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Loss of trabecular bone mineral density in systemic lupus erythematosus.

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Number 12, December 1993, pp 17261734
0 1993, American College of Rheumatology
Objective. To evaluate trabecular bone mineral
density (BMD) in young ambulatory female patients
with systemic lupus erythematosus (SLE).
Methods. Bone mineral density (gm/cm2) at the
lumbar vertebrae (Ll-L4) and at the left femur (neck,
trochanter, intertrochanter, and Ward's triangle) was
measured by dual x-ray absorptiometry in 46 SLE
patients (mean age 31 years, mean disease duration 76
months) and in 108 healthy female controls (mean age 32
years). Twenty-two of the SLE patients were receiving
corticosteroids (CS) at the time of the study.
Results. Lumbar BMD in the SLE patients was
less severely reduced than was BMD at the femoral sites,
but the SLE group was closer to the lumbar fracture
threshold of 0.812 gm/cm2 than was the control group
(P = 0.0009). There were no significant differences
between the SLE patients currently being treated with
corticosteroids and those who were not (P> 0.3). BMD
at Ward's triangle and at the femoral neck was not
significantly reduced in the SLE patients. Total femoral
BMD had a sensitivity of 76% and specificity of 62% in
differentiating the SLE group from the controls. The
From the Department of Medicine, Rheumatic Diseases
Unit, and the Department of Nuclear Medicine, Groote Schuur
Hospital, University of Cape Town, Cape Town, South Africa.
Supported by University of Cape Town Research funds.
Asgar Ali Kalla, MBChB, FCP (SA), MD (UCT): Consultant Rheumatologist, Department of Medicine, Rheumatic Diseases
Unit; Abdul Basier Fataar, MBChB, M.Med (Nuc Med): Chief
Nuclear Radiologist, Department of Nuclear Medicine, Groote
Schuur Hospital; Susan Jane Jessop, MBChB, FF Derm (SA):
Consultant Dermatologist, Department of Medicine, Rheumatic
Diseases Unit; Linda Bewerunge, DipRad: Radiographer, Department of Nuclear Medicine, Groote Schuur Hospital.
Address reprint requests to Asgar Ali Kalla, MBChB, FCP
(SA), MD (UCT), PO Box 30195, Tokai 7966, South Africa.
Submitted for publication June 9, 1992; accepted in revised
form September 22, 1992.
positive predictive value was 61% and the negative
predictive value was 89%. The prevalence of osteopenia
in the SLE patients was 25%.
Conclusion. SLE causes significant trabecular
bone loss, which is not due to corticosteroid therapy.
Osteoporosis is a major cause of morbidity and
mortality in the elderly (1,2). Cortical and trabecular
bone loss occur with menopause (3,4) and with aging
(5,6); menopause-associated and aging-associated
bone loss are referred to as type I osteoporosis and
type I1 osteoporosis, respectively (7). Systemic lupus
erythematosus (SLE) was once considered a fatal
disease of young females (8), but mortality and morbidity are now considerably improved (9). Elderly
women with SLE (10) could be increasingly susceptible to the complications of osteopenia. A recent report
on trabecular bone mass in young patients with SLE
failed to show significant loss due to the disease or to
corticosteroid therapy (11). However, the power of the
study was limited by the small sample size.
We have previously shown that SLE is associated with significant cortical bone loss (12,13). There is
further indirect evidence that bone loss occurs in SLE,
but little is known about its pathogenesis. In 1985,
Dykman et a1 (14) reported on factors associated with
glucocorticoid-induced bone loss. Among their 123
patients with rheumatic diseases, 33% had SLE, 50%
of whom were under 50 years of age. They concluded
that the risk for development of glucocorticoidassociated osteopenia, as measured by single-photon
absorptiometry, was the same in all patient groups.
Hyperparathyroidism secondary to chronic renal failure has been reported in SLE (15,16), but bone mineral
density (BMD) was not measured in those studies.
The demonstration, by Bauss et a1 (17), of
inflammation-mediated osteopenia in rats suggests the
possibility that bone loss in SLE could be a feature of
the inflammatory process. However, it is possible that
protective mechanisms which overcome this negative
effect may be operative in SLE (1 1). A recent in vitro
study (18) showed increased prostanoid activity in
macrophages from patients with rheumatoid arthritis
(RA) and active SLE. Some workers (19,20) have
shown that prostaglandin E, (PGE,) is an essential
cofactor in enhanced production of osteoclastactivating factor. Levels of tumor necrosis factor
(TNF), a potent resorptive substance (21), are lower in
patients with SLE than in patients with RA (22).
