Skip to main content

Medicine Matters rheumatology

Hello, I am Fernando Perez-Ruiz. I am a rheumatologist from Cruces University Hospital in Northern Spain, in the Basque country. I was kindly invited to make a comment on the abstracts that I was interested in during the E-Congress, EULAR 2020, during the COVID-19 pandemic.

So my selection is based on three main topics. First, I will shortly talk about some abstracts on epidemiology and pathophysiology gout. Afterwards, I'll make my comments on some abstracts on diagnosis, specifically, on gout and pyrophosphate arthritis. imaging, and last, I will talk on some abstracts regarding treatment, especially on biologics and outcomes.

So on epidemiology and pathophysiology, I was interested in two abstracts that were based on Mendelian randomization studies. As you may well know, some papers recently published showed that there was no association between CKD, Chronic Kidney Disease, or cardiovascular events associated to hyperuricemia in Mendelian randomization studies compared to observational studies that were positive.

These two studies, from the group of Boston, have shown that in Mendelian randomization studies, there was no evidence of any relationship or causality associating Alzheimer's disease and urate levels. And in addition, there was no relationship between serum urate levels or gout and diabetes.

So to this point, being practically from the clinical point of view, we have no way to recommend the use of urate-lowering therapy to reduce the impact of chronic kidney disease, cardiovascular outcomes, diabetes, or be scared of lowering serum urate levels and inducing Alzheimer's, as was recommended by the recent EULAR recommendations.

Regarding diagnosis and, specifically, imaging with double-energy computed tomography, two papers showed us that double-energy computed tomography has not been shown to be as sensible as thought, because the first studies were using, were selecting patients with very severe gout with a large amount of deposition.

So these two studies, from the US and from Europe, have shown that it is not so sensible, especially at the beginning of the disease-- so during the first to third year of gout symptoms-- that it was not so sensible. It could be useful to differentiate from CPPD decreased calcium pyrophosphate crystal deposition from U8 deposition. But in any way, that can show a causality between deposition and symptoms. So some patients may show CPPD and no relationship with clinical manifestations. So to this point, the usefulness in clinical practice of double-energy CT seems to be blunted and specifically to be used with their most difficult-to-diagnose patients.

Lastly, I would be interested in commenting on some papers on treatment, specifically for papers, two of them on biologics, one of them on treat-to-target strategy, and the last one on the effect of rheumatology, a system of gout patients.

The first two regard to one of the trials in phase 2 with anakinra in gout. The patients were treated with 100 or 200 milligrams a day anakinra versus triamcinolone acetonide, and there was no difference between the two doses of anakinra and their comparator.

So to this point, for patients in which non-steroidals or colchicine is to be used based on clinical grounds, anakinra may be an off-label medication to be used, especially in patients in whom the use of corticosteroids would not be advisable from the clinical point of view. The second study is with a special review, systematic review, of the use of anakinra and other biologics for the treatment of acute inflammation in calcium pyrophosphate crystal arthritis, showing that it could also be useful, but restricted to those patients in which other medications would not be to be used, or refractory cases.

The third study regards to the treat-to-target strategy that has been recommended by most of the rheumatology associations, but not from the American College of Physicians. This is a paper that was authored by Till Uhlig and co-workers in Norwegian, using the data of a prospective cohort of gout patients, showing that during the first year, 85% of the patients could achieve target serum urate levels when prospectively followed up, just mimicking the results from a randomized clinical trial that was recently published by Nottingham University team.

So to this point, treating to target is to be followed as recommended by most of the rheumatology associations and is an easy thing to do when all measures are provided. And what's the usefulness of this approach? In addition to a reduction in the number of flares and the reduction of tophaceous deposition, in the abstract that was authored by Naomi Schlesinger and co-workers from New Jersey showing that those patients who are effectively treated by rheumatologists will use less emergency room devices. So to this point, the appropriate use of UA-lowering therapy and other measures to treat gout by a rheumatologist is associated to a reduction in the use of health care necessities.

So these are the most interesting papers for me. I have to excuse myself, because I didn't select other very interesting abstracts. But it was a very short comment on some especially noticeable studies for me. And I thank you for your kind attention.