Biomedical subjects

K Steindorf

Publications and source records attributed to K Steindorf.

16 recordsLinked to original sources

PubMed2006

Lack of association of herpesviruses with brain tumors.

Gliomas are the most frequent primary brain tumors in humans. Many studies have been carried out on their etiology; however, the only confirmed risk factors are hereditary predisposing conditions and high dose of ionizing radiation. Recently, human cytomegalovirus (HCMV) gene products and nucleic acids were reported to be present in all of 27 glioma samples investigated in contrast to other brain tissues, and it was hypothesized that HCMV might play a role in glioma pathogenesis. To evaluate these findings, samples of 40 gliomas, 31 meningiomas, and 6 acoustic neurinomas (ACNs) were analyzed for the presence of HCMV macromolecules using polymerase chain reaction (PCR) and immunohistochemistry. Additionally, corresponding blood samples from 72 patients were analyzed for the presence of HCMV DNA to check for a possible contamination of tumor tissues with HCMV-infected blood cells. No HCMV DNA sequences were found, neither in brain tumor tissues nor in corresponding blood samples. Immunohistochemistry did not detect HCMV-specific proteins. Addressing a possible role of other herpesviruses as has been suggested in seroepidemiological studies, seroprevalence of antibodies to HCMV, herpes simplex virus (HSV), Epstein-Barr virus (EBV), and varicella-zoster virus (VZV) were determined by enzyme-linked immunosorbent assay (ELISA). Serological analyses of brain tumor patients showed no significant differences in the prevalences of antibodies to HCMV, HSV, EBV, or VZV compared to the general population. Thus, the data of the present study do not support the hypothesis of an association of herpesviruses with the development of primary brain tumors.

Adolescent↗

PubMed2006

Statistical methods for the validation of questionnaires--discrepancy between theory and practice.

OBJECTIVES: Questionnaires used in epidemiological studies should be validated. However, unclarity exists about the appropriate statistical methods and interpretation of validation studies. Thus, we investigated the theory and practice of statistical evaluation approaches. METHODS: Using three platforms, a literature review, own simulations, and a validation study performed by ourselves, we worked out relevant limitations, advantages, and new important aspects of evaluation methods. RESULTS: Our systematic literature review, based on physical activity questionnaires, revealed that correlation coefficients are still the common approach in validation studies, found in 41 of 46 reviewed publications (89.1%). This practice has been criticized in the theoretically oriented literature for more than 20 years. Appropriate evaluation methods as recommended by Bland and Altman were found in only ten publications (21.7%). We showed that serious bias in questionnaires can be revealed by Bland-Altman plots but may remain undetected by correlation coefficients. With our simulations we refuted the argument that correlation coefficients properly investigate whether a questionnaire ranks the subjects sufficiently well. Further, with Bland-Altman analyses we could evaluate differential errors with respect to case-control status in our validation study. Yet, this was not possible with correlation coefficients, because they generally do not identify systematic bias. In addition, we show a potential pitfall in the interpretation of Bland-Altman plots that might occur in specific rare instances. CONCLUSIONS: The commonly used correlation approach can yield misleading conclusions in validation studies. A more frequent and proper use of the Bland-Altman methods would be desirable to improve epidemiological data quality.

Data Interpretation, Statistical↗

PubMed2005

Case-control study of lifetime occupational and recreational physical activity and risks of colon and rectal cancer.

Important aspects of the inverse relation between physical activity and colon cancer risk are still under discussion. In 2000-2003, 239 incident cases of colorectal cancer confirmed by histopathology and 239 hospital-based controls, matched by age and gender, were enrolled. In standardized interviews, data on occupational and recreational physical activity for ages 20, 30, 40, 50 and 60 years were collected from 98 colon cancer cases, 141 rectal cancer cases, and from 193 controls. Besides lifestyle and sociodemographic characteristics, a detailed food frequency questionnaire was assessed. In multivariate logistic regression for colon cancer, significant risk reductions for the highest quartile of total physical activity were found for almost all ages. For lifetime mean physical activity, the multivariate odds ratio for the highest quartile was 0.37 [95% confidence interval (CI) 0.17, 0.83]. For lifelong constantly high-exercisers compared with lifelong non-exercisers an odds ratio of 0.26 (95% CI 0.08, 0.84) was estimated. For rectal cancer, no consistent association with physical activity was found. No confounding effects were observed but the authors found effect modification with total energy intake. These data support an inverse association of colon cancer risk and physical activity which is most expressed if activity is kept up throughout life.

