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Biomedical subjects

I Persson

Publications and source records attributed to I Persson.

At least 55 records · Page 3Linked to original sources
PubMed1999

Risks of breast and endometrial cancer after estrogen and estrogen-progestin replacement.

OBJECTIVE: We studied the risk of breast and endometrial cancer in a cohort of 11,231 Swedish women prescribed different replacement hormone regimens. METHODS: All 10,472 women at risk of developing breast cancer and 8,438 women at risk of endometrial cancer were followed up from the time of the questionnaire in 1987-88 through 1993, by record-linkages to the National Swedish Cancer Registry. Using data from a questionnaire we analyzed the relationships between hormone exposures and cancer risk, with non-compliers and users of less than 1 year as a reference group. RESULTS: For breast cancer, women reporting use of estrogens combined with progestins had evidence of an increased risk relative to women denying intake or taking hormones for less than 1 year; relative risk (RR) = 1.4 (95% confidence interval 0.9-2.3) after 1-6 years of intake, and RR = 1.7 (95% CI 1.1-2.6) after more than 6 years. This excess risk seemed confined to recent exposure. We found no association with intake of estrogens alone using non-compliers and short-term takers as the reference group. The risk of invasive endometrial cancer was increased four-fold in women using medium-potency estrogens alone for 6 years or longer, RR = 4.2 (95% CI 2.5-8.4). Women on such long-term progestin-combined treatment had a lower, non-significant, excess risk (RR = 1.4; 95% CI 0.6-3.3). CONCLUSIONS: We conclude that long-term recent use of estrogen-progestin combined replacement therapy may increase the risk of breast cancer. Exposure to estrogen alone substantially elevates the risk of endometrial cancer, an increase that can be reduced or perhaps avoided by adding progestins.

Breast Neoplasms↗
PubMed1999

Use of oral contraceptives and endometrial cancer risk (Sweden).

OBJECTIVES: To estimate the magnitude and persistence of the protective effect of use of combined oral contraceptives (COCs) and endometrial cancer risk. METHODS: We performed a nation-wide, population-based case-control study among postmenopausal women aged 50-74 years in Sweden, which included 709 subjects with incident, histopathologically verified endometrial cancer, and 3,368 controls with an intact uterus. We used unconditional logistic regression to calculate odds ratios as estimates of relative risks. RESULTS: Use of any sort of oral contraceptive decreased risk for endometrial cancer by 30%, while progestin-only pills reduced risk more markedly. For COCs the reduction in risk was noticeable following 3 or more years of use (OR 0.5, 95% CI 0.3-0.7), and increased with duration of intake, reaching 80% lower risk after 10 years of use. The protective effect of COC use was similar for all degrees of tumor differentiation and invasiveness, and remained for at least 20 years after cessation of use. Subsequent use of hormone replacement did not modify these protective effects. CONCLUSIONS: We conclude that COC use confers a long-lasting protection against endometrial cancer risk which is particularly marked for long-term users.

Age Distribution↗
PubMed1999

Equality and selection for existence.

It is argued that the policy of excluding from further life some human gametes and pre-embryos as "unfit" for existence is not at odds with a defensible idea of human equality. Such an idea must be compatible with the obvious fact that the "functional" value of humans differs, that their "use" to themselves and others differs. A defensible idea of human equality is instead grounded in the fact that as this functional difference is genetically determined, it is nothing which makes humans deserve or be worthy of being better or worse off. Rather, nobody is worth a better life than anyone else. This idea of equality is, however, not applicable to gametes and pre-embryos, since they are not human beings, but something out of which human beings develop.

Beginning of Human Life↗
PubMed1999

Ultrasonographic blood flow measurement in the carotid arteries in postmenopausal women.

