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Biomedical subjects

B A Rosner

Publications and source records attributed to B A Rosner.

At least 55 records · Page 3Linked to original sources
PubMed1996

Birthweight as a risk factor for breast cancer.

BACKGROUND: The mammary gland is largely undifferentiated before birth and may be particularly susceptible to intrauterine influences that could increase the risk of cancer through acceleration of cell proliferation or other pregnancy-related processes. Studies of migrant populations, animal data, and limited epidemiological evidence suggest that breast cancer may originate in utero. In a nested case-control study we assessed whether birthweight and other perinatal factors are associated with risk of breast cancer. METHODS: This case-control study was nested within the cohorts of the two Nurses' Health Studies. We used self-administered questionnaires to obtain information from the mothers of 582 nurses with invasive breast cancer and the mothers of 1569 nurses who did not have breast cancer (controls). Information on risk factors for breast cancer during adulthood were obtained from the nurses; multiple logistic regression analysis adjusted for these risk factors. FINDINGS: Birthweight was a significant predictor of breast-cancer risk. With women who weighed 4000 g or more at birth as the reference category, the adjusted odds ratios for breast cancer were 0.86 (95% CI 0.59-1.25) for birthweights of 3500-3999 g, 0.68 (0.48-0.97) for birthweights of 3000-3499 g, 0.66 (0.45-0.98) for birthweights of 2500-2999 g, and 0.55 (0.33-0.93) for birthweights below 2500 g (p for trend 0.004). Prematurity was not significantly associated with risk of breast cancer. INTERPRETATION: Birthweight is significantly associated with breast-cancer risk, which suggests that intrauterine factors or processes affect the risk of breast cancer in the offspring. High concentrations of pregnancy oestrogens may have an important role in breast carcinogenesis, but other pregnancy hormones or intrauterine factors may also be involved.

Adult↗
PubMed1996

Prospective study of regular aspirin use and the risk of breast cancer.

BACKGROUND: Evidence suggests that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit tumor development in the large bowel. An inverse association between the use of NSAIDs and the incidence of breast cancer has been observed, but this association has not been statistically significant in all studies. PURPOSE: We analyzed data from the prospective Nurses' Health Study to evaluate the influence of aspirin use on breast cancer risk. METHODS: We studied a population of 89,528 female registered nurses who reported no history of breast or other cancers (excluding nonmelanoma skin cancer) and who returned a mailed questionnaire in 1980 that elicited information concerning breast cancer risk factors and current and past aspirin use. Follow-up questionnaires were mailed to the participants every 2 years; the women were followed through 1992. Information concerning current aspirin use was obtained from each biennial questionnaire, except in 1986. Cases of breast cancer were identified through questionnaire responses, and permission was sought for a review of medical records to confirm the diagnoses. Our analysis was based on 2414 cases of invasive breast cancer, which included 2303 cases confirmed with medical records and 111 cases for which no records were obtained. Relative risks (RRs) with 95% confidence intervals (CIs), adjusted for age or age plus other known or potential breast cancer risk factors (i.e., multivariate), were calculated. RESULTS: Regular aspirin use (two or more tablets per week) in 1980 was unrelated to breast cancer incidence during the succeeding 12-year period (with no regular aspirin use as the referent, multivariate RR = 1.03; 95% CI = 0.95-1.12). The corresponding risk estimate for consistent regular aspirin use during the period from 1980 through 1988 was 1.01 (95% CI = 0.80-1.27). The risks were similar for heavy aspirin use (for more than two tablets per day [i.e., > 14 per week] in 1980 and in 1980 through 1988, the multivariate RRs [95% CIs] were 1.05 [0.89-1.23] and 1.09 [0.75-1.60], respectively) and for extended durations of regular use (e.g., for 20 years or more of regular use, multivariate RR = 1.00; 95% CI = 0.71-1.41). CONCLUSION: Our results indicate that regular aspirin use does not reduce the risk of breast cancer.

Adult↗
PubMed1996

Risk factors for breast cancer according to family history of breast cancer. For the Nurses' Health Study Research Group.

