Three polymorphisms associated with low hepatic lipase activity are common in African Americans

We have shown previously that a hepatic lipase allele (designated -514T) is common among African Americans and contributes to low hepatic lipase activity in this population. To identify other hepatic lipase alleles associated with low hepatic lipase activity in this population, the coding region and intron-exon boundaries of the hepatic lipase gene were sequenced in 20 African American men with low hepatic lipase activity. Two polymorphisms (N193S and L334F) were associated with low post-heparin plasma hepatic lipase activity and were much more common in African Americans than in whites. This finding, together with our previous data on the -514T allele, indicates that at least three different hepatic lipase polymorphisms associated with low hepatic lipase activity are common among African Americans. Analysis of hepatic lipase haplotypes revealed that 97% of African Americans have at least one hepatic lipase allele that is associated with low hepatic lipase activity.     

The -514 polymorphism in the hepatic lipase gene (LIPC) does not influence androgen-mediated stimulation of hepatic lipase activity

The -514T allele of hepatic lipase is associated with increased high density lipoprotein-cholesterol levels in men, but not in women. This observation suggests that the -514C to T polymorphism may diminish the response of hepatic lipase to androgens. To test this hypothesis, five -514T and five -514C homozygous men were treated with the anabolic steroid stanozolol for 6 days. The mean increase in hepatic lipase activity was similar in the two groups (45+/-10 vs. 51+/-10 mmol x hr(-1) x l(-1), P = 0.5). To evaluate the association between the -514 polymorphism and hepatic lipase activity at different physiological androgen concentrations, hepatic lipase genotypes and activities were measured in 44 men and 40 premenopausal women. The effect of the -514T allele on hepatic lipase activity was significant and quantitatively similar in both sexes. These data indicate that the -514 polymorphism does not influence the response of hepatic lipase activity to androgens, and that the effects of this polymorphism on hepatic lipase activity are independent of androgen action.     

Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy?

The -514 polymorphism in the hepatic lipase gene (LIPC) is associated with decreased hepatic lipase activity. In the present study, the interaction between body mass index (BMI), the -514 polymorphism, and hepatic lipase activity was examined in 118 white men and in 51 African American men. BMI was significantly positively correlated with hepatic lipase activity in both populations. BMI was similar in men with genetic differences in hepatic lipase activity, indicating that high hepatic lipase activity did not cause increased BMI. The data therefore suggest that high BMI leads to increased hepatic lipase activity. The actions of BMI and the -514 polymorphism on hepatic lipase activity appear to be additive and independent, rather than synergistic. This finding indicates that hepatic lipase activity is a multifactorial trait, determined in part by polymorphism within the LIPC gene as well as by factors that influence BMI.     

Fat distribution and insulin response in prepubertal African American and white children

Ethnic differences in obesity-related disease prevalence may relate to differences in fat distribution or metabolism. We conducted a study in 73 African American and white children to examine the relation between fat distribution and insulin and to determine whether ethnic differences in fat distribution or in adiposity-insulin relations contribute to differences in insulin concentrations. Fasting and postchallenge insulin concentrations were determined by oral-glucose-tolerance test, total body fat by dual-energy X-ray absorptiometry, and subcutaneous abdominal (SAAT) and intraabdominal (IAAT) adipose tissue by computerized tomography. African Americans had greater fasting insulin (x +/- SD: 79 +/- 37 compared with 55 +/- 23 pmol/L, P < 0.01), incremental 30-min insulin (567 +/- 438 compared with 300 +/- 304 pmol/L, P < 0.001), and incremental area under the insulin curve (AUC; 262 +/- 209 compared with 164 +/- 156 pmol/L, P < 0.01). In multiple linear regression, fasting insulin was independently related to total fat within both ethnic groups (model R2 = 0.42 and 0.52 for African Americans and whites, respectively), incremental 30-min insulin to total fat and IAAT in whites only (model R2 = 0.71), and AUC to SAAT in African Americans only (model R2 = 0.49). Adjusting insulin indexes for adiposity did not eliminate the significant effect of ethnicity. In general, relations between adiposity and insulin were stronger in whites than in African Americans. African American children had higher insulin concentrations than white children after total body fat, IAAT, and SAAT were controlled for. However, strong relations between adiposity (total and abdominal) and insulin in both groups suggest that obesity may contribute to disease risk regardless of ethnicity.     

