Even as I post, I'm recovering from my first full-blown Gout attack to my right knee.
I developed an acutely worsening anterolateral right knee pain after a (truncated) 5km run last evening. I initially thought it was a patellar tendon strain as I have a history of tendinosis in this tendon, and it was exquisitely tender proximolaterally. There was no joint effusion.
Sleep was disturbed as it hurt even at rest, which should have alerted me to the inflammatory nature of the pain. I limped the whole morning, despite taking a dose of Arcoxia.
Came to work, planning to ask my surgeon friend to tape my patella medially, still thinking that a laterally tracking patella was the cause. Until I did an ultrasound.
My lateral infra-patellar fat pad was mightily inflamed, and the fat looked unusually hyperechoic. There was an erosion on the lateral edge of the patella. Then the pin dropped: there was a double contour on the lateral end of the cartilage of my lateral femoral condyle, with a hint of intra-cartilage calcification (tramline) as well. It's Gout, and possibly chondrocalcinosis (Pseudogout).
I did what I would do for my patients in the same situation: I injected the inflamed fat (or tophus) with steroid for fast relief; under sonographic guidance, of course.
And I'll have to start treatment. I knew from previous health screens that I have hyperuricaemia, but as I was hitherto asymptomatic, I thought I'll get by with hydration and diet (kidding myself). The recent festive feasting (and weight gain) must have surely done me in.
I'll go with a uricosuric agent, Benzbromarone; with colchicine prophylaxis; and target serum uric acid at below 300 umol/L (5.5 mg/dL). And lose some weight.
Double contour and double tramline signs on cartilage suggesting mixed crystal arthropathy (Gout on cartilage surface, Calcium Pyrophosphate within cartilage substance):
Inflammation (power doppler signals) in the infrapatellar soft tissue, beneath and lateral to the "pancake-shaped" patellar tendon viewed in short axis:
Inflammation in soft tissue lateral to the patellar tendon (not seen), viewed in long axis. The echogenic amorphous material in the midst of the power doppler signals may represent gouty tophus:
Long axis view, patella on the left with surface erosion and adjacent inflammation. Juxta-articular erosions are typically gouty:
Erosion has to be demonstrated on ultrasound in 2 perpendicular planes. Short axis view with patella on the left, lateral femoral condyle on the right:
Needle coming in from the top left, injecting steroid around tophus. Despite removing "cross-beam" imaging, needle is faint as it's 25G: why inflict more pain than is necessary? I'm not masochistic:
The main reason Lesinurad has not been approved for use without a Xanthine Oxidase Inhibitor is the concern that excessive uric acid cascading down the Loop of Henle may damage the kidneys. Uric acid in high concentrations is highly nephrotoxic. Tophaceous Gout sufferers are at high risk for developing renal failure (much like Tumour Lysis Syndrome in oncology), and should remain in the care of a rheumatologist. With inadequate hydration, kidney stones may develop in the susceptible patients.
Even if you do not suffer painful Gout attacks in your joints; even if you are young, otherwise healthy, and think the world as your oyster; you may yet be done in by kidney failure, heat attack and stroke. And these catastrophic events are striking younger and younger, possibly due to our lifestyle and diet.
Ask any rheumatologist, and he/she will tell you that Gout patients are the Numero Uno defaulters. Because when they are relieved of their episodic pain, they don't see why they need to continue on treatment.
Gout is a looming epidemic. Not only is it the "Disease of Kings", some are calling it the "King of Diseases" of our time.
For Gout patients whose kidneys are already impaired, the uricosuric agents don't work, and XOI are the only options for now, to reduce uric acid production. For this same group, Allopurinol is risky in that it may cause potentially life-threatening hypersensitivity reactions, especially in Asians carrying the gene HLA-B5801.
Febuxostat may then be the only option. It's reassuring to know it can be used even in the severely renal-impaired. But it is very costly.
Hopefully a new drug will be developed soon to augment intestinal uric acid excretion via the ABCG2 transporter.