BACKGROUND: Family history of breast cancer is an established risk factor for this disease and is used to identify women at higher risk, although the impact of risk factors for breast cancer among women with a family history is not well defined. PURPOSE: Using a modified extended log-incidence Pike model, we prospectively examined the impact of risk factors for breast cancer among women with and without a family history of the disease. METHODS: Data analyzed were obtained prospectively from the Nurses' Health Study. Two thousand two hundred forty-nine incident cases of invasive breast cancer were identified in a cohort of 89,132 women aged 30-55 years in 1976 followed biennially through 1990 (1.1 million person years of follow-up). With the use of proportional hazards models, we evaluated the association between risk factors for breast cancer and risk among women with and those without a family history of the disease. We then fit a modified extended log-incidence Pike model to these data. RESULTS: Among women with a family history of breast cancer, reproductive risk factors has associations that were different from those observed among women without a family history of the disease. In particular, we observed little protection from later age at menarche, no protection from multiple births when compared with nulliparity, nor from early, as compared with later, age at first birth. Fitting these data to a model of breast cancer incidence on the basis of reproductive risk factors, we observed an adverse effect of first pregnancy on risk of breast cancer among women with a family history of breast cancer that was approximately 50% greater in magnitude than among women without a family history. Additional births after the first birth conveyed little protection for women with a family history. History of benign breast disease, past use of oral contraceptives, and use of postmenopausal hormones showed relative risks that did not differ between women with a family history and those without a family history of the disease. CONCLUSIONS: We observed a consistent increase in risk of breast cancer among women with a mother or sister history of the disease that was exacerbated by first pregnancy. Among women with a family history of breast cancer, the adverse effect of pregnancy persisted so that to age 70 years, parous women were at higher risk of breast cancer than nulliparous women. Among women without a family history of the disease, first pregnancy was associated with a smaller increase in risk, and early pregnancy and higher number of births were each associated with reduced breast cancer incidence.

Adult↗
PubMed1996

Prospective assessment of breastfeeding and breast cancer incidence among 89,887 women.

BACKGROUND: The relation between breastfeeding and breast cancer risk has been examined in many studies; some have reported no association, and others a reduced risk, particularly among premenopausal women. In the only prospective cohort study, no association was found. We have assessed prospectively the association between breastfeeding and incidence of breast cancer among 89,887 women in the US Nurses' Health Study. METHODS: In 1986, participants were asked about the number of months they breastfed for all their children combined. Parous women with no history of cancer were included in this analysis. During 6 years of follow-up (513,015 person-years), 1,459 invasive breast cancer cases were diagnosed. FINDINGS: Relative to women who had never breastfed, no significant overall association was found--after adjusting for established risk factors for breast cancer--between a history of having breastfed and subsequent development of breast cancer (relative risk [RR] 0.93, 95% CI 0.83 -1.03). No inverse trend was observed with duration of breastfeeding; women who breastfed for 2 years of longer had a RR of 1.11 (0.90-1.38). Among women who had given birth only once, women who had breastfed their child experienced a lower incidence of breast cancer (RR 0.68, 0.46-1.00). Among premenopausal women, who tended to be near menopause due to the age structure of the cohort, the RR of breast cancer for those who had lactated was 1.16 (0.89-1.50). Premenopausal women who had lactated for 1 year or more had a RR of 1.10 (0.78-1.57). INTERPRETATION: These data suggest that there is no important overall association between breast-feeding and the occurrence of breast cancer.

Adult↗
PubMed1996

Measurement error models for ordinal exposure variables measured with error.

In dietary epidemiology, the key nutrient variables are often expressed in the quintile scale. The nutrients are often measured with error and it is of interest to consider estimates of relative risk for exposures in the quintile scale corrected for measurement error. In this paper, I propose a measurement error model that relates diet record (true) nutrient values to food frequency (noisy) nutrient values when expressed in the quintile scale. I estimate this measurement error model from validation study data and then apply it to obtain corrected estimates of breast cancer risk in relation to intake of fat and alcohol with use of data from the Nurses' Health Study.

Adult↗
PubMed1996

Coffee consumption and coronary heart disease in women. A ten-year follow-up.

