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J Coresh

Publications and source records attributed to J Coresh.

At least 37 records · Page 2Linked to original sources
PubMed1999

Risk factors for hypercreatinemia in patients with systemic lupus erythematosus.

Renal insufficiency is one of the most severe outcomes of systemic lupus erythematosus (SLE). The aim of this study was to identify baseline predictors of the development of renal insufficiency in a cohort of patients with SLE. 281 patients from the The Hopkins Lupus Cohort (HLC) enrolled between 1987-1994 were followed for the occurrence of renal insufficiency, defined as a serum creatinine 1.6 mg/dl for men and 1.4 mg/dl for women. Over a mean (+/-s.d.) of 3. 3+/-2.1 y of follow up, 46 (16%) of the 281 patients developed renal insufficiency. Using a multivariate Cox proportional hazard model, we found the risk of renal insufficiency associated with younger (0-19 y) or older (40 y) age at baseline (relative risk (95% CI) 5.1 (1.4, 18.8) and 4.1 (2.1, 8.2)) and longer duration of SLE before referral to the cohort (RR 1.25 [1.05, 1.5] for every five years). Additional predictive variables were borderline elevation of serum creatinine at baseline (RR 3.1 (1.4, 6.6) for a serum creatinine 1. 4-1.5 mg/dl for men and 1.2-1.3 mg/dl for women), and mean proteinuria (RR 3.6 (1.8, 7.4) for trace-3+ and 10.6 (3.8, 30.0) for 3+ (urine dipstick level)). Socioeconomic status, race, autoantibodies and complement were not significantly associated with the risk of renal insufficiency. This study supports early referral of SLE patients to rheumatologists and emphasizes the importance of early signs of renal involvement as predictors of later renal insufficiency in SLE patients.

Adolescent↗
PubMed1999

Variants of the insulin receptor substrate-1 and fatty acid binding protein 2 genes and the risk of type 2 diabetes, obesity, and hyperinsulinemia in African-Americans: the Atherosclerosis Risk in Communities Study.

We conducted a community-based case-control study of African-American men and women in the Atherosclerosis Risk in Communities Study. The allele frequencies of the Gly972Arg variant of the insulin receptor substrate-1 (IRS-1) gene and the Ala54Thr variant of the fatty acid binding protein 2 (FABP2) gene were compared in 992 normal control subjects and three patient groups: 1) 321 type 2 diabetic individuals, 2) 260 severely obese individuals, and 3) 258 markedly hyperinsulinemic individuals without diabetes. Allele frequencies of Gly972Arg IRS-1 and Ala54Thr FABP2 were 0.07 and 0.22, respectively; there were no differences in allele or genotype frequencies between patients and control subjects for either gene variant. In weighted linear regression of all patients and control subjects, the presence of the IRS-1 gene variant was associated with a 0.85 (0.42) kg/m2 higher BMI (P = 0.04). In addition, individuals with at least one IRS-1 Arg972 allele and two FABP2 Thr54 alleles had a BMI of 33.3 (7.9) kg/m2, compared with 30.0 (6.3) kg/m2 for those with neither allele (P = 0.05). These results suggest that in African-Americans, these variants in the IRS-1 and FABP2 genes are not associated with the risk of type 2 diabetes, severe obesity, or marked hyperinsulinemia, but that their independent and joint effects may be associated with small increases in BMI.

Arteriosclerosis↗
PubMed1998

Segregation analysis of two-locus models regulating apolipoprotein-A1 levels.

For quantitative traits associated with risk to complex diseases, such as heart disease, single major locus models are likely to be too simplistic. Currently, researchers have begun to use oligogenic models of inheritance, but the resolving power of these models remains to be determined. As the major apoprotein of high density lipoprotein (HDL), apolipoprotein A1 (apo-A1) is generally accepted as a protective factor for coronary artery disease. Although familial aggregation of apo-A1 levels has been reported, the mode of inheritance of apo-A1 remains ill defined. In the present study, we conducted a segregation analysis comparing a series of one-locus and two-locus univariate models for apo-A1 levels in a sample of 137 families ascertained through probands undergoing elective, diagnostic coronary angiography. A two-locus Mendelian model fit these data significantly better than any one-locus model. The incorporation of the second major locus into the model of inheritance leads to a significant improvement in the fit, and a significant decrease of the residual heritability. The best-fitting model included two loci with a reciprocal pattern of epistasis generating 4 distinct genotypic distributions. Taken together, these two major loci account for 58% of the variance of adjusted apo-A1 levels. This demonstration of a second major locus controlling apo-A1 levels may explain the equivocal results obtained from previous studies. This two-locus model may be more powerful for linkage analysis to map one or both of these quantitative trait loci.

