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Current Challenge

Managing Complex Psoriatic Arthritis Case Study: Pt. 3

To follow up on the previous case, a dermatologist has referred to you a 56-year-old female with a 10 year history of psoriasis, who now has developed pain and swelling in both wrists, the right 2nd MCP, left 3rd PIP, and 2nd through 5th DIP joints of both hands. She has prominent morning stiffness involving her hands and feet and when she is first walking about barefoot in the morning, has pain in the balls of her feet and heels.  Upon further questioning, she mentions that she experiences episodic back pain in the upper buttock area, which is worse when she sits for an extended period and improves when she gets up to walk about. She denies history of uveitis or inflammatory bowel symptoms. Her family history is unremarkable for history of psoriasis or rheumatologic disease other than osteoarthritis. She has tried ibuprofen with no benefit. Two years ago she used methotrexate for 6 months for flaring psoriasis, but was taken off it because her transaminases became elevated to 2X ULN. She denies use of alcohol.

Previously her lab results revealed ESR 26, CRP 1.4 (nl to 0.8 mg dL), HLAB27 and RF negative. Hand xrays reveal periarticular osteitis of the left 3rd PIP joint and no erosions. Pelvis xray is normal but MRI reveals bone edema adjacent to the left sacroiliac joint in 2 MRI cuts.

The patient fulfills CASPAR criteria because she has inflammatory arthritis, enthesitis, spondylitis, psoriasis, a negative RF, and periarticular osteitis on xray. Anti-TNF therapy is reasonable at this juncture.

 

Discuss this case further: Rheumbuzz Physician / Medical Professional Discussion Area

Past Challenges

September 17, 2013

To follow up on the previous case, a dermatologist has referred to you a 56-year-old female with a 10 year history of psoriasis, who now has developed pain and swelling in both wrists, the right 2nd MCP, left 3rd PIP, and 2nd through 5th DIP joints of both hands. She has prominent morning stiffness involving her hands and feet and when she is first walking about barefoot in the morning, has pain in the balls of her feet and heels.  Upon further questioning, she mentions that she experiences episodic back pain in the upper buttock area, which is worse when she sits for an extended period and improves when she gets up to walk about. She denies history of uveitis or inflammatory bowel symptoms. Her family history is unremarkable for history of psoriasis or rheumatologic disease other than osteoarthritis. She has tried ibuprofen with no benefit. Two years ago she used methotrexate for 6 months for flaring psoriasis, but was taken off it because her transaminases became elevated to 2X ULN. She denies use of alcohol.

Previously her lab results revealed ESR 26, CRP 1.4 (nl to 0.8 mg dL), HLAB27 and RF negative. Hand xrays reveal periarticular osteitis of the left 3rd PIP joint and no erosiionsA. Pelvis xray is normal but MRI reveals bone edema adjacent to the left sacroiliac joint in 2 MRI cuts. The patient fulfills CASPAR criteria because she has inflammatory arthritis, enthesitis, spondylitis, psoriasis, a negative RF, and periarticular osteitis on xray.

Which of the following treatment approaches is reasonable at this juncture?

  1. Sulfasalazine
  2. Leflunomide
  3. Anti-TNF therapy
  4. All of the above
  5. Leflunomide and Anti-TNF therapy

Rationale:

The answer is not entirely straightforward, and may depend upon criteria such as local insurance dictates and individual preferences of clinician and patient. However, there is good evidence for effectiveness of the anti-TNF therapies in the various clinical domains experienced by the patient: arthritis, enthesitis, spondylitis, and psoriasis. Each of the anti-TNFs have been used in either monotherapy format or in combination with MTX successfully, so the fact that she has had transaminitis related to MTX use historically does not impede us to utilize an anti-TNF as monotherapy. If, after some time, the effect of the anti-TNF should wane, and you are wondering about the possibility of antibodies to the anti-TNF medicine blunting effectiveness, then one could consider either a re-trial of MTX or use of leflunomide to try to dampen antibody formation. Sulfasalazine has been shown to be effective for arthritis but it is not effective for psoriasis or spondylitis and it has not been evaluated regarding effect on enthesitis. Leflunomide is effective for arthritis and psoriasis, but it is not effective for spondylitis, at least as tested in ankylosing spondylitis trials, and it has not been assessed regarding effect on enthesitis. So probably the best response is #3 although those that marked #4 were not unreasonable.

