D-0120, a Novel Oral Selective Uric Acid Transporter Inhibitor, at the 2020 EULAR Online Meeting

It seems that we never have enough different drugs to lower hyperuricemia for the individual patient. Lesinurad is an oral selective uric acid transporter (URAT1) inhibitor, which has both FDA (2015) and EMA (2016) approval and is on the market under the brand name of Zurampic, but isn't sold in Germany for instance [1]. Now comes D-0120, a novel oral selective uric acid transporter (URAT1) inhibitor with one study at the 2020 EULAR Online Meeting. Will there be a market for such a drug?

L. Zhang presented the following study [2]: „OP0205 PHASE I STUDY OF D-0120, A NOVEL URAT1 INHIBITOR IN CLINICAL DEVELOPMENT FOR HYPERURICEMIA AND GOUT“. Daily oral D-0120, at dose levels from 2.5 mg/day to 20 mg/day in 32 healthy volunteers for 7 days was well tolerated. The pharmacokinetics profile demonstrated a dose proportional increase. There had been a significant reduction of serum uric acid levels.

Will there be a market for D-0120? D-0120 showed in a cell model a 150-fold more potent inhibitory activity than lesinurad, which might result in less side effects (hope and speculation!). This might be the pivotal point to go on studying D-0120. There will be patients needing an oral selective uric acid transporter (URAT1) inhibitor, but will there be enough patients to support the another drug of the kind that we already have?

Nevertheless I hope that studies go on and that D-0120 will come to market. That will take some years. In the mean time lesinurad should be available on the German market.

Links and References:

[1] https://en.wikipedia.org/wiki/Lesinurad

[2] L. Zhang1, D. Wyatt2, K. Stazzone1, Z. Shi1, Y. Wang1. OP0205 PHASE I STUDY OF D-0120, A NOVEL URAT1 INHIBITOR IN CLINICAL DEVELOPMENT FOR HYPERURICEMIA AND GOUT. DOI: 10.1136/annrheumdis-2020-eular.5107

.

Rapamycin at the 2017 ACR Annual Meeting in San Diego

I had written about Rapamycin recently as I had visited Easter Island [1]. Rapamycin is a macrolide, which is produced by the bacterium Streptomyces hygroscopicus; samples of this bacterium were taken from Easter Island. The name Rapamycin commemorates Easter Island as Rapa Nui (Great Rapa) is the Polynesian name of Easter Island.

I was surprised that I’ve found three abstracts on Rapamycin at the 2017 ACR Annual Meeting in San Diego.

Olivier Benveniste and colleagues [2] presented a study called [Abstract 5L]: “Rapamycin Vs. Placebo for the Treatment of Inclusion Body Myositis: Improvement of the 6 Min Walking Distance, a Functional Scale, the FVC and Muscle Quantitative MRI”. Conclusion: “Even if the primary endpoint was not reached, these first results showed coherent data in favor of rapamycin. …”

A Japanese group of scientists around Yo Ueda looked at Rapamycin and found, that arthritis in SKG mice can be ameliorated [3].

Earl Sands and colleagues yet looked at another interesting field [4]: “Initial Phase 2 Clinical Data of SEL-212 in Symptomatic Gout Patients: Monthly Dosing of a Pegylated Uricase (Pegsiticase) with Svp-Rapamycin Enables Sustained Reduction of Serum Uric Acid Levels By Mitigating Formation of Anti-Drug Antibodies”. Conclusion: “SEL-212 has been well-tolerated, and, unlike pegylated uricases alone, has mitigated immunogenicity, reduced flare rate and enabled repeated monthly dosing with sustained control of sUA levels in gout patients.”

The abstract of Thomas Winans and colleagues looked at [5]: “mTORC1 Blockade with Rapamycin and N-Acetylcysteine Reduces Anti-Phospholipid Antibody Levels in Controlled Clinical Trials of Patients with SLE”. Conclusion: “These ancillary studies suggest that rapamycin and NAC limit aPL production which should be included as an efficacy outcome in clinical trials of mTORC1 blockade in patients with SLE and APS.”