In light of the above findings, the present study
was designed to determine BMD in patients with
established SLE, with and without corticosteroid therapy. Trabecular BMD was measured at the lumbar
vertebrae, and cortical and trabecular BMD at the
nondominant femur, using dual x-ray absorptiometry
(DXA) .
Forty-six consecutive ambulatory female SLE patients under 50 years of age were studied. They were all
regularly attending an outpatient lupus clinic at Groote
Schuur Hospital between November 1989 and December
1991. The study protocol was approved by the Ethics and
Research Committee at the University of Cape Town (UCT).
Age under 50 years, regular menstruation, ability to walk
without assistive devices, and disease classification according to the American College of Rheumatology (formerly, the
American Rheumatism Association) revised criteria for SLE
(23) were the main basis for selection. Male patients and
pregnant female patients were excluded. Patients were also
excluded if they had undergone total hip replacement for
avascular necrosis (AVN) of the femoral head, if they were
attending the nephritis clinic, or if they were receiving any
form of dialysis. The patients clearly represent a highly
select population of SLE subjects, since confounding variables had to be minimized.
For each patient, data were recorded on age, race,
age at onset of disease, duration of disease, and SLE
diagnostic criteria that were met. A complete physical examination was carried out by a single observer (AAK). The
use of medication, particularly corticosteroids, was carefully
recorded. Functional status was graded according to the
Steinbrocker classification (24). Disease activity was globally evaluated by the observer, but was not scored according to recent techniques (11,25).
BMD was measured with the Hologic (Waltham,
MA) QDR 1000 densitometer, using an x-ray source. The
lumbar spine was measured from L1 to L4, and the mean
lumbar BMD was calculated. The left femur was measured
at 4 different sites (neck, trochanter, intertrochanter, and
Ward’s triangle), and total femoral BMD was calculated
from these values. Radiographs of the hands, hips, and
vertebrae were not obtained, unless specifically indicated
based on symptoms in those areas. The coefficient of variation of the technique at our institution was 0.5%, using a
phantom measured at regular intervals (n = 577) during the
2-year period (1989-1991). In vivo precision is important in
sequential studies of the same individuals over time, but is
irrelevant in cross-sectional studies such as ours.
One hundred eight healthy female volunteers aged
between 18 and 45 years were studied as controls. All of the
controls were independently ambulatory, were not receiving
regular medications, and had regular menstrual cycles.
The SLE patients were divided into 2 groups, corticosteroid-treated and non-corticosteroid-treated.The corticosteroid-treated group represents subjects who were receiving corticosteroid therapy at the time of the study. Time
since stopping corticosteroid therapy was recorded in those
patients who were not currently being treated with corticosteroids but had previously received such treatment at any
stage during the course of their disease. The same criteria
were used for patient selection regardless of corticosteroid
treatment status. In general, patients treated with corticosteroids were started on a regimen of 60 mg/day (-1 mg/kg/
day), reduced gradually over 6 months as dictated by control
of the disease. All patients in the corticosteroid-treated
group had received corticosteroid therapy for longer than 6
months and up to 6 months prior to study. Included in this
group were some patients who had taken corticosteroids for
at least 6 months and had stopped recently (i.e., within the
previous 6 months); similarly, the non-corticosteroidtreated group included a few patients who were taking
corticosteroids but had only begun such treatment within the
previous 6 months. Three of the patients were receiving
immunosuppressive agents, but had normal menstruation.
None of the patients received calcium supplements or vitamin D therapy during the course of the study.