August 19, 2013

A dermatologist has referred to you a 56-year-old female with a 10 year history of psoriasis, who now has developed pain and swelling in both wrists, the right 2nd MCP, left 3rd PIP, and 2nd through 5th DIP joints of both hands. She has prominent morning stiffness involving her hands and feet. When she is first walking about barefoot in the morning, she has pain in the balls of her feet and heels.  Upon further questioning, she mentions that she experiences episodic back pain in the upper buttock area, which is worse when she sits for an extended period and improves when she gets up to walk about. She denies history of uveitis or inflammatory bowel symptoms. Her family history is unremarkable for history of psoriasis or rheumatologic disease other than osteoarthritis. She has tried ibuprofen with no benefit. Two years ago she used methotrexate for 6 months for flaring psoriasis, but was taken off it because her transaminases became elevated to 2X ULN. She denies use of alcohol.

Physical exam reveals weight 217, height 5’5”. Skin exam reveals mild patchy psoriasis lesions on her elbows, behind the ears, and scattered in the scalp – estimated body surface area involvement approximately 2%. Musculoskeletal exam reveals tenderness and swelling in 2-5 DIPs bilaterally, left 3rd PIP, right 2nd MCP, both wrists, left sterno-clavicular joint,  tenderness of the 2nd-5th MTPs bilaterally, and the plantar fascia insertion on the left. She has percussion tenderness over the left upper buttock area.

Laboratory reveals ESR 26, CRP 1.4 (nl to 0.8 mg dL), HLAB27 and RF negative. Hand xrays reveal periarticularosteitis of the left 3rd PIP joint. Pelvis xray is normal but MRI reveals bone edema adjacent to the left sacroiliac joint.

Which of the following statements about this patient and the CASPAR classification criteria for PsA is correct?

  1. The patient fulfills CASPAR criteria because she has inflammatory arthritis and psoriasis
  2. The patient fulfills CASPAR criteria because she has inflammatory arthritis, enthesitis, and psoriasis
  3. The patient fulfills CASPAR criteria because she has inflammatory arthritis, enthesitis, spondylitis, psoriasis, a negative RF, and periarticularosteitis on xray
  4. The patient fulfills CASPAR criteria because she has inflammatory arthritis, spondylitis and psoriasis
  5. The patient fulfills CASPAR criteria because she has inflammatory arthritis, enthesitis, spondylitis and psoriasis

Rationale:

The correct answer is C. The “stem” of the CASPAR classification criteria is that the patient needs to have convincing evidence of inflammatory arthritis, enthesitis, and/or spondylitis before the additional elements of the criteria can be applied. In her case, she has evidence of inflammatory arthritis, enthesitis, and spondylitis based on history, physical exam, and by pelvis MRI. Given this, the additional elements she fulfills are current psoriasis (2 points), a negative RF (1 point) and xray evidence of periarticular osteitis (1 point). Although in the remainder of the statements she fulfills the “stem”, by noting only current psoriasis (yielding 2 points), we do not come up with the additional 3 points necessary to fulfill the criteria.

Reference

Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, et al. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arth Rheum. 2006;54:2665-2673.

July 19, 2013

A 23-year-old female patient comes in with a chief complaint of malaise. Her previous medical history includes lupus nephritis (ISN- class V), diagnosed 6 months ago. Current medications include mycophenolate 1gr/d, hydroxychloroquine. The patient felt well until 7 days ago, when she developed N/V/D, abdominal pain, low grade fever, and achy knees. She has conservative management (hydration and antiemetics) and was taken to the ED for new onset confusion, progressive weakness, and numbness over left side, unable to walk.

Her exam revealed the following:
T:40.1°C, BP:104/56 mm Hg, PR:98  RR:18, O2:100%
Agitated, not oriented
Lungs-decrease breath sounds at bases
Skin- faint petechial rash over legs
MSK-low grade synovitis over 1-3 MCPs, knees
Neurologic examination: no focal abnormalities
CBC: wbc:3.6 HCT:28.4   PLT:48000 
ESR: 45    C3,C4:normal   Cr:1.8
ANA :1:160 speckled pattern
ds DNA ab:320
urine: 3+ blood and protein; 20 - 30 red cells , 10 - 20 white cells per high-power field; 2 – 3 granular casts
Head CT- normal
CXR-min blunting CP angle
LDH- 311*

As an immune compromised patient her possible diagnoses includes NPSLE/CNS lupus; lupus/LN flare with new onset renal failure & hemolytic anemia; infectious endocarditis; or TTP(Thrombotic Microangiopathy).