Short-term effects of a high-sucrose diet on plasma lipid, lipoprotein cholesterol, tissue lipoprotein lipase and hepatic triglyceride lipase in rats

Short-term (2 weeks) effects of a high-sucrose diet on plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities were investigated in rats. Three days of sucrose feeding significantly increased plasma TG (42 +/- 3 mg/dl vs. 56 +/- 2 mg/dl, p = 0.032), while TC increased significantly after 10 days of the diet (50 +/- 2 mg/dl vs. 62 +/- 2 mg/dl, p = 0.0001). HDL-C increased significantly after 3 days of sucrose feeding (36.2 +/- 0.9 mg/dl vs. 42.4 +/- 2.7 mg/dl, p = 0.011). Although LDL-C tended to decrease on days 3, 7 and 10, these changes were not significant. The plasma glucose level did not change during the study. Increased LPL activity in adipose tissue and decreased enzyme activities in skeletal and heart muscles were observed. Adipose tissue LPL returned to the baseline value after 14 days of the diet treatment, while LPL in skeletal and heart muscles remained at the decreased level. HTGL and HTGL/total liver lipase activities were significantly increased after 14 days of the diet. The different responses of lipase activities in various tissues may help to regulate serum lipid and lipoprotein levels in sucrose-fed rats.     

Differences between African American and Caucasian men participating in a community-based prostate cancer screening program

Prostate cancer is a major contributor to morbidity and mortality in the male population, but public awareness of the cancer has been reported as minimal. We evaluated the effectiveness of an educational prostate cancer screening program on 944 men in a midwest urban community. Digital rectal examinations and PSA blood tests were provided at no charge to participants with a grant from the Michigan Department of Community Health. An educational intervention that stressed the importance of prostate cancer early detection and treatment was conducted before screenings. A brief questionnaire administered before and after the videotape and screenings, targeted both knowledge and attitudes concerning prostate cancer. Pre-test results revealed that African American men were significantly (t = 3.7, P = .00) less likely then white men to correctly identify early symptoms of prostate cancer and the basic components of a prostate checkup. Following program involvement, scores significantly improved in all areas and differences were no longer significant between the races. Racial differences were also found for screening preferences and modes of reaching men to participate in screening. African American men were twice as likely as white men to choose private appointments over mass screening (OR = 2.2, P = .00). Radio reached the most African Americans (25%) while newspaper reached the most Caucasians (34%). The decreased level of knowledge among African Americans regarding prostate etiology and clinical factors highlights the need for educational programs to target minority populations. The need for discretion also applies by providing minority-favored access with screening through private appointments.     

Identification of the source of reagent variability in the xanthydrol/urea method

The purpose of this study was to compare seven skinfold equations with underwater weighing (UWW) for estimating body fat in 39 African American [age: 22.8 +/- 3.6 y (x +/- SD); weight: 59.6 +/- 8.3 kg) and 39 white (age: 22.1 +/- 2.9 y; weight: 61.7 +/- 7.3 kg) women. The hypothesis examined was that the equations would produce more accurate body fat estimates in white women, but would be appropriate for use in African American women. Body fat estimated from two quadratic, three linear, and two logarithmic skinfold equations was compared with body fat estimated from UWW; the same procedures were used to evaluate the results in both African Americans and whites. The data were analyzed by using t tests, analysis of variance, Scheffé's honestly significant difference tests, correlations, error assessments, and agreement. The results showed that total error, SEE, and SD values were larger in the African American women than in the white women and were not within acceptable limits listed in the literature. The correlation coefficients were lower in the African American women than in the white women. Agreement between the skinfold equations and UWW, based on deviations from mean differences, was better in the white women. In conclusion, the skinfold prediction equations evaluated in this study were more variable and produced more error when used in African American women. Therefore, population-specific equations for African American women should be used to estimate body fat because they will probably yield more accurate estimates.     