I thought that Rapamycin had its place in transplantation medicine, but now I see that Rapamycin will be useful in Rheumatology, too.

Links and References:

[1] http://rheumatologe.blogspot.de/2017/11/easter-island-and-sirolimus.html

[2] Benveniste O, Hogrel JY, Annoussamy M, Bachasson D, Rigolet A, Servais L, Salem JE, Hervier B, Landon Cardinal O, Mariampillai K, hulot JS, Carlier P, Allenbach Y. Rapamycin Vs. Placebo for the Treatment of Inclusion Body Myositis: Improvement of the 6 Min Walking Distance, a Functional Scale, the FVC and Muscle Quantitative MRI [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). http://acrabstracts.org/abstract/rapamycin-vs-placebo-for-the-treatment-of-inclusion-body-myositis-improvement-of-the-6-min-walking-distance-a-functional-scale-the-fvc-and-muscle-quantitative-mri/. Accessed December 7, 2017.

[3] Ueda Y, Okano T, Yamada H, Ichise Y, Naka I, Takahashi S, Sendo S, Akashi K, Onishi A, Saegusa J, Morinobu A. Inhibition of the Mechanistic Target of Rapamycin Pathway and Glutaminolysis Facilitates the Expansion of Myeloid-Derived Suppressor Cells and Synergistically Ameliorates Arthritis in SKG Mice [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). http://acrabstracts.org/abstract/inhibition-of-the-mechanistic-target-of-rapamycin-pathway-and-glutaminolysis-facilitates-the-expansion-of-myeloid-derived-suppressor-cells-and-synergistically-ameliorates-arthritis-in-skg-mice/. Accessed December 7, 2017.

[4] Sands E, Kivitz AJ, DeHaan Ph.D. W, Johnston L, Kishimoto TK. Initial Phase 2 Clinical Data of SEL-212 in Symptomatic Gout Patients: Monthly Dosing of a Pegylated Uricase (Pegsiticase) with Svp-Rapamycin Enables Sustained Reduction of Serum Uric Acid Levels By Mitigating Formation of Anti-Drug Antibodies [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). http://acrabstracts.org/abstract/initial-phase-2-clinical-data-of-sel-212-in-symptomatic-gout-patients-monthly-dosing-of-a-pegylated-uricase-pegsiticase-with-svp-rapamycin-enables-sustained-reduction-of-serum-uric-acid-levels-by-m/. Accessed December 7, 2017.

[5] Winans T, Kelly R, Lai ZW, Faraone S, Phillips PE, Banki K, Perl A. mTORC1 Blockade with Rapamycin and N-Acetylcysteine Reduces Anti-Phospholipid Antibody Levels in Controlled Clinical Trials of Patients with SLE [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). http://acrabstracts.org/abstract/mtorc1-blockade-with-rapamycin-and-n-acetylcysteine-reduces-anti-phospholipid-antibody-levels-in-controlled-clinical-trials-of-patients-with-sle/. Accessed December 7, 2017.

.

 

A Drink to Eliminate Gout?

I have my doubts, when it comes to a drink to eliminate gout [1]: “THIS 4-INGREDIENT DRINK WILL ELIMINATE YOUR GOUT AND JOINT PAIN FOREVER!”

“Are you aware that cucumber juice helps bring down body temperature”, asks the article. Fever isn’t a problem as long as patients are treated with NSAIDs [Non Steroidal Anti Inflammatory Drugs]. The beverage should also be “effective for removing uric acid crystalization in joints”. First comes treating pain and inflammation, as gout pain is excruciating. Reducing uric acid immediately could mean inducing a new gout attack. However, once the acute gout attack is treated, one can start reducing the level of uric acid.

The juice contains half a medium-sized cucumber, two ribs of celery, a slice of lemon, and a one-inch piece of young ginger root. I like all of it and you’ll get a healthy juice, but that’s it. There isn’t any proof that this reduces pain or removes uric acid. I’ve checked PubMed, really nil!

