Thinking Aloud, Rethinking Gout: RHEUMATOLOGISTS BEWARE, possibly controversial and offensive post ahead😈
2 posts and 2 events prompted me to re-examine Gout, resulting in this protracted 10-day-series on Gout, and culminating in today’s posts.
Some things I was taught early in my medical education tend to stick. 2 axioms came to mind, “Never Say Never”, and “Common Things Occur Commonly”, when I read the 2 posts.
“Never Say Never”:
This rang loudly when I read Dr Cush’s tweet,
“Gout likes to Flare in 1 Joint @ a time; 2 joints possible; 3 joints uncommon and 4 joints NEVER; time to consider other diagnoses”.
Understandably, I found his “NEVER” pronouncement a tad dogmatic.
“Common Things Occur Commonly”:
When I first read and posted this appended article, I quipped tongue-in-cheek that “perhaps the doctors were misdiagnosing Gout as RA”. Gout, being the most prevalent inflammatory arthritides and having the most protean of manifestations earning it the well deserved moniker as today’s Great Mimicker (supplanting Syphilis of old and Lupus of more recent memory), can surely present in polyarticular fashion like RA?
In this prospective study, urate crystals detected on DECT occurred in as many as 20% of random “RA” patients with serum uric acid level over 6mg/dl (that’s current Gout treatment target). This, again, is surprising to me as I was taught that Gout and RA are inversely correlated. It is also telling that a third of the “seronegative RA” patients were DECT-positive for urate, and 70% of DECT-positive were seronegative. DECT-positive also tended to be male and over 60, not your typical RA cohort, but certainly fits Gout’s profile. That they had active disease (DAS>3.2) suggested that their RA treatment might not have been working particularly well.
So, perhaps they are indeed Gout patients after all, misdiagnosed and mismanaged as RA?😲
PATIENTS BEWARE! Your Rheumatologist (myself included) may have misdiagnosed your Gout as:
1) Seronegative RA
2) RS3PE (Relapsing/remitting Seronegative Symmetrical Synovitis with Peripheral Edema)
3) B27-negative Reactive Arthritis
4) Psoriatic Arthritis sine Psoriasis
5) Non-radiographic Ankylosing Spondylitis
6) SAPHO Syndrome
7) Adult-onset Still’s disease
8) Inflammatory Osteoarthritis
9) Pseudogout
10) ?…..
2 events brought it home for me:
Firstly, I saw a flurry of patients presenting with “classical” diagnoses (especially SpA/ReA), with positive serologies even (especially B27), whose inflammatory pain was persistent (at least 3 weeks), with 2 not responding adequately despite combination DMARDs and several switches of targeted therapies (needing high dose steroid for good control). Then, on ultrasound, I saw classical Gout features like double contour sign, juxta-articular erosion or amorphous lesion with hyperaemic rim.
Their serum uric acid levels were not even high by usual laboratory standards (but higher than Gout treatment targets). None had visible tophi. They responded well to ULT, without needing DMARDs or biologics.
Then there is of course the case of me. Over the last 2 years, I had to progressively curtail my running due to persistent right knee and (recently) left ball-of-foot pain, which I attributed to patellar tendinosis (hypoechoic lesion on ultrasound) and plantar bursitis respectively. It wasn’t until I had my first (and hopefully last) “classical” acute Gout flare in my right knee, and a more extensive and meticulous ultrasound revealed those lesions (chronicled in an earlier post), that the diagnosis was clinched. After injecting steroid around the subclinical tophi, and embarking on ULT, I found that even my chronic knee and sole pain disappeared, and I found renewed vigour in my running! This got me thinking that perhaps even the lesion in my patellar tendon is a tophus! I shall monitor the resolution of my tophi sonographically and keep you posted😉
The common thread in these 2 events is that Gout can present not in the classical pictures of:
1) Acute/Critical Gout (severe pain)
2) Intercritical Gout (asymptomatic)
3) Chronic Tophaceous Gout (with or without constant pain).
In fact, if your acute attack does not remit completely within 2 weeks, and you experience persistent pain without visible tophi or overt synovitis, you may not make diagnosis even with the latest generous criteria for Gout. The presence of positive serologies or rheumatic features like enthesitis or psoriasis may be red herrings.
In light of my recent epiphany on Gout, I propose that:
1) Another category of Gout exists, a “Subcritical Gout”, characterised by persistent pain, with our without overt clinical inflammation, but with hyperuricaemia and radiological (ultrasound or DECT) urate deposits. Surely visible tophi don’t just pop up overnight, but start off microscopically and then radiologically. Technically, every Gout patient is tophaceous;
2) Our current definition of hyperuricaemia and our treatment targets are not low enough. Consider that mammals with uricase typically have SUA level below 2mg/dL. We may need to treat hyperuricaemia more aggressively, and not pull back till radiologically-evident tophi have entirely resolved.
Back to you, the patient. If:
1) your profile (age, gender) is atypical of the diagnosed arthritides;
2) your serum uric acid is repeatedly above 6mg/dL (350umol/L);
3) your autoimmune tests (RF, anti-CCP, HLA-B27) all come back negative;
4) your inflammation seems to respond best to high dose steroid;
5) you’re down to your third or fourth targeted therapy for RA;
It’s time to consider Gout.
Talk to your Rheumatologist. He/she may need to re-look the ultrasound of your joints (and adjacent bone and soft tissue), or perhaps order a DECT (which is currently only available at KTPH & SGH). Your friends may be correct after all: your chronic unremitting arthritis is Gout! 😲