CME

“How would you manage these patients with SLE? Cases and
Perspective”

Pembimbing:
dr. Wahyu Djatmiko, Sp.PD, KHOM

Disusun oleh:
Aletha Ayu 1710221018

STAF MEDIK FUNGSIONAL ILMU PENYAKIT DALAM

RSUD PROF.DR. MARGONO SOEKARJO
FAKULTAS KEDOKTERAN
UNIVERSITAS PEMBANGUNAN NASIONAL VETERAN
JAKARTA
2019
 HALAMAN PENGESAHAN
CME
“How would you manage these patients with SLE? Cases and
Perspective”

Disusun oleh:

Aletha Ayu 1710221018

Diajukan untuk Memenuhi Syarat Ujian Kepaniteraan Klinik di

Bagian
Ilmu Penyakit Dalam RSUD Prof.Dr.Margono Soekarjo
Purwokerto

Telah disetujui,
Pada tanggal: 2019

Mengetahui,
Dokter Pembimbing

dr. Wahyu Djatmiko, Sp.PD, KHOM

 Jeanette is a 41-year-old woman with a 5-
year history of mild mucocutaneous and
musculoskeletal lupus. Her symptoms are
reasonably controlled with daily
hydroxychloroquine (HCQ) 300 mg, but
lately she is concerned about “feeling tired
all the time” and has some wrist pain.
Jeanette is currently under a lot of stress
from her work as a Certified Public Accountant. She has been trying to
manage this stress through increased physical activity, which involves a
new kettlebell workout. She feels that regular exercise helps her manage
her fatigue but thinks overexertion might be causing the wrist pain.

Discussion

Systemic lupus erythematosus (SLE) is a complex, multisystem

autoimmune disease associated with a wide range of clinical
manifestations that affects over 300,000 adults in the United States.[2] As
a result of the disease heterogeneity, the prevalence and incidence of SLE
have been challenging to estimate. Recent epidemiologic research using
the American College of Rheumatology (ACR) classification criteria for
SLE and evaluating a wide range of data sources, including lupus
registries, indicates that globally, North America has the highest
estimates for incidence and prevalence (approximately 5.5/100,000 and
75/100,000 person years, respectively).[3-7] These data also show that in
the United States, both incidence and prevalence of SLE are higher in
women compared with men across every ethnic group and age. Incidence
and prevalence of SLE in the United States are highest in African
Americans. Asian and Hispanic populations have higher incidence and
prevalence compared with Caucasians but lower than African Americans.
The overall average age at diagnosis is 39 years, and 34 years for African
American patients with SLE.[7]

Although the causes of SLE are not fully defined, symptoms are likely
driven by the production of pathogenic autoantibodies and dysregulated
immune responses.[8]SLE symptoms vary from mild skin and joint
involvement to life-threatening renal, hematologic, or central nervous
system (CNS) involvement. The most prominent constitutional
symptoms of SLE at disease onset include fatigue, fever, and weight loss.
Fatigue occurs in a majority of patients, further contributing to pain and
psychologic distress.[9] Skin (including the “butterfly rash”) and
musculoskeletal symptoms are common symptoms in 80% and 90% of
patients, respectively,[10] and fever is present in approximately 50% of
patients with active SLE.[11]

The diagnosis of SLE is generally based on clinical and laboratory

findings. The ACR or Systemic Lupus International Collaborating
Clinics (SLICC) Consensus criteria can also be used as further guidance
in identifying clinical features of SLE.[12,13] ACR criteria require the
presence of 4/11 criteria. The SLICC criteria were developed in 2012 and
require the presence of 4/17 criteria (at least one clinical criterion for the
classification of SLE and 1 of the 6 immunologic criteria) or the presence
of biopsy-confirmed lupus nephritis accompanied by antinuclear
antibodies (ANA) or anti-double-stranded (dsDNA) antibodies (Table 1).

