Biomedical subjects

C Svanes

Publications and source records attributed to C Svanes.

36 records · Page 2Linked to original sources

PubMed2000

Trends in perforated peptic ulcer: incidence, etiology, treatment, and prognosis.

After increasing steeply at the beginning of the twentieth century, ulcer perforation incidence during the last decades has declined in the young and in men, and it has risen among the elderly and in women. These changes can be attributed to a cohort phenomenon: Ulcer perforation risk is particularly common in the cohorts born after the turn of the twentieth century and is less common in previous and succeeding birth cohorts. A decline in total incidence is expected with the death of the high risk cohorts. Most ulcer perforations among subjects < 75 years of age can be attributed to smoking. Subjects with a history of ulcer perforation therefore have poorer long-term survival than the general population, most pronounced for younger generations. About one of four ulcer perforations can be attributed to the use of nonsteroidal antiinflammatory drugs, a risk factor of particular importance in the elderly. Ulcer perforation was frequently treated by gastric resection in former days, whereas suture, being the first method introduced in 1887, is the method of choice today. The introduction of antibiotics improved the prognosis of ulcer perforation surgery greatly. Postoperative lethality decreased until 1950 but has remained stable since then. Lethality is higher in the elderly and is higher after gastric than after duodenal perforation. The delay before surgical treatment is a strong determinant for lethality, complication rates, and hospital costs. Treatment delay seems to have increased during the last

Age Factors↗

PubMed1999

Childhood environment and adult atopy: results from the European Community Respiratory Health Survey.

BACKGROUND: Previous literature has indicated that environmental exposures in childhood influence development of atopic sensitization. OBJECTIVE: We sought to study the association between childhood environment and adult atopy. METHODS: Thirteen thousand nine hundred thirty-two subjects aged 20 to 44 years from 36 areas in Europe, New Zealand, the United States, and Australia took part in the European Community Respiratory Health Survey, answering interviewer-led questionnaires and providing blood tests for measurement of specific IgE to grass, house dust mite, cat, and Cladosporium allergens. RESULTS: Atopy was negatively associated with family size (OR = 0. 93; 95% CI = 0.90-0.96 per 1 sib), partly attributable to an independent protective effect of a greater number of brothers (OR = 0.92; 95% CI = 0.89-0.95 per 1 brother). Accounting for total number of siblings, no further influence was detected for number of older or younger siblings. Bedroom sharing was associated with a lower prevalence of atopy, particularly to cat allergen. A protective effect of family size and bedroom sharing could only be detected in subjects reporting no parental allergy (family size, test for interaction P =.012). The presence of a dog in the home in childhood was negatively associated with adult atopy (OR = 0.85, 95% CI = 0. 78-0.92), an effect that remained after adjustment for parental allergy, sibling allergy, and adult pet ownership. CONCLUSION: Subjects from large families with brothers, shared bedrooms, and dogs in childhood were less often atopic as adults. Our findings are consistent with the hypothesis that infectious agents could inhibit development of atopy during childhood. However, in subjects with a strong genetic predisposition, environmental factors in childhood are possibly of less importance.

Adult↗

PubMed1999

Causes of death in patients with peptic ulcer perforation: a long-term follow-up study.

