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Rheumatology

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Does a normal uric acid level rule out a gout flare?

  • No, a normal uric acid level during an acute flare up does not rule out gout 

  • Even if urate crystals have been identified in synovial fluid, a very high leukocyte count > 50,000 should still raise suspicion for concurrent bacterial joint infection 

 

What are the indications for urate lowering therapy?

  • If 1 or more subcutaneous tophi 

  • Evidence of radiographic damage

  • 2 or more gout flare ups annually 

  • Meds that raise urate levels should be discontinued like HCTZ 

 

What is the target urate level to aim for?

  • Urate level <6 

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Acute treatment options for gout?

  • Colchicine, NSAIDs, and glucocorticoids (delivered orally, intramuscularly, or intra-articularly) are all similarly effective

  • Naproxen (500 mg BID) or indomethacin (50 mg TID), best in patients <60 yo w/o renal, CV, or active GI disease

  • Colchicine 1.2 mg PO, followed by a single 0.6-mg dose in 1 hour, continued at 0.6 daily until symptom resolution, contraindicated in CKD, ADRs include GI upset.

  • Prednisone/prednisolone 30 to 40 mg daily until symptom resolution and then taper, use with caution in CHF, DM, PUD

  • Current ACR guidelines support starting urate-lowering therapy (allopurinol) during acute flare (improves future adherence), but only if patient is being treated for the acute flare with one of the above. Allopurinol alone will not treat the acute flare and may prolong the flare duration.

  • https://pubmed.ncbi.nlm.nih.gov/34383428/

  • https://pubmed.ncbi.nlm.nih.gov/32391934

 

When should you stop a patient’s allopurinol? 

  • You do not ever need to stop a patient’s allopurinol or renally-dose for a patient with AKI unless you think that their allopurinol is causing their AKI due to allopurinol hypersensitivity syndrome - rare but potentially fatal constellation of fever, rash, hepatic necrosis, eosinophilia, acute nephritis; this is also why you should test for HLA-B*5801 prior to starting allopurinol in pts of Southwest Asian descent (thanks to Dr. Giattino)

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Normal synovial fluid-

  • Clear/yellow/transparent, Leukocyte count <200/uL; cultures negative

Non inflammatory-

  • Clear/yellow, Leukocyte count 200-2000; cultures negative

Inflammatory-

  • Yellow/opaque/white; leukocyte count 2000-20,000; negative gram stain and culture

Crystal-

  • Yellow/white/translucent/opaque; leukocyte count 10,000-50,000; negative gram stain, positive crystals 

Infectious-

  • Yellow/white/opaque; Leukocyte count >50,000; positive gram stain/positive culture

Hemorrhagic-

  • Red; negative gram stain/culture 

 

Which bacteria can cause a negative culture despite the presence of bacterial infection?

  • Nearly all culture are positive for infection except Neisseria gonorrheae which can be positive in 50% or fewer cases

 

Causes of Mono articular joint infections? 

  • OA, Bacterial infection, Crystal induced, fungi, spirochete (Lyme or syphilis), mycobacteria

 

Causes of oligoarticular (2-4) joint infections? 

  • Disseminated gonorrhea, RF, lyme disease, OA, spondyloarthropathy 

 

Causes of polyarticular infection >5 joints? 

  • Hep A/B, parvovirus, Rubella, HIV, RA, SLE, psoriatic arthritis, crystalline arthritis, OA

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ANA → SLE, Sjogren, Mixed connective tissue disease, Scleroderma 

Anti- smith antibody —> Most specific for SLE

Anti-U1-RNP → Mixed connective tissue disease or SLE (high titers usually seen in MCTD >1:10 000 but does not correlate with disease activity)

Anti-centromere → CREST syndrome → more likely to develop pulmonary hypertension 

Anti-dsDNA antibody → SLE and correlates with disease activity, especially kidney disease

Anti-La/SSB; anti-Ro/SSA antibody —> Sjogren, SLE, RA, sicca syx, neonatal SLE 

Anti-Scl 70 antibody → Systemic sclerosis → more likely to develop pulmonary fibrosis 

Antihistone antibody → Drug induced lupus 

C-ANCA → Granulomatosis with polyangiitis 

P-ANCA (anti MPO) → Churg Strauss (eosinophilic granulomatosis with polyangitis) 

Anti- Jo 1 → Polymyositis and antisynthetase syndrome 

Anti-CCP → RA 

RF → RA, Sjogren, cryoglobinemia, also seen in hep C, endocarditis, SLE 

 

What is the significance of an isolated ANA positive test?

  • Isolated ANA + without specific features or syx and normal exam finding does not establish diagnosis of a connective tissue disease

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Does a negative Rheumatoid factor exclude RA? 

