TRIPASS XR تري باس

 

2

Additional clinical presentation of SLE may include the development of

antiphospholipid antibodies (e.g., lupus anti-β2-glycoprotein, IgG and IgM

anticardiolipin antibodies, and IgG and IgM anti-β2-glycoprotein I) in the blood and

places patients with SLE at increased risk for developing blood clots.

30 Livedo

reticularis is a common feature of antiphospholipid syndrome (APS), which will be

further discussed in the hematologic section. Common symptoms of SLE are

described in Figure 33-1. Other major organ systems may also be affected by SLE,

including the nervous system, cardiovascular, pulmonary, gastrointestinal (GI), renal,

and hematologic.

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Table 33-2

Systemic Lupus International Collaborating Clinics Classification Criteria 2012

for Classifying Systemic Lupus Erythematosus

23

A patient can be classified as having SLE if

he/she

Satisfies 4 of the criteria listed in Table 33-1 including at least

one clinical criterion and one immunologic criterion

Or

Has biopsy-proven nephritis compatible with SLE and with

antinuclear antibody (ANA) or anti-dsDNA antibodies

Clinical and Immunologic Criteria Used in the SLICC Classification Criteria

a

Clinical Criteria

Acute cutaneous lupus (includes lupus

malar rash; do not count if malar

discoid) and the following:

Bullous lupus

Toxic epidermal necrolysis variant of SLE

Maculopapular lupus rash

Photosensitive lupus rash in the absence of dermatomyositis

Or

Subacute cutaneous lupus

Nonindurated psoriaform and/or annular polycyclic lesions

that resolve without scarring, although occasionally with

post-inflammatory depigmentation or telangiectasia

Chronic cutaneous lupus includes the

following:

Classic discoid rash

Localized (above the neck)

Generalized (above and below the neck)

Hypertrophic (verrucous) lupus

Lupus panniculitis (profundus)

Mucosal lupus

Lupus erythematosus tumidus

3.

4.

5.

6.

7.

8.

9.

10.

Chilblains lupus

Discoid lupus/lichen planus overlap

Oral ulcers include the following: (in the

absence of other causes, such as

vasculitis, Behcet’s disease, infection

(herpes virus), inflammatory bowel

disease, reactive arthritis, and acidic

foods)

Palate

Buccal

Tongue

Or

Nasal ulcers

Non-scarring alopecia (in the absence of

other causes such as alopecia areata,

drugs, iron deficiency, and androgenic

alopecia)

Diffuse thinning or hair fragility with visible broken hairs

Synovitis Involving two or more joints

Characterized by

Swelling or effusion

Or

Tenderness in two or more joints and at least 30 minutes of

morning stiffness

Serositis Typical pleurisy for more than 1 day

Or

Pericardial effusion

Or

Pericardial rub

Or

Pericarditis by electrocardiography

Renal (in the absence of other causes,

such as infection, uremia, and

Dressler’s pericarditis)

Urine protein-to-creatinine ratio (or 24-hour protein) representing

500 mg of protein/24 hour

Or

Red blood cell casts

Neurologic Seizures

Psychosis

Mononeuritis multiplex in the absence of other known causes,

such as primary vasculitis

Myelitis

Peripheral or cranial neuropathy, in the absence of other known

causes, such as primary vasculitis, infection, and diabetes

mellitus

Acute confusionalstate, in the absence of other causes, including

toxic/metabolic, uremia, drugs

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Hemolytic anemia

Leukopenia <4,000/mm

3 at least once (in the absence of other known causes,

such as Felty’s syndrome, drugs, portal hypertension, and

1.

2.

3.

4.

5.

6.

thrombotic thrombocytopenia purpura)

Immunologic Criteria

ANA Level above laboratory reference range

Anti-dsDNA Antibody above laboratory reference range (or >2-fold the

reference range if tested by ELISA)

Anti-Sm Presence of antibody to Sm nuclear antigen

Antiphospholipid antibody positivity as

determined by any of the following:

Positive test result for lupus anticoagulant

False-positive test for RPR

Medium- or high-titer anti-β2-glycoprotein antibody level (IgA,

IgG, or IgM)

Positive test result for anti-β2-glycoprotein I (IgA, IgG, or IgM)

Low complement Low C3

Low C4

Low CH50

Direct Coombs’ test In the absence of hemolytic anemia

aCriteria are cumulative and need not be present concurrently.

ELISA, enzyme-linked immunosorbent assay; Anti-dsDNA, anti-double stranded deoxyribonucleic acid; Anti-Sm,

anti-Smith antibodies; RPR, rapid plasma reagin.