I don’t think that this advice is a form of self-help, it’s rather self-torture. Drink it, if you want to drink a healthy juice, but see you doctor if you suffer from gout.

Links:

[1] http://www.natural-remedies8-8-8.cf/2017/10/this-4-ingredient-drink-will-eliminate.html

.

Gout (Part 2) at the ACR 2015 Meeting in San Francisco

There has been a multitude of publications on Gout at the ACR 2015 Annual Meeting in San Francisco. I’ve select my personal highlights and updates. The second part in on studies concerning drugs to reduce inflammation or to lower uric acid.

Let’s first look at what’s new on febuxostat.

Nicola Dalbeth and colleagues presented: “Imaging and Safety Assessments Following Treatment with Febuxostat and Placebo for 2 Years in Subjects with Early Gout”. Conclusion: “This first clinical trial in early gout subjects demonstrated that treatment with febuxostat can achieve a significant reduction in synovitis compared to placebo.” They didn’t see any difference in the RAMRIS erosion and bone edema scores, which might be due to the fact of having restricted the study to patients with early gout.

Pierre-Antoine Juge and colleagues looked at: “Efficacy and Safety of Febuxostat in 55 Gouty Patients with Stage 4/5 Chronic Kidney Disease: Results from a Retrospective Multicenter Study”. Conclusion: “Febuxostat appears efficient in gouty patients with stage 4/5 CKD or renal transplants. However, safety data is not yet validated with respect to renal function. Further studies with larger samples are warranted for assessing this issue.” That leaves us much at the point, where we’ve been before.

The next study is on arhalofenate, a novel urate lowering anti flare therapy in gout. “It lowers serum uric acid (sUA) by blocking URAT1, a tubular UA transporter, and reduces gout flares by blocking the local release of IL-1β.”

Alexandra Steinberg and colleagues presented: “A Study to Evaluate the Efficacy and Safety of Arhalofenate for Preventing Flares and Reducing Serum Uric Acid in Gout Patients”. “Subjects [N=239] were randomized 1:2:2:2:2 to placebo, arhalofenate 600 mg or 800 mg, allopurinol 300 mg or allopurinol 300 mg combined with colchicine 0.6 mg.“ Conclusion: “Arhalofenate at 800 mg significantly decreases gout flares when compared to allopurinol 300 mg. There was no statistical difference in flares between arhalofenate 800 mg and allopurinol 300 mg combined with colchicine. Arhalofenate 800 mg also significantly decreased flares when compared to placebo. These results indicate that Arhalofenate has intrinsic anti-inflammatory activities clinically associated with improvement in gout flares. Arhalofenate sUA lowering activity, while significant compared to placebo, was lower than in the allopurinol 300 mg groups. Arhalofenate was well tolerated and appeared safe. Arhalofenate is currently in development for the treatment of gout as a combination therapy with ULT, both to lower serum uric acid and prevent flares.” The idea might be to suggest a single therapy for flares and lowering uric acid, and achieving this with a single drug. It looks more like a marketing stunt, no matter how much effect there is on IL-1β. Maybe arhalofenate is aiming at too much at the same time. Just a thought. It’s much too early to evaluate this. Arhalofenate might be useful in the time after the first / a flare.

There were two studies on adding lesinurad either to febuxostat or the allopurinol. I guess, you’re not too surprised that these combinations work.

Let’s close this 2nd part with a study on canakinumab.

Naomi Schlesinger and colleagues presented: “A 3-Year Follow-up Study of Canakinumab in Frequently Flaring Gouty Arthritis Patients, Contraindicated, Intolerant, or Unresponsive to Nonsteroidal Anti-Inflammatory Drugs and/or Colchicine”. The authors looked at patients, who were radomized in the two phase 3 studies (N=456), of these 272 patients were followed up in extension studies, where re-treatment was initiated after a flare. Conclusion: “Over 3 years, a mean “on demand” dosing of CAN was 2.68 per pt. Efficacy of CAN was demonstrated […]”.