BACKGROUND: Survival is lower in ulcer perforation patients than in the general population. This study assesses the causes of death in patients treated for peptic ulcer perforation. METHODS: Cause-specific mortality in a population-based cohort of 817 patients treated for ulcer perforation in western Norway during the period 1962-1990 was compared with cause-specific population death rates. Analyses were based on observed and expected mortality curves for major causes of death and on standardized mortality rates (SMRs). Cox regression models were used to analyse possible differences on the basis of sex, birth cohort, surgical procedure, and ulcer location. RESULTS: Ulcer perforation patients experienced increased mortality from neoplasms (SMR = 1.8; 95% confidence interval (CI) = 1.4-2.1), lung cancer (SMR = 3.6; 95% CI = 2.3-4.9), circulatory diseases (SMR = 1.3; 95% CI = 1.1-1.6), ischaemic heart disease (SMR = 1.3; 95% CI = 1.03-1.6), and respiratory diseases (SMR = 1.9; 95% CI = 1.3-2.6). Postoperative deaths accounted for 38% of all excess deaths. Death from recurrent peptic ulcer was increased also in subjects who survived the 1st year after the perforation (SMR = 5.8; 95% CI = 1.2-10.4) but accounted for only a few deaths. The increase in mortality from lung cancer was higher in subjects born after 1910 than in patients of older generations. Excess mortality from lung cancer and from circulatory diseases was higher in male than in female patients. CONCLUSIONS: Increased mortality in ulcer perforation patients could mainly be attributed to smoking-related diseases. This is indirect evidence that smoking may be an important aetiologic factor for ulcer perforation.

Cardiovascular Diseases↗

PubMed1998

Expected survival compared with survival of peptic ulcer patients.

In analyses of patient survival it is often desirable to compare observed survival curves with expected survival curves based on information obtained from the general population. However, current methods of calculating expected survival curves are difficult to interpret and are often poorly documented. We discuss an alternative formulation of the so-called direct method which we recommend for general use. By simulation, we show that the expected survival curve obtained from this method represents the expectation of a Kaplan-Meier curve for a set of random population controls. Thus, the term expected survival does not refer to the expectation of patient survival, but rather to the expected survival curve for a random set of controls. The alternative methods are discussed, and we illustrate the methods in an analysis of long time survival of a population-based sample of peptic ulcer patients.

Age Factors↗

PubMed1998

Hospitalization for lung disease in early childhood and asthma symptoms in young adulthood.

Longitudinal studies have reported an association between early childhood lung disease and adult respiratory disease. This issue has not been addressed in the Nordic countries. We studied the association between hospitalization for lung disease in early childhood and asthma in young adulthood in a Norwegian population sample, while estimating the attributable fraction of childhood hospitalization. A population-based survey in Bergen, Norway included a random sample of 4300 subjects aged 20-44 years, of whom 80% responded. The effect of hospitalization for lung disease before the age of 2 years on asthma in adulthood was analysed by logistic and polytomous logistic regressions, adjusting for related variables. Adjusted attributable fractions were estimated from these models. The risk for different measures of asthma was significantly increased in the 103 persons reporting childhood hospitalization (airways symptoms: OR from 1.9 to 2.9; asthma medication: OR = 2.8). The associations with airways symptoms were stronger in women (OR from 2.6 to 5.3) than in men (OR from 1.4 to 2.4). Given a causal association, adjusted attributable fractions showed that childhood lung disease causing hospitalization explained 4% of asthma symptoms. Early childhood hospitalization for lung disease was related to asthma symptoms in young Norwegian adults, more strongly in women than in men. Only a minor proportion of asthma symptoms in this age group could be related to hospitalization for lung disease in early childhood.

Adult↗

PubMed1998

Birth characteristics and asthma symptoms in young adults: results from a population-based cohort study in Norway.

There is evidence that the origin of obstructive lung disease may be traced back to foetal life. The associations between birth characteristics and asthma symptoms were studied in a random population sample of young Norwegian adults. Respiratory symptoms were recorded in a population-based questionnaire survey. The records of all subjects aged 20-24 yrs were linked with the Medical Birth Registry of Norway. Of 868 subjects born in Norway, there were 690 (79%) responders. The associations between asthma symptoms and birth characteristics were analysed by logistic regression, adjusted for possible confounding factors. Asthma symptoms in young adults were inversely associated with birth weight (odds ratio (OR)wheeze=0.82; 95% confidence interval (CI)=0.69-0.96x500 g increase in birth weight(-1))), and after adjustment for gestational age, birth length, parity and maternal age (ORwheeze=0.69; 95% CI=0.50-0.95x500 g increase in birth weight(-1)). The association did not vary according to adult smoking habits or atopic status and remained when premature and low weight births were excluded (ORwheeze=0.73; 95% CI=0.60-0.90x500 g increase in birth weight(-1)). The association was consistent for all asthma symptoms. Adjusted for birth weight, asthma symptoms were further associated with low gestational age, high birth length and low maternal age. In a random sample of young adults, asthma symptoms were strongly associated with low birth weight, an association driven by the full-term births within the normal birth weight range. The findings show that the risk for adult asthma is partly established early in life and suggest that poor intrauterine growth is involved in the aetiology of asthma.

