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The incidence of systemic lupus erythematosus in baltimore maryland 19701977.

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80
THE INCIDENCE OF SYSTEMIC LUPUS
ERYTHEMATOSUS IN BALTIMORE, MARYLAND,
1970-1977
MARC C. HOCHBERG
The incidence of systemic lupus erythematosus,
based on first hospital discharge diagnosis, in Baltimore, Maryland for the years 1970 through 1977 was
determined for individual sex-race groups and the total
population. Age-specific incidence rates were consistently highest among black females and lowest among white
males: rates for white females exceeded those for black
males through age 54, but then declined for ages 255.
Mean age at diagnosis was significantly lower for black
females versus white females (35.5 versus 41.7 years,
P = 0.005) and for all females versus all males (37.2
versus 44.2 years, P = 0.012). There were no temporal
trends noted in yearly age-adjusted incidence rates
during the 8-year study period. The overall population
incidence of systemic lupus erythematosus was 4.6 per
100,000 per year, representing a twofold increase over a
comparable study done in New York City 15 years ago.
Previous descriptive epidemiologic studies of
systemic lupus erythematosus (SLE) have demonstrated increasing incidence rates from 1.O-7.6 per
From the Rheumatology Division, Department of Medicine, The Johns Hopkins University School of Medicine at the Oood
Samaritan Hospital, and Department of Epidemiology, The Johns
Hopkins University School of Hygiene and Public Health, Baltimore, Maryland.
Supported by grants from the Lupus Foundation of America, the Arthritis Foundation, Maryland Chapter, and The Johns
Hopkins Multipurpose Arthritis Center grant 2-P60-AM20558. Dr.
Hochberg is the recipient of an Arthritis Investigator Award from
the Arthritis Foundation.
Marc C. Hochberg, MD, MPH: Associate Professor of
Medicine, Joint Appointment in Epidemiology.
Address reprint requests to Dr. Marc C. Hochberg, c/o
Good Samaritan Hospital, 5601 Loch Raven Boulevard, Baltimore,
M D 21239.
Submitted for publication March 19, 1984; accepted in
revised form August 7, 1984.
Arthritis and Rheumatism, Vol. 28, No. 1 (January 1985)
100,000 per year during the 20-year period from 1955
to 1974 (1-7). This temporal trend in SLE incidence,
however, may in part be artifactual; that is, the
increase may be due to 1) increased physician knowledge and recognition of the disease, 2) the development of more sensitive diagnostic tests such as antinuclear antibody (ANA) determinations, and 3) diagnosis
of milder cases because of changes in diagnostic
criteria. In addition, comparison of previous studies is
complicated by methodologic differences, especially in
case identification. Studies in New York City (1-3)
and Jefferson County, Alabama (2,3) were based on
hospital discharge records, while those in Rochester,
Minnesota (4) and San Francisco ( 5 ) were based on
both inpatient and outpatient records. Furthermore,
recent studies have not estimated incidence rates by
sex-race groups in nonwhites because of the small
number of cases (43).
Since the ANA test became available in the
1960s and the publication of preliminary criteria for the
classification of SLE in 1971 (8), few other major
technologic advances have been made which would
impact physician diagnosis of SLE. Hence, in a major
metropolitan area with 2 university teaching hospitals
where knowledge is widely disseminated, one would
assume that temporal changes in SLE incidence
during the past decade would probably be more real
than artifactual. Thus, a population-based study of
hospital-diagnosed SLE was done in Baltimore to 1)
estimate the average annual age-specific incidence
rates by sex-race group; 2) explore potential synergistic interaction between the female sex and the nonwhite race in producing higher incidence rates among
nonwhite females; 3) assess possible differences in age
at diagnosis between whites and nonwhites; and 4)
81
SLE IN BALTIMORE, MD
examine recent temporal trends in annual age-adjusted
incidence rates.
METHODS
The records of 19 Baltimore metropolitan area hospitals, 14 hospitals within the Baltimore city limits, and an
additional 5 located in Baltimore County but within the
metropolitan area were reviewed for the period 1970 through
1977, and all patients discharged with a diagnosis of SLE
(Eighth Revision International Classification of Disease,
Code 734.1) (9) were identified. Patient charts were reviewed
by a trained research assistant using a predefined protocol to
obtain the following information: address at time of discharge including zip code, date of birth, sex, race, date of
discharge, marital status, date of diagnosis, number of
previous admissions for SLE, and the presence of the
American Rheumatism Association ( A M ) preliminary criteria for SLE (8). Only the records of Baltimore city residents,
with1 a date of first hospital discharge diagnosis between
January 1, 1970 and December 3 1 , 1977, were considered for
further analysis.