Adult↗

PubMed2001

Nutrient intake patterns in gastric and colorectal cancers.

The purpose of the study was to present the dietary risk pattern in gastric and colorectal cancers, using the same methodological approach in a parallel hospital-based case-control study. In all, 180 cases of colorectal cancer and 80 cases of stomach cancer, confirmed histopathologically, were enrolled from the University Hospital in Cracow. A high intake of carbohydrates was associated with an increased risk of colorectal cancer (OR = 2.45). For stomach cancer, a moderate consumption of carbohydrates markedly increased relative risk (OR = 4.29), while a high intake of carbohydrates increased the risk by 8.73. The patterns of dietary risk factors related to intake of fats were definitively different in both cancer sites. The higher fat consumption was not associated with the higher risk of stomach cancer. A medium intake of fats increased the risk of colorectal cancer by 1.96 and that above 83 g/day by 2.20. In colorectal cancer, the significant protective effect of retinol, carotene and vitamin C has been evidenced, however, only carotene and vitamin E were inversely correlated with stomach cancer.

Case-Control Studies↗

PubMed2000

Combined risk assessment of physical activity and dietary habits on the development of colorectal cancer. A hospital-based case-control study in Poland.

The purpose of the study was to assess the importance of physical activity performed both in occupational settings and in leisure time on the risk of colorectal cancer, considering the possible confounding effects of dietary habits. The hospital-based case-control study was carried out in Poland. In total, 180 incident cases of colorectal cancer were recruited. An equal number of controls, individually matched by gender and age, were chosen from patients with no history of cancer. A food frequency questionnaire combined with quantity of foods eaten was used to assess the usual dietary pattern for 148 food items. The average physical load of the interviewed patients before the occurrence of disease was ascertained by self-assessment. The degree to which patients' recreational time was sedentary was measured by the number of hours spent watching TV. The adjusted risk of colorectal cancer was reduced by half in those active in leisure time (OR 0.45, 95% CI 0.24-0.84). The effect of occupational physical activity was of about the same order of magnitude in terms of risk reduction (OR 0.61, 95% CI 0.29-1.29) and both activities combined acted as independent protective factors. The protective effect of healthy nutrition appeared to be independent from that attributed to physical effort.

Case-Control Studies↗

PubMed2000

Previous infection and other risk factors for acute cerebrovascular ischaemia: attributable risks and the characterisation of high risk groups.

BACKGROUND: Recent reports indicated that previous infection may be a risk factor for ischaemic stroke in younger adults and that the increased mortality of cerebrovascular diseases in winter months may be partly caused by the increased rate of infection during the cold season. METHODS: We performed a 1:1 matched case-control study with 197 cases (83 females, 114 males) aged between 22 and 80 years (median age 65 years) to investigate risk factors for acute cerebrovascular ischaemia, in particular the effect of previous infection. We estimated the impact of risk factors in terms of attributable and absolute risks. RESULTS: All risk factors together, previous infection, hypertension, diabetes mellitus, smoking, coronary heart disease, previous stroke or transient ischaemic attack and family history of stroke yield a summary attributable risk of 0.74 [95% confidence intervals (CI) 0.64-0.83]. Recent infections showed a relative risk of 4.3 (95% CI 1.8-10.5) and an attributable risk of 0.15 (95% CI 0.09-0.21). Seventeen percent of the German population are estimated to be in a high-risk group. This subgroup contributes about 55% of the estimated yearly 120,000 incident cases in the age group 55-84 in Germany. DISCUSSION: Identification of high-risk groups for stroke on the basis of individual risk factor distribution and the estimation of its size is possible and may produce useful results. Reducing the prevalence of infection and early treatment of bacterial infection may lower the incidence of stroke.