Table 1. Criteria for the Classification of SLE[12,13]

ACR Criterion Definition SLICC Clinical Criteria*

Malar rash Fixed erythema, flat or  Acute cutaneous lupus

raised, over the malar
eminences, typically sparing
the nasolabial folds
Photosensitivity Skin rash as a result of
unusual reaction to sunlight,
observed by patient or
clinician
Discoid rash Erythematosus raised patches
with adherent keratotic
scaling and follicular
plugging; atrophic scarring
may occur in older lesions
erythematosus, including
“butterfly rash”
 Chronic cutaneous lupus
erythematosus (eg,
localized/generalized
discoid lupus
erythematosus)
 Oral ulcers (on palate and/or
nose)
 Non-scarring alopecia
 Synovitis (≥ 2 joints) or
tenderness on palpation (≥ 2
joints) and morning stiffness
(≥ 30 min)
 Serositis (pleurisy or
Oral ulcers Oral or nasopharyngeal
ulceration, usually painless,
observed by a clinician
Arthritis Nonerosive arthritis
involving 2 or more
peripheral joints,
characterized by tenderness,
swelling, or effusion
Serositis Pleuritis
 Convincing history of
pleuritic pain or rubbing
heard by a clinician or
evidence of pleural effusion
OR
Pericarditis
 Documented by
electrocardiogram (ECG),
rub, or evidence of
pericardial effusion
pericardial pain for > 1 day)
 Renal involvement
 Urine protein–to-creatinine
ratio (or 24-hour urine
protein) representing 500
mg protein/24 hours
 OR red blood cell casts
 Neurologic involvement
(eg, seizures, psychosis,
myelitis)
 Hemolytic anemia
 Leukopenia (< 4000/μL) or
lymphopenia (< 1000/μL)
 Thrombocytopenia (<
100,000/μL)

Renal disorder Persistent proteinuria greater

than 500 mg/24 hours or >
3+ if quantitation not
performed OR
Cellular casts
 May be red cell, hemoglobin,
granular, tubular, or mixed

Neurologic Seizures OR psychosis

disorder  In the absence of offending
drugs or known metabolic
derangements (uremia,
 ketoacidosis, or electrolyte
imbalance)

Hematologic Hemolytic anemia with

disorder reticulocytosis OR
Leukopenia
 < 4000/mm3 total on 2 or
more occasions OR
Lymphopenia
 < 1500/mm3 on 2 or more
occasions OR
Thrombocytopenia
 < 100,000/mm3 (in the
absence of offending drugs)

ANA Abnormal ANA titer by

immunofluorescence or an
equivalent assay at any point
in time and in the absence of
drugs known to be associated
with “drug-induced lupus”
syndrome

Immunologic Anti-DNA: antibody to SLICC Immunologic

disorders native DNA in abnormal
titer OR
Anti-Sm antibodies: presence
of antibody to Sm nuclear
antigen OR
Positive finding of
antiphospholipid antibody
based on:
 An abnormal serum level of
immunoglobulin G (IgG) or
Criteria
 ANA level above laboratory
reference range
 Anti-dsDNA antibodies
 Anti-Sm antibodies
 Antiphospholipid antibodies
(anticardiolipin and anti-β2-
glycoprotein I
[immunoglobulin A (IgA)-,
IgG-, or IgM-] antibodies;
 immunoglobulin M (IgM)
anticardiolipin antibodies
 On a positive test result for
lupus anticoagulant using a
standard method, or
 On a false-positive serologic
test for syphilis known to be
positive for at least 6 months
and confirmed by Treponema
pallidum immobilization or
fluorescent treponemal
antibody absorption test
false-positive venereal
disease research laboratory
[VDRL] test)
 Low complement (C3, C4,
or CH50)
 Direct Coombs test (in the
absence of hemolytic
anemia)

* Criteria are cumulative and need not be present concurrently.

The goals of SLE treatment are to control disease activity by decreasing

autoimmunity and inflammation, as well as preventing damage to organ
systems. Nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose
glucocorticosteroids, antimalarial medications, immunosuppressants, and
biologic agents are the therapeutic mainstays for treating SLE
symptoms.[14] NSAIDs are used to treat fever, arthritis/arthralgias and
other inflammatory symptoms (serositis). Systemic glucocorticosteroids
are used to treat disease activity and flares with the goal to use the lowest
possible dose for the shortest period of time. Antimalarial medications
such as HCQ are effective in managing SLE by reducing disease activity,
decreasing the risk for flares, and improving mortality.[15] Serious adverse
effects are extremely rare for antimalarials. Data suggest that antimalarial
therapies also improve renal responses when used as adjuvant therapy
with mycophenolate mofetil (MMF) and reduce thrombotic
events.[16] The 2008 European League Against Rheumatism (EULAR)
guidelines recommend that all patients with SLE are candidates for
antimalarial medications unless there are contraindications.
Immunosuppressive agents (eg, azathioprine, MMF, or methotrexate
[MTX]) may be considered for treating disease that is not adequately
controlled by antimalarials.[17]