Adult↗

PubMed1998

Rhythmic patterns in incidence of peptic ulcer perforation over 5.5 decades in Norway.

The incidence of ulcer perforation in 1480 patients treated in the Bergen area of Norway between 1935 and 1990 was analyzed for daily (circadian), weekly (circaseptan), and yearly (circannual) time effects. A circadian rhythm was found overall that was reproducible and fairly stable across seasons, decades, and days of the week. After subgrouping, a circadian rhythm was found in younger patients, males, and duodenal perforations, while a 12 h (circasemidian) rhythm characterized ulcer perforation for women and for gastric ulcers. Duodenal perforations showed highest incidence in the afternoon, while gastric perforations showed a major peak around noon and a secondary peak near midnight. For duodenal ulcer perforation, the circannual pattern was characterized by a 6-month rhythm, with significantly higher incidence in May-June-July and in November-December in most subgroups. A circaseptan rhythm was not found, but there was a significantly higher incidence on Thursday-Friday as compared to Sunday-Monday. The pathophysiological mechanisms underlying the perforation of an ulcer thus seemed to show pronounced circadian and 6-month rhythmic variations, much less so circaseptan or circannual rhythms. While it is likely that exogenous environmental and/or societal factors play a significant role, variations in ulcer perforation may be related to endogenous biological rhythms in pathophysiological factors since the circadian pattern of duodenal perforation follows that for gastric acidity. Knowledge of the temporal patterns in peptic ulcer perforation and associated pathophysiologic factors should prove useful in optimizing the chronotherapeutic management of ulcer disease.

Adolescent↗

PubMed1997

Smoking and ulcer perforation.

BACKGROUND: The use of ulcerogenic drugs is the only well documented risk factor for peptic ulcer perforation, but accounts for only a quarter of the events. Smoking is a well known risk factor for uncomplicated ulcer disease, and patients with ulcer bleeding have increased death rates from smoking related disorders. AIM: To assess the role of smoking in ulcer perforation. SUBJECTS: A total of 168 consecutive patients with gastroduodenal ulcer perforation and 4469 control subjects from a population based health survey. METHODS: The association between ulcer perforation and smoking habits was analysed by logistic regression while adjusting for age and sex. RESULTS: Current smoking increased the risk for ulcer perforation 10-fold in the age group 15-74 years (OR 9.7, 95% CI 5.9 to 15.8) and there was a highly significant dose-response relationship (p < 0.001). The results were similar in men (OR 9.3, 95% CI 4.9 to 17) and women (OR 11.6, 95% CI 5.3 to 25), and for gastric (OR 10.5, 95% CI 4.5 to 25) and duodenal (OR 8.6, 95% CI 4.9 to 15.4) ulcer perforation. No increase in risk was found in previous smokers (OR 0.8, 95% CI 0.2 to 2.2). CONCLUSION: Our findings suggest that smoking is a causal factor for ulcer perforation and accounts for a major part of ulcer perforations in the population aged less than 75 years.

Adolescent↗

PubMed1996

Survival after peptic ulcer perforation: a time trend analysis.