OBJECTIVES: The aim of the present study was to evaluate blood flow in postmenopausal women on hormone replacement therapy (HRT) compared to controls. Blood flow was ultrasonographically measured in the great arteries of the neck instead of in the vessels of the internal genital organs. METHODS: Fifty healthy women with climacteric complaints, at least 6 months postmenopausal, participated in the study. They were randomly divided into two groups. One group received 2 mg estradiol (E2) for 12 days, continued with 2 mg E2 and 1 mg norethisterone acetate for 10 days, followed by 1 mg E2 for 6 days, cyclically during 6 months. The other group received placebo tablets the first 3 months and the same HRT as the first group for the last 3 months. Blood flow was measured ultrasonographically by color flow pulsed Doppler in the common (CCA), internal (ICA) and external (ECA) carotid arteries, before the start of the study, after 3 and 6 months of therapy. RESULTS: CCA and ICA, both low resistance vessels, and ECA, a high resistance vessel, and their waveforms were identified. Pulsatility index did not decrease statistically significant (p > 0.05) in any of the great vessels during 6 months of HRT in this study. There were no differences in blood flow between the HRT-treated group compared to control group during 3 months of therapy, except for the right ECA (p = 0.04). CONCLUSION: The difference in blood flow and wave-forms of the major arteries of the neck were clearly shown, but HRT did not have any important impact on the blood flow in this study. No difference was shown concerning blood flow between the two groups of postmenopausal women, on active therapy or placebo.

Carotid Arteries↗
PubMed1999

Intellectual and physical performance and morbidity in relation to height in a cohort of 18-year-old Swedish conscripts.

To test whether short stature in young men without malformations or chronic childhood diseases is associated with intellectual and physical performance and morbidity, a large cohort of apparently healthy 18-year-old Swedish men was analysed. The original cohort consisted of all men born in 1976 and conscripted in 1994 (n = 38, 900). After exclusion due to growth-affecting disorders or missing data, 32,887 subjects were available for analysis. Short conscripts (height below or equal to -2 SD scores) demonstrated increased overall morbidity compared with taller conscripts (above -2 SD scores). Specifically, short conscripts had more psychiatric and musculoskeletal diagnoses and were more often considered psychologically unsuitable for military service. Mean intellectual performance increased continuously with height; the mean 'standard nine' score was 4.22 for the short men and 5.17 for the rest (p < 0. 001). Short conscripts scored less well than taller conscripts in assessment of psychological functioning during mental stress, and were evaluated as less suitable for leadership positions. Maximal working capacity per kilogramme body weight correlated negatively with height (p < 0.001). In conclusion, short stature was associated with increased morbidity and psychological problems and with lower mean intellectual performance. To what extent this association is direct or indirect needs further evaluation.

Adolescent↗
PubMed1999

Postmenopausal hormone therapy and risk of cardiovascular disease and hip fracture in a cohort of Swedish women.

Postmenopausal estrogen use is associated with a reduced risk of heart disease and hip fracture; in observational studies, different behaviors among hormone users and nonusers may partially explain these results. We examined risk of cardiovascular disease and hip fracture with medium-potency compared with low-potency or short-term estrogen use, and the effect of added progestin, among 9,236 women in Uppsala, Sweden, who responded to a mailed questionnaire in 1987-1988. Using population registries, we identified 213 cases of myocardial infarction, 289 strokes, and 114 hip fractures from 1987-1995. We found a reduced risk of myocardial infarction for medium-potency compared with low-potency or short-term estrogen use (relative risk = 0.75, 95% confidence interval (CI) = 0.56-0.99), with a similar decrease in the subgroup that took estrogens with progestin (RR = 0.69, 95% CI = 0.45-0.90). There was no relation of medium-potency estrogen to stroke (RR = 0.91, 95% CI = 0.71-1.17, and RR = 0.81, 95% CI = 0.61-1.10 for the subgroup taking progestin), and no effect of duration on either heart disease or stroke. We observed a reduction in hip fractures for medium-potency use (RR = 0.65, 95% CI = 0.45-0.95), and for use of combined estrogen-progestin therapy (RR = 0.64, 95% CI = 0.41-1.00). These data support a decreased risk of heart disease and hip fracture for medium-potency estrogen use alone or with progestin; self-selection to hormone use cannot explain these reductions.

Cardiovascular Diseases↗
PubMed1998

Hormone replacement therapy and risk of hip fracture: population based case-control study. The Swedish Hip Fracture Study Group.