Additional labs were taken and include:

The next diagnostic test performed was a peripheral smear.

What is the likely diagnosis?

  1. Pneumonia
  2. Infectious endocarditis
  3. Lupus cerebritis
  4. Thrombotic Thrombocytopenic Purpura (TTP)

Rationale:

The correct answer is D- Thrombotic Thrombocytopenic Purpura (TTP). TTP is pentad of micro-angiopathic hemolytic anemia, thrombocytopenic purpura, fever, neurologic abnormalities and renal disease. It is a rare disease with an incidence of 1-4% (3.7 cases per million). TTP has a delayed diagnosis, poor response, and high mortality, with frequent relapses (30-60%). Independent risk factors for developing 2nd TTP include high disease activity (SLEDAI>10) and lupus nephritis.  Delayed recognition is contributed to a low index of suspicion and delayed symptom evolution.

The etiology of TTP is microthrombus formation with consumption of platelets. High shear stress in the microcirculation and Von Willebrand Factor (vWF) are present. vWF and platelets are prone to form aggregates (micro vascular thrombi). Deficiencies in vWF brand protease ADAMTS-13 and include autoimmune inhibitors and mutations of the ADAMS 13 gene. vWF eads to micro thrombus formation with consumption of platelets, shearing of red cells with hemolysis.

The treatment of choice is Plasma exchange+ pulse steroids. Daily plasma exchange + glucocorticoids, until clinical remission. Testing for ADAMTS 13 enzyme activity and inhibitor are not necessary for diagnosis, but provides useful prognostic information. Ritiuximab has gained favor as an adjunctive agent to treat refractory or relapsing TTP.

References:

Kwok SK et al. Lupus. 2009;18(1):16-21.
Letchumanan P et al. Rheumatology. 2009;48(4):399-403.

Figure Image - Proposed Allopurinol Dosing in CKD

 

May 15, 2013

A 23-year-old Hispanic female has a 6 month history of menometrorrhagia (excess menstrual bleeding), but is without skin rash or arthritis, and her vital signs are stable and without orthostatic changes. She is also without other symptoms or signs that localize a potential source of blood loss (e.g., no hemoptysis, hematemesis or abdominal pain, and she is hemoccult negative).

Her past medical history is otherwise non-contributory, and she has an aunt with an unknown type of arthritis. On initial laboratory evaluation, she is found to have a microcytic anemia with hematocrit of 26.5 (Hgb 8.4), low platelet count of 52,000/uL, modest lymphopenia, and a positive ANA (greater than 1:640). Urinalysis is normal without blood or protein. BUN and creatinine are also within the normal range, and her pregnancy test is negative.‬‬

Which of the following tests are likely to provide the most relevant and urgent data for the patient’s immediate clinical assessment?

  1. Anti-dsDNA, anti-Sm, anti-Ro and La, anti- glycoprotein IIb/glycoprotein IIIa
  2. Peripheral blood smear, reticulocyte count, iron and total iron binding capacity, ferritin, Haptoglobin; LDH; direct Coombs
  3. Antibodies for 2 glycoprotein, cardiolipin, PTT and lupus anti-coagulant
  4. Complement levels; C3 C4, C reactive protein, ESR, serum protein electrophoresis/immunoelectrophoresis
  5. Bone marrow aspirate

Doctor Commentary:

Rationale:

The best answer is B. Admittedly, this is an ambiguous case that is presented with insufficient clinical and laboratory data. In general, menometrorrhagia is present in more than two-thirds of cases of iron-deficiency anaemia in premenopausal women (1). Based on the high titer positive ANA, the patient appears to have an autoimmune diathesis, and this could be related to her primary clinical problem, which is significant anemia and thrombocytopenia. We need to focus on these issues, as this could potentially be life-threatening in the short term, while other abnormalities may need to be addressed in the longer term.

