HeyHippocratesRA, gout, lupus, the vasculitis — a colleague who cites every call.
Clinical decision support that reasons like a rheumatologist while you decide: diagnose RA and treat to target, control the crystal flare, work up the connective-tissue disease, and catch the vasculitis before it costs sight — with the decision rule and exactly what would change it. Built for verified physicians.
Watch it think — in rheumatology.
Two worked examples, reasoned the way it answers: the relevant clinical checks run, the answer is cited, the decision rule is explicit, and what is missing is flagged.
New temporal headache with jaw claudication and transient visual blurring in a 72-year-old, ESR markedly raised — the first move?
Treat suspected giant cell arteritis as a sight-threatening emergency: start high-dose glucocorticoids immediately — do not wait for the temporal artery biopsy, which stays informative for one to two weeks — and give intravenous methylprednisolone when there is visual loss. Confirm with the biopsy or vascular ultrasound, track ESR and CRP, and add tocilizumab as a steroid-sparing agent. Untreated, the fellow eye is at risk within days.
Decision ruleSuspected GCA → high-dose glucocorticoids immediately (IV methylprednisolone if visual loss); biopsy or ultrasound within 1–2 weeks without delaying steroids; ESR/CRP; tocilizumab steroid-sparing.
Not established from this alone — the biopsy, the ophthalmic findings and the inflammatory markers change the certainty and the taper.
A red, hot, swollen first MTP joint that came on overnight, not on any urate-lowering therapy — the flare plan?
Treat the flare early with a single anti-inflammatory chosen by comorbidity: an NSAID, colchicine, or a systemic or intra-articular corticosteroid, with an interleukin-1 inhibitor when those are contraindicated. Do not start urate-lowering therapy during the flare, but continue it if the patient is already established on it. Once the flare settles, begin allopurinol low and titrate to a target serum urate below 6 mg/dL, with flare prophylaxis for the first months.
Decision ruleAcute gout → NSAID / colchicine / steroid (by comorbidity); do not start ULT mid-flare but continue if established; after settling, allopurinol titrated to urate below 6 mg/dL with prophylaxis.
Not established from this alone — renal function, comorbidity and the flare pattern change the drug and the urate target.
Illustrative simulations. The physician always decides.
The answers rheumatologists actually look up.
The exact questions your field searches for — answered in the format the knowledge base speaks: the answer, the decision rule, what's missing, and the source.
Rheumatoid arthritis — how do I diagnose and treat to target?
Diagnose with the ACR/EULAR 2010 classification — the joint count and distribution, RF and anti-CCP, acute-phase reactants and symptom duration — after excluding mimics. Start a disease-modifying drug early, methotrexate as the anchor, and treat to a target of remission or low disease activity measured with a composite score, escalating to a biologic or JAK inhibitor when the target is missed. Early control changes the trajectory.ACR/EULAR
Decision ruleACR/EULAR 2010 to classify; start a DMARD early (methotrexate anchor); treat to target remission or low activity by composite score; escalate to biologic or JAK if the target is missed.
Missing data: the antibody status, the disease-activity score and comorbidity change the drug and the pace.
Gout — the acute flare and when to start urate-lowering therapy?
Treat the flare with an NSAID, colchicine, or a corticosteroid, matched to renal function and comorbidity. Start urate-lowering therapy — usually allopurinol — for recurrent flares, tophi, urate stones or radiographic damage, titrating to a serum urate below 6 mg/dL, or below 5 with tophi. Give flare prophylaxis when starting, and do not stop urate-lowering therapy that is already running during an acute attack.ACR · gout
Decision ruleFlare: NSAID / colchicine / steroid by comorbidity. Start ULT (allopurinol) for recurrent flares, tophi, stones or damage → titrate to urate below 6 (below 5 if tophi) + prophylaxis; never stop established ULT mid-flare.
Missing data: the renal function, the flare frequency and the tophus burden change the threshold and the target.
Systemic lupus — the diagnosis and initial workup?
Use the ANA as the entry criterion — a negative ANA makes SLE very unlikely — then apply the EULAR/ACR 2019 weighted classification across the clinical and immunologic domains. Confirm with specific antibodies (anti-dsDNA, anti-Sm), complement levels, a blood count and a urinalysis to catch nephritis. Hydroxychloroquine is the backbone for nearly everyone, with immunosuppression scaled to organ involvement.EULAR/ACR 2019
Decision ruleANA as entry (negative makes SLE unlikely); EULAR/ACR 2019 weighted criteria; confirm dsDNA/Sm + complement + urinalysis for nephritis; hydroxychloroquine backbone; immunosuppression by organ.
Missing data: the antibody profile, the complement and the urinalysis change the diagnosis and the treatment.
Giant cell arteritis — recognizing it and the emergency treatment?
Suspect giant cell arteritis in anyone over 50 with a new headache, scalp tenderness, jaw claudication or visual symptoms and a raised ESR or CRP. Start high-dose glucocorticoids at once — intravenous when vision is threatened — because the risk is irreversible blindness; the temporal artery biopsy or ultrasound stays informative for one to two weeks after steroids begin. Tocilizumab spares steroid exposure over the long taper.ACR · vasculitis
Decision ruleOver 50 + new headache / jaw claudication / visual change + high ESR or CRP → glucocorticoids immediately (IV if visual loss); biopsy or ultrasound within 1–2 weeks; tocilizumab steroid-sparing.
Missing data: the biopsy, the ophthalmology exam and the markers change the certainty and the taper.
What it knows in rheumatology
Your whole practice, one specialist brain — grounded in specialist-written, cited knowledge.
A generalist rheumatology colleague across inflammatory arthritis, crystal disease, connective-tissue disease, vasculitis and spondyloarthritis — cited, non-directive, always with the decision rule.
Deep specialist agents for vasculitis, lupus and connective-tissue disease, inflammatory myositis and pediatric rheumatology — each its own specialist voice and knowledge base — plus your own uploaded materials.
Why not just use OpenEvidence or ChatGPT?
A large language model answers any clinical question with total confidence and no idea whether it is right. A search engine finds papers. HeyHippocrates reasons inside your specialty from a knowledge base a specialist in your field wrote and signed, and tells you the decision rule and what is missing.
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Questions rheumatologists ask
It reasons in the frameworks you use — the ACR/EULAR criteria, treat-to-target, the ACR gout guideline and the EULAR/ACR lupus criteria — and always shows the reasoning, the decision rule and what would change it. The decision always stays your call.
Both. Fellows use it to pressure-test a plan and learn the decision rule; attendings use it as a fast, cited second opinion in clinic and on consults. Access is gated to verified physicians.
Vasculitis, lupus and connective-tissue disease, inflammatory myositis and pediatric rheumatology each have their own deep specialist agent on the Pro plan, on top of the full rheumatology scope on Basic.
No. It is physician-facing clinical decision support — a cited thinking partner. It does not diagnose, does not treat, and gives no patient-facing advice. The decision always stays with you.
Every answer is grounded only in specialist-written, cited rheumatology knowledge — traceable to a named source — and always states the decision rule plus what data is missing, instead of a confident guess.