OBJECTIVE: To determine the relative risk of hip fracture associated with postmenopausal hormone replacement therapy including the effect of duration and recency of treatment, the addition of progestins, route of administration, and dose. DESIGN: Population based case-control study. SETTING: Six counties in Sweden. SUBJECTS: 1327 women aged 50-81 years with hip fracture and 3262 randomly selected controls. MAIN OUTCOME MEASURE: Use of hormone replacement therapy. RESULTS: Compared with women who had never used hormone replacement therapy, current users had an odds ratio of 0.35 (95 % confidence interval 0.24 to 0.53) for hip fracture and former users had an odds ratio of 0.76 (0.57 to 1.01). For every year of therapy, the overall risk decreased by 6% (3% to 9%): 4% (1% to 8%) for regimens without progestin and 11% (6% to 16%) for those with progestin. Last use between one and five years previously, with a duration of use more than five years, was associated with an odds ratio of 0.27 (0.08 to 0.94). After five years without hormone replacement therapy the protective effect was substantially diminished (-7% to 48%). With current use, an initiation of therapy nine or more years after the menopause gave equally strong reduction in risk for hip fracture as an earlier start. Oestrogen treatment with skin patches gave similar risk estimates as oral regimens. CONCLUSIONS: Recent use of hormone replacement therapy is required for optimum fracture protection, but therapy can be started several years after the menopause. The protective effect increases with duration of use, and an oestrogen-sparing effect is achieved when progestins are included in the regimen.

Administration, Cutaneous↗
PubMed1998

Body size in different periods of life and breast cancer risk in post-menopausal women.

Adult obesity has been associated with an increased risk of post-menopausal breast cancer, but it is unclear whether this relationship reflects a causal role of obesity during childhood and adolescence, of weight gain during adult life or of adult obesity per se. In a population-based case-control study in all of Sweden, we included 3,345 (84% of all eligible) women aged 50-74 years with invasive breast cancer, and 3,454 (82% of all selected) controls of similar age. Mailed questionnaires and telephone interviews were used to collect detailed information on anthropometric measures. Odds ratios were estimated through multiple logistic regression. Women with the leanest somatotype at age 7 had about a 3-fold higher risk of breast cancer than the most obese (P for trend 0.0009). A suggested protective effect of a high body mass at age 18 and a detrimental influence of body mass 1 year prior to data collection largely reflected the effect of weight gain after age 18, a strong predictor of breast cancer risk. Among women at least 20 years post menopause, those who had gained 30 kg or more since age 18 had an odds ratio of 2.04 (95% confidence interval 1.20-3.48) of breast cancer compared with those who had maintained their weight unchanged. The effect of weight gain was unequivocal among non-users but not among users of hormone replacement therapy. Our findings have important implications, suggesting weight preservation as a means for prevention of post-menopausal breast cancer as well as a causal role of childhood body build in breast cancer etiology.

Age Factors↗
PubMed1998

Variation in the efficacy of hormone replacement therapy in the prevention of hip fracture. Swedish Hip Fracture Study Group.

Use of postmenopausal hormone replacement therapy (HRT) has been associated with a reduced risk of osteoporotic fractures. However, it is uncertain whether this risk reduction is modified by other risk factors for hip fracture. In a population-based case-control study in Sweden, we investigated the association between HRT and hip fracture risk within categories of age, body measures and lifestyle factors in postmenopausal women, 50-81 years of age. Mailed questionnaires and telephone interviews were used to collect data. Of those eligible, 1328 incident cases with hip fracture (82.5%) and 3312 randomly selected controls (81.6%) answered the questionnaire. Ever use of HRT in women less than 75 years old was associated with an odds ratio (OR) of 0.66 (95% confidence interval: 95% CI 0.50-0.87) for hip fracture compared with OR 0.40 (95% CI 0.21-0.77) in women 75 years or older. We found a significant interaction between HRT and both weight and physical activity (p < 0.05). The protective effect of HRT was particularly pronounced in lean women: compared with never HRT users, ever users weighing under 60 kg had an OR of 0.44 (95% CI 0.30-0.66) whereas women weighing more than 70 kg had an OR of 0.91 (95% CI 0.53-1.56). Women with low recent leisure physical activity (less than 1 h/week) similarly benefited more from HRT for hip fracture prevention than women with a higher degree of recreational physical activity. The observed interactions with weight and physical activity suggest that HRT has the best protective effect against hip fracture among high-risk women.

Age Factors↗
PubMed1998

Association of family history and other risk factors with breast cancer risk (Sweden).