Apolipoprotein A-I↗
PubMed1998

Serum creatinine levels in the US population: third National Health and Nutrition Examination Survey.

This report describes the distribution of serum creatinine levels by sex, age, and ethnic group in a representative sample of the US population. Serum creatinine level was evaluated in the third National Health and Nutrition Examination Survey (NHANES III) in 18,723 participants aged 12 years and older who were examined between 1988 and 1994. Differences in mean serum creatinine levels were compared for subgroups defined by sex, age, and ethnicity (non-Hispanic white, non-Hispanic black, and Mexican-American). The mean serum creatinine value was 0.96 mg/dL for women in the United States and 1.16 mg/dL for men. Overall mean creatinine levels were highest in non-Hispanic blacks (women, 1.01 mg/dL; men, 1.25 mg/dL), lower in non-Hispanic whites (women, 0.97 mg/dL; men, 1.16 mg/dL), and lowest in Mexican-Americans (women, 0.86 mg/dL; men, 1.07 mg/dL). Mean serum creatinine levels increased with age among both men and women in all three ethnic groups, with total US mean levels ranging from 0.88 to 1.10 mg/dL in women and 1.00 to 1.29 mg/dL in men. The highest mean creatinine level was seen in non-Hispanic black men aged 60+ years. In the total US population, creatinine levels of 1.5 mg/dL or greater were seen in 9.74% of men and 1.78% of women. Overall, among the US noninstitutionalized population, 10.9 million people are estimated to have creatinine values of 1.5 mg/dL or greater, 3.0 million have values of 1.7 mg/dL or greater, and 0.8 million have serum creatinine levels of 2.0 mg/dL or greater. Mean serum creatinine values are higher in men, non-Hispanic blacks, and older persons and are lower in Mexican-Americans. In the absence of information on glomerular filtration rate (GFR) or lean body mass, it is not clear to what extent the variability by sex, ethnicity, and age reflects normal physiological differences rather than the presence of kidney disease. Until this information is known, the use of a single cutpoint to define elevated serum creatinine values may be misleading.

Adolescent↗
PubMed1998

Creatinine clearance as a measure of GFR in screenees for the African-American Study of Kidney Disease and Hypertension pilot study.

Serum creatinine and endogenous creatinine clearance (CrCl) are widely used measures of renal function. This study compares the precision, bias, and sources of error in using different CrCl measures to estimate the glomerular filtration rate (GFR) in 118 men and women screened for the African-American Study of Kidney Disease and Hypertension (AASK) pilot study. We measured serum creatinine, 24-hour CrCl, and CrCl during timed clearance periods conducted simultaneously with an 125I-iothalamate GFR study. Serum creatinine was measured using two different kinetic rate Jaffe methods (CX3 and Hitachi). After standardization for body surface area, the different measures of renal function available for each individual were compared with the 125I-iothalamate GFR simultaneous to the CrCl. In a subset of 50 participants, the CrCl measures were compared with a follow-up GFR (fGFR). The mean 125I-iothalamate GFR was 65.2 (SD, 26.4), with a range of 11 to 122 mL/min/1.73 m2. The mean +/- SD percentage differences from the GFR were -9%+/-22% for the Cockcroft-Gault estimated CrCl, 1%+/-29% for the 24-hour CrCl, and 8%+/-16% for the CX3 simultaneous CrCl. The Hitachi method overestimated serum creatinine and underestimated GFR. Compared with an fGFR, the mean +/- SD differences were 2%+/-19% for the first GFR, -6%+/-20% for the Cockcroft-Gault estimated CrCl, 10%+/-28% for the 24-hour CrCl, and 14%+/-29% for the CX3 simultaneous CrCl. Thus, the increased precision with which the timed CrCl predicted its simultaneous GFR did not extend to improved ability to predict a future GFR. The fractional excretion of creatinine, measured as the ratio of the CX3 simultaneous CrCl to 125I-iothalamate clearance, increased with decreasing GFR but was lower than expected (mean +/- SD of 1.21+/-0.16 for GFRs between 20 and 40 mL/min/1.73 m2). The lower fractional excretion explains why the 24-hour and Cockcroft-Gault CrCls did not overestimate GFR, but the reasons for this lower excretion are uncertain. Creatinine assay specificity and calibration are important sources of variability that must be examined in any CrCl measure of GFR. We conclude that despite requiring substantially more time and effort, neither the outpatient 24-hour urine nor the timed CrCl offered increased precision over a calculation based on serum creatinine, sex, age, and weight in predicting GFR.