Adult↗

PubMed1999

Wegener's granulomatosis associated with renal cell carcinoma.

OBJECTIVE: To determine the frequencies and types of malignant neoplasms occurring before or simultaneously with the diagnosis of Wegener's granulomatosis (WG), and to test for the presence of "Wegener's autoantigen," proteinase 3 (PR3), in malignant tissues from WG patients to ascertain whether an association exists between malignancy and WG. METHODS: A retrospective statistical analysis was performed on the medical records of 477 patients with WG as compared with a control group of 479 patients with rheumatoid arthritis (RA). A murine monoclonal antibody was used to test malignant tissues for the presence of PR3. RESULTS: A malignant neoplasm was found in 23 patients in the WG group and in 18 patients in the control group. The odds ratio for malignant neoplasm in the WG group was 1.79 (P = 0.0876, 95% confidence interval [95% CI] 0.92-3.48). Seven patients with renal cell carcinoma were found in the WG group compared with 1 patient in the control group, for an odds ratio of 8.73 (P = 0.0464, 95% CI 1.04-73.69). Simultaneous occurrence of cancer and WG was observed in 14 patients with WG compared with 1 control patient, for an odds ratio of 18.00 (P = 0.0059, 95% CI 230-140.67). Furthermore, the diseases occurred simultaneously in 5 of the 7 patients with both WG and renal cell carcinoma, but not in the single patient in the control group with RA and renal cell carcinoma. PR3 could not be detected in any of the 8 malignant tissue samples (4 renal cell carcinomas) investigated in the patients from the WG group. CONCLUSION: The close temporal association between renal cell carcinoma and WG suggests that malignancy is, in some cases, a trigger for the development of WG. However, since PR3 was not found in malignant tissues from the WG patients, the immunopathologic mechanisms leading to autoimmunity and vasculitis remain unclear.

Adult↗

PubMed1998

Estimation of the cumulated exposure to polychlorinated dibenzo-p-dioxins/furans and standardized mortality ratio analysis of cancer mortality by dose in an occupationally exposed cohort.

For a cohort of 1189 male German former herbicide and insecticide workers with exposure to polychlorinated dibenzo-p-dioxins and -furans (PCDD/F), we report an extended standardized mortality ratio (SMR) analysis based on a new quantitative exposure index. This index characterizes the cumulative lifetime exposure by integrating the estimated concentration of PCDD/F at every point in time (area under the curve). Production department-specific dose rates were derived from blood levels and working histories of 275 workers by applying a first-order kinetic model. These dose rates were used to estimate exposure levels for all cohort members. Total mortality was elevated in the cohort; 413 deaths yielded an SMR of 1.15 (95% confidence interval [Cl] 1.05, 1.27) compared to the mortality of the population of Germany. Overall cancer mortality (n = 124) was significantly increased (SMR = 1.41, 95% Cl 1.17, 1.68). Various cancer sites showed significantly increased SMRs. The exposure index was used for an SMR analysis of total cancer mortality by dose. For 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) a significant trend (p = 0.01) for the SMRs with increasing cumulative PCDD/F exposure was observed. The SMR in the first exposure quartile (0-125.2 ng/kg x years) was 1.24 (95% Cl 0.82, 1.79), increasing to 1.73 (95% Cl 1.21, 2.40) in the last quartile (> or = 2503.0 ng/kg x years). For all congeners combined as toxic equivalencies (TEQ) using international toxic equivalency factors, a significant increase in cancer mortality was observed in the second quartile (360.9-1614.4 ng/kg x years, SMR 1.64; 95% Cl 1.13, 2.29) and the fourth quartile (> or = 5217.7 ng/kg x years TEQ, SMR 1.64, 95% Cl 1.13, 2.29). The trend test was not significant. The results justify the use of this cohort for a quantitative risk assessment for TCDD and to a lesser extent for TEQ.

Adult↗

PubMed1998

Quantitative cancer risk assessment for dioxins using an occupational cohort.