Lipoprotein lipase activity and plasma triglyceride clearance are elevated in endurance-trained women

Numerous studies have examined factors regulating high-density lipoprotein cholesterol (HDL-C) levels in male endurance athletes, but few studies have examined HDL-C regulation in female athletes. The present study compared lipid and lipoprotein concentrations, postheparin lipolytic activities, and the clearance rate (K2) of triglycerides following an intravenous fat infusion in 12 female distance runners (aged 33 +/- 9 years, mean +/- SD) and 13 sedentary women (33 +/- 9 years). Runners were leaner and had greater maximum oxygen uptake values than controls. Runners also had nonsignificantly lower triglyceride (53 +/- 15 v 65 +/- 13 mg/dL) and higher HDL-C (62 +/- 14 v 52 +/- 8 mg/dL, P = .06). Lipoprotein lipase activity (LPLA) was 33% greater (P < .05) and fat clearance (K2) was 27% faster (P < .01) in the trained women, and LPLA correlated directly with K2 (r = .61) and HDL-C (r = .62) in this group (P < .05 for both). K2 was directly related to HDL-C in the athletes (r = .57, P = .06), and also when the active and sedentary women were combined (r = .43, P < .05). These results suggest that increased LPLA and enhanced plasma triglyceride clearance may contribute to the HDL-C levels of physically active premenopausal women.     

Effects of leptin adipose tissue lipoprotein lipase in the obese ob/ob mouse

OBJECTIVE: To characterize the adaptations of lipid metabolism, with special emphasis on tissue lipoprotein lipase, to negative energy balance brought by chronic treatment of obese ob/ob mice with leptin. DESIGN: According to a 2 x 2 factorial analysis, lean and obese C57BL/6J mice were subcutaneously infused with leptin (100 micrograms.kg-1.day-1) or vehicle (phosphate-buffered saline) during seven days. RESULTS: Cumulative food intake and final body weight of vehicle-infused obese mice were twofold higher than in lean controls. Leptin decreased cumulative food intake and body weight of obese, but not lean mice. Lipoprotein lipase (LPL) activity in white inguinal and epididymal and brown interscapular adipose tissues of control obese mice was at least twofold higher than in lean mice, but comparable in the vastus lateralis muscle. Leptin treatment of obese mice significantly lowered LPL activity to that of lean mice in all tissues examined. Vehicle-infused obese mice had higher liver triglyceride content and were hypertriglyceridemic compared to lean mice, and triglyceride concentrations in plasma and liver were decreased proportionally after leptin treatment. Leptin lowered glycemia and insulinemia of obese mice to lean levels and decreased plasma corticosterone. Leptin infusion had no notable effect on tissue lipoprotein lipase nor plasma variables of lean mice. CONCLUSIONS: Leptin infusion abolished hyperinsulinemia in the ob/ob mouse, an effect that was probably responsible for the concomitant normalization of adipose LPL activity. This study shows that decreased LPL activity, plasma triglyceride concentrations and hepatic triglyceride production constitute some of the adaptive peripheral adaptations of lipid metabolism, which accompany the reduction in fat mass accretion brought by leptin treatment of the obese ob/ob mouse.     

Common variants in the promoter of the hepatic lipase gene are associated with lower levels of hepatic lipase activity, buoyant LDL, and higher HDL2 cholesterol

Increased hepatic lipase (HL) activity is associated with small, dense, low density lipoprotein (LDL) and low high density lipoprotein2 (HDL2) cholesterol (-C) levels. A polymorphism in the promoter region of the HL gene (LIPC) is associated with HDL-C levels. To test whether this association is mediated by differences in HL activity between different LIPC promoter genotypes, the LIPC promoter polymorphism at position -250 (G-->A), HL activity, LDL buoyancy, and HDL-C levels were studied in white normolipidemic men and men with coronary artery disease (CAD). The less common A allele (frequency=0.21 and 0.25 in normal and CAD subjects, respectively) was associated with lower HL activity (P<0.005 by ANOVA) and buoyant LDL particles (P相似文献   

Lipoprotein lipase gene mutations D9N and N291S in four pedigrees with familial combined hyperlipidaemia