OBJECTIVE--To assess the relationship between coffee consumption and risk of coronary heart disease (CHD) among women. DESIGN--Prospective cohort study with coffee consumption measured in 1980, 1984, and 1986, and follow-up through 1990. SETTING--Female registered nurses in the United States. PARTICIPANTS--A total of 85,747 US women 34 to 59 years of age in 1980 and without history of CHD, stroke, or cancer. MAIN OUTCOME MEASURE--Ten-year incidence of CHD (defined as nonfatal myocardial infarction or fatal CHD). RESULTS--During 10 years of follow-up we documented 712 cases of CHD. After adjustment for age, smoking, and other CHD risk factors, we found no evidence for any positive association between coffee consumption and risk of subsequent CHD. For women drinking six or more cups of caffeine-containing coffee per day in 1980, the relative risk was 0.95 (95% confidence interval, 0.73 to 1.26) compared with women who did not consume this beverage. Similarly, there was no association when the first 4 years of follow-up were excluded, when nonfatal and fatal CHD end points were examined separately, or when we updated coffee consumption in 1984 or 1986 and examined only CHD during the next 2-year interval. Further, there was no association with caffeine intake from all sources combined or with decaffeinated coffee consumption. CONCLUSIONS--These data indicate that coffee as consumed by US women is not an important cause of CHD.

Adult↗
PubMed1994

A prospective study of cigarette smoking and risk of colorectal adenoma and colorectal cancer in U.S. women.

BACKGROUND: A positive correlation between smoking and colorectal cancer has been reported for men, but not for women, who began smoking in substantial numbers in the late 1940s and early 1950s. We hypothesized that smoking acts as an initiator of colorectal neoplasia and that an association with cancer in women has been missed because of the long period between initiation and diagnosis of cancer. PURPOSE: Our purpose was to assess the association between smoking and risk of colorectal adenoma and colorectal cancer in women and to estimate the minimum induction period between the onset of smoking and cancer diagnosis. METHODS: Our data came from the ongoing Nurses' Health Study, in which current and lifetime smoking histories and other potential confounding factors were assessed by questionnaire at baseline and at 2-year intervals. We documented 586 new cases of colorectal cancer from 1976 to 1990 from a group of 118,334 women and 564 new cases of adenoma among 12,143 women who had a first colonoscopy or sigmoidoscopy between 1980 and 1990. We then assessed the relative risk (RR) of small adenoma, large adenoma (> or = 1 cm), and colorectal cancer in terms of pack-years of smoking. RESULTS: The amount smoked in the prior 20 years was related to the prevalence of small adenomas (multivariate RR = 1.45; 95% confidence interval [CI] = 1.25-1.68; P < .0001) and less strongly with large adenomas (RR = 1.31; 95% CI = 1.17-1.47; P < .0001), adjusting for age, intake of saturated fat, dietary fiber, folate, and alcohol, body mass, family history of colorectal cancer, and pack-years of cigarettes smoked within the prior 20 years. Pack-years of cigarettes smoked more than 20 years in the past was associated with risk of large adenoma (multivariate RR for a 20 pack-year increment = 1.29; 95% CI = 1.01-1.64; P trend = .04), but not of small adenoma (RR = 1.11; 95% CI = 0.93-1.34). Cigarette smoking was unrelated to colorectal cancer until 35 years after smoking began, but then became progressively more strongly related with time. Among women who had started smoking more than 10 cigarettes per day 35-39 years in the past, the RR for cancer was 1.47 (95% CI = 1.07-2.01), progressing to 1.63 (95% CI = 1.14-2.33) after 40-44 years and 2.00 (95% CI = 1.14-3.49) after 45 years. CONCLUSIONS: Because the minimum induction period for colorectal cancer appears to be at least 35 years, an association between smoking and colorectal cancer in women may just now be showing up. IMPLICATIONS: Our findings suggest that cigarette smoking may be a previously unrecognized, preventable cause of colorectal cancer among women.

Adenoma↗
PubMed1994

An optimal rule for screening subjects for clinical trials in the presence of within-person variability.