The survival of 1098 patients with ulcer perforation in Norway during the period 1952-1990 was compared with expected survival. Cox regression models incorporating population mortality rates, were used to analyse effects of sex, age, year of birth, and year at risk on excess mortality. Survival was lower in patients than in the general population through a follow-up period of 38 years. Relative survival was lower in women as compared to men, due to more delayed treatment. Long-term survival was lower after praepyloric perforations than after the other perforation types. Relative survival was higher in patients treated 1952-1970 than in those treated more recently. However, adjustment for year of birth revealed a decline in short-term mortality with calendar time, which is in accordance with improved management during the study period. Relative mortality, particularly long-term mortality, was higher in younger birth cohorts, suggesting a shift towards more serious etiologies.

Cohort Effect↗

PubMed1996

Incidence of multiple sclerosis in Møre and Romsdal, Norway from 1950 to 1991. An age-period-cohort analysis.

We have examined the time trends in multiple sclerosis incidence over the past four decades from 1950 to 1991 in Møre and Romsdal County, Norway. Incidence rates by year of birth, year of onset and year of diagnosis according to sex, age and clinical course were studied. All patients with multiple sclerosis diagnosed by August 1992 were included, giving a total of 419 patients (171 men, 248 women) with onset of multiple sclerosis in the period 1950-91. Mean age at onset was 33.2 years, and mean age at diagnosis was 39.2 years. The incidence rate by year of onset increased from 2.87 per 100 000 in the period 1950-54 (men 3.06, women 2.67) to 5.57 per 100 000 in 1985-91 (men 3.75, women 7.94) (P<0.001). The incidence was particularly high in the period from 1975 to 1985. Major period- or cohort-effects in incidence, apart from the general increasing trend, could not be identified by an age-period-cohort analysis.

Adolescent↗

PubMed1996

Ulcer bleeding and perforation: non-steroidal anti-inflammatory drugs or Helicobacter pylori.

Non-steroidal anti-inflammatory drug (NSAID)-exposure increases the risk for ulcer perforation by a factor of 5-8. Recent data from Norway indicate that NSAID exposure is more common in gastric than in prepyloric, pyloric and duodenal perforation. Twenty to 40% of patients with gastric perforation have used NSAIDs; attributable risks are not published. The risk for ulcer bleeding is increased by a factor of 3-5 in NSAID users, with similar effects for stomach and duodenum. NSAID exposure accounts for 20-35% of ulcer bleedings. There is little knowledge about the role of Helicobacter pylori in ulcer complications, a limited importance of the bacteria is indicated in the etiology of both perforation and bleeding. Ulcer complications have a multifactorial origin. NSAIDs account for a limited part of the events. H. pylori infection may play a still undocumented role. Smoking, alcohol and aspirin are other important causal factors.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1995

Incidence of perforated ulcer in western Norway, 1935-1990: cohort- or period-dependent time trends?

Previous reports have shown that peptic ulcer mortality follows birth cohorts. To the authors' knowledge, temporal variation in ulcer incidence has not been studied. Therefore, they present incidence data for a defined area of western Norway where 1,312 patients born between 1845 and 1975 were treated for ulcer perforation between 1935 and 1990. A rise and subsequent fall in incidence was observed in successive birth cohorts for both sexes, with the highest incidence observed for males born between 1900 and 1919 and females born between 1920 and 1929. Age-period-cohort analyses based on Poisson regression techniques were adapted to provide a statistical tool for testing specific cohort and period effects. Age-cohort models without period effects explained the variations in incidence for both sexes and all ulcer locations, suggesting cohort-dependent etiology. A cohort pattern in prevalence of smoking partly explained the cohort pattern in perforation risks for both sexes. No period effects were seen that could be attributed to the increase in the sale of non-steroidal anti-inflammatory drugs, to the introduction of antibiotics around 1950, or to World War II. Susceptibility to ulcer perforation seems to follow birth cohorts, and major etiologic factors should be sought in prenatal life, in childhood, or in life-style patterns that follow birth cohorts.