The mainframe computer at UCT was used for all
Table 1. Trabecular bone mineral density (BMD; gm/cm2) at the
lumbar vertebrae and cortical and trabecular BMD at 4 femoral sites
in normal female volunteers and in female patients with systemic
lupus erythematosus (SLE)*
(n = 108)
Above threshold
for fracture
Femoral BMD
Ward’s triangle
Total femur
Age, years
Height, cm
Weight, kg
(n = 46)
1.04 f 0.13
0.23 t 0.13
0.86 f 0.13
0.71 ? 0.1
1.1 f 0.15
0.69 f 0.16
0.95 f 0.12
32 f 8
162 f 7
59 f 12
0.83 ? 0.11
0.66 0.11
1.05 ? 0.15
0.66 f 0.17
0.87 t 0.12
31 f 7
157 t 25
59 f 18
* Values are the mean
f 0.11
k 0.11
0.0009 11
O.OOO9 11
O.oo00 19
Table 2. Trabecular bone mineral density (BMD; gm/cm2) at the
lumbar vertebrae and cortical and trabecular BMD at 4 femoral sites
in the systemic lupus erythematosus (SLE) patients who were or
were not taking corticosteroids at the time of study*
femoral measurements in the total SLE group as well as the
2 corticosteroid treatment subgroups.
(n = 22)
Lumbar BMD
Femoral BMD
Ward’s triangle
Total femur
Age, years
Height, cm
Weight, kg
Disease duration,
(n = 24)
1.0 2 0.12
0.96 t 0.08
0.84 2 0.09
0.68 t 0.1
1.09 2 0.12
0.68 t 0.18
0.88 t 0.1
32 t 6
160 2 8
66 t 16
84 (13-204)
0.82 f 0.12
0.64 t 0.11
1.02 2 0.15
0.65 f 0.16
0.86 +- 0.13
31 + - 8
153 f 32
54 t 18
60 (7-242)
* Values for disease duration are the mean (ranges); other values are
the mean f SD.
statistical calculations. The SAS package (26,27) and BMDP
statistics software (28) were used for all conventional analyses. Analysis of variance was used for univariate comparisons. Multivariate discriminant analysis was used to evaluate the sensitivity and specificity of the measurement of
BMD at the various sites in the diagnosis of SLE and to
predict corticosteroid treatment. Stepwise multiple regression analysis was used to predict lumbar BMD from femoral
measurements and Ward’s triangle BMD from lumbar and
There were 46 SLE patients eligible for study.
Their mean ? SD age was 31 ? 7 years, and the mean
? SD disease duration was 76 .t 66 months. The age of
the 108 controls was 32 ? 8 years (P = 0.5). Twentytwo of the SLE patients were currently receiving
corticosteroid therapy, while 24 had not received such
therapy in the 6 months prior to the study. Of these, 5
had previously received corticosteroid therapy, but
had stopped 12-155 months (mean 42 months) earlier.
Bone mass at several of the sites measured was
significantly different between the controls and the
SLE patients. Patients with SLE were generally characterized by a loss in BMD at the lumbar vertebra and
proximal left femur. This was seen at primarily cortical
(intertrochanter) as well as primarily trabecular (trochanter, total femoral, lumbar) bone sites. Ward’s
triangle was the least affected (Table 1). None of the
SLE patients had a BMD reading that was below the
theoretical fracture threshold of 0.812 gm/cm2, but
SLE patients seemed more likely to develop fracture
at the lumbar vertebrae ( P = 0.0009) if bone loss were
to continue. Differences were statistically significant at
p :0.009
1.2 1.15 1.25
1.15 1.2
1.05 -
Figure 1. Box plots of lumbar bone mineral density in normal controls and in patients with systemic lupus erythematosus
(SLE) divided according to whether they were currently receiving corticosteroid (CS) treatment and according to whether
they had ever received such therapy. Boxes represent the interquartile ranges (25-75%); horizontal lines within the boxes
represent the means; vertical lines outside the boxes complete the ranges (except for outlying values, represented by
circles). Medians are not shown. As seen in the pairs of box plots shown in the middle and on the right, there were no
significant dierences between CS-treated and non-CS-treated patients, irrespective of stage of use (NS = not significant).
p = 0.0000
Figure 2. Box plots of total femoral bone mineral density in normal controls and in patients with systemic lupus
erythematosus (SLE) divided according to whether they were currently receiving corticosteroid (CS) treatment and
according to whether they had ever received such therapy. Boxes represent the interquartile ranges (25-75%); horizontal
lines within the boxes represent the means; vertical lines outside the boxes complete the ranges (except for outlying values,
represented by circles and stars). Medians are not shown. As seen in the pairs of box plots shown in the middle and on the
right, there were no significant differences between CS-treated and non-CS-treated patients, irrespective of stage of use
(NS = not significant).