In screening subjects for a continuous variable, such as blood pressure (BP), for eligibility for clinical trials, multistage rules are often used to select subjects within a target range. Multiple readings may be taken over successive visits, and the subject must meet eligibility criteria at each visit. We present an optimal rule that minimizes the number of clinic visits needed per eligible subject or the overall number of screening visits needed to achieve a given sample size of eligible subjects. We illustrate these methods with the design of phase I of the Trials of Hypertension Prevention (TOHP), which attempts to identify subjects with mean diastolic BP in the range 80- < 90 mm Hg over three screening visits. The optimal rule requires only 73% of the visits needed with a no-screening rule in which all subjects are examined at each visit, and the average BP at all screening visits is used as a criterion. The optimal rule requires only 36% of visits needed in a more standard approach in which a subject must have an observed mean diastolic BP of 80- < 90 mm Hg on each of three consecutive visits. Alternatively, one may minimize the expected cost of screening per eligible subject when screening visits differ in cost. Examples are given of optimal rules with differing relative costs per visit.

Adult↗
PubMed1993

Family history, age, and risk of breast cancer. Prospective data from the Nurses' Health Study.

OBJECTIVE: To examine prospectively the risk of breast cancer as influenced by a maternal history of breast cancer, the mother's age at diagnosis, or a sister's history of breast cancer. DESIGN: Prospective cohort study with biennial follow-up. SETTING/PARTICIPANTS: 117,988 women in the Nurses' Health Study aged 30 to 55 years in 1976, followed up through 1988 (1.3 million person-years of follow-up). RESULTS: We identified 2389 incident cases of invasive breast cancer. Compared with women without a maternal history of breast cancer, the age-adjusted relative risk (RR) of breast cancer was highest among women whose mother was diagnosed before the age of 40 years (RR, 2.1 [95% confidence interval, 1.6 to 2.8]). The RR decreased with advancing maternal age at time of diagnosis to 1.5 (95% confidence interval, 1.1 to 2.2) for maternal diagnosis after the age of 70 years. Having a sister with a history of breast cancer also was related to increased risk; for women with one sister with breast cancer compared with those with one sister without such a history, the age-adjusted RR was 2.3 (95% confidence interval, 1.6 to 3.4). Women whose mother and sister both had a history of breast cancer had an RR of 2.5 (95% confidence interval, 1.5 to 4.2) compared with those without a family history. These associations did not differ appreciably when stratified by age; menopausal status; history of benign breast disease; body mass index; age at menarche; or parity or age at first birth of the women at risk. The results remained unchanged when we controlled for these risk factors in multivariate models. Despite slightly greater mammography surveillance and earlier detection of tumors among women with a family history of breast cancer, detection bias is unlikely to account for more than a small part of the observed association. CONCLUSIONS: Risk of breast cancer is approximately doubled among women whose mother had breast cancer diagnosed before the age of 40 years or who have a sister with breast cancer, and remains elevated even for those whose mothers were diagnosed with breast cancer at the age of 70 years or older. However, the risk associated with a mother or sister history of breast cancer is smaller than suggested by earlier retrospective studies. Overall, within this population of middle-aged women, only 2.5% of breast cancer cases are attributable to a positive family history.

Adult↗
PubMed1993

Screening rules for determining blood pressure status in clinical trials. Application to the trials of hypertension prevention.

Multistage blood pressure screening rules are often used to select subjects for clinical trials. Multiple blood pressure readings are taken over successive visits, and the subject must meet eligibility criteria at each visit. In this paper, the authors present methods which depend on the distribution of the subject's underlying blood pressure values (the predictive value approach) or, alternatively, the subject's observed mean over all screening visits (the empirical predictive value approach) given the observed mean after one or more visits. The authors apply these methods to data from Phase I of the Trials of Hypertension Prevention, which attempts to identify subjects with mean diastolic blood pressures in the range 80-89 mmHg over three screening visits. The estimated efficiency of these rules is evaluated in terms of the number of clinic screening visits needed per eligible subject. Relative to reexamining all subjects at each visit (no screening), these approaches can reduce the number of visits required by 27%. This is in contrast to the standard rule in which a subject must have an observed mean diastolic blood pressure of 80-89 mmHg on each of three consecutive visits, which requires twice as many clinic visits per eligible subject as not screening. Thus, the approach presented is useful in identifying eligible subjects for clinical trials in an efficient manner.

