Updates in Rheumatology for the Busy Hospitalist

The neon of Las Vegas may have framed this year’s clinical update at SHM Converge 2025, but the real spotlight fell on the everyday rheumatologic dilemmas that land patients in our wards. Kimberly Trotter, MD, an assistant professor of medicine at the University of Chicago’s rheumatology section in Chicago, distilled four high-impact disease clusters—gout, rheumatoid arthritis (RA), systemic lupus erythematosus, and vasculitis—into pragmatic lessons meant to shorten length of stay, avert diagnostic detours, and preserve organ function.

National data show that nearly half of rheumatology-related admissions stem from osteoarthritis, but the acute issues that consume hospitalists’ attention are gout (13%), rheumatoid arthritis (8%), and a miscellany of systemic disorders such as lupus and vasculitides. Recognizing these entities early shortens stays; missteps add an average of two days, particularly when gout flares are overlooked.   This recap is tailored to hospitalists who need fast clinical traction rather than casino flash.

Gout: Know when to tap, when to treat

Hospitalization itself is a gout trigger—volume shifts, diuretics, and dietary changes conspire to ignite flares. Classic monoarthritis of the lower limb reaches maximum agony within 24 hours, but beware polyarticular or spinal involvement. Aspirate any hot, swollen joint unless septic arthritis has already been ruled out; crystal confirmation prevents both undertreatment and steroid overuse. First-line therapy pivots on timing: colchicine is valuable only if it’s started no more than 36 hours from symptom onset (1.2 mg to start, 0.6 mg after an hour, then 0.6 mg once or twice daily; halve frequency in stage 3 chronic kidney disease. Beyond that window, reach for nonsteroidal anti-inflammatory drugs (NSAIDs) or prednisone 40 mg with a taper over five to 10 days; avoid dose packs, which can boomerang flares. Continue outpatient urate-lowering agents during flares—holding allopurinol or febuxostat invites post-discharge crises. IL1 blockade (anakinra) matches standard therapy in efficacy and may rescue patients with contraindications to steroids or NSAIDs, but costs run high.

Pearls

• Podagra is virtually pathognomonic, yet gout can coexist with infection—tap before you treat.
• Never taper steroids too briskly; rebound pain is real.
• Starting allopurinol during a flare is acceptable if long-term therapy is indicated and renal function allows.

RA: The great mimicker

RA admissions may reflect articular pain, pulmonary nodules, interstitial lung disease, pericarditis, or accelerated atherosclerosis. Extra-articular disease can masquerade as an infection and drive soaring C-reactive protein (CRP), so hospitalists must rule out sepsis before escalating immunosuppression. Low-dose prednisone (10 to 20 mg) or targeted intra-articular steroids quell acute synovitis; higher doses (40 mg or higher) are for threatening systemic flares. Continue baseline glucocorticoids to prevent adrenal crisis, but pause methotrexate, anti-tumor-necrosis-factor agents, and Janus kinase inhibitors until infection is excluded. For new-onset RA, remember that rheumatoid factor and anti-cyclic-citrullinated-peptide are diagnostic aids—extreme CRP suggests you are chasing the wrong zebra.

Pearls

• Viral hepatitis, parvovirus, Lyme, and endocarditis can all yield false-positive rheumatoid factor—think broadly.
• Keep an eye on methotrexate toxicity in chronic kidney disease; reduce the dose or hold if estimated glomerular filtration rate is less than 30 mL/min.
• RA patients die more often from cardiovascular disease than from their arthritis; flag high-risk profiles for post-discharge follow-up.

Systemic lupus erythematosus: flare versus fail

Systemic lupus erythematosus favors young women but strikes all sexes and races; minority men often present with more severe organ damage. Inpatient admissions commonly arise from nephritis, serositis, infection, or thrombotic events. Antinuclear antibody negativity virtually excludes lupus, so avoid “just in case” testing; instead, order complements C3 and C4 and anti-double-stranded-DNA when flare is suspected, as hypocomplementemia and rising double-stranded DNA titers track disease activity. Treat musculoskeletal or cutaneous flares with NSAIDs or prednisone at up to 20 mg; organ-threatening disease warrants 40 to 60 mg (or pulse methylprednisolone) plus a steroid-sparing agent. Hydroxychloroquine is the cornerstone therapy, is not immunosuppressive, and should continue through infections—consult ophthalmology to schedule annual retinal exams after five years.

Pearls

• Fever in lupus may signal infection, flare, or both; trending CRP (often low in pure flare) and procalcitonin can help.
• Nephritis may present subtly—order spot protein and creatinine ratios liberally.
• Thrombosis risk skyrockets with antiphospholipid antibodies; prophylactic anticoagulation merits discussion.

Vasculitis: Size matters

Giant Cell Arteritis (Large Vessel)

In patients over 50 years old with new temporal headaches or jaw claudication, treat giant cell arteritis (GCA) as a vision-threatening emergency. Start IV methylprednisolone 500 to 1,000 mg/day for three days for visual symptoms, then oral prednisone 40 to 60 mg. Temporal artery biopsy remains confirmatory but should not delay steroids; obtain within two weeks of treatment. Tocilizumab is a validated steroid-sparing option. Normal erythrocyte sedimentation rate and CRP almost rule out GCA, yet rare seronegative cases exist.

ANCA Associated Vasculitis (Small Vessel)

Think granulomatosis with polyangiitis, microscopic polyangiitis, or eosinophilic granulomatosis with polyangiitis when hematuria, pulmonary infiltrates, sinus disease, or mononeuritis multiplex cluster together. Labs: erythrocyte sedimentation rate, CRP, creatinine, urinalysis, myeloperoxidase, proteinase 3 anti-neutrophil cytoplasmic antibodies (ANCA, as in ANCA-associated vasculitis), and anti-glomerular basement membrane antibodies if indicated. Imaging and, crucially, tissue biopsy define the diagnosis; “no biopsy, no vasculitis,” unless biopsy is strongly contraindicated. Begin high-dose steroids once infection is excluded; rituximab now rivals cyclophosphamide for induction with fewer long-term harms, and avacopan (a C5a inhibitor) is emerging as adjunctive therapy. Plasma exchange is no longer routine after negative data from the PEXIVAS clinical trial.

Pearls

• Vessel size predicts organ pattern: large, like GCA, targets cranial and limb arteries; small, like ANCA, prefers kidney, lung, and otolaryngological regions.
• ESR and CRP are highly sensitive but nonspecific; falling markers do not always equal remission.
• Early steroid-sparing biologics curb cumulative glucocorticoid toxicity—coordinate rheumatology follow-up before discharge.

In a city known for doubling down, Dr. Trotter reminded us that the safest bet in rheumatology is early recognition, judicious steroid use, and continuity of evidence-based disease-modifying therapy. By integrating these pearls into daily practice, hospitalists can tilt the odds toward shorter stays and better long-term outcomes—no dice required. 

Dr. Migliore is an assistant professor of medicine at Columbia University College of Physicians and Surgeons, director of general medicine perioperative, and consult services, and medical director of surgery and surgical step-down at Columbia University Medical Center in New York.