1. Health Disparities in SLE
Those we can address as health professionals
Those we can address as citizens
Those that are immutable

2. The Lupus Initiative Curriculum: Note to Reviewers
Suggested changes from previous reviewers have been compiled but are not reflected in the slides that follow.
Any revisions you recommend will be added to those already received and, following this round of review,
A small panel of lupus educators will evaluate all comments received and decide what will be incorporated into the final slide modules.
Thank you for your participation in this process. Sharing your expertise helps ensure the best educational materials are available to future medical and health professionals.

3. Distribution of US Population Race and Ethnicity 2008 and 2050

4. Problems with Available Data Sets
Many studies have small numbers of patients and may not be representative
Many studies have data from 30–40 years ago
Many studies of racial/ethnic differences relate to the general population, not specifically to those with SLE
Access to healthcare and disease outcome may vary geographically, so some data sets may not be broadly applicable

5. Why There Is a Problem Mortality Odds ratio compared with females
P value
Odds ratio compared with females
Male (ns)
Odds ratio compared with whites
Black (ns)
Hispanic (ns)
Odds ratio
Below the poverty line
Disease activity at baseline <.001
Poverty and lack of education are public health concerns
Adapted from LUMINA

6. Who Gets SLE?
Women > men: 2–3:1 before puberty; 9:1 after menarche; 2:1 after menopause
African ancestry, Hispanics, Asians: whites ~3–4:1

7. Ascertainment Matters
We were wrong for a long time and thought blond women got lupus.
First study showing blacks have more lupus

8. Why Women? Genetics A 2nd X chromosome (increased incidence in XXY)
Demethylation of TLR7, CD40 ligand (epigenetics)
Hormones
Estrogen is permissive (altered estrogen metabolism in blacks to more estrogenic compounds)
Androgen is protective

9. Why Certain Races/Ethnicities?
Genetics
Different risk alleles in different populations:
PTPN22 in whites
FcRIII158F (low binding) in Asians
FcRIIB in all (the allele confers a loss of function as the protein is not in lipid rafts. Interestingly, it protects against malaria)

10. Are There Nongenetic Risk Factors?
The incidence of many autoimmune diseases is increasing. This appears to be true for lupus also.
There have been many speculations why; none is proven:
Hygiene hypothesis
Estrogen exposure
Vitamin D deficiency
Obesity

11. Prevalence Rate (%) Vitamin D Deficiency by Race and Gender
We are all Vitamin D deficient, but blacks, Hispanics and Asians more so

12. Patients with 25-D Levels <10 ng/mL
25-D Levels are Low in Black and Hispanic Lupus Patients and Inversely Correlates with Disease Activity
Patients with 25-D Levels <10 ng/mL
25-D Levels (ng/mL)
Blacks
Asians
Whites
Hispanics
Blacks
Asians
Whites
Hispanics
25-D Blood Levels (ng/mL)
SLEDAI

13. Major Manifestations Blacks have
More renal disease with more pure membranous disease
Cardiovascular events at an earlier age; more carotid plaque, more hypertension but lower cholesterol and triglycerides
More discoid disease
Hispanics have
Cardiovascular events at an earlier age
Asians have
More hemolytic anemia and more thrombocytopenia
Northern Europeans have
More skin manifestations than Southern Europeans

14. Serology Chinese More anti-DNA than blacks or whites More anti-Ro
Less anticardiolipin
Blacks
More anti-Sm than Chinese or whites
More anti-U1RNP

15. Presentation in Different Groups
Age
Antibodies
Organs
Blacks
Younger
Sm, RNP
Discoid, kidney
Asians
Kidney
Hispanics
malar rash, kidney
Whites
Older
Skin, CNS
Men ?
Pediatric
Kidney, CNS
These data are based on relatively small studies. It does appear that disease is more active in blacks and Hispanics at time of diagnosis. Whether this has to do with properties of the disease or issues relating to the healthcare system and physicians is not clear. It is important to recognize that untreated lupus progresses. Treat before there is irreversible tissue damage.

