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Notes Washed Up in a BottleDon. W. MacCorquodale M.D. M.S.P.H.Periodic Notes From the Field on Philosophy and Science. |
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FROM THE RED-FACED DEPARTMENTIn the last issue of Notes Washed Up in a Bottle, I wrote that most Cuban-Americans are black. I am grateful to a reader who pointed out correctly that the statement is simply not true. The overwhelming majority of Cuban-Americans are white. FERTILITY, FAMILY PLANNING, AND REPRODUCTIVE HEALTHThe National Center for Health Statistics recently reported the findings from the National Survey of Family Growth of 2002, which involved interviewing American women aged 15-44 years. Here are some of the findings I found of special interest:
COMMENT: There are no surprises here, although I found the association between educational attainment and sexual behavior interesting. I suspect that it really reflects something more complex, namely, the influence of social class. MATERNAL MORTALITY
Maternal mortality declined from 800 deaths per 100,000 live births in 1900 to 7.1 deaths per 100,000 live births in 1998. It has remained relatively constant for the past 25 years. Deborah Rosenberg and her colleagues conducted a study to compare maternal deaths to other women of high risk status to assess the factors associated with mortality and to examine the magnitude of the Black-White maternal mortality differential (Rosenberg D et al. Disparities in mortality among high risk pregnant women in Illinois . Ann. of Epidemiology 2005; 16: 26-32). High risk pregnant women were identified using Illinois 's vital records data for 1994 to 1998. A woman was classified as a maternal death by certain diagnoses on the death certificate and by an interval or less than 1 year between delivery and death. High risk survivors were defined as having at least one of the following medical characteristics or one of the following complications of labor and delivery:
The final sample consisted of nearly 77,000 high risk pregnant women: 28 pregnancy related deaths and slightly more than 76,600 high risk survivors. Women who had a pregnancy-related death were more likely to be 35 years of age or older (32% vs. 16%), unmarried (59% vs. 31%), multiparous (70% vs. 49%), African-American (52% vs. 17%), and to have received late or no prenatal care (26% vs. 15%). For African-American and Hispanic women, the risks for death were 5.6 (95% CI, 4.3-7.3) and 1.5 (95% CI, 0.98-2.2) times that of White women. For women > 35 years of age, the risk of death was 2.5 (95% CI, 1.9-3.2), times that of women aged 20-34 years, and for unmarried women, the risk was 2.8 (98% CI, 2.2-3L6) times greater than for married women. For women who had no prenatal care or late entry into care the risks of death were 5.3 (95% CI, 2.2-13.1) and 1.7 (95% CI, 1.1-2.8) times that of women who began care in the first trimester. For multiparous women, the risk of death was approximately 2-4 times that of women who were nulliparous. The mortality rate for women with pregnancy induced hypertension (PIH) was 13.7 per 10,000; African-American and Hispanic women with a diagnosis of PIH were 9.9 (95% CI, 4.4-22.2 and 7.9 (95% CI, 3.2-19.6) times more likely to die than were White women with the same diagnosis. The overall mortality rate for women with hemorrhage was 16.5 per 10,000; African-American and Hispanic women with a diagnosis of hemorrhage were 4.7 (95% CI, 1.3-16.8) and 3.7 (95% CI, 0.8-16.7) times more likely to die than were White women with the same diagnosis The authors wrote that this study is the first population-based study that compares maternal deaths to pregnant women with severe morbidity rather than to women whose infants comprise the entire birth cohort. They added that restricting the comparison group to high risk survivors controls for potential confounding by risk status. COMMENT: I found this a most interesting article, however, I was struck by the wide confidence intervals associated with the estimates of various risk factors, for example, “African-American and Hispanic women with a diagnosis of PIH were 9.9 (95% CI, 4.4-22.2) and 7.9 (95% CI, 3/2-1.6) times more likely to die than were White women with the same diagnosis.” I suspect that the numbers of cases in those individual cells were quite small, which resulted in imprecise estimates. EFFECTIVENESS OF SCREENING FOR PROSTATE CANCERJohn Concato and his colleagues conducted a nested case-control study to assess whether or not screening with the prostate specific antigen, PSA, with or without digital rectal examination, DRE, improved survival for prostate cancer (Concato J et al. The effectiveness of screening for prostate cancer. Archives of Int. Medicine, January 9, 2006). In a case-control analysis of the effect of screening on survival, exposure to prior screening tests is compared among people with cancer who died (case patients) vs. a representative sample of people (controls) who are still alive with or without the same cancer. A lower frequency of screening among case patients as compared with controls provides evidence supporting a protective effect of screening on mortality. Potential cases patients were men in the cohort, who had been diagnosed with prostate cancer between Jan. 1, 1991, and Dec. 31, 1995, and who were identified using pathology databases at 10 Veterans Administration Medical Centers in New England . Control patients were selected at random from the remaining cohort still receiving VA care, matched 1:1 for each case based on VA facility and age. Men with prostate cancer were eligible to be selected as controls, using the criterion that control patients had to be alive on the date of death of the corresponding matched case patient. The primary analysis examined “definite” PSA screening tests and overall mortality. Standard methods for calculating sample sized determined that 498 case and 498 controls would detect an odds ratio of 0.67 as a protective effect of screening with a P = 0.05 and 80% power. A secondary analysis addressed cause-specific (prostate cancer) mortality as the outcome. Among the cohort, 1425 men were diagnosed as having prostate cancer between 1991 and 1995. Follow-up for mortality through 1999 identified 501 case patients who died, exceeding the required sample size of 498. For each case patient, a control patient (n= 501) was randomly selected from the cohort and matched by age and site. Definite screening with PSA occurred in 70 cases (14%) and 65 controls (13%). These data correspond to an unadjusted, match OR of 1.10 (95% CI; 0.75 – 1.62, p = .62. Evidence of a benefit of screening would have included a “deficit” of screening among case patients vs. control patients. After adjusting for race and comorbidity, the OR for screening remained statistically nonsignificant at 1.08 (95% CI; 0.71 – 1.64). Black race (OR, 3.18, 95% CI; 1.74-5.83) and comorbidity (OR, 1.46, 95% CI: 1.31-1.64) were associated with mortality. A secondary analysis examined the association of screening and cause-specific mortality. Overall, 136 (275) of 501 case patients had evidence of death due to prostate cancer. The adjusted OR for screening with PSA or DRE was 1.13 (95% CI; 0.63 – 1.78). The authors commented that the 4- to 9-year period for mortality ascertainment is consistent with the study design because finding unscreened men who died relatively soon after diagnosis is needed to establish a benefit of screening. COMMENT: I found the results of this study rather surprising. I would have expected that increased screening would have detected a large number of indolent prostatic cancers among older men that would not have resulted in death from prostate cancer. Had this occurred, the study would have demonstrated a spurious benefit from PSA screening. I am anxious to see this study replicated. |
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