I think both flares and urate lowering therapies were addressed in the studies. Gout still is a challenge. I hope that studies will also look at the problem of adherence to drugs.

References:

Dalbeth N, Saag KG, Palmer W, Choi H, Hunt B, MacDonald P, Thienel U, Gunawardhana L. Imaging and Safety Assessments Following Treatment with Febuxostat and Placebo for 2 Years in Subjects with Early Gout [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/imaging-and-safety-assessments-following-treatment-with-febuxostat-and-placebo-for-2-years-in-subjects-with-early-gout/. Accessed November 16, 2015.

Steinberg A, Chera H, Choi YJ, Martin R, McWherter C, Zhang Y, Boudes P. A Study to Evaluate the Efficacy and Safety of Arhalofenate for Preventing Flares and Reducing Serum Uric Acid in Gout Patients [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/a-study-to-evaluate-the-efficacy-and-safety-of-arhalofenate-for-preventing-flares-and-reducing-serum-uric-acid-in-gout-patients/. Accessed November 16, 2015.

Juge PA, Truchetet ME, Ottaviani S, Vigneau C, Loustau C, Cornec D, Pascart T, Cornec-Legall E, Florien M, Bailly F, Schaeverbeke T, Saraux A, Dieude P, Flipo RM, Jean-Baptiste G, Richette P, Lioté F, Bardin T, Chales GH, Ea HK. Efficacy and Safety of Febuxostat in 55 Gouty Patients with Stage 4/5 Chronic Kidney Disease: Results from a Retrospective Multicenter Study [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/efficacy-and-safety-of-febuxostat-in-55-gouty-patients-with-stage-45-chronic-kidney-disease-results-from-a-retrospective-multicenter-study/. Accessed November 16, 2015.

Saag KG, Bardin T, So A, Khanna P, Storgard C, Baumgartner S, Fung M, Bhakta N, Adler S, Kopicko J, Becker MA. Analysis of Gout Subjects Receiving Lesinurad and Allopurinol Combination Therapy By Baseline Renal Function [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/analysis-of-gout-subjects-receiving-lesinurad-and-allopurinol-combination-therapy-by-baseline-renal-function/. Accessed November 16, 2015.

Dalbeth N, Jones G, Terkeltaub R, Khanna D, Kopicko J, Adler S, Bhakta N, Fung M, Storgard C, Baumgartner S, Perez-Ruiz F. Efficacy and Safety in Patients with Tophaceous Gout Receiving Lesinurad and Febuxostat Combination Therapy: Interim Analysis of an Extension Study [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/efficacy-and-safety-in-patients-with-tophaceous-gout-receiving-lesinurad-and-febuxostat-combination-therapy-interim-analysis-of-an-extension-study/. Accessed November 16, 2015.

Schlesinger N, Bardin T, Bloch M, Lheritier K, Machein U, Junge G, So A, Alten R. A 3-Year Follow-up Study of Canakinumab in Frequently Flaring Gouty Arthritis Patients, Contraindicated, Intolerant, or Unresponsive to Nonsteroidal Anti-Inflammatory Drugs and/or Colchicine [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/a-3-year-follow-up-study-of-canakinumab-in-frequently-flaring-gouty-arthritis-patients-contraindicated-intolerant-or-unresponsive-to-nonsteroidal-anti-inflammatory-drugs-andor-colchicine/. Accessed November 16, 2015.

 .

Gout (Part 1) at the ACR 2015 Meeting in San Francisco

There has been a multitude of publications on Gout at the ACR 2015 Annual Meeting in San Francisco. I’ve select my personal highlights and updates. The first part leaves out studies on drugs.