Based on chart review, cases were required to fulfill
at least 4 of the preliminary criteria for SLE to be included in
subsequent analyses.
The population data were derived from the 1970 and
1980 United States censuses of the city of Baltimore. Both
the 1970 and 1980 censuses reported numbers of persons by
age group, sex, and either white or black race. Population
denominators for each year of the study were estimated by
linear extrapolation using 1970 and 1980 as benchmarks.
Age-specific annual incidence rates of hospital-diagnosed SLE were calculated for each sex-race group per year
from 1970 through 1977. Ten-year age groups were used,
except for a single group for those below age 15 and one for
tho!je age 65 and above. The overall age-adjusted average
annual incidence rates for each sex-race group were calculated using the direct method and the total 1980 Baltimore
city population as the standard. Standard errors were calculated using the methods of Chiang (10). Time trend analysis
of mean age at diagnosis and yearly age-adjusted incidence
rates for each sex-race group were conducted using Spearman’s rank-order correlation coefficient (R,) (1 1). Finally,
Rothman’s synergy index (12) was determined to evaluate
the possible interaction between sex and race as independent
risk factors for the development of SLE.
RESULTS
A total of 302 incident cases of SLE were
identified among Baltimore city residents discharged
during the 8-year study period (Table 1). Black females
were most commonly affected, accounting for 63% of
cases; females comprised 87% of cases, giving an
overall crude sex ratio of 6:1. There was no significant
temporal trend in the total number of cases diagnosed
per year during the study period (R, = -0.44, P >
0.05).
The patterns of the age-specific average annual
Table 1. Number of hospital-diagnosed incident cases of systemic
lupus erythematosus by sex-race group and year in Baltimore city
residents, 1970-1977*
Year
WM
1970
1971
1972
1973
1974
1975
1976
1977
1
0
0
1
1
BM
WF
BF
Total
1
3
6
9
4
3
2
3
3
3
10
9
11
8
8
10
7
9
21
28
31
22
17
29
27
15
38
46
46
34
28
42
38
30
Total
7
33
72
190
302
0
* WM = white males; BM = black males; WF = white females; BF
=
black females.
incidence rates varied between the individual sex-race
groups (Table 2 and Figure 1). Incidence rates were
lowest among white males, and too few cases were
identified during the study period to allow an adequate
description of the age distribution except to note that
no cases were identified in persons age 24 and under.
The overall crude rate among white males was 0.45 per
100,000 per year. Incidence rates among black males
showed a unimodal distribution with maximum rates
occurring in the 45-54 and 55-64 age groups; the
overall crude rate was 2.08 per 100,000 per year.
Incidence rates were consistently greater among black
males compared with white males in all age groups; the
overall crude race ratio for males was 4.6:l (Table 3).
Age-specific incidence rates among white females showed a bimodal distribution with peaks in the
15-24 and 45-54 age groups; rates declined precipitously above age 55. The overall crude rate was 3.94
per 100,000per year and the crude rate limited to the
15-54 age groups combined was 6.05 per 100,000per
year. Incidence rates were consistently greater among
white females compared with white males; the overall
crude sex ratio among whites was 8.8:l (Table 3).
Age-specific incidence rates for black females
showed a unimodal distribution with the maximum
rate of 21.6 per 100,000per year occurring in the 25-34
age group. Incidence rates were higher among black
females than any of the other 3 sex-race groups.
Comparison of black female with black male rates
showed the greatest differences in the 15-34 age
groups with an overall crude sex ratio of 5.1 :1. Similar
comparison of black female rates with white female
rates showed variable patterns with age; the overall
crude race ratio for females was 2.7:l (Table 3).
Overall age-adjusted average annual incidence
rates were 0.42,2.50,3.93,and 11.42for white males,
82
HOCHBERG
Table 2.
Average annual age-specific incidence rates of systemic lupus erythematosus by sex-race group in the city of Baltimore, 1970-1977
White females
Black males
White males
Total
Black females
~~~
Age group
5 14
15-24
15-34
35-44
45-54
55-64
265
Overall crude rate
Overall age-adjusted rate?
Standard error
No.
Rate*
0
0
2
2
0
2
1
-
No.