Figure 33-1 Common symptoms of systemic lupus erythematosus. (Source: Haggstrom, Mikael/Wikipedia

Commons/Public Domain. http://www.commons.wikipedia.org/wiki/File:SymptomsofSLE.png. Accessed

July 26, 2015.)

Nervous System

SLE affects both the central nervous system (CNS) and peripheral nervous system.

The CNS manifestations affect approximately two-thirds of patients with SLE.

30

Collectively, both have been described as neuropsychiatric syndromes. The

pathology of the syndromes is not well understood. The syndromes may be ascribed

to the autoimmune nature of SLE, where the immune anti-neuronal antibodies attack

the neurons causing neuronal damage and leading to cognitive dysfunction, or the

production of antiphospholipid antibodies that damage blood vessels and may cause

clots in the brain.

28 Neuropsychiatric manifestations are nonspecific and variable.

They may occur in less than 40% of patients with SLE, while the remaining events

represent complications of the disease, therapies and therapy-related side effects,

infections, and metabolic abnormalities.

31 Patients with SLE can present with higher

rates of anxiety and depression. Depression is more common in those experiencing

changes in appearance and limitations from complications and medication-related

side effects.

32 Other manifestations include migraine headaches, memory loss, and

seizures. Less common symptoms may also occur, such as psychosis, confusion,

peripheral neuropathy, mood disorders, autonomic dysfunction, movement disorders,

Guillain–Barre, and cerebrovascular disease.

27 Diagnosis and laboratory tests for

neuropsychiatric events related to SLE continue to be challenging, as well as the

therapies used for them.

33

Cardiovascular

Patients with SLE are at increased risk of morbidity and mortality from

cardiovascular disease, especially associated with atherosclerosis. Premature

atherosclerosis is associated with longer lupus disease duration, more damage, and

less aggressive immunosuppressive therapy.

34,35 They are at higher risk for

myocardial infarction or stroke compared to the healthy population. In addition,

pericarditis and pericardial effusion are the most common cardiac complications

associated with SLE, occurring in approximately 45% of patients.

28,29,30,36 They range

from mild-to-severe symptomatology. Patients may present with fever, dyspnea,

tachycardia, and congestive heart failure. Other clinical features that may occur in

more than 80% of patients with SLE include left ventricular dysfunction, segmental

wall motion abnormalities, nonspecific ST-T wave changes, and decreased ejection

fraction.

2 Valvular abnormalities can also be common and are linked to

antiphospholipid antibodies. The most common

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abnormality is diffuse thickening of the mitral and aortic valves followed by the

presence or absence of nonbacterial vegetations (Libman–Sacks), valvular

regurgitation, and stenosis.

2 Modifiable risk factors, in addition to comorbid disease

screening, include reducing long-term steroid use as it is linked to the development of

hypertension, smoking cessation, reducing homocysteine levels with folate

supplementation, and preventing thrombosis with aspirin or anticoagulation in

patients with APS.

27 These will help to reduce cardiovascular risk and control

disease activity by reducing the inflammatory atherogenic effects.

CASE 33-1

QUESTION 1: T.C. is a 45-year-old Hispanic woman with hypertension, hypercholesterolemia, and an 18-

year history of SLE. For the first 10 years after the diagnosis of SLE, she had frequent SLE flares and was

treated with high-doses of prednisone. As a result, she developed steroid-induced diabetes and osteoporosis.

Though her SLE has been relatively stable over the past 2 years, she has not been feeling well 1 month ago.

T.C. denies symptoms consistent with her usual SLE flares, but she reports a sharp chest pain that worsens

when lying down and improves when leaning forward, significant fatigue and shortness of breath with minor

activity. She feels better after resting but has not returned to her previous energy level. She reports good

adherence with her medications, which include the following:

Alendronate 70 mg weekly

Hydrochlorothiazide 25 mg every morning

Hydroxychloroquine 400 mg daily

Lisinopril 40 mg daily

Metformin 1,000 mg twice daily

Simvastatin 40 mg daily

Acetaminophen 650 mg prn pain

Findings from an examination of the patient are unremarkable, except for elevated blood pressure. Lupus

anticoagulant antibodies are within normal limits. What is the most likely cause of T.C.’s complaints of fatigue

and positional chest pain?

Patients with long-standing SLE are at increased risk for cardiovascular disease.

Given that T.C.’s SLE is stable, cardiovascular disease is the most likely cause of

her current symptoms.