We consider a cohort of 1189 male German factory workers (production period 1952-1984) who produced phenoxy herbicides and were exposed to dioxins. Follow-up until the end of 1992 yielded a significantly increased standardized mortality ratio (SMR) for total cancer (SMR 141; 95% confidence interval 117-168). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) concentrations up to 2252 ng/kg body fat were measured in 275 cohort members. Other higher chlorinated dioxins and furans also occurred in high concentrations. For quantitative analysis, the integrated TCDD concentration over time was used as an exposure variable, which was calculated using results from half-life estimation for TCDD and workplace history data. The other congeners were expressed as toxic equivalency (TEQ) and compared to TCDD using international toxic equivalency factors. Poisson and Cox regressions were used to investigate dose-response relationships. Various covariables (e.g., exposure to beta-hexachlorocyclohexane, employment characteristics) were considered. In all analyses, TCDD and TEQ exposures were related to total cancer mortality. The power model yielded a relative risk (RR) function RR(x) = (1 + 0.17x)0.326 for TCDD (in microgram/kilogram blood fat x years)--only a slightly better fit than a linear RR function--and RR(x) = (1 + 0.023x)0.795 for TEQ. Investigations on latency did not show strong effects. Different methods were applied to investigate the robustness of the results and yielded almost identical results. The results were used for unit risk estimation. Taking into account different sources of variation, an interval of 10(-3) to 10(-2) for the additional lifetime cancer risk under a daily intake of 1 pg TCDD/kg body weight/day was estimated from the dose-response models considered. Uncertainties regarding the dose-response function remain. These data did not indicate the existence of a threshold value; however, such a value cannot be excluded with any certainty.

Adult↗

PubMed1997

A topographic analysis of atrophic gastritis and stomach cancer risk. A clinicoepidemiological study in Poland.

The purpose of this cross-sectional study was to assess the relation between intestinal and diffuse stomach cancer at its various locations with topography of atrophic gastritis. The study population consisted of 3435 patients who reported over the period of 1991-1994 for the first time to gastroenterological outpatient clinics of 7 university medical centers in Poland. Among these subjects there were 131 histologically proved consecutive cases of gastric carcinoma. The reference group consisted of 1540 patients among whom endoscopic examination did not reveal peptic ulcers, polyps, deformations of antrum or bulbus duodenum and mucosa erosions. Gastroscopy on gastric cancer patients and the reference group was performed and biopsy specimens were obtained from the tumour and from the antrum and stomach corpus distant from the tumour. Among the gastric cancer cases there was a higher prevalence of atrophic gastritis in the intestinal than in the diffuse type. The highest prevalence of atrophic gastritis irrespective of its degree and stomach area was observed in the tumour-area of intestinal cancer located distally (78.9%), and the lowest in the tumour-free area in diffuse proximal cancer (18.5%). Prevalence of atrophic pangastritis (atrophic gastritis present both in the corpus and antrum) was also highest in intestinal distal cancer (69.2%) and lowest in diffuse proximal cancer (21.7%). The age-adjusted correlation coefficients between gastritis score in the tumour-area and tumour-free area were highly significant. It was shown that only atrophic pangastritis was significantly associated with gastric cancer irrespective of its histology and location (OR = 3.8, 95% CI:2.4-6.0), however, it was much stronger related to the intestinal gastric cancer (OR = 5.9, 95% CI: 3.1-11.0), than to the diffuse carcinoma (OR = 2.2, 95% CI: 1.1-4.3).

Adult↗

PubMed1996

Cancer mortality in German male workers exposed to phenoxy herbicides and dioxins.

In an occupational cohort study, the relation between exposure to phenoxy herbicides, and contaminants (dioxins and furans) and cancer mortality was investigated. A total of 2,479 workers from four plants in Germany were included, with a mortality follow-up until the end of 1989 (for one cohort, until the end of 1992). A total of 484 deaths were recorded yielding a standardized mortality ratio (SMR) of 101 (95 percent confidence interval [CI] = 92-111) for total mortality, and an SMR of 119 (CI = 100-141) for all malignant diseases. A variety of herbicides was produced, including those which are known to have been contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). High dioxin and furan exposure (in particular, exposure to TCDD, but also to higher chlorinated dioxins) had occurred in two of the four plants as shown by blood-fat measurements in a sample of workers. Mortality from all neoplasms increased with latency and was highest in the largest plant where the highest TCDD blood levels were recorded. An increased mortality in the total cohort from respiratory cancer (SMR = 154, CI = 115-202), cancer of the buccal cavity and pharynx (SMR = 295, CI = 135-560), and non-Hodgkin's lymphoma (SMR = 326, CI = 119-710) was observed. Our findings are consistent with results from other cohorts which showed an increased overall cancer mortality and mortality of respiratory cancer after long-term exposure to these phenoxy herbicides and dioxins.