Rate
2
4
3
6
8
6
4
0.87
1.21
-
0.99
0.50
0.45
0.42
0.16
0.34
1.25
1.56
3.52
4.97
5.06
4.35
2.08
2.50
0.43
No.
Rate
No.
Rate
No.
Rate
0
16
10
12
17
9
8
-
8
45
53
34
24
15
11
1.45
12.46
21.57
16.63
12.95
11.08
8.75
10.54
11.42
0.83
10
65
68
54
49
32
24
0.53
5.28
7.69
7.63
6.22
4.56
3.08
4.40
4.62
0.26
5.55
4.73
6.87
7.23
3.71
2.33
3.94
3.93
0.46
* Rates per 100,000 population per year.
t Adjusted to the 1980 Baltimore total population using the direct method.
black males, white females, and black females, respectively (Table 2). Comparison of these age-adjusted
rates reflects a marked sex effect and a somewhat less
pronounced racial effect (Table 3 ) . To evaluate the
possibility of additive interaction or synergism between sex and race as risk factors for high incidence,
Rothman's index of interaction was determined (Table
4). The age-adjusted incidence rate for white males
was set as the background risk of developing SLE in
the absence of either factor, that is, female sex or
black race. The calculated values of 1.97 for all age
groups and 2.11 for age groups 15-54 (corresponding
to reproductive or childbearing years in females) are
significantly different from 1.0 and suggest a definite
synergistic interaction between female sex and black
race.
*
*
DISCUSSION
The incidence of systemic lupus erythematosus
in several communities in the United States has been
reported previously (1-5), and these studies have been
recently reviewed (13). This study represents the
largest epidemiologic study of SLE in terms of number
a
a
a
The distribution of age at diagnosis among the
sex-race groups is also shown in Table 2. The median
age at diagnosis was 36, 46, 42, and 33 years for white
males, black males, white females, and black females,
respectively. The mean age at diagnosis was significantly younger for black females compared with white
females (35.5 5 15.7 years versus 41.7 k 17.4 years; t
= -2.79, P = 0.005) and for all females compared with
all males (37.2 16.3 years versus 44.2 16.9 years; t
= -2.51, P = 0.012).
There were no significant trends in either the
annual age-adjusted incidence rates or the mean age at
diagnosis for any of the sex-race groups during the
study interval.
5.0
Table 3. Ratios of average annual age-specific incidence rates of
systemic lupus erythematosus between sex-race groups
0
0, 1.0
a
w 0.5
n
cn
0.2
:
"
Femalemale
Age group
5 14
U
0.19
Black
I
I
I
I
I
1
10
20
30
40
50
60
I
I
70 80
AGE
Figure 1. Average annual age-specific incidence rates of systemic
lupus erythematosus in Baltimore (city), 1970-1977, for white males
(01, black males (B), white females (O), and black females (O),
Note that the ordinate axis is a 3-cycle logarithmic scale.
15-24
25-34
35-44
45-54
55-64
265
Overall crude ratio
Overall age-adjusted
ratio
* N o cases present
4.3
9.9
13.8
4.7
2.6
2.2
2.0
5.1
4.6
B1ack:white
White
-*
5.4
5.7
Male
3.7
4.7
8.8
9.3
5.1
8.7
4.6
5.9
-
in denominator of ratio.
1.8
2.9
-
Female
2.2
4.6
2.4
1.8
3.0
3.7
2.7
2.9
83
SLE IN BALTIMORE, MD
Table 4. Calculation of Rothman’s synergy index (12)*
Age-adjusted
average annual incidence ratet
All ages$
White males
Black males
White females
Black females
Ages 15-549
White males
Black males
White females
Black females
Relative rate
(RR)
0.42
2.50
3.93
11.42
5.95 =
9.36 =
27.19 =
0.46
2.41
5.85
15.93
1.00 = RRW
5.24 = RRlo
12.72 = RRol
34.63 = RRII
1.00 =
RRII - RRW
S=
RR + RRol - 2RRw
t Rates per 100,000 per yea??
j: S = 1.97 (95% confidence intervals: I .46. 2.66).
S = 2. I 1 (95% confidence intervals: 1.52, 2.93).
* Synergy index
=
s
of incident cases identified, as well as denominator
population, and provides updated information on agespecific average annual incidence rates by sex-race
group, as well as new information on differences in
mean age at diagnosis between individual sex-race
groups and evidence of synergy between the female
sex and the black race in producing the highest incidence rates of SLE in black females.
