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Biomedical subjects

D W Cramer

Publications and source records attributed to D W Cramer.

107 records · Page 6Linked to original sources

Tubal infertility and the intrauterine device.

To study the association between intrauterine devices (IUDs) and pelvic inflammatory disease, we compared contraceptive histories in 4185 while women--283 nulliparous women with primary tubal infertility, 69 women with secondary tubal infertility, and 3833 women admitted for delivery at seven collaborating hospitals from 1981 to 1983. The relative risk of tubal infertility associated with IUD use was calculated by means of multivariate logistic regression to control for confounding factors, including region, year of menarche, religion, education, smoking, and reported number of sexual partners. The adjusted risk of primary tubal infertility associated with any IUD use before a first live birth was 2.0 (95 per cent confidence limits, 1.5 to 2.6) relative to nonuse. Users of the Dalkon Shield had an adjusted risk of 3.3 (1.7 to 6.1), users of the Lippes Loop or Saf-T-Coil had a risk of 2.9 (1.7 to 5.2), and users of copper IUDs had a risk of 1.6 (1.1 to 2.4). Women who reported having only one sexual partner had no increased risk of primary tubal infertility associated with IUD use. The adjusted risk of secondary tubal infertility associated with use of a copper IUD after a first live birth was not statistically significant (1.5; 95 per cent confidence limits, 0.8 to 3.0), whereas the risk from similar use of noncopper devices was significant (2.8; 1.3 to 5.9). We conclude that tubal infertility is associated with IUD use, but less so with copper IUDs.

Adult↗

Epidemiology of complete molar pregnancy.

The epidemiology of complete molar pregnancy is dominated by two strong factors. The first is the wide geographic variation in incidence, from less than 1 per 1,000 deliveries in the United States and Canada to about 1 per 100 deliveries in Indonesia and other Asian countries. The second factor is maternal age, with an increasing risk of molar pregnancy with increasing maternal age. Both genetic and environmental factors may underlie these two risk factors. The genetic factors may include chromosomal defects that occur as a consequence of oocyte aging. The environmental factors probably include nutrition. Although many aspects of nutrition deserve further study, some new research suggests that a focus on vitamin A metabolism may be especially profitable.

Female↗

Dietary animal fat in relation to ovarian cancer risk.

Food and beverage frequency questionnaires were administered to 215 white women with epithelial ovarian cancer and to 215 control women matched by age, race, and residence. Women with ovarian cancer favored foods higher in animal fats and consumed significantly greater amounts of animal fat and significantly less vegetable fat compared with control subjects. Adjusted for potential confounding due to differences between case and control subjects in weight and parity, there was a significant trend for increasing risk for ovarian cancer with increasing animal fat consumption. No major differences were noted between patients and control subjects in coffee, alcohol, and tobacco use. Dietary factors may partially explain variation in the international incidence of this disease and suggest a new pathway for its etiology.

Alcohol Drinking↗

Mumps, menarche, menopause, and ovarian cancer.

Clinical history of mumps during childhood, age at menarche, and age at natural menopause were obtained in 119 postmenopausal women with ovarian cancer and 109 postmenopausal control subjects from the general population. Case subjects differed significantly from control subjects in being less certain whether they had had mumps and in being less likely to recall the age at infection. In both groups, a significant inverse correlation was observed between age at menarche and menopause in subjects with a positive clinical history for mumps but not in subjects with a negative clinical history for mumps. The correlation was strongest in case subjects who said they had had mumps, especially those who were nulliparous. We speculate that the mumps virus may be a determinant of reproductive span and, through its potential to cause a depletion of oocytes, increase the risk for ovarian cancer.

Age Factors↗

Determinants of ovarian cancer risk. I. Reproductive experiences and family history.

Reproductive experiences and family history were assessed in 215 white females with epithelial ovarian cancer and in 215 control women matched by age, race, and residence. Pregnancy exerted a strong protective effect against ovarian cancer, which increased with the number of live-born children. After adjustment for parity, an effect of age at first live birth and breast-feeding was not apparent. Menstrual events did not differ significantly between cases and controls, although cases were more likely to have had an earlier menopause and less likely to have had a surgical menopause. Women with ovarian cancer had more frequently used menopausal hormones in cyclic fashion compared to controls. Regarding family history, women with ovarian cancer more frequently reported consanguinity in their ancestry and a highly frequency of primary relatives with cancer of the colon, lung, ovary, and prostate gland.

Consanguinity↗

Determinants of ovarian cancer risk. II. Inferences regarding pathogenesis.