The role of the lipoprotein lipase (LPL) gene in familial combined hyperlipidaemia (FCH) is unclear at present. We screened a group of 28 probands with familial combined hyperlipidaemia and a group of 91 population controls for two LPL gene mutations, D9N and N291S. LPL-D9N was found in two probands and one normolipidaemic population control. LPL-N291S was found in four probands and four population controls. Subsequently, two pedigrees from probands with the D9N mutation and two pedigrees from probands with the N291S mutation were studied, representing a total of 24 subjects. Both LPL gene mutations were associated with a significant effect on plasma lipids and apolipoproteins. Presence of the D9N mutation (n = 7) was associated with hypertriglyceridaemia [2.69 +/- 1.43 (SD) mmol L-1] and reduced plasma high-density lipoprotein cholesterol (HDL-C) concentrations (0.92 +/- 0.21 mmol L-1) compared with 11 non-carriers (triglyceride 1.75 +/- 0.64 mmol L-1; HDL-C 1.23 +/- 0.30 mmol L-1, P = 0.03 and P = 0.025 respectively). LPL-D9N carriers had higher diastolic blood pressures than non-carriers. LPL-N291S carriers (n = 6) showed significantly higher (26%) apo B plasma concentrations (174 +/- 26 mg dL-1) than non-carriers (138 +/- 26 mg dL-1; P = 0.023), with normal post-heparin plasma LPL activities. Linkage analysis revealed no significant relationship between the D9N or N291S LPL gene mutations and the FCH phenotype (hypertriglyceridaemia, hypercholesterolaemia or increased apo B concentrations). It is concluded that the LPL gene did not represent the major single gene causing familial combined hyperlipidaemia in the four pedigrees studied, but that the LPL-D9N and LPL-N291S mutations had significant additional effects on lipid and apolipoprotein phenotype.     

Myelosuppressive changes from single or repeated doses of radioantibody therapy: effect of bone marrow transplantation, cytokines, and hematopoietic suppression

Apolipoprotein E phenotype (APOE phenotype) has been demonstrated to be a genetic determinant of cardiovascular disease. This atherogenicity may be a reflection of the association of APOE phenotype and plasma lipoprotein concentrations. The Coronary Artery Risk Development in Young Adults (CARDIA) Study affords the opportunity to assess the frequency of apolipoprotein E alleles in population-based samples of African Americans and whites in the United States and to compare the associations of APOE phenotype with lipoprotein and apoprotein concentrations. Data from 3,485 African-American and white men and women between the ages of 25 and 37 years who attended the fourth CARDIA Study examination in 1992-1993 were used in this analysis. African-American men and women had significantly higher frequencies of E2 and E4 phenotype and thus higher frequencies of *epsilon2 and *epsilon4 alleles (p < 0.005). Men and women of both races with APOE4 phenotype generally had higher low density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a) concentrations and lower high density lipoprotein cholesterol concentration, and individuals with APOE3 phenotype had the lowest triglyceride concentration. Major differences between African Americans and whites were observed in the distribution of APOE phenotypes and *epsilon alleles, but APOE phenotype was associated with similar differences in lipoprotein and apoprotein concentrations in both races. The data suggest that APOE phenotype may be a risk factor for cardiovascular disease in both African Americans and whites because it is associated similarly with an adverse lipoprotein profile.     

Central markers of body fat distribution are important predictors of plasma lipids in elderly men and women

We determined the contribution of body fat distribution, peak VO2, fat mass, and dietary intake to variation in plasma lipids in elderly individuals. Volunteers were a healthy cohort of older Caucasian women (n = 75, mean age +/- SD, 72 +/- 5 years) and older men (n = 101, 72 +/- 5 years). We determined fat mass from underwater weighing, fat patterning from waist circumference, as well as peripheral and truncal skinfolds, exercise capacity from peak VO2, and dietary intake from three-day food diaries. Plasma lipid levels were measured in the fasting state and included total cholesterol, high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), and fasting triglycerides. Older women weighted less than older men, but had higher fat mass, truncal, and peripheral skinfolds. Waist circumference and peak VO2 were lower in older women than older men. Older women had higher total cholesterol (217 +/- 31 vs. 197 +/- 30; p < 0.01), HDL-C (54 +/- 12 vs. 49 +/- 14; p < 0.05), and LDL-C (133 +/- 26 vs. 121 +/- 27; p < 0.01) when compared with older men. No gender differences were noted in fasting triglycerides. Truncal skinfolds were the best predictor of plasma lipids in older men, accounting for between 9% and 30% (r2) of the variation in plasma lipids. Similarly, in older women, central markers of fatness (i.e., waist circumference and truncal skinfolds) were the best predictors of plasma lipids (r2 = 3% to 24%). Total fat mass, peak VO2 and dietary intake were not independent predictors of plasma lipids in older men and women. Indices of central body fatness, rather than total fat mass, peak VO2 or dietary intake are stronger predictors of plasma lipids in healthy older men and women.     

