Research agenda
| No | Research question | Comment with respect to a T2T approach |
|---|---|---|
| 1 | What is the optimal target serum urate level to manage gout? | SUA level of <6 mg/dL (<360 µmol/L) or <5 mg/dL (<300 µmol/L) are not data driven, a valid and reliable cut-off will facilitate a targeted approach. |
| 2 | Is the current recommended target serum urate level a valid endpoint? | This important question should be addressed by taking the scientific evidence and the patient point of view into account. A laboratory parameter might not adequately reflect the signs and symptoms of the patient. |
| 3 | How often should the serum urate level be measured to optimally control disease? | Definition of time intervals to measure SUA is mandatory to adapt therapy based on the treatment target. |
| 4 | How does frequency of serum urate measurement impact on the management of patients with gout? | Frequency of measurements should be feasible and aim to avoid overassessment and underestimation. No trial exists at all to address impact of measurement on the management of patients with gout. |
| 5 | Are very low serum urate levels dangerous (such as by causing neuropsychiatric disease, eg, dementia)? | The knowledge about valid upper and lower thresholds of SUA is mandatory to follow a T2T approach. |
| 6 | What are the consequences of lowering serum urate levels? | A T2T approach in patients with gout must address potential harmful consequences (like occurrence of acute attacks while initiating ULT). |
| 7 | Is it possible to develop a composite disease activity measure that might serve as a better target for management of gout disease activity in clinical practice? (GDAI=gout disease activity index). | More than the SUA level influences disease activity in patients with gout. Therefore, it seems likely that a composite instrument is addressing the patients need more accurate. |
| 8 | Does an elevated serum urate level cause chronic kidney disease? | The relationship between gout and chronic kidney disease is bidirectional and whether it is a causal relation or an association is still a matter of debate. It still has to be shown that lowering of SUA prevents renal function from further deterioration (and vice versa). |
| 9 | How often should renal function be measured? | Frequency of measurements should be feasible and aim to avoid overassessment and underestimation. |
| 10 | What is the optimal management of gout in patients with multiple comorbidities? | Determination of treatment target and strategy to adapt the therapy depends on occurrence of many factors, that is comorbidities. Multidisciplinary management should agree upon an achievable treatment target. |
| 11 | Is there any diagnostic utility to aspirating joints in patients with intercritical gout? | The absence of crystals in the synovial fluid is one of the targets that are linked to lowering SUA. Serial joint aspiration studies confirmed the disappearance of crystals with effective ULT. The value of this laboratory finding in patients with absent of gout attacks is questionable. |
| 12 | Should monitoring by ultrasound or CT be used in gout? | Diagnostic utility of imaging procedure has been studied to diagnose but has not been extensively studied to monitor the disease. Since deposition of MSU crystals in the tissue is a consequence of increased levels of SUA imaging procedure might serve as a surrogate marker in the management of gout. |
| 13 | How is the treatment of both acute and chronic manifestations of gout best integrated into a T2T strategy? | Whether the artificial partition between acute and chronic stages is helpful in treating patients with gout is still a matter of debate. However, research on implementations strategies focused on setting a target and adapting the treatment accordingly is strongly needed. |
| 14 | What is the optimal timing of initiating treatment for acute gout attacks? | The start of the treatment and prescheduled adaptation process within the treatment strategy is a crucial point that is not yet well defined in studies. Especially, initiating ULT during an acute gout attack remains a matter of debate. |
| 15 | What is the optimal strategy to eliminate tophi? | The outcome ‘size and number of tophi’ is difficult to assess. There is no consensus about the optimal tool to assess this outcome reliable and sensitive to change. However, assessment of tophi is crucial to assess adaptation process within the treatment strategy. |
| 16 | Should urate lowering therapy be initiated after the first gout attack? | Whether ULT therapy should be initiated after the first gout attack or after a subsequent attack remains controversial. Studies should be conducted to address this question, so as to optimise treatment |
| 17 | Is there any effect of treating asymptomatic hyperuricaemia? | Studies are warranted to assess whether T2T approach is also applicable for patients with asymptomatic hyperuricaemia. |
| 18 | What is the role of surgery in the treatment of tophi? | Pharmacological interventions are the cornerstone in the T2T approach, but the value of surgical procedures has not been investigated. |
| 19 | Does a T2T approach improve the adherence of patients to their treatment? | Adherence to treatment is low in patients with gout. In a T2T approach, patients do have increased visits at least in the beginning of their disease. One important question is whether this approach is increasing the adherence of patients to their treatment |
MSU, monosodium urate; SUA, serum uric acid levels; T2T, target-to-target; ULT, using urate-lowering therapy.