Entrapment of surface epithelium within the ovarian stroma was proposed as an initial event in the pathogenesis of cystadenocarcinoma of the ovary. Subsequent events, including differentiation, proliferation, and eventual malignant transformation of the entrapped epithelium, may occur as a consequence of stimulation by estrogen or estrogen precursors. These events were more likely when the steroid producing stroma itself had been stimulated by high gonadotropins. Animal experiments suggested that gonadotropin excess and stromal stimulation may result by disturbing normal feedback inhibition between ovary and pituitary or by destroying ovarian follicles. By analogy, in humans, a number of common chemicals and drugs may increase gonadotropins by enhancing estrogen degradation in the liver or by directly stimulating production by the pituitary. Elevated gonadotropins may also result via mechanisms that cause primary ovarian failure including pelvic irradiation, exposure to chemicals or metabolites toxic to follicles, or ovarian infections such as mumps.

Cell Differentiation↗

Factors affecting the association of oral contraceptives and ovarian cancer.

We investigated the relation between epithelial ovarian cancer and the use of oral contraceptives in a case-control study of 144 white women under the age of 60 who had ovarian cancer and 139 white women under 60 who were selected from the general population. We observed a decreased risk for ovarian cancer associated with the use of oral contraceptives in subjects 40 through 59 years of age at the time of the study. The relative risk, adjusted for parity, was 0.11, with 95 per cent confidence limits of 0.04 to 0.33. In contrast to the findings in older women, a decreased risk for ovarian cancer associated with oral-contraceptive use was not found in women under 40. In this group, the adjusted relative risk associated with any use of oral contraceptives was 1.98, with 95 per cent confidence limits of 0.74 to 5.27. The lowest risk for ovarian cancer associated with the use of oral contraceptives was observed in older parous subjects and in women who had discontinued use more than 10 years previously.

Adult↗

Ovarian cancer and talc: a case-control study.

Opportunities for genital exposure to talc were assessed in 215 white females with epithelial ovarian cancers and in 215 control women from the general population matched by age, race, and residence. Ninety-two (42.8%) cases regularly used talc either as a dusting powder on the perineum or on sanitary napkins compared with 61 (28.4%) controls. Adjusted for parity and menopausal status, this difference yielded a relative risk of 1.92 (P less than 0.003) for ovarian cancer associated with these practices. Women who had regularly engaged in both practices had an adjusted relative risk of 3.28 (P less than 0.001) compared to women with neither exposure. This provides some support for an association between talc and ovarian cancer hypothesized because of the similarity of ovarian cancer to mesotheliomas and the chemical relation of talc to asbestos, a known cause of mesotheliomas. The authors also investigated opportunities for potential talc exposure from rubber products such as condoms or diaphragms or from pelvic surgery. No significant differences were noted between cases and controls in these exposures, although the intensity of talc exposure from these sources was likely affected by variables not assessed in this study.

Adolescent↗

Trends in the incidence of endometrioid and clear cell cancers of the ovary in the United States.

An increase in reported incidence of endometrioid and clear cell cancers of the ovary occurred in the United States during the 1970s, while no change occurred in the overall incidence of ovarian cancer. The authors can not rule out that this was due to a shift in the criteria for histologic classification or improved coding, although these seem unlikely to account entirely for the change. In the four areas where the trend for endometrioid and clear cell cancers of the ovary was examined, the per cent increases in their occurrence were correlated with the per cent increases in the occurrence of carcinoma of the uterine corpus. The concomitant trends and the biologic similarities between these histologic types of ovarian cancer and the uterine cancers suggest that common etiologic factors may be involved. The role of postmenopausal estrogen use in the etiology of ovarian cancer must be clarified by further epidemiologic studies, but such studies should take tumor histology into consideration.

Adenocarcinoma↗

Review of epidemiologic studies of endometrial cancer and exogenous estrogen.

Epidemiologic literature on the association of exogenous estrogen and endometrial cancer is reviewed. Descriptive studies have documented fluctuations in the incidence of endometrial cancer, mainly of localized disease, associated with estrogen use. Etiologic studies have established an association between estrogen use during menopause and the occurrence of endometrial cancer. Although the association appears to be a valid one, several biases may have falsely increased the magnitude of this association. The association also appears to be strongest for local disease and weakest for the most invasive disease, which implies that the etiology for the more invasive endometrial cancers is largely unaccounted for by estrogen use. A need for a prospective study to define other potential risks and benefits of estrogen therapy is clear. However, appreciation of factors known to modify the risk of endometrial cancer from exogenous estrogen can help the clinician to use these preparations judiciously.

Dose-Response Relationship, Drug↗