Adolescent↗

PubMed1994

Adverse effects of delayed treatment for perforated peptic ulcer.

OBJECTIVE: The authors assessed the consequences of delayed treatment for ulcer perforation with regard to short-term and long-term survival, complication rates, and length of hospital stay. SUMMARY BACKGROUND DATA: Important adverse effects of delayed treatment have not been studied previously. Conflicting results have been given with regard to short-term survival. METHODS: One thousand two hundred ninety-two patients operated on for perforated peptic ulcer in the Bergen area between 1935 and 1990 were studied. The effect of delay on postoperative lethality and complications adjusted for age, sex, ulcer site, and year of perforation was analyzed by stepwise logistic regression. The effect of delay on duration of hospital stay adjusted for potential confounding factors was analyzed by Cox proportional hazards regression. Observed survival was estimated by the Kaplan-Meier method, and expected survival was calculated from population mortality data. RESULTS: Adverse effects increased markedly when delay exceeded 12 hours. Delay of more than 24 hours increased lethality sevenfold to eightfold, complication rate to threefold, and length of hospital stay to twofold, compared with delay of 6 hours or less. The reduced long-term survival for patients treated more than 12 hours after perforation could be attributed entirely to high postoperative mortality. CONCLUSIONS: Delayed treatment after peptic ulcer perforation reduced survival, increased complication rates, and caused prolonged hospital stay. To improve outcome after ulcer perforation, an effort should be made to keep delay at less 12 hours, particularly in elderly patients.

Age Factors↗

PubMed1993

Perforated peptic ulcer over 56 years. Time trends in patients and disease characteristics.

Perforated gastroduodenal ulcer was studied in 1483 patients in the Bergen area during the years 1935-90 to discover time trends in age and sex, disease characteristics, treatment, and outcome. The male:female ratio fell from 10:1 to 1.5:1, median age increased from 41 to 62 years. Most perforations were found in the duodenum in 1935-64, and in the pyloric and praepyloric area in 1965-90. There was a 10% occurrence of gastric ulcers throughout the study period. Ulcer site was related to age (more gastric and less duodenal perforations with increasing age) and sex (more pyloric and less duodenal ulcers among women). There were twice as many perforations in the evening compared with the early morning. The diurnal variation was more pronounced for duodenal and pyloric than for gastric and praepyloric perforations. Circadian and seasonal variation of ulcer perforation did not change during the 56 years studied. Treatment delay increased from median five hours to median nine hours. Infective complications and mortality fell with the introduction of antibiotics around 1950. General complications has increased in recent years because of the increase of elderly patients. Among patients who died, the proportion with associated disease rose from 27 to 85% during the study period.

Adult↗

PubMed1990

Trends in and value and consequences of radiologic imaging of perforated gastroduodenal ulcer. A 50-year experience.

The trends in and value and consequences of radiologic imaging in 1128 patients with perforated gastroduodenal ulcer have been studied over the 50-year period 1935-1985. The proportion of patients undergoing plain X-ray studies increased from 4% in the first 5-year period (1935-1939) to 94% in the last (1980-1985). Pneumoperitoneum was found in 77% of those undergoing X-ray studies. Water-soluble contrast studies were introduced in 1960, and in the three 5-year periods 1970-1985 from 8% to 13% underwent such imaging. Leakage was demonstrated in 60% of those undergoing contrast studies. Contrast studies have had a limited role in the pretreatment evaluation of these patients. The frequency of pneumoperitoneum was fairly constant over the 50-year period, and the only patient characteristic that influenced the occurrence of free gas in the abdominal cavity was age, with a higher proportion of patients with pneumoperitoneum in old patients. Any radiologic study increased treatment delay by at least 2 h.

Adult↗

PubMed1989

A multifactorial analysis of factors related to lethality after treatment of perforated gastroduodenal ulcer. 1935-1985.