Lifestyle modifications such as smoking cessation, diet, weight loss, and

physical activity are recommended as nonpharmacologic management
strategies for patients with SLE.[14] Aerobic physical activity in particular
has shown particular efficacy for managing symptoms of fatigue and is a
recommended lifestyle modification strategy to reduce the risk for
cardiovascular disease.[8]

Case 1 Continues

You conduct a focused medical history, which includes questions about

Jeanette’s current medications. When you ask the patient to describe
whether she is currently taking her antimalarial medications, she does not
respond and instead tells you that her primary care provider prescribed
oral prednisone, which she takes when she needs “a little extra” pain
relief. Physical examination reveals that the patient has a low-grade
fever, tenderness and swelling in several proximal interphalangeal joints
and both wrists, and active Raynaud's phenomenon. Jeanette tells you
that while she normally needs a nap for an hour or so each day, at the
moment she “wants to sleep all day.”

Discussion

Raynaud’s phenomenon, a vasospastic process that is triggered by cold

exposure, is present in up to 50% of patients with SLE.[11] While fever is
likely due to SLE in this case, infectious complications can develop in up
to 50% of patients with SLE, especially involving the skin, respiratory,
and urinary systems.[11] The impaired immune function in SLE
predisposes patients to infections, the majority of which are caused by
bacteria.[18] Additionally, viral infections including Epstein-Barr virus,
cytomegalovirus, and varicella-zoster virus can be challenging to
distinguish from active SLE.[19] To reduce the risk for morbidity and
mortality associated with infections, it is important to keep
influenza, Pneumococcus, hepatitis B virus, and tetanus vaccinations up
to date as part of routine patient monitoring.[17] Patients who are
immunosuppressed or taking high-dose glucocorticosteroids should not
receive live vaccines.

Low- and nonadherence to HCQ are common in patients with SLE. Up to

75% of SLE patients do not take their medications as
prescribed.[20] Several factors contribute to low medication adherence in
 SLE, including depression, higher SLE activity, fear of treatment side
effects, cognitive deficits, lower socioeconomic status, polypharmacy,
and the high cost of medications.[21,22] Patients with increased disease
severity may also be less likely to adhere to antimalarial medication due
to loss of confidence in treatment efficacy or, conversely, become
comfortable about missing, delaying, or reducing antimalarial doses.
Patients may also become comfortable with their level of functioning and
rationalize new symptoms, as in Jeanette’s case (ie, explaining joint pain
in terms of strain from a new physical workout). Low- and nonadherence
to medications are significant drivers of poor patient outcomes, including
poor disease control, decreased quality of life, and a higher rate of
outpatient rheumatology, primary care, and emergency room
visits.[22] Conversely, medication adherence in SLE reduces disease

Clinical Disease Activity Serologic Disease

Activity

Inflammatory manifestations Autoantibodies

 Mucocutaneous (skin rashes, oral/nasal ulcers,  Anti-dsDNA
alopecia)  Anti-C1q
 Musculoskeletal (polyarthritis, myositis)
 Serositis
 Glomerulonephritis
 Neurological (cerebritis, seizures, neuropathies,
myelitis, others)
 GI and ophthalmic manifestations

Noninflammatory manifestations (autoantibody-  Decreased serum

mediated) complement
 Hematologic (cytopenia)  Increased complement
 Some neurologic manifestations (eg, cognitive split products
dysfunction, psychosis, myasthenia gravis)
 aPL-mediated ischemic/microischemic lesions

activity and risk for flares.

