ObjectivesHospitalisation is a risk factor for flares in people with gout. However, the predictors of inpatient gout flare are not well understood. The aim of this study was to develop a prediction model for inpatient gout flare among people with comorbid gout.MethodsWe used data from a retrospective cohort of hospitalised patients with comorbid gout from Wellington, Aotearoa/New Zealand, in 2017 calendar year. For the development of a prediction model, we took three approaches: (A) a clinical knowledge-driven model, (B) a statistics-driven model and (C) a decision tree model. The final model was chosen based on practicality and performance, then validated using bootstrap procedure.ResultsThe cohort consisted of 625 hospitalised patients with comorbid gout, 87 of whom experienced inpatient gout flare. Model A yielded 9 predictors of inpatient gout flare, while model B and C produced 15 and 5, respectively. Model A was chosen for its simplicity and superior C-statistics (0.82) and calibration slope (0.93). The final nine-item set of predictors were pre-admission urate >0.36 mmol/L, tophus, no pre-admission urate-lowering therapy (ULT), no pre-admission gout prophylaxis, acute kidney injury, surgery, initiation or increase of gout prophylaxis, adjustment of ULT and diuretics prior to flare. Bootstrap validation of the final model showed adequate C-statistics and calibration slope (0.80 and 0.78, respectively).ConclusionWe propose a set of nine predictors of inpatient flare for people with comorbid gout. The predictors are simple, practical and are supported by existing clinical knowledge.

Objective: The objective of this study was to investigate the hypouricemic effects of green tea extract (GTE) in healthy individuals.Methods: This study comprised 1-week control, 2-week interventional, and 1-week follow-up periods. Participants were assigned randomly at the interventional period to consume GTE at 2 (GTE2), 4 (GTE4), or 6 (GTE6) g/d. Levels of serum uric acid (SUA), uric acid clearance, and serum antioxidant power (using trolox equivalent antioxidant capacity assay) were measured at both ends of each study period.Results: Of 30 participants, 11, 11, and 8 received GTE2, GTE4, and GTE6, respectively. After 2 weeks of consumption, the mean SUA level tended to decrease in all groups, with no statistical significance. Serum uric acid reduction was greatest in GTE2 (from 4.81 ± 0.81 mg/dL to 4.64 ± 0.92 mg/dL, 3.53%). Uric acid clearance decreased significantly in GTE2 (from 11.37 ± 6.41 mL/min per 1.73 m 2 to 7.44 ± 2.74 mL/min per 1.73 m 2 , 34.56%, P < 0.05) and GTE4 (from 8.36 ± 3.41 mL/min per 1.73 m 2 to 5.78 ± 2.33 mL/min per 1.73 m 2 , 30.86%, P < 0.05). Serum antioxidant capacity (TEAC) increased significantly in GTE6 (from 32.77 ± 3.39 mg/mL to 35.41 ± 3.17 mg/mL, 8.06%, P < 0.05). There was no significant change in creatinine clearance. Gastrointestinal adverse events were common, but usually mild, with no medical treatment required.Conclusions: Green tea extract may modestly lower SUA level and decreases uric acid clearance. Green tea extract also significantly elevated serum antioxidant capacity with a positive dosage effect. The effect of GTE on SUA in healthy individuals was short term. The effects of GTE on urate handling in patients with hyperuricemia or gout need to be determined. P < 0.001 for all participants. The analysis was compared with the previous value. FIGURE 3. Antioxidant effect of GTE consumption, determined by the TEAC assay. *P < 0.05 for the GTE2 group, ¶ P < 0.05 for the GTE6 group, § P < 0.05 for all participants. The analysis was compared with the previous value.

The hyperuricemic effect of pyrazinamide and ethambutol was due primarily to a decrease in UACl, which was reversible, and had no negative effect on the renal function. Arthralgia was uncommon and required no specific treatment.

Objectives To develop and validate a gout flare risk stratification tool for people with gout hospitalised for non-gout conditions. Methods The prediction rule for inpatient gout flare was derived from a cohort of 625 hospitalised people with comorbid gout from New Zealand. The rule had four items: (1) no pre-admission GOut flare prophylaxis, (2) no pre-admission Urate-lowering therapy, (3) Tophus and (4) pre-admission serum urate &gt;0.36 mmol/l within the previous year (GOUT-36 rule). Two or more items are required for the classification of high risk for developing inpatient gout flare. The GOUT-36 rule was validated in a prospective cohort of 284 hospitalised people with comorbid gout from Thailand and China. Results The GOUT-36 rule had a sensitivity of 75%, specificity of 67% and AUC of 0.71 for classifying people at high risk for developing inpatient gout flare. Four risk groups were developed: low (no items), moderate (one item), high (two items) and very high risk (three or four items). In a population with frequent (overall 34%) in-hospital gout flare, 80% of people with very high risk people developed flare, while 11% of low-risk people had inpatient flare. Conclusion GOUT-36 rule is simple and sensitive for classifying people with high risk for inpatient gout flare. The rule may help inform clinical decision and future research on the prevention of inpatient gout flare.