There are several considerations that must be addressed efficiently. Is the blood loss an acute or chronic problem? Also, is there evidence of acute hemolysis, and is there a physiologic response that seeks to compensate for the low hematocrit? The peripheral smear can provide essential information that may otherwise be overlooked, as we need to look for mechanical shear-associated changes to red cells, which might indicate that there is acute hemolysis or even disseminated intravascular coagulopathy, or TTP, which could each also explain the abnormally low platelet count. I also failed to mention other potentially important clues such as MCV and MCH and red cell distribution (2). The reticulocyte count of course will suggest whether there is an appropriate bone marrow response to produce new red cells, while measuring ferritin, iron and iron binding capacity can suggest whether there are adequate iron stores to replace the red cell loss. Serum haptoglobinlevels will be reduced with hemolysis, and LDH can be raised when released from damaged red cells. The direct Coombs test is of course useful for assessing for local deposition of anti-red cell antibodies.

In addition, there are also several other potential red flags embedded in the case history. Could this patients also have an be anti-phospholipid syndrome, and this often occurs concurrent with autoimmune thrombocytopenia (ATP), in which antibodies to integrin molecules, such as glycoprotein IIb/IIIa, are common. Yet the most severe complications of ATP (i.e., intracranial bleed) are generally associated with much lower platelet levels, so this may be a relatively compensated state. As for the bone marrow aspiration, SLE can initially present with aplastic anemia, but this is less common and may not be as potentially emergent as other of the diagnoses mentioned above. The review by Hepburn et al. provides a more complete overview of the differential diagnoses associated with cytopenias in SLE patients (3).

References:

  1. Palacios S.The management of iron deficiency in menometrorrhagia.GynecolEndocrinol. 2011 27 Suppl 1:1126-30. doi: 10.3109/09513590.2012.636916.
  2. http://labtestsonline.org/understanding/analytes/cbc/tab/test
  3. Hepburn AL, Narat S, Mason JC. The management of peripheral blood cytopenias in systemic lupus erythematosus.Rheumatology (Oxford). 2010 49(12):2243-54. doi: 10.1093/rheumatology/keq269.

 

April 17, 2013

A 29-year-old female presents to the office with inflammatory back pain. She has noted the pain which is worse in the am and associated with 2 hours of morning stiffness for the last 5 years. She also reports intermittent pain and swelling in the L knee.  Her symptoms improve with exercise and NSAIDs but she cannot tolerate the NSIADs because of crampy abdominal pain and loose bowel movements. She has lost 5 pounds over the last 8 months, despite no decline in appetite.  She denies any history of psoriasis, uveitis, or inflammatory bowel disease. Her father, age 55, has low back pain but she is estranged from him and does not know the underlying diagnosis or his current or past treatment.

On exam, she is a thin female in NAD.  Skin: without lesions. General exam: normal. MSK: slight swelling and tenderness in the L knee without effusion. Shober score: 12.5 cm and positive Patrick’s test on the R side. The remainder of the exam is normal.

She is a non-smoker.

Data: CRP: 22; HLAB27 positive; X-ray of SI joints, lumbar, thoracic and cervical spine- normal.

What is the most accurate statement about her back disease?

  1. Although her x-rays are negative, the diagnosis is most consistent with axial spondyloarthritis and she has significant risk factors for disease progression.
  2. The intolerance to NSAIDs indicates the presence of Crohns’ disease and she should have a colonoscopy performed.
  3. Females with axial spondyloarthritis show more x-ray damage and functional loss compared to males.
  4. Female patients with axial spondyloarthritis are less likely to have children compared to women in the general population.

Doctor Commentary:

Rationale:

The correct answer is D. Female patients with axial spondyloarthritis are less likely to have children compared to women in the general population.

Studies have shown that females with ankylosing spondylitis tend to be undiagnosed, show less xray changes and more functional impairment than male counterparts. Significant factors for progression include baseline syndesmophytes, smoking, disease duration, and positive family history. She had none of these risk factors. Female AS patients are also less likely to have children. Intolerance to NSAIDs can cause abdominal cramping without inflammatory bowel disease so it is not necessary to perform a colonoscopy unless symptoms persist off NSAIDs.

March 15, 2013

A 55-year-old woman with RA is failing methotrexate 20mg per week and prednisone 15 mg per day. She is also on a daily NSAID.

She has high disease activity and markers of poor prognosis. She has agreed to start (add) a TNF inhibitor.

Her husband has recently recovered from a painful attack of shingles and she wants to discuss issues of vaccination as she herself had shingles in her left thoracic area 3 years ago.

With regards to the shingles vaccine (Zostavax), which of the following is the correct answer?

