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C H A P T E R 1 2
Rheumatology
Molly Forlines Mary Ann Picone Anthony M. Iuso Michael A. Ciaramella
Rheumatoid Arthritis and Systemic Lupus
Erythematosus
Rheumatoid arthritis (RA) and systemic lupus erythematosus
(SLE) are autoimmune diseases with rheumatologic
manifestations that can often mimic the symptoms of multiple
sclerosis (MS). Marrie et al recently included RA in a systematic
review of epidemiological studies assessing the relation between
autoimmune diseases and MS. 1 Their review included three
studies (two population based) that addressed the incidence of
RA in MS populations and calculated an estimated incidence of
0.21%. Additionally, they included 17 studies assessing the
prevalence of RA in MS and calculated an estimated prevalence
of 2.92%. Two of the studies included found the prevalence of
RA before MS diagnosis to be 0.22% to 1.17%.
2,3
The review
also included 11 studies that assessed the relation between MS
and SLE and estimated an incidence rate of SLE in MS
populations to be 0.02% to 0.35% and a prevalence of 0.14% to
2.90%.
1,4,5
The analysis by Marrie et al, although not definitive, suggests that
the incidence and prevalence of RA and SLE in MS is not
significantly different from that of RA and SLE in the general
population. However, there have been a number of similar trends
found in all three autoimmune diseases. The three conditions
share rheumatologic symptoms, and new evidence suggests the
possibility of a similar pathogenesis between RA, SLE, and MS.
Most notably, all three are significantly more likely to occur in
females than in males, particularly females of childbearing age.
6-8
On a cellular level, all three are characterized by excess
Th1/Th17 cytokine production, B lymphocyte involvement, and
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the role of tumor necrosis factor (TNF) and extracellular vesicles.
3,9-11
For the rheumatologist, there is a great deal of overlap between
both the clinical manifestations of RA, SLE, and MS and their
subsequent treatment. However, some common RA and SLE
treatments can exacerbate MS symptoms and even advance the
disease. The following chapter will explore the signs and
symptoms of these diseases, their treatments, and the implications
of some of these treatments in MS.
Rheumatoid Arthritis
RA is among the most common chronic inflammatory diseases
and primarily involves the joints. 12 Like MS, RA has many extra-
articular manifestations that must be considered during diagnosis
and treatment, such as rheumatoid nodules, pulmonary
involvement, vasculitis, and other systemic comorbidities. If left
untreated, joint destruction and inflammation can lead to
decreased physical function and the inability to carry out basic
tasks or maintain employment. 13 The exact etiology of RA is
unknown. It appears to involve multiple cell types such as T and
B cells and genes such as class II MHC genes.
14
RA should be suspected if an adult patient presents with
inflammatory polyarthritis. The location and duration of morning
stiffness can suggest an alternative diagnosis, as patients with RA
should report pain and/or stiffness in the peripheral joints (not the
low back) for at least 30 minutes, with pain improving with
activity.
15,16
If symptoms of arthritis have been present for less
than 6 weeks, they may be due to an acute viral polyarthritis
rather than RA; the longer the symptoms persist, the more likely
an RA diagnosis becomes. In addition to performing a complete
physical examination to assess for synovitis and the presence and
distribution of swollen or tender joints, the laboratory tests
indicated in Table 12.1 should also be considered. Diagnosis is
also confirmed by exclusion of similar diseases such as psoriatic
arthritis, acute viral polyarthritis, polyarticular gout, and SLE.
13
Systemic Lupus Erythematosus
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SLE is a chronic inflammatory disease of unknown etiology that
can impact virtually every organ. Like MS, SLE preferentially
affects females of childbearing age and is less prominent in
prepubescent and postmenopausal women, suggesting that female
sex hormones may play a role in pathogenesis. 8 Physical
symptoms include mucosal ulcers, inflammatory polyarthritis,
photosensitivity, and, most commonly, acute cutaneous lupus
erythema, which presents as erythema in a malar distribution over
the cheeks and nose and is commonly referred to as “the butterfly
rash.” 17 Patients with SLE are at risk for developing
neuropsychiatric manifestations, which involves depression,
encephalopathy, coma, and psychosis and occurs in
approximately 50% of patients with SLE. 18 Like RA, SLE
involves T and B cell activity and is associated with class II MHC
genes.
19
SLE is diagnosed based on clinical and laboratory findings, but
the clinical heterogeneity and lack of pathognomonic features can
deter a definitive diagnosis. Additionally, patients may present
with only a few clinical indications of SLE, which often resemble
other autoimmune diseases or infections. 19 Demographics should
be considered when evaluating a patient for SLE. Like MS, it is
more common in women of childbearing age. However, MS is
more common in women of European descent, whereas SLE
disproportionately affects African Americans, Asians, and
Hispanic Americans. In addition to routine laboratories and
urinalysis, abnormalities in antinuclear antibodies,
antiphospholipid antibodies, C3 and C4 or CH50 complement
levels, and erythrocyte sedimentation rate and C-reactive protein
levels could support a diagnosis of SLE.
How Do RA and SLE Compare With MS?
Patients with MS present with pain in the extremities but not
specifically the joints. 20 MS is classified as an immune-mediated
inflammatory demyelinating disease of the central nervous
system, and clinical features are far less specific than that of RA
or SLE. Patients with MS report migraines, painful tonic spasms,
and neuropathic pain. 21 The most useful diagnostic tool in
support of an MS diagnosis is magnetic resonance imaging (MRI)
and would demonstrate multifocal areas of demyelination with
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loss of oligodendrocytes and astroglial scarring. Disease
progression is monitored through annual MRIs.
22
A key feature of MS is the presence of oligoclonal bands (OCBs)
found in the cerebrospinal fluid (CSF) obtained during a lumbar
puncture. OCBs are found in up to 95% of patients with clinically
definite MS.
22,23
A positive CSF analysis is based on the presence
of OCBs or by an increased immunoglobulin G (IgG) index
without an increased IgG index in blood serum; if there is an
increased IgG index present in blood serum, alternative diagnoses
should be considered. Apart from the presence of OCBs, the CSF
appearance and pressure are normal. It should be noted that the
presence of OCBs in the CSF alone is not enough to confirm a
diagnosis of MS; up to 8% of CSF samples from patients without
MS contain the bands. 22 This is especially important given that
CSF samples from patients with neuropsychiatric SLE have been
shown to contain OCBs. 23 Please refer to Table 12.1 for
similarities and differences in the diagnoses of these three
diseases.
Table 12.1
Diagnostic Results for Rheumatoid Arthritis (RA), Systemic Lupus
Erythematosus (SLE), and Multiple Sclerosis (MS)
19,22-25
Test RA SLE MS
Antinuclear
antibody
Positive in
40%-45% of
patients at a
dilution of
1:40
Recommended
that tests be
run at a
dilution of
1:160
Positive in
virtually all
patients at some
time during
course of
disease at all
dilutions
If negative but
suspicion of
SLE high, more
antibody testing
necessary
Insignificant at
all dilutions
Rheumatoid
factor (RF)
Positive
50%-70% of
the time
Higher the
titer, stronger
likelihood of
RA
Positive in
20%-30% of
patients with
SLE
Negative
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