Given the complexity of SLE clinical presentations, effective patient-
provider communication is a key strategy that can support adherence to
pharmacologic therapy. Clinicians should not assume that patients are
taking their medications, including antimalarials, as prescribed. It is
important to ask specific questions of patients about their adherence to
antimalarial therapy, including whether patients have missed or delayed
HCQ doses and if so, how often. However, patients might not be
forthcoming about low- or nonadherence. Other strategies for
determining adherence include measuring plasma HCQ levels. As HCQ
has a long elimination half-life, low blood HCQ concentrations represent
a feasible marker of low adherence and can be reliably quantified via
high-performance liquid chromatography (HPLC).[21] Once poor
adherence is uncovered, clinicians should discuss patient concerns, such
as fears about HCQ side effects. Clinicians should also provide education
about safely and effectively using medications, discuss alternative dosing
options (eg, reduce the daily number of HCQ doses), and work to build
trust and boost patients’ self-efficacy by anticipating and listening to
patient concerns about treatment.[20]

Discussion

Although the presenting pattern of symptoms often prevails throughout

the disease course, SLE is characterized by unpredictable periods of
exacerbation and remission, in which flares of disease activity contribute
to progressive damage and considerable morbidity.[23] Although ANA are
evaluated as part of the approach to diagnosis for patients with suspected
SLE (Table 2), they are not routinely monitored. Serologic monitoring
parameters for lupus disease activity include the presence of anti-dsDNA
antibodies and low C3 and/or C4 (Table 2).[14]

Table 2. Clinical and Serologic Disease Activity in SLE[24]

Assessment of disease activity, organ involvement, risk factors (ie,

infection, cardiovascular disease), and complications is an important
aspect of the standard of care for monitoring and managing patients with
SLE, and new clinical manifestations such as arthritis or skin lesions
should be noted and documented.[14,17] EULAR and the British Society
for Rheumatology guidelines recommend assessing patients with inactive
disease at 6- to 12-month intervals for complete blood count (CBC) with
differential, erythrocyte sedimentation rate (ESR), C-reactive protein
(CRP), serum albumin, serum creatinine (or estimated glomerular
filtration rate [eGFR]), and urinalysis and urine protein/creatinine
ratio.[14,25] These routine laboratory parameters are also recommended for
patients presenting with evidence of active disease. Serum evidence of
leukopenia, anemia, or thrombocytopenia may reflect active disease,
while ESR and CRP elevations can also reflect increased disease activity
and accrued damage; however, elevations in acute phase reactants are
common in patients with SLE and might not be reliable markers of
disease activity.[26,27] Patients with active disease are evaluated as
frequently as required by the active manifestation being treated, on
average every 1 to 3 months.

Complement levels are also associated with active disease. Low C3/C4
and/or elevated C3/C4 activation products may indicate active
lupus/lupus nephritis, which is a severe complication of SLE that
increases morbidity, including end-stage renal disease, and
mortality.[11] There is a lifetime prevalence of kidney involvement for
approximately 50% of SLE patients.[2] Assessment to exclude kidney
involvement should include urinalysis with examination for urinary
sediment, serum creatinine, eGFR, and protein-to-creatinine ratio to
assess severity of glomerular disease.[17]Increased serum titer of anti-
dsDNA and low complement levels (ie, CH50, C3, C4) are indicative of
flare.[23]

Discussion

Flares are common occurrences throughout the course of SLE and can
result in organ damage. Although accepted definitions of flare are
inconsistent, they are broadly defined as measurable increases in or
worsening of disease activity in one or more organ systems.[29] Flares are
typically categorized as mild, moderate, or severe, and high SLEDAI
scores are predictive of SLE damage accumulation and mortality (Table
3).
Table 3. Examples of Mild, Moderate, Severe Flares[25]

Mild Moderate Severe

SLEDAI < 6 SLEDAI 6-12 SLEDAI > 12

And/or And/or And/or

Clinically stable with no life- More serious manifestations Organ- or life-threaten

threatening organ
involvement (eg, arthralgia,
fatigue, mucocutaneous
lesions, recurrent episodes of
ulcers, mild pleuritis)
including fever, lupus-
related rash, cutaneous
vasculitis, alopecia with
scalp inflammation,
arthritis, pleurisy,
pericarditis
(eg, widespread rash,
myositis, severe pleur
and/or pericarditis, as
enteritis, myelopathy,
psychosis, acute confu
optic neuritis)

Predictors of flare include young age at SLE diagnosis (< 25 years),

lupus nephritis prior to baseline visit, and immunosuppressive treatment
for SLE.[30] Based on data from the belimumab trials, predictors of
moderate-to-severe flares in patients being treated with standard
therapies included renal, neurologic, or vasculitic involvement, elevated
anti-dsDNA, or high B lymphocyte stimulator levels, and low C3.[23]