  1. Because she is only 55 she is not a candidate for Zostavax.
  2. Because she is on methotrexate and prednisone administration of Zostavax, a live vaccine, is contraindicated.
  3. Because of her past history of Zoster she does not need and is not a candidate for Zostavax.
  4. She is a candidate for Zostavax and it can be administered no less than 2 weeks prior to initiating her anti-TNF drug.
  5. She is a candidate for Zostavax and it can be administered no less than 4 weeks prior to initiating her anti-TNF drug.

Doctor Commentary:

Rationale:

The correct answer is 4: She is a candidate for Zostavax and it can be administered no less than 2 weeks prior to initiating her anti-TNF drug.

Let’s break this down. The vaccine for Zoster has been a great advance in preventing dermatomal zoster and its attendant complications in eligible people. The FDA approves this vaccine for individuals 50 years of age and older but the ACIP (Advisory Committee on Immunization Practices - part of the CDC) recommends it for individuals over the age of 60.

Our patient is at high risk for shingles (i.e. RA and immunosuppressive therapy) and she is a good candidate by age though she may or may not be reimbursed for it. The recent guidelines on Zoster vaccine from the ACR recommend the vaccine for older RA patients receiving non-biologic DMARD therapies, or before DMARD or biologic treatments are started. The CDC has recommended that individuals receiving lower dose prednisone (< 20 mg/day) or methotrexate and azathioprine at doses used for rheumatic diseases may safely receive the vaccine (http://www.rheumatology.org/publications/hotline/2012_09_12_herpeszoster.asp).

While patients with previous Zoster were excluded from the pivotal trial recent studies suggest the vaccine is safe in such populations (Schmader KE, Levin MJ, Gnann JW, Jr., et al. Efficacy, safety, and tolerability of herpes zoster vaccine in persons aged 50-59 years. Clin Infect Dis. 2012;54(7):922-8) and expert opinion favors vaccine after the first 2-3 years. Finally we believe it is wise and advisable to vaccinate this patient before starting the biologic since current biologic therapy is a contraindication for live vaccines. The recommended waiting period is two weeks. Recent studies have suggested that Zostavax may be both safe and efficacious in patients on biologic therapies but their retrospective design does not permit any change in the guidelines yet (JAMA. 2012;308(1):43-9).

February 15, 2013

A 38-year-old man with focal glomerulosclerosis and a creatinine of 4.4 has begun to experience more frequent attacks of gout. He has had four attacks over the past 6 months, the last one involved 4 joints and required 12 days of high dose prednisone therapy to resolve.

He had presented with nephrosis 3 years previously, and his kidney disease did not respond to corticosteroids in combination with cyclosporine or mycophenolate.

He is a high school football coach and physical education teacher, but was forced to go part time for health issues (fatigue, joint pains and the frequent gout flares). His insurance drug benefits will end shortly, he is applying for disability benefits.

On examination BP 133/78. Bilateral mild pitting edema. Tophi in bilat olecranon bursa, overlying 2nd mcp on the left, 3rd pip joint on the right and bilateral 1st MTP joints + intradermal tophacious deposits on finger pads.

He has no known medication allergies and does not drink alcohol or smoke cigarettes.

He has been placed on the transplant list following a recent renal biopsy.

Medications: atorvastatin, clonidine, enalapril, biweekly erythropoietin and furosemide. He has required frequent doses of prednisone to treat the attacks of gout.

Laboratory studies notable for: creatinine 4.4, Hgb 9.8, Albumin 2.9, urate 8.9.

For treatment of the hyperuricemia you suggest:

  1. Delay treatment until after the renal transplant
  2. Allopurinol 100 mg once every other day
  3. Allopurinol 50 mg then titrate to dose that reduces the serum urate to
  4. Allopurinol 300 mg once daily
  5. Febuxostat 40 mg once daily
  6. Pegloticase 8 mg every 3 weeks, continue until tophi resolved

Doctor Commentary:

Rationale:

The correct answer is 3: Allopurinol 50 mg then titrate to dose that reduces the serum urate to < 6.

A severe hypersensitivity reaction is more common in chronic kidney disease (CKD), with an overall prevalence of 1-4/1000 (estimated). The mortality rate is 25%. Oxypurinol is renally secreted, with levels higher in CKD. Thus, the dose adjustment should give lower oxypurinol levels and fewer hypersensitivity reactions.1, 2

Figure Image - Proposed Allopurinol Dosing in CKD

Based on estimated oxypurinol levels achieved with assumed appropriate allupurinol dose of 300 mg.