Chang-Fu Kuo an colleagues presented: “Impact of Gout on the Risk of Atrial Fibrillation”. They’ve looked at “45,378 incident gout patients and 45,378 age-, sex-, practice-, registration year- and index year-matched controls”. Results: “The prevalence of AF at index date in gout patients (male, 72.3%; mean age, 62.4 ± 15.1 years) was 7.42% (95% confidence interval [CI], 7.18%–7.66%) and in matched controls 2.83% (95% CI, 2.67%–2.98%). […]” Conclusion: “This population-based study indicates that gout is independently associated with a higher risk of AF at diagnosis and the risk is also higher after the diagnosis.” Hart data, that detecting and treating hyperuricaemic patients is warranted!

Paras Karmacharya and colleagues looked at: “Seasonal Variation in Acute Gouty Arthritis: Data from Nationwide Inpatient Sample”. Conclusion: “Unlike previous studies, our analysis found the peak incidence of acute gout in the fall with its peak in the month of November. […]. They should have left it at this, but they speculate in their conclusion: “Various environmental (temperature, humidity, diet, physical activity) and biochemical factors (low cortisol levels, high absolute neutrophil counts and plasminogen activator inhibitor-1) have been implicated for the seasonal variation. There have been conflicting data on the correlation of the incidence of acute gouty arthritis with environmental factors such as temperature or humidity.” I take out of this abstract, that there is an interesting seasonal variation, which could be useful for campaigns on lowering uric acid levels and/or gout.

Jeewoong Choi and colleagues presented: “Dietary Patterns (DASH, Prudent, Western Diets) and the Risk of Gout in US Women – the Nurses Health Study”. DASH stands for: Dietary Approaches to Stop Hypertension. The diet lowers blood pressure, reduces cholesterol, and improves insulin sensitivity. And these is based on research. Conclusion: “The Western dietary pattern is associated with an increased risk of gout, which explains the rising burden of gout in Western countries. In contrast, the DASH diet and prudent dietary pattern are associated with a lower risk of gout.  The DASH diet appears to offer an attractive additional nutritional approach for gout, as it also reduces blood pressure in hypertension (present in 74% of gout patients) and is also recommended to prevent CVD (a common comorbidity of gout).” I call this good news for people, who do not like to take medications.

MaryAnn Zhang and colleagues discussed: “Do Omega-3 Fatty Acids Reduce Risk of Recurrent Gout Attacks?” Conclusion: “Dietary ω-3 FA-rich fish consumption had a protective effect for recurrent gout attacks in the community, whereas ω-3 FA supplementation alone, as taken in a self-directed manner, did not.” Why do I like this study? Because I’m opposed to nutraceuticals. ω-3 FA supplements had a p-value of 0.98. ω-3 FA-rich Fish had a p-value of 0.02 in favour of the fish diet.

It’s interesting how many new aspects on gout surface each year at the big meeting! The second part will be on drugs in gout therapy.

References:

Kuo CF, Grainge MJ, Zhang W, Doherty M. Impact of Gout on the Risk of Atrial Fibrillation [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/impact-of-gout-on-the-risk-of-atrial-fibrillation/. Accessed November 16, 2015.

Karmacharya P, Pathak R, Aryal M, Giri S, Donato A. Seasonal Variation in Acute Gouty Arthritis: Data from Nationwide Inpatient Sample [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/seasonal-variation-in-acute-gouty-arthritis-data-from-nationwide-inpatient-sample/. Accessed November 16, 2015.

Choi J, Lu N, Zhang Y, Rai SK, Curhan GC, Choi HK. Dietary Patterns (DASH, Prudent, Western Diets) and the Risk of Gout in US Women – the Nurses Health Study [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/dietary-patterns-dash-prudent-western-diets-and-the-risk-of-gout-in-us-women-the-nurses-health-study/. Accessed November 16, 2015.

The DASH Diet: http://dashdiet.org/what_is_the_dash_diet.asp

Zhang M, Zhang Y, Terkeltaub R, Chen C, Neogi T. Do Omega-3 Fatty Acids Reduce Risk of Recurrent Gout Attacks? [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). http://acrabstracts.org/abstract/do-omega-3-fatty-acids-reduce-risk-of-recurrent-gout-attacks/. Accessed November 16, 2015.