Adult↗
PubMed1993

Folate, methionine, and alcohol intake and risk of colorectal adenoma.

BACKGROUND: Reduced methylation of DNA may contribute to loss of the normal controls on proto-oncogene expression. In humans, hypomethylation of DNA has been observed in colorectal cancers and in their adenomatous polyp precursors. Accumulation of DNA methylation abnormalities, observed during progression of human colorectal neoplasia, may be influenced by certain dietary factors. The apparent protective effect of fresh fruits and vegetables, the major folate sources, on colorectal cancer incidence suggests that a methyl-deficient diet contributes to occurrence of this malignancy. Low dietary folate and methionine and high intake of alcohol may reduce levels of S-adenosylmethionine, which is required for DNA methylation. PURPOSE: To determine if dietary factors that may influence methyl availability are related to colorectal adenomas, we prospectively examined the association of folate, methionine, and alcohol intakes and risk of colorectal adenoma. METHODS: We assessed dietary intake for a 1-year period for women of the Nurses' Health Study, started in 1976, and for men of the Health Professionals Follow-up Study, started in 1986--using a semiquantitative food frequency questionnaire. Adenomatous polyps of the left colon or rectum were diagnosed in 564 of 15,984 women who had had an endoscopy between 1980 and 1990 and in 331 of 9490 men who had undergone an endoscopy between 1986 and 1990. RESULTS: High dietary folate was inversely associated with risk of colorectal adenoma in women (multivariate relative risk [RR] = 0.66; 95% confidence interval [CI] = 0.46-0.95 between high and low quintiles of intake) and in men (RR = 0.63; 95% CI = 0.41-0.98) after adjusting for age, family history, indications for endoscopy, history of previous endoscopy, total energy intake, saturated fat intake, dietary fiber, and body mass index. Relative to nondrinkers, drinkers of more than 30 g of alcohol daily (about two drinks) had an elevated risk of adenoma (in women, RR = 1.84, 95% CI = 1.19-2.86; in men, RR = 1.64, 95% CI = 0.92-2.93). Methionine intake was inversely associated with risk of adenomas 1 cm or larger (RR = 0.62; 95% CI = 0.46-0.85, combining men and women). CONCLUSIONS: Folate, alcohol, and methionine could influence methyl group availability, and a methyl-deficient diet may be linked to early stages of colorectal neoplasia. A dietary pattern that increases methyl availability could reduce incidence of colorectal cancer. IMPLICATIONS: These data support efforts to increase dietary folate in segments of the population having diets with low intakes of this nutrient.

Adenoma↗
PubMed1993

Intake of trans fatty acids and risk of coronary heart disease among women.

Trans isomers of fatty acids, formed by the partial hydrogenation of vegetable oils to produce margarine and vegetable shortening, increase the ratio of plasma low-density-lipoprotein to high-density-lipoprotein cholesterol, so it is possible that they adversely influence risk of coronary heart disease (CHD). To investigate this possibility, we studied dietary data from participants in the Nurses' Health Study. We calculated intake of trans fatty acids from dietary questionnaires completed by 85,095 women without diagnosed CHD, stroke, diabetes, or hypercholesterolaemia in 1980. During 8 years of follow-up, there were 431 cases of new CHD (non-fatal myocardial infarction or death from CHD). After adjustment for age and total energy intake, intake of trans isomers was directly related to risk of CHD (relative risk for highest vs lowest quintile 1.50 [95% Cl 1.12-2.00], p for trend = 0.001). Additional control for established CHD risk factors, multivitamin use, and intakes of saturated fat, monounsaturated fat, and linoleic acid, dietary cholesterol, vitamins E or C, carotene, or fibre did not change the relative risk substantially. The association was stronger for the 69,181 women whose margarine consumption over the previous 10 years had been stable (1.67 [1.05-2.66], p for trend = 0.002). Intakes of foods that are major sources of trans isomers (margarine, cookies [biscuits], cake, and white bread) were each significantly associated with higher risks of CHD. These findings support the hypothesis that consumption of partially hydrogenated vegetable oils may contribute to occurrence of CHD.