  • No, patients may have seronegative RA. 

  • A positive RF alone is NOT enough to diagnose RA

 

What is the major cause of death in patients with RA?

  • Cardiovascular disease 

 

What should all patients with RA undergoing general anesthesia undergo? 

  • Must get Cervical X ray to rule out atlantoaxial subluxation 

 

RA Treatment?

  • First line- NSAIDs and low dose oral or intraarticular steroids (symptom management- have no impact on disease progression) 

  • DMARDs- MTX is in the initial DMARD used → should be instituted immediately in patients with erosive disease

    • MTX is absolutely contraindicated in pregnancy 2hereas hydroxychloroquine and sulfasalazine can be used in pregnancy. 

  • Biologic therapy- indicated when disease control is not achieved by DMARD therapy only. You would add biologics to MTX → Infliximab, Entanercept, Adalimumab, Golimumab

  • Surgical intervention → Severe pain, functional disability, ruptured tendons 

Developing an effective treatment algorithm for rheumatoid arthritis - PubMed (nih.gov)

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What is required for the diagnosis? 

  • Antibody to Ro/SSA and La/SSB along with classic findings is sufficient for diagnosis 

 

In unclear cases, gold standard for diagnosis ? 

  • Lip biopsy of minor salivary gland. 

 

What do you have to worry about in pregnant women with Anti-Ro/La antibody?

  • Neonatal heart block 

 

What lymphomas are Sjogren patients at higher risk of developing relative to the general population?

 

What is the main treatment? 

  • Symptomatic relief- artificial tears, artificial saliva, mouth lubricant 

 

When is immunosuppressive therapy indicated? 

  • It is only indicated in patients with severe systemic manifestation

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What is the gold standard for the diagnosis of hip or knee OA? 

  • An X ray of the hip or knee. Hand x rays are not usually recommended. Hand exam is much more specific 

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What tests should you consider if a patient has an explosive psoriatic arthritis flare up  vs severe flare up? 

 

Does the extent of skin involvement correlate with joint disease?

  • No , there is no correlation between extent of skin involvement and severity of joint disease

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What are the features of reactive arthritis? 

  • Conjunctivitis, enesthitis, urethritis, sacroilitis, arthritis

  • “ The classic triad of can’t see, can't pee, can't climb the tree- conjunctivitis, urethritis, and arthritis” is only seen in one third of the patients” 

 

What is the first line treatment for reactive arthritis? 

  • Chronic antibiotic therapy is NOT indicated. It is usually self limited and will resolve in 6 months. First line treatment is supportive with NSAIDs or steroid injections

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What is the treatment?

  • First line- NSAID (they are disease modifying in ankylosing spondylitis) 

  • Glucocorticoid injections for enthesitis and persistent synovitis 

  • TNF inhibitors for inadequate control of axial disease with NSAIDs. MTX, hydroxychloroquine and sulfasalazine are NOT considered treatments for ankylosing spondylitis 

  • Sulfasalazine for peripheral joint disease

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What is the significance of HLA-B27 testing?

  •  It cannot be used independently to exclude or confirm diagnosis of ankylosing spondylitis or other spondylopathy. 

  • It is not diagnostic on its own, however can tell us the risk of spondyloarthritis in uncertain situations.

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What medications associated with it?

  • Hydralazine, Procainamide, Isoniazid, Minocycline, TNF inhibitors 

 

Classic presentation of drug induced lupus?

  • Fever, serositis, arthritis 

 

Antibodies seen with Drug induced lupus? 

  • ANA can be positive. However anti-dsDNA and anti-smith antibodies would be negative. 

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When to order the SLE antibodies and what are they for? 

  • ANA should be ordered before ANY sub serology testing. If the ANA is positive, then specific subserologies are indicated based on clinical scenario:

    • Anti–DS DNA: 95% specific for SLE and ~50% to 60% sensitive. Found in more severe disease, especially the kidney. Antibody levels follow disease activity and are good to monitor during tx

    • Anti-Ro/SSA and anti-La/SSB antibodies: Sensitive for MCTD. Levels do not correlate with disease activity

    • Anti-Smith: Most specific for SLE (99%) but have low sensitivity and do not correlate with disease activity

    • Anti–U1-ribonucleoprotein: Associated with photosensitive rash

    • Low C3 and C4 often associated with an active flare up. 

 

What is a characteristic feature of lupus facial rash? 

  • Does NOT involve the nasolabial fold. 

 

Treatment of SLE?

  • NSAID and hydroxychloroquine for arthritis

  • Hydroxychloroquine should be continued indefinitely to prevent flare ups. Even if a quiescent state of disease should be continued. 