16. Progression of Disease
Differences in affected organs: more renal disease and more membranous nephropathy in blacks
Rate of accumulation of damage is higher in blacks and Hispanics
Damage accrual relates to poverty. There may be a genetic component also: lack of DRB1*0301 in Hispanics, presence of DQB1*0201 in whites.
Mortality rate is higher in blacks, Hispanics, Asians

17. Renal Disease Is a Major Cause of Morbidity and Mortality
There is more renal disease in pediatric-onset SLE and in blacks
60% of patients with adult-onset SLE develop renal disease
80% of patients with pediatric-onset SLE develop renal disease
50% of ESRD in SLE is in blacks, although they account for <25% of affected individuals

18. Multivariate Predictors of Progression of Proliferative Lupus Nephritis
Proverty, health insurance, and hypertension are not immutable

19. Hypertension
Predictors of hypertension in patients from the LUMINA cohort by multivariable logistic regression analyses (n = 382)
Hypertension and renal disease are a bad combination. We must treat hypertension

20. Total Age-Adjusted Coronary Heart Disease Mortality Among US Females Age 35 and Older, 1998
SLE increases the risk of coronary heart disease in all groups

21. Factors Related to Outcome
Patient issues
Inactivity
Self-efficacy (related to poverty and education)
Adherence to therapeutic regimen
Obesity
Physician issues
Willingness to engage patients in therapy decisions
Willingness to discuss exercise and diet (both black and white MDs less likely to discuss these topics with black patients)
Cultural competency
Issues for both patient and physician
Communication (language barriers)
Health education

22. Factors Related to Outcome
Societal issues
Access to healthcare
Poverty
Education

23. Survival in Patients with Severe Lupus Nephritis on the Basis of Race
P <.029, black vs white; NS for black vs other and for other vs white).

24. Renal Transplants Transplant access
Blacks < Hispanics < whites receive transplants
Organ donation less in blacks (both living and cadaver)
Medicaid is a risk for no transplant

25. Transplant Survival Black recipients (n = 1304)
Non-black recipients (n = 1149)

26. Renal Transplants Transplant outcome
Both adult and pediatric blacks do less well (almost double mortality in black children)
More recurrent disease in blacks
Reasons for poor outcome
Poverty
Hypertension less well controlled in blacks
Blacks have a longer time on dialysis
It is not yet clear if there is a genetic component to transplant outcome in SLE: IL-6, rantes, CCR5, TNF, CTLA-4,TLR4 (both donor & recipient)

27. Cardiovascular Outcome
Contributing problems
Hypertension
Diabetes
Adequate medical management
Whites > blacks and Hispanics
Management
Access to cardiac catheterization
Men > women
Whites > minority
Physicians less likely to discuss exercise, diet with blacks

28. Estimated Age-Adjusted Prevalence of Overweight and Obesity among US Females Ages 20–74 Years, 1988–1994
Source: NHANES III [1988–94] (not specific for SLE patients)

29. Treatment
Are there important racial/ethnic differences in how to use medications or in response?
Mycophenolate
Higher dose needed in blacks (3 vs 2 gm)
Cyclophosphamide
? less good renal response in blacks
Rituximab
? greater response in blacks
Antihypertensive medication
Beta blockers less effective in blacks

30. Treatment Genetic contribution to efficacy and toxicity TPMT
Toxicity and efficacy of azathioprine levels lower in women, minorities
P450
Efficacy of cyclophosphamide: no evidence of racial differences

31. Medication Adherence No difference in taking medications Blacks
Hispanics
Whites
Follow-up visit
57%
53%
62%
Prescription
87%
95%
84%
Reason for lack of follow-up:
Whites: feel better
Blacks, Hispanics: difficulty making appointment

32. Clinical Research
Minority patients are underrepresented in clinical studies

33. Clinical Trials
Concept of “the good study patient” emphasizes someone who is compliant and has a strong social network
No difference among racial/ethnic groups in willingness to participate in clinical trials if previously enrolled
Physicians need to put more effort into enrolling minorities in clinical research and clinical trials. Patient education is a useful recruitment strategy

34. Conclusions—You Can Make a Difference as a Physician and a Citizen
Remediable issues: patient and physician
Hypertension
Diabetes
Self-efficacy
Access to organ donation
Access to cardiac catheterization
Engagement in clinical research and clinical trials
Obesity
Cultural competency
Societal issues
Stress
Poverty/access to healthcare/insurance

35. Physician Misconceptions
Conscious misconceptions:
There are no disparities
63% of physicians think the healthcare system has no racial or ethnic bias (compared with 43% of the entire population and 25% of blacks)
Minorities are unlikely to engage in clinical studies
Unconscious misconceptions:
Minorities engage in unhealthy behaviors
Smoking, immunizations, fruit and vegetable intake are not different between blacks and whites
Minorities are unable/unwilling to participate in their own care

36. Recommendations (The IOM Model)
Inform healthcare professionals on the nature and extent of disparities
Use treatment guidelines to avoid unconscious bias
Implement patient education programs
Include measures of racial and ethnic disparities in performance measures