Biomedical subjects

Tomas Riman

Publications and source records attributed to Tomas Riman.

7 recordsLinked to original sources

PubMed2006

Use of hormone replacement therapy before and after ovarian cancer diagnosis and ovarian cancer survival.

Use of hormone replacement therapy (HRT) has been hypothesized to affect survival of epithelial ovarian cancer (EOC). We studied 5-year survival in patients with invasive EOC and borderline ovarian tumors (BOT) according to HRT use before and after diagnosis in a prospective nation-wide cohort study of 799 women diagnosed with EOC (n = 649) and BOT (n = 150) aged 50-74 years in 1993-1995 in Sweden. Cox regression was used to obtain multivariate age-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Multivariate models included indicator variables for age, tumor stage, grade and histological subtype. After 5 years of follow-up, 45% of the patients with EOC and 93% of the patients with BOT were alive. For women with BOT there were no associations between HRT-use pre- or postdiagnosis and survival. There was no overall difference in 5-year EOC survival according to use HRT before diagnosis (multivariate HR = 0.83, 95% CI = 0.65-1.08), except for serous EOC (HR = 0.69, 95% CI = 0.48-0.98). Analyses of different HRT preparations, duration and recency of use did not reveal any variations in pattern of survival. We observed a better survival for EOC-patients who used HRT after diagnosis (multivariate HR = 0.57, 95% CI = 0.42-0.78). We conclude that HRT-use prior to diagnosis of EOC does not affect 5-year survival, except for a possible survival advantage in serous EOC. Women using HRT after diagnosis had a better survival than women with no use, but we cannot rule out that this latter finding may reflect a subtle selection process.

Aged↗

PubMed2006

A prospective study of the transient decrease in ovarian cancer risk following childbirth.

Epidemiologic evidence shows that the risk of ovarian cancer is decreased following childbirth. We examined the time points when the decreased risk of postpartum maternal ovarian cancer reaches the lowest point and whether the protective effect diminishes over time. A case-control study nested within the Swedish Fertility Register included 10,086 cases of epithelial ovarian cancer recorded in the Swedish Cancer Register from 1961 to 2001. From the Fertility Register, 49,249 eligible subjects matched to the cases by age were selected as controls. The analysis contrasted risk between adjacent parities through logistic regression models that included indicator variables representing each year of age, age at delivery, and time since delivery. Compared with nulliparous women, uniparous women had a transient decrease in maternal ovarian cancer risk at 2 years after delivery (spline-derived odds ratio, 0.71; 95% confidence interval, 0.53-0.95, for those delivered at age 25 years) and maintained a lower risk for 4 years postpartum. Similar transient decreases were observed in biparous women compared with uniparous women and in women with three parities compared with biparous women. The protective effect of childbearing seemed to diminish with time. The transient decrease in postpartum ovarian cancer risk may define the latent period required for pregnancy hormones in clearing out ovarian cells that have undergone early stages of malignant transformation. The period before the risk increases again could indicate the period required for ovarian cancer induction.

Adolescent↗

PubMed2004

Some life-style factors and the risk of invasive epithelial ovarian cancer in Swedish women.

The objective of this nationwide case-control study was to examine body mass index (BMI), alcohol use, coffee consumption, cigarette smoking, and leisure-time physical activity in relation to epithelial ovarian cancer (EOC) risk. Subjects were 655 newly diagnosed EOC cases and 3899 population controls, all 50-74 years of age at recruitment between 1993 and 1995. Data were collected through mailed questionnaires. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. Women with a BMI > or = 30 kg/m2 compared with those with a BMI < 22 kg/m2 appeared to have an elevated EOC risk (OR = 1.37, 95% CI: 1.01-1.85), particularly of mucinous (OR = 2.76, 95% CI: 1.15-6.61) and clear-cell histologies (OR = 2.68, 95% CI: 0.96-7.48). The OR for EOC among coffee users reporting > or = 6 daily cups compared with non-users was 0.68 (95% CI: 0.42-1.10). Alcohol consumption was unrelated to EOC risk. Compared to non-smokers the ORs of EOC among current smokers were 0.70 (95% CI: 0.52-0.94) for those who smoked 1-10 cigarettes/day and 0.74 (95% CI: 0.53-1.02) for heavier smokers, while former smokers were at an unaltered risk (OR = 0.83, 95% CI: 0.66-1.04). Reduced EOC risks were observed among women in the highest compared with the lowest physical activity levels both at age 18-30 years (OR = 0.67, 95% CI: 0.52-0.87) and during the last years preceding study enrollment (OR = 0.68, 95% CI: 0.53-0.87). We conclude that women may avoid an excess risk of EOC through maintaining a normal BMI and reduce their risk by participation in leisure-time physical activity. The use of coffee, alcohol, or cigarette smoking does not appear to increase the risk of EOC.

Aged↗

PubMed2004

Review of epidemiological evidence for reproductive and hormonal factors in relation to the risk of epithelial ovarian malignancies.