Age Factors↗
PubMed1993

A comparison of prospective and retrospective assessments of diet in the study of breast cancer.

Fat intake was examined in relation to risk of breast cancer using dietary questionnaires administered both before and after the diagnosis of breast cancer. Among the Nurses' Health Study cohort members who completed a food frequency questionnaire and were free of cancer in 1986, 398 were diagnosed with breast cancer during 2 years of follow-up. These cases and 798 age-matched controls (cohort members who also completed a dietary questionnaire in 1986 but did not develop breast cancer) were sent another food frequency questionnaire in 1989 inquiring about their diet in 1985. Three hundred cases and 602 controls responded to the second questionnaire. The age-adjusted analysis using the prospective (1986) questionnaire demonstrated no appreciable associations between breast cancer incidence and intakes of total fat (odds ratio (OR) between highest and lowest quintiles = 0.87; 95% confidence interval (CI) 0.54-1.40) and saturated fat (OR = 0.97; CI 0.64-1.46). The age-adjusted analysis using the retrospective (1989) questionnaire suggested positive associations between breast cancer incidence and intakes of total fat (OR = 1.43; 95% CI 0.90-2.27) and saturated fat (OR = 1.38; 95% CI 0.89-2.13). When nutrients were adjusted for total energy intake, the direction and magnitude of the differences between the prospective and retrospective analyses were similar to the analyses unadjusted for energy intake. These results suggest that case-control studies of diet and breast cancer may yield biased associations between fat intake and the risk of breast cancer.

Adult↗
PubMed1993

Recall and selection bias in reporting past alcohol consumption among breast cancer cases.

Recall and selection bias are well-recognized potential problems in case-control studies of alcohol and cancer, but few analyses have attempted to assess the direction and the magnitude of these potential biases. We thus examined alcohol consumption in relation to risk of breast cancer using dietary questionnaires administered both before and after the diagnosis of breast cancer in the Nurses' Health Study (United States). Among cohort members who completed a dietary questionnaire in 1986 and who were free of cancer, 616 were diagnosed with breast cancer during follow-up to December 1989. These cases and 1,277 controls (a random sample of cohort members who did not develop cancer up to 1990) then were sent another questionnaire inquiring about their diet in 1985. Four hundred and ninety-four cases (80.2 percent) and 999 controls (78.2 percent) responded to the second questionnaire. The analysis based on the prospective (1986) questionnaire demonstrated an elevated risk of breast cancer among women who drank 30 or more g of alcohol daily (about two drinks) relative to nondrinkers (odds ratio [OR] = 1.55, 95 percent confidence interval [CI] = 1.01-2.39). The analysis based on the retrospective questionnaire also indicated a similar but slightly attenuated elevation of risk of breast cancer among women who drank at least 30 g daily (OR = 1.42, CI = 0.85-2.40). In these data, bias due to selection and recall had only minor effects on reported intake of alcohol consumption.

Adult↗
PubMed1993

Effect of strenuous exercise on platelet activation state and reactivity.