Several instruments have been developed to assess disease activity and

flare. Several versions of the SLEDAI are in use: the Safety of Estrogens
in Systemic Lupus Erythematosus National Assessment (SELENA)-
SLEDAI (an instrument specific to flare measurement), SLEDAI-2K,
and Hybrid-SLEDAI. It is important to be mindful of the version of the
SLEDAI you are using as your score is likely to be different depending
on the instrument used. In addition to SLEDAI, other instruments used in
clinical trials and in research include the British Isles Lupus Assessment
Group (BILAG) and the Revised Systemic Lupus Activity Measure
(SLAM-R). However, these instruments are complicated to use and
difficult to score and have not been adopted in practice.[29] Moreover,
physician-completed indices typically assess SLE disease activity via
clinical and/or laboratory findings and not the extent to which the disease
impacts patient health-related quality of life and functioning. Patient-
reported outcomes (PRO) measures provide additional information
concerning disease impact on health-related quality of life and
functioning that are not captured by physician assessment.[31] PRO
instruments used in research settings include the Medical Outcomes
Study Short Form 36 (SF-36) and SLE-specific tools such as Lupus
Quality of Life (LupusQoL) and LupusPRO. The Lupus Impact
Tracker (LIT) is a short tool that can be integrated into clinical practice to
assess disease impact on patients and support constructive dialog with
patients about treatment planning and disease management.[32] While
symptoms of mild flare can be subtle and may require minimal or no
intervention to control, severe flares are clinically significant and require
a change in treatment.

Case 1 Continues

Laboratory findings (Table 4) and disease activity assessment of the

patient using SLEDAI indicates worsening disease activity. Your
diagnosis is SLE with an arthritis flare and you recommend a short
course of oral prednisone 10 mg/day. You also suggest that Jeanette keep
a daily diary of her symptoms to monitor fatigue and pain. You see
Jeanette again for follow-up at 4 weeks and again at 8 weeks after
initiation of prednisone; however, at 8 weeks, neither the patient’s
symptoms nor disease activity measures have improved. You increase
steroid dosing to 20 mg/day, and after 3 months, there is some
improvement but steroid toxicities start to become apparent.

Table 4: Relevant Laboratory Results

Laboratory Test Results

Hemoglobin 12.2 (11.5-15.5 g/dL)

White blood cell count 5.3 (4-11 x109/L)

Platelet count 180 (150-450 x109/L)

ESR 33 (< 20 mm/h)

CRP 14 (< 5 mg/L)

eGFR > 60 ( > 90 mL/min/1.73m2)

C3 72 (80-180 mg/dL)

C4 6 (10 -45 mg/dL)

dsDNA 525 (< 30 IU/mL)

Urinalysis Without abnormalities

Discussion

Patients with moderate SLE, especially with high anti-dsDNA and low
complement, who do not respond to HCQ and short-course prednisone,
may require additional therapy. MTX is a disease-modifying
antirheumatic drug (DMARD) approved for treating rheumatoid arthritis
(RA). Although not approved for the treatment of SLE, it can be used to
alleviate joint pain and swelling in mild SLE, as well as lupus skin
rashes.[33] The persistent serologic unrest evident in Jeanette’s case makes
MTX not an ideal therapeutic option for this patient. Abatacept is
currently approved for RA and has shown some efficacy in patients with
SLE refractory to conventional therapies but is also not US Food and
Drug Administration (FDA)-approved for this indication,[34] although
clinical trials investigating abatacept in SLE arthritis are currently
ongoing. Use of etanercept in SLE is limited by concerns of increasing
disease activity.[36] Intravenous (IV) or subcutaneous belimumab is an
anti-B-lymphocyte stimulator (BlyS; also known as anti-B-cell activating
factor [BAFF] or anti-CD257) monoclonal antibody that is FDA
approved as add-on therapy for adults with persistently active SLE with
skin and/or joint disease that do not respond to standard therapies. There
are currently no data comparing the effectiveness of belimumab to other
agents in SLE, nor are there data to establish the most effective
combination strategy.