each of the lumbar vertebrae (P < 0.01) (data not
Table 2 shows the BMD at different sites in the
SLE patients divided according to current treatment
or lack of treatment with corticosteroids. There were
no significant differences between the 2 subgroups at
any of the sites measured. Figure 1 shows box plots
depicting the mean and range of values for lumbar
BMD in the controls and SLE subgroups. SLE patients were also stratified according to whether they
had ever used corticosteroids at any stage of the
disease. The 3 sets of plots show clearly that while the
disease seems to have a definite effect on BMD, this is
unlikely to be due to current or past corticosteroid
therapy. Findings of BMD at the femoral sites were
similar with respect to the effect of corticosteroid
therapy (Figure 2). Values for the individual SLE
patients are shown in Figure 3.
The corticosteroid-treated and non-corticosteroid-treated SLE subgroups were comparable in
terms of height and age, but disease duration was
longer in the treated subgroup (mean 84 months, range
13-204 months) than in the untreated subgroup (mean
60 months, range 7-242 months) (P = 0.006). The
overall mean duration of disease in the SLE group was
76 months. Mean weight was, not surprisingly, higher
in the corticosteroid-treated patients (P < 0.05).
Discriminant analysis was used to determine
which of the measurements best predicted the presence
of SLE. The underlying diagnosis was the dependent
variable, while each of the measurements, including
age, height, and weight constituted the independent
variables. Total femoral BMD discriminated the patient group from the controls at step l , with a sensitivity of 76% and a specificity of 62%. The inclusion of
a reduced intertrochanteric BMD lowered the sensitivity to 54%, but increased the specificity to 74%.
Fortunately, the diagnosis of SLE is not dependent
only on measurement of BMD, since the positive
predictive value at step 1 was only 61%. Surprisingly,
the negative predictive value was 89%. The prevalence
of reduced total femoral BMD (Baye’s theorem) was
25%. When the 2 SLE subgroups were subjected to
discriminant analysis, none of the variables, including
disease duration, showed any predictive value.
All of the patients were in Steinbrocker functional class I or 11. None of the patients was using
assistive devices for any activities of daily living.
None was receiving thiazide diuretics, thyroid replacement medication, calcitonin, bisphosphonates, fluoride, calcium supplements, vitamin D, or other substances likely to interfere with bone metabolism. The
mean t SD weight of the SLE patients was 59 ? 18 kg
and that of the controls was 59 ? 12 kg (P = 0.9). The
mean height of the SLE patients was 157 ? 25 cm and
that of the controls was 162 7 cm (P= 0.01). Height
and weight did not feature as predictors in the discriminant analysis.
mldpolnts ever-cs
1 .oo
Total Femoral
.. ......
........ .
w 0..
M 0.0
Std. Dev.
p = 0.9
Figure 3. Frequency histograms of lumbar and total femoral bone
mineral density in 46 systemic lupus erythematosus patients, 27 of
whom had received corticosteroids at some time in the course of
their disease (ever-cs) and 19 of whom had not. M denotes the mean
value for the group. The differences between the ever-cs and the
never-cs groups were not statistically significant.
Multiple regression analysis was used to further
characterize the SLE group as well as the 2
corticosteroid-treated subgroups. When lumbar BMD
was used as the dependent variable, total femoral
BMD was the best predictor in the total group (R2 =
0.39) as well as the corticosteroid-treated subgroup
(R2 = 0.31). In the non-corticosteroid-treated subgroup, trochanteric BMD was the best predictor of
lumbar BMD (R2 = 0.65). When we used Ward’s
triangle as the dependent variable, the combination of
intertrochanteric, total femoral, and femoral neck
BMD predicted 79% of the variation in Ward’s triangle
BMD in the total SLE group and 89% of the variation
in the corticosteroid-treated subgroup. In the noncorticosteroid-treated subgroup, 76% of the variation
in Ward’s triangle BMD was explained by a variation
in trochanteric BMD. Clearly, then, corticosteroid
therapy, though not the primary cause of bone density
loss, was having some influence on bone metabolism
in the SLE patients, predominantly at the proximal
femur, representing cortical and trabecular bone.
Our findings for lumbar BMD differ significantly
from those in a previous report, despite similarities in
study populations, criteria for diagnosis, and measurement techniques (11). Our data suggest that SLE
causes generalized osteopenia, since we have previously reported significant cortical bone loss in SLE
(12,13). Although our study did not evaluate the relationship to disease activity or some of the other
potential mechanisms of bone loss in SLE, we believe
the findings are pertinent and justify further evaluation
and elucidation. The study by Dhillon et a1 (11) did not
show any relationship between SLE disease activity as
measured by the British Isles Lupus Assessment
Group score and lumbar BMD.