Black People↗
PubMed1998

Familial aggregation of renal disease in a population-based case-control study.

Family history of renal disease has been associated with an increased risk of end-stage renal disease (ESRD). It is uncertain whether this risk is mediated by familial aggregation of risk factors for ESRD, such as diabetes and hypertension. The association of ESRD with familial aggregation of renal disease was examined in a large, population-based case-control study conducted in Maryland, Virginia, West Virginia, and Washington, DC. The number of first-degree relatives who were affected with any type of renal disease was compared between 689 newly treated ESRD patients registered in the Medicare ESRD program (92% of all eligible incident cases presenting between January and July of 1991) and 361 control subjects without ESRD who were selected by random-digit dialing (90% response rate). Patients and control subjects were frequency matched by age; patients with ESRD caused by polycystic kidney disease and other known hereditary kidney diseases were excluded. Analysis was conducted using multiple logistic regression. After controlling for the proband's age, gender, race, family size, socioeconomic status, and personal and family histories of diabetes and hypertension, having one first-degree relative with renal disease increased the odds of ESRD by 1.3 (95% confidence interval, 0.7 to 2.6) and having two or more affected first-degree relatives increased the odds of ESRD by 10.4 (95% confidence interval, 2.7 to 40.2). These data support familial aggregation of renal disease in excess of that predicted by clustering of diabetes and hypertension within families, suggesting that either genetic susceptibility or environmental exposures shared within families increase the risk of developing ESRD. This risk is also much higher when two or more first-degree relatives have renal disease. Unraveling the molecular basis of this increase in risk may provide new avenues for treatment and prevention of ESRD.

Adult↗
PubMed1998

Epidemiology of cardiovascular risk factors in chronic renal disease.

Treatment and prevention of cardiovascular disease in the general population has benefited greatly from the identification of cardiovascular disease risk factors. Given the particularly high risk of cardiovascular disease and total mortality among patients with chronic renal insufficiency (CRI) and end-stage renal disease (ESRD), it is important to assess the role of traditional and nontraditional risk factors for cardiovascular disease. This review discusses the foundations of risk factor epidemiology and briefly summarizes the evidence regarding cardiovascular risk factors in renal disease. Diabetes and hypertension have a very high prevalence in patients with CRI. Patients with CRI and ESRD also have a higher frequency of cardiac dysfunction and left ventricular hypertrophy, which further increase the risk of cardiovascular disease. Finally, patients with renal disease have a higher prevalence of less established risk factors, including low HDL, and high triglycerides, lipoprotein(a), and homocysteine, where prospective studies and clinical trials are needed to provide a scientific basis for reduction of cardiovascular risk among patients with renal disease.

Cardiovascular Diseases↗
PubMed1997

A comprehensive analysis of complex traits in problem 2A.

We used descriptive analysis to investigate the relationship between affection status and five quantitative traits (Q1-Q5) in Problem 2A and results suggested the five quantitative traits fall into two groups. The first group comprised three strongly correlated traits, Q1-Q3, which underlie affection status, and the second group comprised Q4 and Q5, which are not directly related to affection status. Segregation and linkage analyses of traits Q1-Q3 and affection status from the first replicate detected one of the major loci for Q1 (MG1) linked to marker 14 on chromosome 5 (D5G14). Because our segregation analysis failed to show evidence of a major locus effect on Q2, and we overlooked the interaction between MG3 and sex, we did not detect either MG2 or MG3. Using Haseman-Elston sib-pair analysis [Haseman and Elston, 1972], we also examined the statistical power of Q1 and type I error rate (using the environmental factor as an index), for the remaining 199 replicates in the context of a genome screen.

Chromosome Mapping↗
PubMed1997

Further trends in the etiology of end-stage renal disease in African-Americans.