BACKGROUND: It has been hypothesized that platelets are activated, or made more activatible, by strenuous exercise and that these changes may play a role in the genesis of exercise-induced coronary ischemia. Previous studies have yielded conflicting results but have used assays (eg, platelet aggregation, plasma platelet factor 4, and plasma beta-thromboglobulin) that are subject to methodological problems. METHODS AND RESULTS: In the present study, a whole blood flow cytometric method was used to study the platelet activation state and reactivity of 12 physically active and 12 sedentary individuals before and after standardized treadmill exercise testing. The peptide gly-pro-arg-pro (GPRP) was included in this assay to prevent fibrin polymerization and platelet aggregation, thus allowing the measurement of the reactivity to thrombin of individual platelets in the physiological milieu of whole blood. A panel of fluorescent-labeled monoclonal antibodies was used to monitor activation-dependent platelet surface changes: downregulation of glycoprotein (GP) Ib (6D1) and upregulation of GMP-140 (S12), the GPIIb-IIIa complex (PAC1), and GPIV (OKM5). In samples obtained before exercise, platelets not exposed to thrombin showed no evidence of in vitro activation. In the sedentary subjects, exercise caused a consistent and significant augmentation of the platelet activation state and reactivity as judged by the binding of 6D1 in the presence of thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P = .001), and 0 U/mL (P = .004) and by the binding of OKM5 in the presence of thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P = .029), and 0 U/mL (P = .035). Exercise increased the binding of PAC1 at only a single thrombin concentration (0.005 U/mL, P = .027) and did not alter the binding of S12 at any thrombin concentration. In contrast, in the physically active subjects, exercise failed to cause a consistent alteration in either platelet activation state or platelet reactivity. No significant differences were found between the 12 male and 12 female volunteers. CONCLUSIONS: Strenuous exercise in sedentary subjects but not physically active subjects resulted in both platelet activation and platelet hyperreactivity. These changes were more readily detected with monoclonal antibodies directed against GPIb (6D1) and, to a lesser extent, GPIV (OKM5) rather than those directed against the GPIIb-IIIa complex (PAC1) and GMP-140 (S12). Platelet activation by thrombin, generally regarded as the most physiologically important agonist, can be studied in whole blood in a clinical setting through the use of the peptide GPRP.

Adult↗
PubMed1993

The value of the chest X-ray in making the diagnosis of bronchial asthma.

Although bronchial asthma is one of the most common chronic illnesses of children and young adults, it remains underdiagnosed. To assess the value of the chest X-ray in helping to make the diagnosis of asthma at the primary care level, we studied the medical records of 58 patients aged 18-40 with the diagnosis of mild to moderate asthma and for whom both simple spirometry-forced one-second expiratory volume (FEV1) and/or peak expiratory flow rate (PEFR)--and a chest X-ray had been performed. Only 21 of 58 (36%) had spirometry indicative of asthma (SPI+) while 34 of 58 (59%) had abnormal chest X-rays (CXR+)--"increased markings" and/or "low diaphragm." Although CXR+ discriminated between asthmatic patients and a normal control group, no difference was found between asthmatic patients and a group of patients with acute bronchitis. Nonetheless, the number of asthmatic patients with CXR+ and SPI - (n = 23) was significantly larger than the number with CXR- and SPI+ (n = 10), which indicates that for mild asthma the chest X-ray may be more sensitive than spirometry even though not as specific. These results were surprising at the time of the investigation. Subsequently, however, the importance of the inflammatory response in asthma came to light, which rendered the results more interesting than surprising. We conclude that the chest X-ray has value in making the diagnosis of mild bronchial asthma.

Acute Disease↗
PubMed1992

Type of postmenopausal hormone use and risk of breast cancer: 12-year follow-up from the Nurses' Health Study.

We prospectively examined the use of hormone replacement therapy in relation to breast cancer incidence in a cohort of women 30 to 55 years of age in 1976. During 12 years of follow-up (480,665 person-years) among postmenopausal women, 1,050 incident cases of breast cancer were documented. Overall, past users of replacement estrogen were not at increased risk. After adjustment for established risk factors, type of menopause, age at menopause, and current age, the rate ratio (RR) was 0.91, 95 percent confidence interval (CI) = 0.78-1.07. The risk of breast cancer was elevated significantly among current users (RR = 1.33, CI = 1.12-1.57); after adjusting for age, we observed no evidence of increasing risk with increasing duration of use among current users (P trend = 0.41), or among past users (P trend = 0.46). Women currently using unopposed estrogen (RR = 1.42, CI = 1.19-1.70), estrogen and progesterone (RR = 1.54, CI = 0.99-2.39), or progesterone alone (RR = 2.52, CI = 0.66-9.63), were all at increased risk of breast cancer compared with never users. These data suggest that long-term past use of estrogen replacement therapy is not related to risk, that current estrogen use increases risk of breast cancer to a modest degree, and that the addition of progesterone does not remove the increased risk observed with current use of unopposed estrogen.

Adult↗