Diltiazem concentrations in plasma vs PR intervals on electrocardiogram in 8 men

AIM: To develop an acute tolerant model in describing relationship between diltiazem (Dil) concentrations in plasma and PR intervals on ECG in men. METHOD: Both plasma concentrations of Dil and changes of ECG were simultaneously determined after po Dil 90 mg in 8 men. RESULTS: A two-compartmental pharmacokinetic model with first-order input gave a good fitting for the plasma concentration of Dil. Corresponding pharmacokinetic parameters were estimated: t1/2 beta, 5.9 +/- 1.0 h; MRT, 15.9 +/- 1.0 h; t0, 0.38 +/- 0.07 h; tmax, 2.7 +/- 0.4 h, and Cmax, 161 +/- 60 micrograms.L-1. The good fittings for plasma concentration-effect data were obtained with tolerant model E = S x C/(1 + T/T50). The pharmacodynamic parameters were given as follows: S, 829 +/- 293 s.g-1.L; Kt0, 0.037 +/- 0.024 h-1 and T50, 10 +/- 4 micrograms.L-1. CONCLUSION: Relationship between Dil concentrations in plasma and PR interval changes in men after po 90 mg was described using an acute tolerant model.     

Physical activity and plasma lipoprotein lipid concentrations in men

Twenty-three apparently normal untrained men aged 20--55 participated in a 4-month self-regulated training programme ending in a marathon run. Fasting plasma and lipoprotein lipid concentrations, adipose tissue lipoprotein lipase activity, anthropometric data, alcohol consumption, smoking habits, weekly mileage run and performance on a bicycle ergometer were recorded before and after the training period. Training induced an increase in high density lipoprotein cholesterol (HDL-C) concentration which was not directly related to concomitant decreases in mean very low density lipoprotein cholesterol (VLDL-C) concentration or mean total skinfold thickness. The degree of the changes in VLDL lipids and HDL-C levels were related to pretraining values, and changes in HDL-C and VLDL triglycerides (VLDL-TG) were also associated. Initial total skinfold thickness correlated inversely with the change in VLDL-TG levels during training. The pretaining concentration of VLDL-C was related to the corresponding value for HDL-C after training. The magnitude of exercise-induced changes in VLDL-C and HDL-C levels are more related to pre-training levels than to changes in measured exercise parameters, indices of obesity or adipose tissue lipoprotein lipase activity. However, the level of adiposity of subjects at the beginning of the study influenced the response of VLDL-TG levels to increased physical activity. The data suggest that VLDL contributes to the increase in HDL-C levels with exercise but is not the major source of the increment.     

Ethnic differences in electrocardiographic left ventricular hypertrophy in young and middle-aged employed American men

In the United States population, black men have higher prevalence rates of electrocardiographic (ECG) high QRS voltage, more ST-segment and T-wave abnormalities, and more ECG left ventricular hypertrophy (LVH) than do white men. Reasons for these differences have not been fully elucidated. The prevalence rate of ECG LVH and associated characteristics were compared in black and white men in the Chicago Heart Association Detection Project in Industry population study. Data were from 1,391 black men and 19,126 white men (age range 20 to 64 years) employed by 84 Chicago organizations. ECG LVH was defined by the presence of both high QRS (Minnesota code 3.3) and ST-T abnormality (code 4.1-4.3 or 5.1-5.3). Black men had a significantly higher prevalence rate of ECG LVH than did white men in each 15-year age group (15.9 vs 2.4, 14.6 vs 2.8, and 35.7 vs 12.5/1,000 in the 20- to 34-, 35- to 49-, and 50-to 64-year age groups, respectively; p < 0.01 for each comparison). Multiple logistic regression analyses indicated that systolic blood pressure and age were associated positively with ECG LVH (p < 0.01) in both black and white men. Men with history of hypertension and receiving drug treatment had a greater likelihood of having ECG LVH than did those with history of hypertension but not receiving drug treatment, possibly because those with more severe hypertension were more likely to have been prescribed medication. Serum cholesterol, cigarettes smoked/day, 1-hour post-load plasma glucose and education were not consistently related to ECG LVH.(ABSTRACT TRUNCATED AT 250 WORDS)     