Publications in the past year have continued to shed light on the etiology of the excess risk of end-stage renal disease end-stage renal disease among African-Americans. Prospective data now show that even mild elevations in blood pressure are associated with an increased risk of end-stage renal disease. The prevalence of hypertension among African-Americans has been declining, but remains much higher than among White people. Management of hypertension is the best avenue to prevent much of the excess burden of end-stage renal disease, but the relative merits of different agents and levels of blood pressure control are still under study. In addition, individuals with human immunodeficiency virus-related end-stage renal disease represent a small but rapidly growing number of patients that are predominantly African-American. Studies are underway to examine ethnic differences and risk factors for the earlier stages of renal disease as well as genetic mutations for non-Mendelian forms of end-stage renal disease.

AIDS-Associated Nephropathy↗
PubMed1997

Evaluation of serum creatinine for estimating glomerular filtration rate in African Americans with hypertensive nephrosclerosis: results from the African-American Study of Kidney Disease and Hypertension (AASK) Pilot Study.

Measurement of GFR is considered the standard for estimating renal function. However, standardized accurate GFR methodology is expensive and cumbersome; therefore, estimates of GFR based on serum creatinine concentration have been employed. The purpose of the study presented here was to assess the accuracy and precision of using serum creatinine measurements to estimate GFR in the screen cohort of The African-American Study of Kidney Disease and Hypertension (AASK) Pilot Study. GFR was estimated by four methods: 100/serum creatinine, Cockcroft-Gault equation, creatinine clearance from 24-h urine collection, and a new regression equation derived from the pilot study data. These methods were compared with renal clearance of 125I-iothalamate GFR (GFR1) in 193 hypertensive (diastolic blood pressure > or = 95 mm Hg) African-American screen (142 men, 51 women). A second GFR (GFR2) was performed in 98 screen who were eligible (GFR1 25-70 mL/min per 1.73 m2) for the pilot study. Accuracy was assessed by the difference of 125I-iothalamate GFR-estimated GFR (delta GFR), and precision was estimated from the combined root mean squared error (CRMSE) and the coefficient of determination (r2). The results for accuracy (+/- SD) and precision were as follows: (1) 100/Scr, delta GFR = -0.76 +/- 16.5, CRMSE = 16.5, r2 = 0.69; (2) Cockcroft-Gault, delta GFR = 9.56 +/- 14.9, CRMSE = 17.7, r2 = 0.66; 3) 24-h creatinine clearance, delta GFR = 0.79 +/- 20.7, CRMSE = 20.7, r2 = 0.49; 4) New equation delta GFR = -0.08 +/- 12.8, CRMSE 12.7, r2 = 0.75. In comparison, a second GFR (GFR2, N = 98) had delta GFR = 1.36 +/- 8.48, CRMSE 8.6, r2 = 0.75. Estimates based on 100/SCr and the new equation were the most precise. It was concluded that GFR estimated by serum creatinine is superior to outpatient 24-h urine creatinine clearance in this population. Serum creatinine values can be used to provide a reasonably accurate estimate of GFR in hypertensive African Americans.

Adult↗
PubMed1996

Adjusting survival curves for confounders: a review and a new method.

When reporting results from survival analysis, investigators often present crude Kaplan-Meier survival curves and adjusted relative hazards from the Cox proportional hazards model. Occasionally, the investigators will also provide a graphical representation of adjusted survival curves based on regression estimates and the average covariate values in the study groups. In this paper, the authors review the limitations of this approach and examine alternative approaches to obtaining adjusted survival curves that have been proposed. Furthermore, a new method to obtain multivariate adjusted survival curves is described. This method is based on direct adjustment of the observed conditional probability of survival at the time of each event. When an unexposed group is used as a standard for adjusting an exposed group, the survival curve in the exposed group is adjusted to the covariate distribution among the unexposed at the time of the event. This method has the advantage over the average covariate method of allowing for the possibility that the adjusted survival curves differ in shape. The method can handle multiple fixed or time-dependent categorical covariates as well as left truncated data, and it allows for estimation of confidence intervals. The authors have written a macro in SAS language that produces the adjusted survival estimates and graphs. This macro is available on request and can be downloaded through the World Wide Web.

Coffee↗
PubMed1996

Exercise thallium tomography predicts future clinically manifest coronary heart disease in a high-risk asymptomatic population.