CASE 33-1, QUESTION 2: What tests would best confirm your suspicion?

Electrocardiograms (EKGs), exercise stress tests, and echocardiograms. Cardiac

stress test is also considered a best way to determine the presence and extent of her

cardiovascular disease, especially for symptomatic patients.

CASE 33-1, QUESTION 3: Along with a referral to a cardiologist, which of the following treatments would

you recommend that T.C. initiate at this time?

Aspirin is recommended because her most likely diagnosis is cardiovascular

disease. She has no evidence of active SLE, so aspirin would be the most

appropriate treatment at this time to prevent risk of thrombosis. Premature

atherosclerosis with cardiovascular events tends to manifest as a late complication

for patients with SLE. Oral anticoagulants may be considered for T.C. if she has

developed antiphospholipid antibodies and APS.

CASE 33-1, QUESTION 4: Late in the disease course of SLE, what is the most common cause of high

mortality rates?

Early in the disease course, mortality is primarily from inflammation affecting

organ systems. Over time, mortality tends to be mostly from coronary artery disease

and complications of chronic steroid therapy and immunosuppression. SLE disease

could elevate the LDL and reduce the HDL levels in addition to treatment with

systemic steroids that could worsen the cholesterol profile.

Pulmonary

Pulmonary involvement occurs in 30% of patients with SLE.

30 Pleuritis or pleural

inflammation is the most common pulmonary manifestation of SLE. It is associated

with chest pain, cough, and dyspnea. Pleural effusions are typical findings and are

usually linked with antinuclear antibody (ANA)-positive exudates with low

complement.

37 Alveolar hemorrhage is a common occurrence in patients with SLE,

particularly in those with high titers of anti-dsDNA antibodies and active

extrapulmonary disease.

30 Another respiratory complication is identified as the

“shrinking lung syndrome,” which can occur in 25% of SLE patients.

2

It is

characterized as progressive dyspnea (worse in the supine position) and weakness of

the diaphragm and respiratory muscles. Acute lupus pneumonitis and pulmonary

hypertension, although rare, could also develop as pulmonary complications.

Gastrointestinal

Nonspecific GI symptoms include abdominal pain, nausea, vomiting, diarrhea, and

stomach upset. These are reported in 25% to 40% of patients with SLE, which could

be disease-related or from medication side effects.

2 Other clinical manifestations

include dyspepsia and peptic ulcers.

Renal

Up to 70% of all SLE patients will develop some form of renal complication, which

is a poor prognostic indicator. Approximately 60% will have kidney involvement in

the first 10 years of the disease.

18 Thirty-five percent of patients will develop

nephrotic syndrome or lupus nephritis (LN) by the time of SLE diagnosis.

38

It is a

serious kidney complication, which increases the risk of renal failure, cardiovascular

disease, and mortality.

39 LN is caused by inflammation and deposits of immune

complexes consisting of anti-dsDNA in the glomeruli. It includes proteinuria (>0.5

g/24 hours) and/or hematuria, described as active urinary sediment (>5 RBCs per

high-power field, pyuria, or cell casts), in addition to a significant creatinine

clearance reduction. For patients with inactive sediment and >500 mg/day of

proteinuria, monitoring is recommended with urinalysis every 3 to 6 months for 3

years. More frequent monitoring, such as every 3 months, is preferred for patients

with anti-dsDNA antibodies and/or hypocomplementemia.

40

Aside from performing a urinalysis, a renal biopsy is required in all lupus patients

with evidence of kidney involvement to determine the histologic subtype of LN and

the extent of disease severity.

41,42 Pathology reports can elucidate the extent of

inflammatory (reversible) and chronic (irreversible scarring) changes. LN can be an

ongoing disease, with flares often requiring repeat biopsy and repeat treatment (refer

to Chapter 28, Chronic Kidney Disease for Lupus Nephritis, Case 28-4).

Hematologic

Hematologic disorders can occur in patients with SLE. The most common

hematologic manifestation is normochromic, normocytic anemia, which is often

overlooked in young menstruating women. Iron deficiency may also develop. A

common cause of anemia is suppressed erythropoiesis from chronic inflammation.

Patients may have a positive Coombs test without apparent hemolysis.

42 Leukopenia

and thrombocytopenia are also common manifestations

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that can develop as part of the disease process, or may be a side effect of the

pharmacologic treatment for SLE. Oftentimes, leukopenia consists of lymphopenia,

not granulocytopenia.