Adipose Tissue↗

PubMed1996

[Controlled clinical studies for topographic analysis of atrophic gastritis and stomach cancer].

The purpose of this cross-sectional study was to assess the relation between intestinal and diffuse stomach cancer at its various locations with topography of atrophic gastritis. The study population consisted of 3435 patients who reported over the period of 1991-94 for the first time to gastroenterological outpatient clinics of 7 university medical centers in Poland. Among these subjects there were 131 histologically proved consecutive cases of gastric carcinoma. The reference group consisted of 1540 patients among whom endoscopic examination did not reveal peptic ulcers, polyps, deformations of antrum or bulbus duodenum and mucosa erosions. Among the gastric cancer cases there was a higher prevalence of atrophic gastritis in the intestinal than in the diffuse type. The highest prevalence of atrophic gastritis irrespective of its degree and stomach area was observed in the tumour-area of intestinal cancer located distally (78.9%), and the lowest in the tumour-free area in diffuse proximal cancer (18.5%). Prevalence of atrophic pangastritis (atrophic gastritis present both in the corpus and antrum) was also highest in intestinal distal cancer (69.2%) and lowest in diffuse proximal cancer (21.7%). For other types of cancer the prevalence rates of atrophic pangastritis was 50.0% in intestinal proximal cancer and 37.5% in diffuse distal carcinoma. The age-adjusted correlation coefficients between gastritis score in the tumour-area and tumour-free area were highly significant. It was shown that only atrophic pangastritis was significantly associated with gastric cancer irrespective of its histology and location (OR = 3.8, 95% CI:2.4-6.0), however, it was much stronger related to the intestinal gastric cancer panga (OR = 5.9, 95% CI: 3.1-11.0), than to the diffuse carcinoma (OR = 2.2, 95% CI: 1.1-4.3).

Adult↗

PubMed1995

Lung cancer deaths attributable to indoor radon exposure in West Germany.

BACKGROUND: There is substantial epidemiological and experimental evidence that exposure to radon at levels found in underground mines can cause lung cancer. Although radon levels measured in homes are normally substantially lower, there is concern about the presence of a known lung carcinogen in a residential setting. METHODS: Using national survey data on radon concentrations in homes in the former West Germany, the proportion and absolute numbers of lung cancer deaths attributable to radon are estimated. As lung cancer risk models derived directly from residential radon studies are not yet available, the risk model developed recently by Lubin et al. from a joint analysis of 11 underground miners' studies is applied. For an estimate of the impact of smoking on radon-attributable lung cancers, three different approaches are used and compared. RESULTS: Our analysis shows that after adjusting for dosimetry differences between mines and homes about 7% of all lung cancer deaths in the western part of Germany may be due to residential radon. This corresponds to a total of about 2000 deaths (95% CI: 500-8200), 400 in females and 1600 in males. Adjusting for the intermediate relationship for smoking and radon, the attributable risk is estimated to be about 4-7% for smokers and 14-22% in non-smokers. CONCLUSIONS: Our analysis basically confirms the results of former calculations with regard to the total number of lung cancer deaths attributable to radon in West Germany. However, we show that the standard practice that applies the same model to smokers and non-smokers may result in biased estimates for these groups.

Air Pollution, Indoor↗

PubMed1995

Cigarette use and the estimation of lung cancer attributable to radon in the United States.