BACKGROUND: Exercise testing, even when combined with radionuclide perfusion imaging, does not accurately predict future clinical coronary heart disease (CHD) in low-risk asymptomatic populations. We hypothesized that these tests would perform better in a higher-risk population with a high prevalence of occult CHD. Siblings of persons with premature CHD represent such a group in whom it would be advantageous to identify affected individuals before the occurrence of clinically manifest CHD. METHODS AND RESULTS: Exercise thallium scintigraphy was performed in 264 asymptomatic individuals less than 60 years of age who had a sibling with documented CHD before age 60. Despite an average age of only 46 years at the time of screening, 19 of 264 siblings developed clinical CHD (sudden death in 1, myocardial infarction in 10, coronary revascularization in 8) over a mean of 6.2 years (range, 1 to 9 years) of follow-up. Abnormal thallium scans were observed in 29% of men and 9% of women, while abnormal exercise ECGs occurred in 12% and 5% respectively. Of men >/= 45 years of age, 45% had an abnormal exercise ECG, thallium scan, or both. In contrast, only 3% of women < 45 years of age had an abnormal test result. Although abnormal exercise ECGs and thallium scans were both predictive of future clinical CHD, the thallium scan was associated with a higher relative risk. After adjustment for age, sex, and exercise ECG results, the relative risk of developing clinical CHD was 4.7 for an abnormal scan. Siblings with a concordant abnormal exercise ECG and thallium scan had a relative risk of 14.5. These siblings were all men > 45 years of age at the time of screening and had a strikingly high incidence of CHD (6 of 12, 50%). CONCLUSIONS: Exercise thallium scintigraphy appears to be useful in the risk assessment of asymptomatic siblings of patients with premature CHD, particularly in male siblings who are 45 years of age or older.

Adult↗
PubMed1996

Race and sex differences in the distribution of cerebral atherosclerosis.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the influence of race, sex, and other risk factors on the location of atherosclerotic occlusive lesions in cerebral vessels. Previous angiographic studies of patients with stroke or transient ischemic attack (TIA) suggest that extracranial atherosclerosis is more common in whites and intracranial disease is more common in blacks. Noninvasive techniques such as duplex ultrasound, transcranial Doppler (TCD), and magnetic resonance angiography (MRA) allow vascular assessment of a more representative proportion of patients than does conventional angiography alone. METHODS: Consecutive patients evaluated at a community hospital for stroke or TIA over a 2-year period were reviewed. Lesions were defined as a 50% or greater atherosclerotic stenosis by angiography, duplex ultrasound, or TCD, or a moderate stenosis by MRA. RESULTS: Whites were more likely than blacks to have extracranial carotid artery lesions (33% versus 15%, P = .001), but the proportion of patients with intracranial lesions was similar (24% versus 22%). Men were more likely to have intracranial lesions than women (29% versus 14%, P = .03). When multivariate logistic regression analysis was used, white race was the only predictor for extracranial carotid artery lesions, and male sex was the only predictor for intracranial lesions. The cause of stroke/TIA was extracranial carotid artery disease in 8% and intracranial disease in 8% of all patients in the study. CONCLUSIONS: The distribution of cerebral atherosclerosis is influenced by race and sex but not by other vascular risk factors. In our patient population, intracranial disease is as common a cause of cerebral ischemia as extracranial carotid disease.

Aged↗
PubMed1995

The contribution of urinary cations to the blood pressure differences associated with migration.

People living in unacculturated societies have a low average blood pressure and little rise in blood pressure with age. In a community-based survey in southwestern China, the authors assessed the contribution of urinary cation excretion to differences in blood pressure between an unacculturated group (Yi farmers) and migrants to an urban environment, as well as urban controls from a different ethnic group (Han). In March 1989, blood pressure and overnight urinary electrolyte levels were measured on 3 consecutive days in 313 Yi farmers, 265 Yi migrants, and 253 urban Han residents, all male. Of the urinary electrolytes, a higher sodium:potassium ratio best explained the higher blood pressure in the migrants. Yi farmers had lower systolic (106.7 mmHg vs. 114.8 mmHg, respectively) and diastolic (66.2 mmHg vs. 71.3 mmHg, respectively) blood pressures than Yi migrants. However, even after adjustment for age, body mass index, alcohol intake, and urinary sodium, potassium, calcium, and magnesium excretion, Yi farmers continued to have lower average blood pressures than Yi migrants. In pooled analyses of all three groups, urinary sodium and calcium were positively related and urinary potassium and magnesium were inversely related to blood pressure. Migration is associated with a higher blood pressure that is only partially explained by higher levels of adiposity and alcohol and sodium intake and lower levels of potassium and magnesium intake.