Ovarian cancer is the leading cause of mortality related to gynecologic malignancies in Sweden but there is no current screening program. Based upon epidemiological research there is evidence that certain reproductive factors are associated with ovarian cancer risk. Most studies generally indicate that each childbirth incurs a 15-20% risk reduction. Women who have used oral contraceptives for 5 years or longer experience about half the risk of ovarian cancer compared with never users. Breastfeeding seems to be protective while age at menarche and at menopause are less consistent risk predictors. Tubal ligation and hysterectomy seem to reduce ovarian cancer risk by up to 80%. Although some studies found endometriosis, polycystic ovarian syndrome (PCOS) and pelvic inflammatory disease (PID) to be positively related to ovarian cancer, the role of these factors is not yet established. Most recent studies observed an approximately 50% ovarian cancer risk increase among ever users of hormone replacement therapy (HRT) compared with never users, and the risk increased further with long-term use. There is less information concerning separate estrogen and progestin effects of HRT and ovarian cancer risk. Although the cause of ovarian cancer remains obscure, hypotheses relating to "incessant" ovulation, excessive gonadotropin secretion, retrograde carcinogen transportation, apoptosis and estrogen/progestin imbalance have been invoked as etiological explanations. All these hypotheses find various epidemiological support. The aim of this review is to summarize the epidemiological findings on reproductive factors and ovarian cancer risk. These findings are considered in the context of etiologic hypotheses and some new research areas are suggested.

Adult↗

PubMed2003

Hormone replacement therapy and epithelial ovarian cancer: is there and association?

Recently it was estimated that about one-third of postmenopausal British women aged 50-64 years currently uses hormone replacement therapy (HRT) for treatment of climacteric symptoms and for other medical reasons. To reduce an excess risk of endometrial cancer induced by oestrogens, modern HRT regimens contain either sequential or continuous progestogens. The protective effect of parity and oral contraceptive use observed in the majority of epidemiological studies on epithelial ovarian cancer (EOC) suggest that hormonal factors are likely to operate in ovarian carcinogenesis. However, the studies where HRT was examined in relation to the risk of EOC have reported conflicting results. The objective of this epidemiological review is to evaluate the risk of EOC in relation to the use of HRT, with particular focus on the few studies where oestrogens and progestogens in HRT were assessed separately. Further, the findings regarding HRT and EOC risk will be discussed in the context of available aetiological hypotheses. Finally, any clinical implications are commented upon.

Case-Control Studies↗

PubMed2002

Risk factors for invasive epithelial ovarian cancer: results from a Swedish case-control study.

This case-control study evaluated reproductive and other factors in relation to epithelial ovarian cancer (EOC) risk. Between 1993 and 1995, the authors recruited 655 EOC cases and 3,899 population controls aged 50-74 years who were born in and residents of Sweden. Data were collected through mailed questionnaires. Odds ratios were estimated by unconditional logistic regression. Parity reduced EOC risk (odds ratio = 0.61, 95% confidence interval (CI): 0.46, 0.81) for uniparous compared with nulliparous women. The risk of EOC decreased with incomplete pregnancies, early menopausal age, late age at first birth, and unilateral oophorectomy; increased with family history of ovarian cancer; and was not associated with menarcheal age, lactation, irregular menses, and menopausal symptoms. Histology-specific odds ratios of EOC for ever compared with never users of oral contraceptives were: serous, 0.56 (95% CI: 0.42, 0.74); mucinous, 1.96 (95% CI: 1.04, 3.68); endometrioid, 0.71 (95% CI: 0.49, 1.03); clear cell, 0.66 (95% CI: 0.31, 1.43); and all EOCs, 0.73 (95% CI: 0.59, 0.90). Prolonged oral contraceptive use reduced EOC risk, with persistent protection up to 25 years after the last use. Ever use of hormone replacement therapy increased EOC risk (odds ratio = 1.41, 95% CI: 1.15, 1.72). Among etiologic hypotheses, the retrograde transportation hypothesis accommodates most epidemiologic findings concerning EOC risk.

Age Factors↗

PubMed2002

Hormone replacement therapy and the risk of invasive epithelial ovarian cancer in Swedish women.

BACKGROUND: Estrogen replacement therapy (ERT), which is mainly used to relieve climacteric symptoms, increases a woman's risk for uterine endometrial cancer and epithelial ovarian cancer (EOC). Estrogens are often combined with progestins in hormone replacement therapy (HRT) to reduce the risk of uterine endometrial cancer. Data on the association between HRT including progestins and EOC risk are limited. This nationwide case-control study examined EOC risk in relation to HRT regimens with sequentially added progestins (HRTsp) and continuously added progestins (HRTcp). METHODS: Between 1993 and 1995, we enrolled 655 histologically verified incident case patients with EOC and 3899 randomly selected population controls, all 50-74 years of age. Data on HRT use were collected through mailed questionnaires. Multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by the use of unconditional logistic regression. RESULTS: Risks of EOC were elevated among ever users as compared with never users of both ERT (OR = 1.43, 95% CI = 1.02 to 2.00) and HRTsp (OR = 1.54, 95% CI = 1.15 to 2.05); risks were elevated for serous, mucinous, and endometrioid subtypes. For all EOC types combined, the greatest risk increases were seen with hormone use exceeding 10 years. Ever use of HRTcp was not associated with increased EOC risk relative to HRTcp never use (OR = 1.02, 95% CI = 0.73 to 1.43). The risk of EOC was elevated among HRTsp ever users as compared with HRTcp ever users (OR = 1.78, 95% CI = 1.05 to 3.01). ORs for EOC after ever use of low-potency estrogens were 1.18 (95% CI = 0.89 to 1.55) for oral and 1.33 (95% CI = 1.03 to 1.72) for vaginal applications, but no relationship was seen between EOC risk and duration of use. CONCLUSION: Ever users of ERT and HRTsp but not HRTcp may be at increased risk of EOC.

Adenocarcinoma, Clear Cell↗