African American-white differences in lipids, lipoproteins, and apolipoproteins, by educational attainment, among middle-aged adults: the Atherosclerosis Risk in Communities Study

Measures of socioeconomic status have been shown to be related positively to levels of high density lipoprotein (HDL) cholesterol in white men and women and negatively in African American men. However, there is little information regarding the association between educational attainment and HDL fractions or apolipoproteins. The authors examined these associations in 9,407 white and 2,664 African American men and women aged 45-64 years who participated in the Atherosclerosis Risk in Communities Study baseline survey, and they found racial differences. A positive association for HDL cholesterol, its fractions HDL2 and HDL3 cholesterol, and its associated apolipoprotein A-I was found in white men and white women, but a negative association was found in African American men, and there was no association in African American women. In whites, there was also an inverse association of low density lipoprotein (LDL) cholesterol and apolipoprotein B with educational attainment. With the exception of African American men, advanced education was associated with a more favorable cardiovascular lipid profile, which was strongest in white women. Racial differences in total cholesterol (women only), plasma triglycerides, LDL cholesterol, apolipoprotein B (women only), HDL cholesterol, HDL2 and HDL3 cholesterol, and apolipoprotein A-I were reduced at higher levels of educational attainment. Apart from triglycerides in men and HDL3 cholesterol in women, these African American-white lipid differences associated with educational attainment remained statistically significant after multivariable adjustment for lifestyle factors. Lipoprotein(a) showed no association with educational attainment. These findings confirm African American-white differences in lipids, lipoproteins, and apolipoproteins across levels of educational attainment that were not explained by conventional nondietary lifestyle variables. Understanding these differences associated with educational attainment will assist in identifying measures aimed at prevention of cardiovascular disease.     

Proton magnetic resonance spectroscopy of linear nevus sebaceus syndrome

OBJECTIVE: The potential effect of ethnicity on the serum lipid profile and lipoprotein(a) [Lp(a)] was studied in a population with chronic spinal cord injury (SCI). STUDY DESIGN: The distribution and correlates of high density lipoprotein (HDL) cholesterol and Lp(a) were studied in a population of 600 subjects with chronic SCI. RESULTS: Mean +/- SEM serum HDL cholesterol was significantly higher in the African American group than in the white and Latino groups (47 +/- 1 vs 40 +/- 1 and 38 +/- 1 mg/dL, p < .0001, respectively). The African American group had a lower serum total to HDL cholesterol ratio than white and Latino groups (4.46 +/- .153 vs 5.18 +/- .168 and 5.40 +/- .140 mg/dL, p < .01, respectively). Mean serum Lp(a) levels were significantly higher in the African American group than in Latino or white groups (29 +/- 2 vs 18 +/- 1 and 15 +/- 1 mg/dL, p < .0001, respectively). Age, duration of SCI, and level and completeness of lesion had no significant effect on serum Lp(a) level. CONCLUSIONS: In a population with chronic SCI, those in the African American group had the highest serum HDL cholesterol concentrations, the lowest serum total to HDL cholesterol ratios, and elevated levels of serum Lp(a) compared with the Latino and white groups. In a population of individuals with chronic SCI, ethnicity was shown to have a major effect on serum lipids and may be used to assist in the determination of cardiovascular risk.     