Pathogenetically, SLE could result in bone loss
through several mechanisms, e.g., effects on the kidneys (interfering with vitamin D hydroxylation or as a
result of secondary hyperparathyroidism), immobility
due to arthritis, conscious avoidance of sunshine,
inflammation-mediated osteopenia, or as a complication of corticosteroid therapy. Although secondary
hyperparathyroidism has been associated with tendinous laxity in SLE (16), the effect on bone mass in
SLE is not known. It is surprising that a recent study
using DXA was unable to demonstrate any significant
bone loss among SLE patients (1 1). Our results suggest that age and premenopausal status were unlikely
to have been responsible for the negative findings of
that investigation. The most likely reason for the
improved power of our study is the larger sample size;
our study represents the largest series of BMD measurements at the proximal femur and lumbar vertebrae
in patients with SLE.
The literature is replete with studies of osteoporosis in RA (29-31), but lacking in studies of BMD
or osteoporosis in SLE (11). Factors implicated in the
bone loss in RA include age, menopausal status, sex
hormone status, vitamin D deficiency, disability, and
corticosteroid therapy (6,32-37). There is experimental evidence that a bone resorption-stimulating factor,
which has been measured in the serum of patients with
RA (38), has some characteristics of parathyroid hormone and osteoclast-activating factor (39). Lymphokines and other inflammatory mediators such as kinins, interleukins, and TNF also stimulate bone
resorption in inflammatory disease (21,40). There is
some question about the suitability of comparisons
between RA and SLE, since RA is generally thought
to cause severe disability (41). However, osteoporosis
in RA probably occurs independently of disability,
age, and menopause (32-37).
Robinson et a1 (42) have suggested that the resorptive factor in RA may be PGE,. The possibility that
the bone loss of RA (32-37,43,44) and SLE (12,13) may
be partly explained by inflammation is strongly supported by the demonstration of inflammation-mediated
osteopenia in rats (17). However, protective mechanisms which overcome this negative effect are likely to
operate in some SLE patients (11). Further support
comes from an in vitro study of 55 patients with RA and
10 with active SLE, which demonstrated increased prostanoid activity in both groups (18). This finding is significant, since it suggests that inflammation-mediated
osteopenia is a common pathway for bone resorption
in patients with RA and SLE. Yoneda and Munday (19)
and Dominiquez and Mundy (20) have shown that PGE,
is the essential cofactor in enhanced production of
osteoclast-activating factor from macrophages. Previously, when we compared metacarpal measurements in
patients with RA and SLE, periosteal resorption was
more severe in SLE while endosteal resorption was
characteristic of RA (12), suggesting possible differences
in the mechanism of osteoporosis in the 2 diseases.
Our finding of similar bone mass in corticosteroid-treated and non-corticosteroid-treated patients is similar to recent findings in corticosteroidtreated patients with RA (44). Some of our treated
patients no longer required corticosteroid therapy, but
the very insignificant probability value (P > 0.5) as
well as the sensitivity of the BMD measurement
technique (45,46), make the likelihood of a Type I1
(beta) error seem small. Guyatt et a1 (47), in a critical
review of the literature, drew attention to the defective
methodology of many early studies of corticosteroidinduced osteopenia, in which confounding variables
were not adequately addressed. It is not clear whether
some form of reparative process plays a role in young
corticosteroid-treated patients, since microscopic
studies of the endosteal surface (48) have shown that
corticosteroids impair bone formation, resulting in
uncoupling. Corticosteroids have also been shown to
reduce absorption of calcium from the gut (49). It is
possible that corticosteroids improve arthritis in SLE,
thereby improving overall function. Alternatively, by
reducing inflammation, they may overcome the effect
of inflammation-mediated osteopenia by reducing
PGE:, or osteoclast-activating factor levels. TNF levels are considered to be low in active SLE (21). It is
interesting that Saville and Kharmosh (50), several
years ago, proposed that corticosteroids may have a
protective effect on bone in premenopausal RA patients. It should also be remembered that corticosteroid treatment is generally reserved for patients with
severe disease, which may further confound the issue.