43 Patients with SLE may also develop a thrombotic disorder

known as APS. APS is characterized by the development of autoantibodies to

phospholipids present in the serum. Antiphospholipid antibodies interfere with the

coagulation system, particularly protein C and the function of endothelial cells.

13 APS

features are described as venous or arterial thrombosis, miscarriages or spontaneous

abortions, and thrombocytopenia from antiphospholipid antibodies.

27 The European

League Against Rheumatism (EULAR) recommends low-dose aspirin in individuals

with SLE and antiphospholipid antibodies as primary prevention of thrombosis and

pregnancy loss.

7 Long-term use of oral anticoagulants is considered as secondary

prevention of thrombosis in nonpregnant patients with SLE and thrombosis

associated with APS. On the other hand, unfractionated or low-molecular-weight

heparin and aspirin should be used in pregnant patients with SLE and APS.

Lymphadenopathy could be a common presentation in SLE, where it may occur in

15% to 26% in patients. Diffuse lymphadenopathy, however, is a very rare

occurrence.

44,45 Lymph node biopsy may be considered to exclude alternative

diagnoses.

DIAGNOSIS

Diagnosis is based on the presence of 4 or more of the 11 criteria, either serially or

simultaneously, of the ACR classification. The revised criteria yields a sensitivity of

83% and a specificity of 96% for SLE diagnosis but are associated with several

weaknesses.

22,46 For instance, many patients with biopsy-proven LN do not meet the

criteria. Also, there have been numerous advances in imaging, serologic, and

cerebrospinal fluid testing that resulted in an outdated CNS definition. The Systemic

Lupus International Collaborative Clinics (SLICC) guidelines propose new criteria

for the disease.

23 According to the SLICC criteria, a person is diagnosed with SLE

when there is presence of at least 4 of the 11 criteria, of which one must be a clinical

criterion and one an immunologic criterion.

23 Furthermore, the classification can also

be made from a biopsy confirming LN and presence of antinuclear antibodies (ANA),

or anti-dsDNA antibodies. Both anti-Smith (anti-Sm) and anti-dsDNA antibodies are

highly specific for SLE, but anti-Sm antibodies lack sensitivity.

1 Anti-dsDNA and

anti-Sm antibodies are found in approximately 70% and 30% of patients with SLE,

respectively.

47 Other markers, such as the lupus anticoagulant and IgG and IgM

antibodies to anticardiolipin are specific for APS. Their presence may increase the

risk for thrombosis or miscarriages. When compared to the ACR classification, the

SLICC criteria have higher sensitivity (97%) but not specificity (84%) (Table 33-

2).

18

The diagnostic workup can be challenging because of the complexity of the disease

and overlapping features of many other autoimmune diseases, such as polymyositis,

rheumatoid arthritis, and scleroderma. The workup includes an assessment of the

clinical presentation, physical examination, diagnostic, and laboratory tests.

Approximately 80% of patients have skin involvement manifesting as

photosensitivity, alopecia, malar and discoid rash (thick, red, scaly patches on the

skin), and ulcers in the oral and nasal cavities or in the vagina, all of which are part

of the ACR criteria.

22

CASE 33-2

QUESTION 1: P.J., a 26-year-old, obese (80 kg, 5-feet tall) African-American woman, presents to the

emergency department complaining of chest pain. It is a sharp and substernal pain, but with a component that is

diffuse and aggravated by deep aspiration. Two months ago she presented to the emergency department with a

6-week history of fatigue, low-grade fevers, hair loss, joint pain, and oral ulcers. Her laboratory tests showed a

positive ANA test result. Blood cultures were negative for infection. The urinalysis was negative for blood, and

the urine culture was negative for infection. A chest x-ray showed non-pulmonary infiltrates. Her symptoms

improved after a 10-day tapering course of prednisone. Feeling better, P.J. decided not to follow-up with her

physician’s appointment last week. Today, the medical resident’s examination reveals an ill-appearing woman,

with a temperature of 100.5°F (38.06°C), oral ulcers, alopecia, and tachycardia with distant heart sounds. What

signs and symptoms exhibited by P.J. are consistent with SLE?

According to the “1997 Update of the 1982 American College of Rheumatology

Revised Criteria for Classification of Systemic Lupus Erythematosus,” the diagnosis

of SLE is satisfied when 4 of 11 criteria are present. The criteria contain 4

cutaneous, 4 systemic, and 3 laboratory components (Table 33-1). P.J. meets criteria

with the presence of a positive ANA test result, oral ulcers, presumed pericarditis,

and presumed arthritis (joint pain). Furthermore, her clinical features are consistent

with SLE including fatigue, alopecia, and low-grade fevers (infection ruled out).