Residential exposure to radioactive radon and its decay products has been estimated to account for 10-12% of all lung cancer deaths in the U.S. It has been difficult to evaluate fully the impact of cigarette smoking, the most important cause of lung cancer, on this estimate, because factors for patterns of tobacco use have not been included in the risk models, since risk models are derived from studies of underground miners exposed to radon and detailed data on smoking are limited. Lung cancer risk estimates for exposure to radon progeny in smoker and non-smoker populations are obtained by applying the same risk model to each population group, thereby assuming the joint effects of smoking and exposure to radon progeny are multiplicative. However, in miners, joint relative risks (RR) for the two exposures are most consistent with an intermediate relationship between multiplicative and additive, so that the present approach likely results in an overestimate of risk in smokers and an underestimate of risk in nonsmokers. Lubin et al. (National Institutes of Health Publication No. 94-3644, 1994) present an ad hoc approach for adjusting risk models to incorporate smoking status. The approach is based on the relative magnitude of the effects of radon progeny in smokers and nonsmokers and therefore may not be applicable to non-miner populations if the proportion of smokers and the RR for smoking differ. We show that the modification can be derived explicitly by assuming an arithmetic mixture model for the joint RR for smoking and exposure to radon progeny. In this way, smoking parameters in the population of interest (the proportion of smokers and the RR of smoking) can be used directly to adjust radon progeny risk models and obtain risk estimates that are specific for smokers and nonsmokers. With an intermediate RR relationship for smoking and radon progeny, the attributable percentage of lung cancer deaths from residential radon may be twofold greater in non-smokers than in smokers.

Air Pollution, Indoor↗

PubMed1994

Nitrate in drinking water. A case-control study on primary brain tumours with an embedded drinking water survey in Germany.

BACKGROUND: Nitrate is known to be a precursor in the endogenous formation of N-nitroso compounds which are thought to be associated with the development of brain tumours. METHODS: We conducted a population-based case-control study on the aetiology of primary brain tumours in adults in which the nitrate concentration in drinking water was investigated as a quantitative variable. For this purpose, an additional drinking water survey was performed. RESULTS: Analysis of 173 incident cases and 418 controls did not show any relationship between exposure to nitrate in drinking water and risk of developing primary brain tumours. We found mean nitrate concentrations of 15.98 mg/l (SD 15.61) in the drinking water history of the cases and of 16.16 mg/l (SD 15.72) for controls. In addition, we compared the quantitative history of nitrate contamination of the study participants to a semi-quantitative assessment by a stick method. Although we found good agreement between these methods we would recommend the use of detailed water surveys for retrospective studies on contaminants in drinking water. CONCLUSION: The results suggest the absence of an association between nitrate levels in drinking water and the risk of brain tumours. However in order to draw definite conclusions quantitative prospective studies are needed.

Adult↗

PubMedDate not supplied

Risk of colorectal cancer from alcohol consumption at lower vitamin intakes. A hospital-based case-control study in Poland.

The purpose of the study was to assess the relation between the simultaneous exposure to alcohol and consumption of micronutrients that have protective properties against colorectal cancer. A hospital-based case-control study of colorectal cancer was carried out between January 1998 and November 1999 at the University Hospital in Krakow, Poland. In total, 180 incident cases of colorectal cancer, confirmed by histopathology, were recruited and an equal number of controls, individually matched by gender and age (+/-5 y), were chosen amongst patients with no history of cancer. A food-frequency questionnaire for 148 food items, combined with the quantity of foods eaten, was used to assess the normal dietary pattern. The data confirmed the reported inverse association between the intake of retinol, thiamine, or antioxidant micronutrients (vitamins C, E) and the occurrence of colorectal cancer. Alcohol intake was found to be an important risk factor for this cancer site, and the risk escalated in parallel with increased intake of retinol, carotene, vitamins C and E, but with high consumption of alcohol ran a noticeably high risk of colorectal cancer (OR= 6.79; 95% CI: 2.08-22.18). The risk was markedly lower, however, among alcohol drinkers who reported a high intake of micronutrients (OR = 1.35; 95% CI: 0.39-4.67). The data suggest that a combination of high consumption of alcohol and low intake of retinol and antioxidant vitamins may considerably increase the risk of colorectal cancer.

Adult↗