However, no repeatedly documented relationship between Oxy levels and reactions exists. Most reactions happen early, more rapidly with repeat dosing, suggesting an allergic reaction. If adhered to, <30% patients will lower their urate levels to 6.0 mg/dL. There is no clear evidence that dose adjustment decreases hypersensitivity reactions.2-5

Figure Image - Allopurinol dosing in CKD

References:

  1. Hande, et al. Am J Med. 1984;76:47-56.
  2. Hung, et al. PNAS. 2005;102:4134-39.
  3. Dalbeth, et al. J Rheum. 2006;33:1646-50.
  4. Vazquez-Mallado. Ann Rheum Dis. 2001;60:981-83.
  5. Silverberg, et al. ACR. 2009.

Discuss this case further: Rheumbuzz Physician / Medical Professional Discussion Area

January 15, 2013

A 55-year-old man presents with several weeks of fever, arthralgias, and a rash described as non-blanching papules (figure).  He has lost 7 pounds. His past medical history is unremarkable. He takes no medications and his social and sexual history is non-contributory. On screening examinations he has a mild anemia of 11.0 grms of hemoglobin, WBC of 5500 /mm3 with a normal differential.  A complete metabolic profile is normal with a creatinine clearance of 70ml/min. His ESR is 66 mm/hr and a urinalysis shows trace protein with numerous RBCs with a dysmorhic appearance. An ANA is negative but his RF is + at 120 iu. and C3 and C4 are moderately depressesed at 11mg% and 12mg%. and ANCA shows +CANCA pattern by IFA but negative EIA to PR3.

Doctor Commentary:

Rationale:

I would obtain serologies for HCV, HBV and HIV and order blood cultures. This case actually represents a case of strep viridans endocarditis with immune complex GN. Finally, a positive IFA ANCA without confirmatory EIA to PR3 or MPO should not be considered a true paositive. Such results are well reported with certain infections especially SBE. Always think of the “must rule outs.”

Discuss this case further: Rheumbuzz Physician / Medical Professional Discussion Area

December 18, 2012

What is the best serum urate-lowering therapeutic option for this patient at this time?

  1. Start allopurinol at 100 mg/day and gradually escalate the dose to achieve a serum urate level
  2. Start allopurinol at 100 mg/day without further dose increases because of his decreased renal function.
  3. Discuss with his transplant nephrologist, about the possibility of switching his azathioprine to mycophenolate mofetil prior to initiating allopurinol.
  4. Start febuxostat at 40 mg/day and then increase dose to achieve a serum urate level

Doctor Commentary:

References:

  1. Stamp L, Searle M, O’Donnell J, Chapman P. Gout in solid organ transplantation: a challenging clinical problem. Drugs 2005; 65:2593–2611.
  2. Cummins D, Sekar M, Halil O, et al. Myelosuppression associated with azathioprine-allopurinol interaction after heart and lung transplantation. Transplantation 1996; 61:1661–1662.
  3. Navascues RA, Gomez E, Rodriguez M, Laures AS, Baltar J, Grande JA. Safety of the allopurinol-mycophenolate mofetil combination in the treatment of hyperuricemia of kidney transplant recipients. Nephron 2002; 91:173–174.

Series Objectives

  1. Describe evidence-based strategies and guidelines for managing the risk of infection associated with immunosuppressive therapy in patients with rheumatic disease.
  2. Apply evidence-based guidelines for screening rheumatic disease patients who are potential candidates for immunosuppressive therapy.
  3. Identify comorbidities in patients with rheumatic disease and develop strategies for their prevention or treatment.
  4. Compare and contrast evidence-based treatment strategies with regard to clinical outcomes and adverse effects in patients with rheumatic disease.
  5. Recognize the early signs and symptoms of rheumatic disease that may lead to timely diagnosis and initiation of appropriate therapy.

Target Audience

This activity is designed for rheumatologists, primary care physicians, and other clinicians, including allied health professionals, nurse practitioners, and physician assistants, who treat patients with rheumatic diseases.

Activity Director

Leonard H. Calabrese, DO
Professor of Medicine
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University
R.J. Fasenmyer Chair of Clinical Immunology
Vice Chairman, Department of Rheumatic and Immunologic Diseases
Orthopaedic and Rheumatologic Institute
Cleveland Clinic
Cleveland, OH