Breast carcinoma survival analysis for African American and white women in an equal-access health care system

BACKGROUND: This retrospective review of breast carcinoma cases in the Department of Defense (DoD) Central Tumor Registry evaluated differences in survival patterns between African American and white women treated in U.S. military health care facilities. The study examined the effects of age, stage of cancer, tumor size, grade, lymph node involvement, waiting time between diagnosis and first treatment, marital status, military dependent status, alcohol usage, tobacco usage, and family history of cancer. METHODS: Researchers reviewed the tumor registry records of 6577 women (5879 whites and 698 African Americans) diagnosed with breast carcinoma. The patients, ages 19-97 years, were diagnosed between 1975 and 1994. A hazard ratio (relative risk of mortality) model compared African American and white patients, adjusting for various combinations of covariates; impact of independent variables on the risk of death; prognostic factors significantly associated with survival; disease free and overall survival times; effects of ethnicity, stage, and age on survival; and trends in stage at diagnosis. A P value (2-sided) of less than 0.05 was considered statistically significant. RESULTS: After adjustment for age, the risk of death was 1.45 (95% confidence interval [CI], 1.20-1.76) times greater for African American women than for white women. Adjustment for stage reduced the risk to 1.41 (95% CI, 1.16-1.70); further adjustment for demographic variables and most clinical variables had no effect. Still, African American women treated in the military health care facilities had a better survival rate than African American women represented in the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In our study, the 5-year risk of death, from any cause, was 1.37 for African American women with breast carcinoma; in other words, the mortality rate for African American women was 24.77% compared with 18.08% for white women. In the latest SEER data, the 5-year relative risk of death for African American women compared with white women is 1.86. The mortality rate in SEER is 34.2% for African American women and 18.4% for white women. The survival rate for white DoD beneficiaries is comparable to that for white women in SEER. CONCLUSIONS: These observations suggest that ready access to medical facilities and the full complement of treatment options that are standard for all DoD patients improve survival rates for African American women. However, a significant unexplained difference in survival still exists between African American and white military beneficiaries.     

Racial differences in rate of CD4 decline in HIV-1-infected homosexual men

OBJECTIVE: To determine whether racial differences exist in the rate of CD4 lymphocyte decline in HIV-1-infected homosexual men. DESIGN: Prospective cohort study. STUDY POPULATION: Non-Hispanic white (n = 321) and black (n = 102) HIV-1-seropositive homosexual and bisexual men were recruited from the Baltimore/Washington, DC metropolitan areas between 1984-1985 and 1987-1990, and evaluated semiannually. MAIN MEASUREMENTS: Changes in CD4 lymphocyte count and CD4 percentage over time were analysed using linear regression methods for the 271 white and 69 black participants who had at least four semiannual CD4 lymphocyte measurements. RESULTS: Rate of decline in CD4 lymphocyte count over 6 months was much slower among black than white seroprevalent men at all levels of baseline CD4 count (baseline 201-400 x 10(6)/l: + 0.24 versus -17.7 x 10(6)/l; 401-600 x 10(6)/l: -11.3 versus -23.9 x 10(6)/l; 601-800 x 10(6)/l: -15.1 versus -35.2 x 10(6)/l; > 800 x 10(6)/l: -4.3 versus -42.7 x 10(6)/l for black versus white, respectively), although this was only statistically significant for the lowest and highest strata of baseline CD4 count. These racial differences persisted after adjustment for recruitment period (1984-1985 or 1987-1990), follow-up duration, age and zidovudine therapy or Pneumocystis carinii pneumonia prophylaxis. Similar findings were observed among the 70 white and 11 black seroconverters. Black participants were also less likely than a subgroup of white participants matched on baseline CD4 lymphocyte count to be HIV-1 p24 antigen-positive. However, after acid dissociation of samples initially p24 antigen-negative, there were no significant differences in the prevalence of p24 antigenemia at enrollment or after 1 year of follow-up. CONCLUSIONS: This analysis suggests a more gradual decline in CD4 lymphocyte count among black than white Americans. The clinical significance of and reasons for this are unclear, but the lower prevalence of p24 antigenemia due to immune complexing among black Americans suggests that racial differences in the immune response to HIV may exist. Additional studies are needed to validate these findings in a larger cohort of non-whites, and to assess their relationship with other measures of cell-mediated immune function.