The sensitivity of the DXA technique in measuring trabecular bone is well established (45,46,51).
The lateral projection offers little advantage in young
subjects, in whom aortic calcification and osteophytes
are less likely to confound calcium status (52). Our
study was not able to demonstrate any significant
relationship of BMD to duration of disease. In RA
(5334) and postmenopausal osteoporosis, it is reported that maximal bone loss occurs within the first 5
years. We were not able to adequately evaluate this
aspect of bone loss in SLE, which would require
longitudinal evaluation of the same patients at a future
date, as well as larger numbers. Patients with early
disease should also be studied.
Although none of the patients manifested any of
the symptomatic complications of osteopenia, they
were significantly closer to the fracture threshold than
were the normal controls. Asymptomatic fractures were
not excluded by radiographic studies, but they were not
seen on the densitometric image. The lower peak bone
mass of our patients puts them at greater risk for fracture
after menopause (55). SLE may begin in old age (lo), and
survival in SLE has been considerably improved in
recent years (9,56,57). This is due to multiple factors, but
it implies that more female patients with SLE are likely
to reach menopause. Estrogens are known to aggravate
SLE (58), so alternative bone-conserving strategies need
to be considered. Our findings do not support the need
to replace prednisone with deflazacort in these patients (59,60).However, we believe there is a need to
evaluate agents such as calcitonin and bisphosphonates
in controlling bone loss in SLE. The use of calcium
supplements with or without vitamin D should be encouraged for these patients, especially in light of recent
evidence that this may protect against fracture (61).
Some studies have failed to show any beneficial effects
of calcium and vitamin D in preventing corticosteroidrelated bone loss (62).
There are no data on femoral BMD in SLE
previously reported in the literature. Ours is the first
description of reduced total femoral BMD in SLE
patients studied using dual-energy techniques. BMD at
Ward’s triangle is generally considered the most predictive of hip fracture (63,64), so the risk of fracture at
the femur may not be increased in our subjects. We
experienced difficulties in accurately localizing the
Ward’s triangle area with our machine at the time of
scanning of some subjects. This may explain the
apparent lack of demineralization in that region in our
patients. If SLE patients are prone to microfracture as
a result of osteopenia, this could explain the pathogenesis of AVN of the femoral head in patients with SLE
(65,66), which may manifest several years after discontinuation of corticosteroid therapy (66).
The results of regression analysis confirm that
corticosteroids do have an effect, though not a primary
one, on bone metabolism. However, contrary to some
reports (67-69), this effect seems to be accentuated at
the femur but not at the vertebrae. It is not clear to us
why different femoral sites are predictive of lumbar
BMD and Ward’s triangle BMD according to treatment or lack of treatment with corticosteroids. Lumbar BMD was a poor predictor of Ward’s triangle
BMD in this study. The discriminant analysis suggests
that the underlying disease was the most important
determinant of bone loss in SLE.
Further research is needed in order to evaluate
the prevalence of complications of osteopenia in SLE
and to prevent these in elderly patients. In addition,
carefully planned studies are needed to clarify the
controversy regarding corticosteroid-induced bone
loss. This is important since these potentially lifesaving drugs are sometimes denied to patients who
could benefit from them, because of likely adverse
effects, particularly osteoporosis. Careful attention to
the potential mechanisms would help in the development of strategies for prevention. Lower salivary
testosterone levels (70) would not explain the differences in BMD among SLE patients, since the changes
were not confined to corticosteroid-treated patients.
Comparisons with young, corticosteroid-treated patients with other rheumatic diseases, with asthma, and
with organ transplants would add to our knowledge
about corticosteroid-induced osteoporosis.
Based on the results of the present study, we
conclude that systemic lupus erythematosus causes
significant trabecular bone loss at the lumbar vertebrae
and the left femur, high-dose corticosteroids do not
appear to cause significant trabecular bone loss in
SLE, and trabecular bone loss in SLE is most likely an
effect of inflammatory substances, rather than disability or aspects of therapy. Caution should be exercised
in interpreting negative results that may be derived
from studies using small samples of subjects. Finally,
we believe that further, careful research of bone
metabolism in SLE is needed.
We wish to express our thanks to the normal volunteers and SLE patients who agreed to participate in the
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loss, lupus, trabecular, systemic, erythematosus, density, mineraly, bones
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