    • Annual eye exam needed for those on hydroxychloroquine 

  • Life threatening disease→ Steroids, Mycophenolate or cyclophosphamide 

  • Vitamin D and calcium supplements for all patients. 

  • Bisphosphonates indicated in those with osteoporosis or osteopenia only. 

 

What medications can be used in pregnancy?

  • Prednisone and hydroxychloroquine

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Treatment of SLE flare?

  • Depends on severity → Typically pulse dose steroids (methylpred 0.5 mg/kg) x 3 days with taper

  • Continue home hydroxychloroquine

  • Consider immunosuppressive agents such as cyclophosphamide

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How do you diagnose APLS?

  • Lupus anticoagulant, anticardiolipin antibodies, anti-B2-glycoprotein antibodies

  • >1 arterial, venous, or small vessel thrombosis

  • Pregnancy morbidity

 

What is the treatment for APLS?

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What is the primary cause of morbidity and mortality in patients with SScl? 

  • Pulmonary disease 

 

What are the features of a scleroderma crisis? 

  • HTN with microangiopathic hemolytic anemia, thrombocytopenia, AKI with mild proteinuria and bland urine. 

  • Prednisone can precipitate a scleroderma crisis. 

  • This is the only case where ACE/ARB is used in AKI-  Prescribe ACE inhibitors for scleroderma renal crisis regardless of the serum creatinine level; continue even in the setting of kidney failure.

  • Do NOT use steroids to treat scleroderma

 

What are the differentiating factors between diffuse and limited scleroderma?

  • Limited scleroderma- No scleroderma renal crisis, pulmonary hypertension is more common 

  • Diffuse scleroderma- scleroderma renal crisis can be present, interstitial lung disease is more common 

 

How is early Raynaud from Scleroderma differentiated from primary Raynaud disease?

  • Nailfold capillary destruction and dilated capillary loops are seen in raynaud with scleroderma but NOT primary raynaud 

 

What pulmonary testing is needed for those with scleroderma?

  • All patients have to undergo PFT and high resolution CT at the time of diagnosis 

  • PFT with DLCO should be repeated every 6-12 months 

  • Annual echo

  • RHC is required for definitive diagnosis of pulmonary arterial hypertension 

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Which vasculitides are associated with which size vessels?

  • Large: Takayasu, Giant cell (GCA)

  • Medium: Polyarteritis nodosa, Kawasaki

  • Small (ANCA-associated): Granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis

  • Small (immune-associated): Cryoglobulinemic vasculitis, IgA vasculitis, hypocomplementemic urticarial vasculitis

 

Polyarteritis nodosa kidney disease- No involvement of glomerulus- no urine erythrocyte casts, but hematuria or proteinuria may occur 

 

For eosinophilic granulomatosis with polyangiitis - cannot make diagnosis in the absence of eosinophilia 

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Giant Cell Arteritis treatment?

  • Treat with high dose steroids plus tocilizumab. Must treat immediately to prevent vision loss. Obtain biopsy in less than 2 weeks. 

 

Takayasu treatment?

  • Steroid treatment, can also use steroid sparing agents like MTX or azathioprine 

 

Polyarteritis Nodosa treatment?

  • Steroid and cyclophosphamide for severe organ threatening disease. 

  • Must check for hepatitis B and treat any underlying infection 

 

Granulomatosis with polyangiitis/Microscopic polyangiitis treatment?

  • Treat with steroids, Rituximab preferred over cyclophosphamide 

 

IgA vasculitis treatment?

  • Usually self limited 

  • Treat with steroid or cyclophosphamide if severe or persistent glomerulonephritis 

 

HCV associated cryoglobulinemia vasculitis treatment?

  • Treat underlying hepatitis C 

  • In severe disease, treat with prednisone, cyclophosphamide and plasmapheresis

 

Behcet disease treatment?

  • Steroid as first line 

  • Steroid sparing agent if major disease manifestation (Uveitis, GI involvement, CNS or large artery involvement) 

  • Colchicine or apremilast for oral ulcers  

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What is the treatment?

  • CBT and aerobic exercise 

  • Medical treatment: pregabalin, duloxetine. DO NOT use OPIOIDS or NSAID 

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What is the first line treatment?

  • Intra-artiuclar steroid injections, NSAIDs, colchicine or steroids in acute disease

 

What X-ray finding is seen with CPP?

  • Chondrocalcinosis

  • Although an x-ray without chondrocalcinosis DOES NOT rule out CPP

 

What is the treatment of chronic CPP?

  • Low dose colchicine, low dose NSAID or low dose steroid

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