CASE 33-2, QUESTION 2: After P.J. has started treatment and further laboratory tests are performed,

what other specialists would you involve in her care at this time?

Rheumatologist and cardiologist because of P.J.’s pericarditis. The cardiologist

could evaluate the patient’s modifiable cardiovascular risk factors, such as

hypertension, dyslipidemia, and obesity. Pericarditis with pericardial effusion is

most commonly associated with cardiovascular involvement and SLE. Symptoms

could include sharp chest pain and fluid around the heart, worsened with deep

breathing and certain body positions. Endocarditis, myocarditis, and valvular disease

are less common. Over time, other specialists including gastroenterologist,

neurologist, pulmonologist, and nephrologist may be considered as part of P.J.’s

multidisciplinary team.

PHARMACOLOGIC AND NONPHARMACOLOGIC TREATMENTS

The management approach for SLE will depend on the severity of the disease and

organ involvement. A therapeutic plan is created based on clinical guidelines for the

management, treatment, and monitoring of SLE. It should include considerations for

pharmacologic and non-pharmacologic approaches with clearly defined goals. Since

there is currently no cure for SLE, the goals of therapy are to prevent flares, treat

active symptoms of disease, minimize drug toxicity, and reduce risk of complications

and organ damage. An effective and successful therapeutic plan is individualized

based on the patient’s needs, symptoms, lifestyle, and disease complications. Patients

should be regularly monitored by their providers every 3 to 6 months.

NSAIDs and COX-2 Inhibitor

Treatment options will differ depending on the level of severity of SLE. For mild

disease, nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) and selective

cyclooxygenase-2 (COX-2) inhibitor, such as celecoxib, are used. Because of their

ability to inhibit

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the release of prostaglandins and leukotrienes, NSAIDs and the COX-2 inhibitor

possess anti-inflammatory, analgesic, and antipyretic properties. They are effective

in reducing swelling, relieving muscle and joint pain, fever, as well as pleuritic chest

pain.

26,48 Patients with antiphospholipid antibodies and are at increased risk of

thrombosis or atherosclerotic disease may benefit from low-dose aspirin for primary

prevention, or long-term anticoagulation therapy for secondary prevention.

7 Longterm use of NSAIDs is encumbered with GI, cardiovascular, and renal issues.

Common GI side effects include dyspepsia, heartburn, and nausea. More serious GI

symptoms such as stomach bleeding and mucosal lesions may occur. Cardiovascular

side effects associated with NSAIDs may include hypertension and the risk of

myocardial infarction. Fluid retention and acute tubular necrosis with kidney failure

may also occur with long-term use, especially in elderly patients.

As a class, NSAIDs work in the same manner; however, not every agent has the

same effect on every patient. When a NSAID is used, it needs to be titrated to its

maximal dose over 1 to 2 weeks. The agent should not be discontinued until the

patient has been on the maximal dose for at least 2 weeks, which is the amount of

time NSAIDs reach maximal efficacy.

27 Although all NSAIDs appear to work in the

same way, not every agent has the same effect on every person. In addition, patients

may do well with one NSAID for a period of time, then may not derive further benefit

from it for some unknown reason. Switching the patient to a different NSAID could

produce the desired effects. NSAIDs may be appropriate for chronic pain

management in aspirin users provided that appropriate GI prophylactic measures are

used in high-risk patients. Patients should use only one NSAID at any given time to

really know its benefits.

Celecoxib, a COX-2 inhibitor, is more selective in the inhibition of

cyclooxygenase, which is involved in the transformation of arachidonic acid to

prostaglandin precursors. Celecoxib has the same efficacy as NSAIDs; however, it

possesses a milder GI side effect profile. It does not have a direct effect on

platelets.

49 Therefore, it is preferred over NSAIDs in patients with

thrombocytopenia. There have been many studies and case reports correlating COX2 inhibitors with cardiovascular risks (e.g., stroke and heart attack), especially with

rofecoxib (Vioxx), which was removed from the U.S. market.

49–51

CASE 33-2, QUESTION 3: Which of the following treatments would P.J. benefit from using at this time?

P.J. could benefit from high-dose NSAIDs. Traditionally, the initial treatment for

SLE pericarditis (inflammation of the lining of the heart or pericardium) is high-dose

NSAIDs such as ibuprofen. Patients with SLE are at increased risk for coronary heart

disease from increased cardiovascular risk factors (i.e., chronic inflammation,

dyslipidemia, obesity, and physical inactivity). SLE patients with recurrent

pericarditis will need to be on immunosuppressive medications.