One thousand one hundred and twenty-eight patients treated for perforated gastroduodenal ulcer during the years 1935-1985 were studied at the Haukeland University Hospital. The majority of patients (97.7%) were treated surgically. The data was analyzed by contingency tables and chi square testing, and a stepwise logistic regression analysis was performed in order to reveal interactions between variables and to elucidate time trends in lethality rates. The total postperforation lethality was 7.4%, the postsurgical death rate was 6.6%, and the death rate among conservatively treated patients was 42.3%. Lethality was significantly influenced by year of hospital admission and increased markedly with the age of the patients. For all age groups, the lethality decreased markedly with time. Treatment delay was associated with a moderate but significant increase in lethality. In patients with gastric ulcer the lethality was 3.6 times higher than in those with duodenal ulcer. The death rate was similar in the duodenal and pyloric ulcer groups. Death rate decreased with time in both stomach ulcer, duodenal, and pyloric ulcer patients. There was no sex difference and no difference between patients treated with simple suture or gastric resection.

Duodenal Ulcer↗

PubMed1988

Epithelial restitution and cellular proliferation after gastric mucosal damage caused by hypertonic NaCl in rats.

Hypertonic NaCl enhances gastric cancer in rats induced by N-nitroso compounds. This study was designed to examine the structural changes and alterations in mitotic activity occurring after mucosal exposure to hypertonic NaCl. Wistar rats were given one ml of 4.5 M NaCl by gastric tube and groups of 4-5 animals were sacrificed at different time intervals up to 120 h. An i.p. injection of thymidine was given 1 h before death. Samples of antral and corpus mucosa were prepared for microscopy and autoradiography. Hypertonic NaCl caused uniform destruction of surface mucous cells and pits in the corpus and antrum. Epithelial restitution with the formation of a thin epithelial layer occurred within one h of damage. The mucosa changed towards normal within 24-48 h. The distance between mucosal surface and the replicating cells decreased during the first 2 h. The proliferation zone remained in the middle of the glandular layer throughout the experiment. The proliferative activity increased during the first 24 h after mucosal damage. The number of labelled cells per unit area of mucosa was somewhat larger in the corpus than the antrum, but in the corpus the distance between proliferating cells and mucosal surface was double that of the antrum. Hypertonic NaCl causes a series of changes in the gastric mucosa. The increased mitotic activity can only partly explain the cocarcinogenic effect, since N-nitroso-induced adenocarcinomas occur predominantly in the antrum while the mitotic activity is maximal in the corpus.

Analysis of Variance↗

PubMed1984

Gastric blood flow determination: intramural distribution and arteriovenous shunting of microspheres.

Total and regional gastric blood flows were measured in 23 anesthetized cats by labeled 10-micron (range 8-12 microns) and 15-micron (range 12-20 microns) microspheres. Total blood flow correlated closely with the gastric venous outflow. Flow estimates by 10-microns spheres were 2.95% lower than simultaneous 15-micron estimates. Approximately 2% of the 10-micron spheres and 0.1% of the 15-micron spheres were shunted through the gastric vasculature. The diameter distribution of 6,245 embolized spheres, measured by microscopy, corresponded to that of the injectate, except for a lack of the smallest spheres. Within the mucosa, the 10-microns spheres predominantly lodged in the glandular layer, whereas larger spheres gradually lodged more basally; 50% of the 15-microns population appeared in the lamina propria below the gland bases. Vasodilation did not alter the intramucosal distribution. Spheres in the subglandular lamina propria represented blood flow mainly to the glandular layer. It is therefore essential for reliable estimation of blood flow to the glandular layer of the mucosa that the lamina propria is completely included in the specimens. The submucosa contained only 0.5% of the 10-microns and 2.2% of the 15-micron embolized spheres. Spheres of 10.5-17 microns in diameter are considered the most suitable for determination of gastric blood flow.

Animals↗