OBJECTIVES: Women with a family history of breast cancer have an increased risk for the disease. However, the combined impact of family history and other risk factors on breast cancer risk is unclear. We conducted a large epidemiologic study to examine this issue. METHODS. In a population-based case-control study in all of Sweden, 3,345 women aged 50 to 74 years with invasive breast cancer (84 percent of all eligible), and 3,454 controls of similar age (82 percent of all selected) were included. Mailed questionnaires and telephone interviews were used to collect detailed information on potential breast cancer risk factors. Odds ratios (OR) and 95 percent confidence intervals (CI) were estimated through multiple logistic regression. RESULTS: Women with a history of breast cancer in any first-degree relative had an increased risk of breast cancer compared with those without such a history (OR = 1.96, CI = 1.67-2.30). There was no clear indication of a differential impact of hormonal risk factors (age at menarche, parity, age at first birth, age at menopause, use of exogenous hormones, and weight gain) or body build at age seven among women with and without a positive family history. Yet, benign breast disease and height clearly were related to breast cancer risk in subjects without a family history, whereas seemingly not so in women with a family history. Formal tests for interaction between family history and these factors, however, did not prove statistically significant. CONCLUSIONS: Our findings indicate that established risk factors entail similar associations with breast cancer risk among women with and without family history of the disease.

Aged↗
PubMed1998

Recent trends in breast cancer incidence in Sweden.

Breast cancer incidence in Sweden during the period 1984-93 shows no clear trend in women aged below 40 years but a transient increase at ages 50-69 years, probably as a result of mammography screening. Our data give no indication that use of oral contraceptives or replacement hormones have affected nationwide breast cancer incidence rates.

Adult↗
PubMed1998

Hormonal aspects of epithelial ovarian cancer: review of epidemiological evidence.

Epithelial ovarian cancer is fairly common with high rates in Scandinavia, intermediate rates in western Europe and North America and low rates in the developing countries and in Japan. The 5-year survival rate is less than 40%. Increasing parity consistently gives a strong protection against epithelial ovarian cancer. A lesser degree of protection is probably derived from incomplete pregnancies and lactation. Ages at menarche and menopause are most probably weak predictors of epithelial ovarian cancer risk. Ever users of oral contraceptives (OC) have 30% lower risk compared to never users. The protection increases with duration of OC use, being about 50% after 5 years. The reduced risk among past OC users persists for at least 10 years after cessation of use. Results concerning hormone replacement therapy (HRT) and epithelial ovarian cancer risk are conflicting, but most data point to a weak or no association, but as an increasing number of women use HRT it still seems important to resolve any potential effect. Infertility adds to epithelial ovarian cancer risk in nulliparous women, while temporary fertility problems in parous women do not appear to increase risk. A possible independent risk effect of fertility drug use has not been easy to assess and remains unresolved. It has been particularly difficult to separate the effects of fertility drugs from those of infertility. Tubal ligation and hysterectomy convey protection against epithelial ovarian cancer, possibly through a suppressed ovarian hormone production. The causes of epithelial ovarian cancer are poorly understood, but reproductive hormones are thought to be involved in the aetiology. For a long time the 'incessant' and 'gonadotrophin' hypotheses have been promoted in relation to carcinogenesis. Both hypotheses find support in ovarian cancer epidemiology, and recent progress in molecular biology adds to the understanding of possible aetiological mechanisms. Another hypothesis focuses on the retrograde transport of contaminants or carcinogens through the Fallopian tubes. It is important to establish if the same risk factors apply to the various histological types of ovarian cancer, as particularly the mucinous ovarian tumours seem to present with different risk factors. Another question to resolve is if sporadic vs. inherited cases carry distinct risk profiles. As the hypotheses above do not explain all of the results derived from ovarian cancer epidemiology, there is a need to test additional hypotheses to possibly define preventive programmes and to come closer to the cause of ovarian cancer.

Adenocarcinoma↗
PubMed1998

Oral contraceptive use: interview data versus pharmacy records.