The database used in this study represented
patients with SLE who were Baltimore city residents
at the time of first hospital diagnosis, who fulfilled 4 or
more of the preliminary ARA criteria for SLE, and
were discharged from Baltimore area hospitals. Patients with SLE discharged during the study interval
who were either first diagnosed before 1970 and/or did
not reside in the city of Baltimore were excluded from
analyses; they represented an additional 153 cases.
The method of case selection used is similar to
that employed by Siegel and Lee (l), who justified
their method on the assumptions that patients with
SLE would require hospital care because of severity of
illness and/or difficulty in diagnosis and would use
local facilities for medical care (3). More recent studies
in Rochester, Minnesota (4) and San Francisco (5)
used both inpatient and outpatient records which were
linked through computerized patient registries. Since
the assumption of Siegel and Lee relating to the
requirement of hospital care for diagnosis is no longer
valid, especially in major urban areas with educated
internists and rheumatologists, it is likely that the
database used in this study is biased due to a systemat-
ic underestimation of incident cases of SLE in patients
who either have mild disease not requiring hospitalization and/or were diagnosed and managed completely
as outpatients during the study period.
In an attempt to quantify the degree of underestimation, the author surveyed the faculty of the Johns
Hopkins Rheumatology Division. Of 121 private patients with SLE who were seen during the 12-month
period from July 1983 through June 1984 and were
under regular followup in our university-based private
patient clinic, 11 (9.1%) had never been hospitalized
(14). There was a suggestion of racial influence in the
proportion of patients never having been hospitalized,
10.7% of 103 whites versus none of 18 blacks, but this
is not statistically significant (P = 0.24, Fisher’s exact
2-tailed test). Whether this underestimation of the
number of incident cases applies equally to all 4 sexrace groups in the community is unknown; it is possible that white patients with higher socioeconomic
status may seek care earlier in their illness and be
more likely to be diagnosed and managed as outpatients by private rheumatologists than blacks with
lower socioeconomic status. This is suggested by the
private patient data noted above; however, the inaccuracies inherent in attempts to generalize these results
to other populations are recognized.
Another potential source of underestimation of
incident cases is that patients with SLE might have
been discharged with other listed discharge diagnoses.
Examples would include other connective tissue disorders such as unspecified collagen vascular disease or
mixed connective tissue disease, or glomerulonephritis or lupus nephritis. These reporting errors might be
attributable to physician misdiagnosis or coding errors
by medical records personnel. Unfortunately, we did
not review any such records and are therefore unable
to estimate the potential impact on the data presented.
The patterns of the age-specific incidence rates
of SLE in Baltimore, based on first hospital discharge
diagnosis of SLE, are largely comparable with those
patterns noted by Siegel and Lee in New York City
and Jefferson County, Alabama (1-3). Among 65 cases
in white females identified in the New York City study
area, the peak incidence rate of 4.4 per 100,000 per
year occurred in the 25-34 year age group, while in the
present study, the peak incidence rate of 7.23 per
100,000per year occurred in the 45-54 year age group.
This suggests an increase in the age at diagnosis among
white females over the 15-year interval separating
these studies. This is supported by an increase in the
median age at diagnosis, which rose from 39.7 among
HOCHBERG
93 cases diagnosed between 1949 and 1968 (3) to 42
among 72 cases in this study. It is important to note,
however, the significant decline in incidence rates
above age 54 among white females in this study (Table
2 and Figure l), compatible with the well-recognized
sex effect occurring during the reproductive years
which is associated with rates varying from 4.73-7.23
per 100,000 per year between ages 15 and 54.
Incidence rates increase 8.5-fold with puberty
in black females and reach maximum values in the 2534 year age group followed by a steady exponential
decline. The median age at diagnosis of 33 years in
black females is in agreement with that reported by
Siegel and Lee in 35 cases diagnosed between 1949 and
1968 (3). The significant difference in mean age at
diagnosis between black and white females noted in
this study has not been previously reported. Others
have noted differences in the racial distribution of
patients with late-onset SLE compared with patients
with young-onset (15). In this study there was no
significant difference in the frequency of diagnosis at
or above age 55 among white females compared with
black females; 17 (23.6%) of 72 cases versus 26
(13.7%) of 190 cases (P = 0.08, Fisher’s exact test).