Antimalarials

Antimalarials are currently the mainstay therapy for SLE, in particular

hydroxychloroquine sulfate (Plaquenil) and chloroquine. They work through

immunomodulation by downregulating the production of TNF alpha and other

proinflammatory cytokines.

52 Hydroxychloroquine is preferred over chloroquine

because it is associated with less corneal deposition (opacities) and retinopathy

risks.

33 Ocular side effects occur in a dose-dependent manner where the risk is low

when hydroxychloroquine’s dose is less than 600 mg daily and less than 6.5

mg/kg/day. It has anti-inflammatory effects and is used to reduce the time to flare-ups,

constitutional (i.e., fever and rashes), skin, fatigue, and joint symptoms.

53

Additionally, hydroxychloroquine has antithrombotic and lipid-lowering effects,

which can help patients with SLE.

54 Other ocular symptoms may include blurred

vision, night blindness, missing or blanched out areas in the central or peripheral

fields, light flashes and streaks, and photophobia. Hydroxychloroquine-related side

effects may also include a bull’s eye appearance in the macular region.

33 The

manufacturer recommends eye exams should be performed at baseline and

subsequently every 3 months with long-term hydroxychloroquine treatment. In

contrast, the American Academy of Opthalmology (AAO) proposes more flexible eye

exam criteria. The AAO recommends patients who are at low risk (those taking

hydroxychloroquine less than 6.5 mg/kg/day dose for a treatment duration of less than

5 years) be checked at baseline and then, if normal, every 5 years. Patients who are

at high risk (those taking hydroxychloroquine more than 6.5 mg/kg/day dose for >5

years, aged more than 60 years old or pediatric patients, or those with existing retinal

disease and kidney or liver disease) should be evaluated at baseline and then

annually.

55 Patients should be screened for the presence of “premaculopathy”

antimalarial retinopathy, or retinal toxicity during scheduled eye exams because it is

a reversible stage as long as hydroxychloroquine is discontinued.

Patients may need to take hydroxychloroquine for months to experience the

maximal effect. For SLE, the initial oral hydroxychloroquine dose is 400 mg given

daily for 3 to 6 months depending on patient response, then tapered to 200 mg daily

for maintenance therapy. If the patient does not have any benefit from

hydroxychloroquine after 6 months, the drug should be discontinued.

CASE 33-3

QUESTION 1: R.W., a 54-year-old Caucasian woman with a 30-year history of SLE, returns to her

rheumatologist for evaluation. She has received prednisone, hydroxychloroquine, and azathioprine in the past.

Her SLE has been stable for 2 years. Feeling well, R.W. discontinued all of her medications more than 1 year

ago. She recently returns from a family vacation in the Caribbean. Having been out in the sun for a few hours

on the first day, she developed an erythematous eruption over photo-exposed areas of her face, ears, and legs

despite the application of sunscreen. R.W. returns home, and the lesions are healing. Though she is fatigued,

she feels well enough to return to work. You determine that her rash is because of photosensitivity. What would

be the best next step in the management of R.W.?

The next appropriate step is to initiate a short-course of low-dose prednisone

because it can be used to treat a photosensitive rash from SLE. The rash may occur

because with SLE, the body’s immune system does not function properly, and the

inflammatory response works to damage the patient’s own tissues. Prednisone is a

corticosteroid that helps to reduce the inflammation and immune response, thereby

preventing further damage to the tissues in the body.

CASE 33-3, QUESTION 2: The rash resolves; however, R.W. continues to complain of fatigue and

arthralgia. No other clinical signs or symptoms consistent with SLE flare emerge. Laboratory test results reveal

continued elevation of anti-dsDNA antibody titers and suppressed complement levels. What is your next step in

managing R.W.?

Hydroxychloroquine should be initiated as it is effective for long-term treatment of

SLE with rash, fatigue, and arthralgias. Hydroxychloroquine is often prescribed in

combination with steroids to reduce the dose required of the steroids. It is prescribed

for skin rashes, mouth ulcers, and joint pain. Hydroxychloroquine improves SLE by

decreasing autoantibody production, protecting against

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the damaging effects of ultraviolet light from the sun and other sources, and

improving skin lesions. Several studies have reported the benefits of

hydroxychloroquine in treating symptoms of SLE, preventing disease flares, and its

association with less organ damage.