Immunosuppressant therapy is used in more moderate-to-severe nonrenal

cases of SLE when high-dose corticosteroids or antimalarial medications
have failed to control disease activity or to reduce flares. Current options
include cyclophosphamide, azathioprine, and MMF. These agents exert
suppressant effects on the immune system by reducing T-cell and B-cell
proliferation as well as via DNA and RNA
disruption.[35] Cyclophosphamide is not approved for SLE but is typically
used as induction treatment for severe SLE and can be followed by other
maintenance therapies such as azathioprine or MMF.[36] Although MMF
has not been specially evaluated in nonrenal lupus, accumulating data
suggest that MMF combined with steroids can reduce moderate and
severe SLE disease activity as well as renal and nonrenal
flares.[19,37] These agents are generally well tolerated, with side effects
including myelosuppression, hepatotoxicity, renal dysfunction, increased
risk of infection, and cancer.

Cyclophosphamide has been associated with amenorrhea, especially with

high doses, and risk for infertility.[38] MMF is better tolerated and less
toxic than cyclophosphamide.[39,40] In fact, due to its less severe side
effect profile, the 2012 ACR Clinical Practice Guidelines for Lupus
Nephritis established MMF as the preferred induction agent compared
with cyclophosphamide for patients in whom fertility preservation is a
major consideration.[41]

Discussion

Patient perspective is a critical consideration in the context of treatment

planning and flare management. Clinicians and patients need to work
together to make decisions about appropriate treatment strategies based
on clinical evidence that balances risks and expected outcomes with
patient preferences and values.[42] As data continue to accumulate on
treat-to-target strategies with the goal to achieve the lupus low disease
activity state (LLDAS) (Figure 1), physicians might start to consider
LLDAS and remission as the correct targets aimed at decreasing long-
term morbidity and mortality in SLE.

Figure 1. Lupus Low Disease Activity State[43]

Case 1 Conclusion

Jeanette would prefer to avoid injectable therapies (IV or subcutaneous)

at this time. You initiate treatment with MMF, 1000 mg twice daily. At
follow-up, Jeanette is tolerating her medication and both her symptoms
and SLEDAI scoring have improved. When you see her at future follow-
up visits, in addition to monitoring therapeutic drug levels, you provide
additional education about strategies for managing fatigue and avoiding
sun exposure and periodically assess her general education needs on
SLE.
Which of the following laboratory tests would you include as part of your
evaluation of Jeanette to gauge disease activity?

Your Peers Chose: ANA

17%
Anti-Ro/La, anti-ribonucleoprotein (RNP)
18%
Anti-dsDNA titer
62%
Anti-Sm
3%
Anti-dsDNA titers fluctuate with disease activity and are considered the
most useful laboratory tests to predict flare. EULAR guidelines
recommend that anti-dsDNA antibodies be monitored every 3 to 6
months or at each visit.[17]

Question 2 of 3
Which of the following is the next best step before prescribing MMF to
the patient?

Your Peers Chose:

Discuss with the patient the benefits and risks of all treatment options
available
73%
 Tell the patient she has to adhere to her treatment if she wants to
improve
13%
Tell the patient to follow up in 6 months
6%
Inform the patient that MMF is the best option for her and provide an
informational handout on the drug
8%
Shared decision-making is a key component of patient-centered SLE
management.[42]

Question 3 of 3
What would you now recommend as the next best approach in treatment?

Your Peers Chose:

Reassure the patient that tapering remains the right course of action
18%

Suggest a steroid dose that satisfies both you and the patient
10%
Acknowledge the challenge of tapering and suggest that it is time to
consider treatment with belimumab
68%
Start the patient on rituximab 4%

Belimumab has shown efficacy for reducing disease activity and steroid
use in patients with SLE when used in combination with standard of
care. [60]

Below are all the test questions with an explanation of the correct
answer.

1. Terrence is a 33-year-old man with a 5-year history of systemic lupus

erythematosus (SLE). He has stopped taking his SLE medications
because he feels that they are not effective and are only making his
disease worse. He complains of fever, fatigue, and joint pain. Which of
the following is the next best step to get this patient back on track with
his treatment regimen?

Answer: Discuss the risks and benefits of his treatment options

Effective patient-clinician interaction and shared decision making enable
patients to actively participate in their treatment plan decisions. This
sharing of information and recognition of patient preferences can lead to
more favorable outcomes as well as adherence to medication. It is
important for healthcare providers to educate patients on their disease,
treatment options, and medication-related complications. Once the
patient is well informed, he or she can contribute to the decision-making
process of the treatment plan, help set treatment goals, and feel more
empowered to ask questions to better understand SLE. Medication
adherence, in turn, is more likely when patients are informed and
engaged in their care.