Adult↗
PubMed1995

Segregation analysis of HDL3-C levels in families of patients undergoing coronary arteriography at an early age.

HDL cholesterol (HDL-C) level is a risk factor for coronary heart disease. Studies have shown a strong genetic influence on HDL-C levels in addition to environmental influences, but no definite major gene control has been demonstrated. Since HDL subfractions may better reflect the actions of distinct metabolic alterations than total HDL2 we tested the hypothesis that the amount of cholesterol in the denser HDL3 subfraction (HDL3-C) is under the control of a major gene. The study population included 676 family members of 116 probands who underwent coronary arteriography at an early age (men < or = 50 and women < or = 60 years). HDL3-C level was measured by using enzymatic methods after preparative ultracentrifugation at a density of 1.125 g/mL. HDL3-C was adjusted for age, gender, alcohol consumption, and smoking, which combined accounted for 3% of its variance. Segregation analysis was conducted on adjusted HDL3-C by using regressive models. The familial correlations for HDL3-C levels were spouse .03 +/- .08, parent-offspring .14 +/- .05, and sibling .24 +/- .05. The data strongly supported a codominant mendelian model, with the common allele coding for lower HDL3-C levels and the rarer allele (frequency, 25%) coding for higher HDL3-C levels. This major gene explained 34% of the variation in HDL3-C levels and 9% of the variation in total HDL-C levels. These results suggest that HDL3-C levels exhibit clearer genetic control than total HDL-C and may therefore be a useful target for further genetic studies.

Adult↗
PubMed1995

Survival on dialysis among chronic renal failure patients treated with a supplemented low-protein diet before dialysis.

Concerns have been raised about the possibility of protein restriction resulting in malnutrition and poor subsequent survival on dialysis. However, no studies have examined patients treated with protein restriction to determine their subsequent survival on dialysis. This study prospectively monitored 67 patients with established chronic renal failure (mean initial serum creatinine of 4.3 mg/dL) who were treated with a very low-protein diet (0.3 g/kg per day) supplemented with either essential amino acids or a ketoacid-amino acid mixture and observed closely for clinical complications. Forty-four patients required dialysis. Once dialysis was started, dietary treatment was no longer prescribed. The cumulative mortality rate during the first 2 yr after starting dialysis was 7% (95% confidence interval, 0 to 16%). During this period, only two deaths occurred compared with 11.5 deaths expected on the basis of national mortality rates adjusted for age, sex, race, and cause of renal disease (P = 0.002). However, the protective effect was limited to the first 2 yr on dialysis. Thereafter, mortality rates increased, resulting in a total of 10 deaths during 96.4 person-years of follow-up, which was not significantly lower than the 14.9 deaths expected (P = 0.25). Extrapolation of sequential serum creatinine measurements made before dietary treatment suggests that the improved survival cannot be due to the early initiation of dialysis. Although the lack of an internal control group and data on dialysis lends uncertainty, the large difference in mortality rate between these patients and the nationwide experience indicates that protein restriction and close clinical monitoring predialysis does not worsen and may substantially improve survival during the first 2 yr on dialysis. These findings point out the importance of studying predialysis treatments as a means for lowering mortality on dialysis.

Adult↗
PubMed1994

Minimum sample size estimation to detect gene-environment interaction in case-control designs.

As genetic markers become more available, case-control studies will be increasingly important in defining the role of genetic factors in disease causality. The authors estimate the minimum sample size needed to assure adequate statistical power to detect gene-environment interaction. One assumption is made: the prevalence of exposure is independent of marker genotypes among controls. Given the assumption, six parameters (three odds ratios, the prevalence of exposure, the proportion of those with the susceptible genotype, and the ratio of controls to cases) dictate the expected cell sizes in a 2 x 2 x 2 table contrasting genetic susceptibility, exposure, and disease. The three odds ratios reflect the association between disease and 1) exposure among non-susceptibles; 2) susceptible genotypes among nonexposed individuals; and 3) the gene-environment interaction itself, respectively. Given these parameters, the number of cases and controls needed to assure any particular Type I and Type II error rates can be estimated. Results presented here demonstrate that case-control designs can be used to detect gene-environment interaction when there is both a common exposure and a highly polymorphic marker of susceptibility.

Case-Control Studies↗