. In April 1974 the boundaries of administrative areas were radically revised, but mortality data for the old districts were still compiled up to 1978. In this paper we review the material available for small districts and its uses and limitations for research into the causes of cancer. It is argued that these data covering 29 years deserve to be more widely used both for generating clues and for testing hypotheses about the aetiology of cancer and other chronic diseases.
We have compared estimation of alveolar carbon monoxide measured either as end-expired or mixed-expired carbon monoxide tension with two spectrophotometric estimations of venous blood carboxyhaemoglobin (COHb). Estimation of mixed-expired carbon monoxide proved more convenient for patients than the end-expired method, and this estimation of carbon monoxide exposure discriminated between non-smokers and smokers as well as measurements of COHb. The technique is bloodless, economical, and simple to perform. It should prove a valuable method for validating reported smoking habits of people attending smoking advisory centres and for epidemiological surveys of smoking.
This paper reviews briefly some industrial applications which may result in occupational exposure of the workforce to preformed N-nitroso compounds. It considers exposure to nitrate in more detail, discussing epidemiological evidence which lends support to the hypothesis that high nitrate ingestion is related to high mortality from gastric cancer, through the formation in vivo of carcinogenic N-nitroso compounds. It presents the preliminary findings in a census-based mortality study of industrial workers exposed to nitrate-containing dust in the manufacture of fertilizers.
Cardiovascular mortality and morbidity were assessed, after a mean follow-up period of 5 years, in an unselected series of 159 adults presenting with the nephrotic syndrome between 1972 and 1975. 60% of the deaths were attributed to terminal renal failure, and the incidence of deaths from ischaemic heart-disease (IHD) was not significantly above normal. The proportion of patients experiencing angina and intermittent claudication and the prevalence of ischaemic electrocardiographic changes did not differ significantly from those of a London control population. At follow-up, hypertension was significantly more common (p less than 0.001) in male nephrotic patients than in controls. Earlier reports of a greatly increased incidence of IHD in unselected patients with the nephrotic syndrome were not confirmed. Routine treatment of hyperlipidaemia in the nephrotic syndrome is not, therefore, recommended.
Although various factors have been implicated in the aetiology of oesophageal cancer, one factor common to many countries is the consumption of alcoholic beverages. In England and Wales mrtality from oesophageal cancer declined rapidly during the early part of this century but both mortality and incidence have increased in recent years. The generation of males born in 1906 had lower mortality than any preceding or succeeding generation. It is suggested that ages 20 to 30 may be critical in the development of oesophageal cancer and that the 1906 cohort was less exposed to alcohol than other generations. The international analysis suggests that ethyl alcohol itself rather than any specific alcoholic beverage is associated with this cancer.
A method is described for the determination of a measure of relative risk from vital statistical data. If the frequency of disease in a population is linearly related to the level of exposure to a given factor, then a measure of the relative risk can be estimated from the slope and intercept of the regression line. For example, when the exposure is measured in terms of the proportion of the population exposed to the factor, then the relative risk is equal to (Formula: see text). This offers an indirect but simple and inexpensive method for estimating relative risk. It should be used with caution, particularly where confounding factors may be responsible for the apparent association between disease and factor. Applications of the method to estimate the relative risk of (a) circulatory diseases in women using oral contraceptives and (b) ovarian cancer in women with different average family sizes, both yielded relative risk estimates comparable with those obtained from case-control and prospective studies.
A clear inverse relation between average completed family size and mortality from ovarian cancer in different populations of women is seen from one country to another; for successive generations of women living within the same country; in married and single women; and in different social, religious, immigrant, and ethnic groups. The findings suggest that pregnancy--or some component of the child-bearing process--protects directly against ovarian cancer. This protection seems to persist throughout life. The more-than-twofold increase in the age-standardised ovarian-cancer death-rate in England and Wales since 1931 can be explained largely by changes in the average completed family size.
This paper reviews routine data-collecting systems and methods for disease surveillance in England and Wales. It discusses population-based correlation studies, which seek to explain disease trends by relating routine health statistics to possible causative agents on a secular, geographical, or occupational basis. It describes recent developments in linking information collected by routine general purpose systems as a means of identifying and following individuals exposed to potential hazards.