.

Gout - some extreme pictures

Recently we treated a patient with gout. Let me first thank this gentleman for agreeing to publish his x-ray charts and pictures of his hands.
He had been pretreated in an outside hospital. So, the uric acid already had been lowered from about 13.8 to 8.0 mg/dl. ESG and CRP were only slightly elevated.

The x-ray charts show multiple joint involvement and tophi destroying bones 

In the pictures one can see the uric acid deposits under the skin and swelling of joints

It will take quite some time to mobilize the uric acid deposits as pegloticase isn't appoved in Germany.

07.09.2015
Here is another X-ray chart about the destruction, gout tophi may cause. At some places the bone has gone completely.

A New Venture into the World of Gout

Any rheumatologist having crossed Gout Creek must feel motivated to write about gout. Has anyone else?

Well I've crossed Gout Creek (New Zealand, South Island) and there have been some interesting new studies, so I feel very motivated to put a few ideas together.

We all know that alcohol isn't doing good to gout patients, but beer and liquor are tought to be more harmful than for instance a glass of wine. A new study questions this dogma.

T. Neogi and colleagues published the following study: "Alcohol quantity and type on risk of recurrent gout attacks: An internet-based case-crossover study" (Link: http://www.amjmed.com/article/S0002-9343(14)00032-1/abstract). Results: The study included 724 participants with gout (mostly men). The risk of recurrent gout attack was 1.36 for > 1-2 and 1.51 for > 2-4 alcoholic beverages higher compared with no alcohol consumption in the 24 hours prior to the gout attack. Consuming wine, beer, or liquor, all had lead to an increased risk of gout attack. The author's concluded: "Episodic alcohol consumption, regardless of type of alcoholic beverage, was associated with an increased risk of recurrent gout attacks, including potentially with moderate amounts. Persons with gout should limit alcohol intake of all types to reduce the risk of recurrent gout attacks."

I don't think that the "dogma" has been fully refuted, but it seems to be a good idea to point out to gout patients that it's better to avoid alcohol in any form. "Really, no alcohol at all?" As most people have a all or nothing attitude, allowing a teeny weeny bit of wine might ease the way to keep gout patients out of harm.

There have been some interesting papers at the EULAR 2013 Meeting in Madrid, link: http://rheumatologe.blogspot.de/2013/07/gout-at-eular-2013-meeting-in-madrid.html.

I hadn't yet written on interesting studies on gout, which had been presented at the ACR 2013 Meeting in San Diego. I'll dicuss a couple of these studies here.

J.M.A. Wijnands and colleagues presented an abstract [No. 90]: "Insufficient Evidence For An Increase In Prevalence and Incidence Of Gout: A Systematic Review and Meta-Regression Analysis." Methods: "Pubmed, Embase and Web of Science were systematically searched for primary studies on the prevalence and incidence of gout in the general population." Conclusion: "There was insufficient evidence for an increase in prevalence or incidence of gout in recent years." That's reassuring to hear, but I see more patients with more severe gout in recent years, maybe the rate of referral has changed.

Seong-Kyu Kim and collegues looked at [No. 93]: "Higher Consumption Of Sugar-Sweetened Soft Drinks Increases The Risk Of Hyperuricemia In Korean Population: The Korean Multi-Rural Communities Cohort Study." The study was superbly powered with N=9400. Conclusion: "Higher consumption of sugar-sweetened soft drinks increased the risk of hyperuricemia in the Korean population, showing a differential linear trend for hyperuricemia according to gender."

M. De Vera and colleagues presented [No. 210]: "Medication Adherence In Patients With Gout: A Systematic Review." Conclusion: "This is the first systematic review of medication adherence, with particular focus on gout patients. Adherence rates may vary according to methods used to measure adherence. Overall, synthesis of current evidence suggest that medication non-adherence is substantial in gout. Findings highlight the importance of discussing adherence with gout medications during health care professional encounters with gout patients." Among the studies included in this review, allow me to quote: Zandman 2013. N=7,644, follow up after 6 years, proportion of days covered: more than 80% - 17% of patients were still adherent!