BACKGROUND: If women tend to forget and underreport their past oral contraceptive (OC) use, but the recall among cases is enhanced by the presence of disease, recall bias may explain some reported health effects of OC use. METHODS: Two different sources of information on lifetime OC use were compared for 427 (84%) of a community-based sample of 511 women aged 20-34: (i) structured interviews, using a life event calendar and picture display as memory aids, and (ii) a register of all prescriptions dispensed by pharmacies in the county since 1970. RESULTS: Interview data and pharmacy records showed high levels of agreement for any OC use, current use, time since first and last use, total duration of use, and for duration of use in different 'time windows'. But there was a tendency to under-report specific kinds of OC used in the past. CONCLUSION: Underreporting of OC use among non-cases would usually introduce little or no bias (as compared to pharmacy records) for this kind of interview and women. However, it may be preferable to use interviews for current OC use, and pharmacy records for specific kinds of OC used in the past.

Adult↗
PubMed1997

Hormone replacement therapy and the risk of breast cancer. Nested case-control study in a cohort of Swedish women attending mammography screening.

There is concern that hormone replacement therapy (HRT) increases the risk of breast cancer. We undertook a case-control study of this risk relationship within a cohort of 40- to 74-year-old women in Uppsala County, Sweden, who participated in mammography screening. Incident cases of breast cancer were ascertained during 5 years of follow-up. In all, 435 cases (87% invasive, 13% in situ cancers) were detected, 313 through screening and 122 through clinical diagnosis. As controls, 1,740 women were selected randomly. Information on risk factors and use of HRT was obtained through interviews before the start of follow-up. Multivariate analyses revealed an increased risk among users of any type of HRT for more than 10 years, the odds ratio (OR) being 2.1 (95% confidence interval [CI] 1.1-4.0), as well as when restricting analyses to cases diagnosed through mammography screening. After stratification for compound type, risk estimates were apparently higher among women reporting estradiol-progestin combined treatment vs. estradiol or conjugated estrogens alone, with ORs for more than 10 years of intake being 2.4 (95% CI 0.7-8.6) and 1.3 (95% CI 0.5-3.7), respectively. Analyses through a model including both compound type and length of hormone intake confirmed a significant excess risk linked to treatment for more than 10 years, OR = 2.6 (95% CI 1.3-5.1). Our results indicate a moderately increased risk of breast cancer after many years of HRT and, hypothetically, a further enhancement of the risk with added progestins.

Adult↗
PubMed1997

Risk of endometrial and breast cancer in patients with diabetes mellitus.

Diabetes mellitus patients have metabolic and endocrine alterations that could contribute to an increased incidence of hormone-related cancers. We assessed the incidence of endometrial and breast cancer among 80,005 women and the incidence of breast cancer among 73,847 men (total of 153,852 patients) identified in the Swedish In-patient Register as having been hospitalized for diabetes mellitus in the period 1965-1983. These patients underwent follow-up through 1989 via the Swedish Cancer Register and other nation-wide Swedish registers. The outcome measures were standardized incidence ratios (SIR) based on age-, sex- and calendar period-specific incidence rates from the entire Swedish population. To minimise the effect of selection bias, we excluded from the calculation of incidence ratios the first year of observation and cases diagnosed incidentally at autopsy. Only first cancers were considered for the estimates. A total of 328 endometrial cancers (SIR = 1.8; 95% confidence interval [CI] = 1.6-2.0), 1,145 female breast cancers (SIR = 1.3; 95% CI = 1.2-1.4) and 13 male breast cancers (SIR = 2.0; 95% CI = 1.0-3.4) were observed. We conclude that compared with the general population, patients with diabetes mellitus have an increased incidence of endometrial and breast cancers.

Adult↗
PubMed1997

In vitro kinetics of two human CYP1A1 variant enzymes suggested to be associated with interindividual differences in cancer susceptibility.

A genetic polymorphism (A4889-->G) in the human CYP1A1 gene which creates an Ile462-->Val amino acid substitution has been suggested to cause altered enzymatic properties of CYP1A1. Since several epidemiological studies have shown an association between the CYP1A1-Val allele and lung cancer, we considered it of importance to evaluate the in vitro kinetic properties of the two CYP1A1 variants after expression of each cDNA in yeast. No differences were found in K(m) or Vmax for CYP1A1 dependent O-dealkylation of ethoxyresorufin and 3-hydroxylation of benzo(a)pyrene between the two variants. The data indicate that the Ile/Val polymorphism in human CYP1A1 is not functionally important.

Benzo(a)pyrene↗