The difference in mean age at diagnosis may,
however, be due to bias in case identification if
hospitalization for diagnosis of SLE was more likely in
younger blacks than whites, especially below age 34,
because of differences in medical practice patterns
and/or severity of illness. Socioeconomic factors
might also be important in this regard; an association
of low socioeconomic status with black race and
decreased survival in patients with SLE was the
reason for an apparent association of black race with
decreased survival in a recent multicenter study (16).
Thus, if socioeconomic status differed between racial
groups, as it would be expected to, differential access
to public clinic versus private practitioner care might
influence the probability of hospital admission for
diagnosis and care of SLE. We took into consideration
whether SLE was the primary discharge diagnosis or
simply a listed comorbid diagnosis on the medical
record. Overall, 36 (1 1.9%) of the 302 incident cases
had SLE listed as a secondary diagnosis; there were
no statistically significant differences in the frequency
of this parameter between sex-race groups. Despite
these possible biases, the difference in age at diagnosis
might in fact represent host differences in immune
response (17) related to the development of SLE. In
any event, this difference is comparable with that
noted in mean age at death among black and white
females in an 1 1-year study of mortality from SLE in
the United States (18).
Comparison of the age-specific incidence rates
between the sex-race groups reveals interesting sex
and race ratios (Table 3). Excess female incidence,
especially among blacks where adequate numbers of
cases occurred, was most striking in the reproductive
years through age 34. The importance of endocrine
factors related to sex hormones has been repeatedly
noted in patients with SLE, with emphasis on their
possible role in pathogenesis and expression of disease
(19-24). Excess incidence in blacks is less striking but
noteworthy and confirms the data of Siegel and Lee
(1-3). Increased prevalence (1-3,5) and mortality
(13,18,25) among blacks compared with whites with
SLE has also been noted. The synergistic interaction
of female sex and nonwhite race in producing the
highest mortality rates from SLE (18,25), as well as
from systemic sclerosis (26) and polymyositis/dermatomyositis (27) in nonwhite females has previously
been reported. The present data demonstrate a significant interaction of female sex and black race in producing higher incidence rates in black females not only
in the childbearing years, but also throughout the
overall age spectrum. Racial differences in sex hormone production and metabolism (28), as well as
immune reactivity (17) may interact with the sex
factors (20) in ways which remain to be elucidated.
This study found no evidence of temporal
trends in either yearly age-adjusted incidence rates
among the sex-race groups or mean age at diagnosis.
The absence of temporal trends in incidence rates is
consistent with our observation of declining mortality
rates from SLE (18) in the setting of improvement in
survivorship during a time interval which included this
study period (29). Furthermore, the absence of secular
trends in mean age at diagnosis is consistent with our
observation of increasing mean age at death from SLE
(18) associated temporally with improved prognosis
among SLE patients.
The absence of a temporal increase in hospitaldiagnosed SLE incidence rates in this study does not
necessarily imply a stability of overall population
rates, since increasing numbers of cases may be diagnosed and managed on an outpatient basis. Such data
were not obtained in this study, so the possibility of an
increase in total SLE cannot be excluded.
The overall population average annual ageadjusted incidence rate, based on first hospital discharge diagnosis of 4.62 per 100,000 per year (95%
confidence intervals: 4.10, 5.14) is lower than those
SLE IN BALTIMORE, MD
reported for Rochester, Minnesota (5.7 per 100,000per
year) (4) and San Francisco (7.6 per 100,000 per year)
(5). ‘These studies, as noted above, included both inhospital and outpatient diagnosed cases in well-defined populations and would be expected to have
higher incidence rates since all cases of SLE do not
require hospitalization for diagnosis. The overall rate
in Baltimore is more than double that of 2.0 per
100,000 per year in New York City (3) and confirms
the increase in incidence rates of SLE noted previously. Although this increase may, in large part, be
explained by increased physician diagnosis because of
doctor and patient awareness and more sensitive laboratoiry tests, a true increase in incidence cannot be
excluded. Nonetheless, SLE can no longer be considered a rare disease, with an incidence in young white
females below age 25 and in black females below age
34 which may be comparable to or exceed that of
definite rheumatoid arthritis (30). Continued research
toward the development of both primary and secondary prevention strategies (31) is clearly warranted.
ACKNOWLEDGMENTS
The author wishes to thank Sheila Brown for abstracting patient records, Katherine vanDyke for assistance
in computer programming and data analysis, and Cathay
Insley for preparation of the manuscript.
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