K. Logee and colleagues presented [No. 214]: "Use Of Dual-Energy Computed Tomography In Evaluation Of Axial Gout." Nice pictures! Conclusion: "Dual-energy CT can be used to visualize the presence of axial MSU deposition. This may lead to appropriate diagnosis and management of axial gout while avoiding invasive procedures and erroneous treatment." I think, we're still far away from the second half of the authors' conclusion.

P. Sunkureddi and colleagues presented the following study [No. 1177]: "Efficacy and Safety Of Canakinumab Pre-Filled Syringe Versus Triamcinolone Acetonide In Acute Gouty Arthritis Patients." Conclusion: "CAN-PFS (Canakinumab pre-filled syringe) was superior to TA (triamcinolone acetonide) in relieving pain and reducing risk of new attacks, and had a safety profile similar to CAN-LYO (Canakinumab lyophilized powder). The safety profile was also consistent with that observed in previous CAN-LYO studies. Efficacy and safety of the two CAN (Canakinumab) formulations were comparable." I know that this study won't have much impact on daily life, but I think it's an important study for the one patient we all might see in the next years, where everything else had failed.

K.G. Saag and colleagues looked at [No. 1178]: Effect Of Febuxostat On Serum Urate Levels In Gout Subjects With Hyperuricemia and Moderate-To-Severe Renal Impairment: A Randomized Controlled Trial." Conclusion: "In subjects with moderate-to-severe renal impairment, FEB (febuxostat) urate-lowering was efficacious, with no emergent serious safety issues at 12 m (months). The sUA (serum uric acid) was significantly reduced in subjects receiving either regimen of FEB compared to PLB (placebo)." I guess, febuxostat is now fully established, though the high price might still be a problem.

S. Baumgartner and colleagues looked at [No. 1189]: "Allopurinol Dose Titration and Efficacy: A Large-Scale, 6-Month, Multicenter, Prospective Study." Conclusion: " In this large, multinational, prospective observational study of gout, optimal allopurinol dose escalation occurred infrequently. Fewer than 50% of patients overall achieved target sUA level greater than 6.0 mg/dL and the majority of those with a baseline dose of or higher than 300 mg/day did not increase their dose. These data, consistent with published literature, likely reflect real-world circumstances in which a significant proportion of patients fail to reach sUA targets with allopurinol therapy as currently used." PDCA! We have good plans (plan), we put them into practice (do), we have to check more consequently (check), and act - increase the dosage. Hopefully, patients won't leave this quality improving cycle.

F. Perez-Ruiz and colleagues presented [No. 1191]: Low-Dose Anakinra Is Effective For The Prophylaxis Of Acute Episodes Of Inflammation In Severe Tophaceous Gout." Conclusion: "This pilot study is, to our knowledge, the first to prospectively explore in pre-established doses the efficacy of low-dose anakinra for the prophylaxis of AEIs in patients with severe comorbidities and difficult to treat tophaceous gout."

R.T. Keenan and colleagues presented [No. 1193]: "Target Tophus Size and Complete Response Rates In Patients Treated With Open-Label Pegloticase For Chronic Gout Refractory To Conventional Therapy." Conclusion: "Many small and medium subcutaneous tophi resolved within the first 6 months of pegloticase therapy. These data show that substantial incremental benefit in tophus response for unresolved small to medium tophi can be gained with 9–12 months of therapy in UA responders." I have seen patients, who would benefit from pegloticase, but there are problems with getting an appoval by insurance companies as it's an off-label use.

There were lots of interesting studies on gout at both the EULAR 2013 Meeting in Madrid and the ACR 2013 Meeting in San Diego. Let's hope that we can counsel patients even better now.

Picture of tophous gout