Gout treatment remains suboptimal. Identifying populations at risk of developing gout may provide opportunities for prevention. Our aim was to assess the risk of incident gout associated with obesity, hypertension and diuretic use. We conducted a systematic review and meta-analysis of prospective and retrospective cohort studies in adults (age ≥ 18 years) from primary care or the general population, exposed to obesity, hypertension or diuretic use and with incident gout as their outcome. A total of 9923 articles were identified: 14 met the inclusion criteria, 11 of which contained data suitable for pooling in the meta-analysis. Four articles were identified for obesity, 10 for hypertension and six for diuretic use, with four, nine and three articles included respectively for each meta-analysis. Gout was 2.24 times more likely to occur in individuals with body mass index ≥ 30 kg/m² (adjusted relative risk 2.24 (95% confidence interval) 1.76–2.86). Hypertensive individuals were 1.64 (1.34–2.01) and 2.11 (1.64–2.72) times more likely to develop gout as normotensive individuals (adjusted hazard ratio and relative risk respectively). Diuretic use was associated with almost 2.5 times the risk of developing gout compared to no diuretic use (adjusted relative risk 2.39 (1.57–3.65)). Obesity, hypertension and diuretic use are risk factors for incident gout, each more than doubling the risk compared to those without these risk factors. Patients with these risk factors should be recognised by clinicians as being at greater risk of developing gout and provided with appropriate management and treatment options.

Giant cell arteritis (GCA), if untreated, can lead to blindness and stroke. The study’s objectives were to (1) determine a new evidence-based benchmark of the extent of diagnostic delay for GCA and (2) examine the role of GCA-specific characteristics on diagnostic delay. Medical literature databases were searched from inception to November 2015. Articles were included if reporting a time-period of diagnostic delay between onset of GCA symptoms and diagnosis. Two reviewers assessed the quality of the final articles and extracted data from these. Random-effects meta-analysis was used to pool the mean time-period (95% confidence interval (CI)) between GCA symptom onset and diagnosis, and the delay observed for GCA-specific characteristics. Heterogeneity was assessed by I 2 and by 95% prediction interval (PI). Of 4128 articles initially identified, 16 provided data for meta-analysis. Mean diagnostic delay was 9.0 weeks (95% CI, 6.5 to 11.4) between symptom onset and GCA diagnosis (I 2 = 96.0%; P < 0.001; 95% PI, 0 to 19.2 weeks). Patients with a cranial presentation of GCA received a diagnosis after 7.7 (95% CI, 2.7 to 12.8) weeks (I 2 = 98.4%; P < 0.001; 95% PI, 0 to 27.6 weeks) and those with non-cranial GCA after 17.6 (95% CI, 9.7 to 25.5) weeks (I 2 = 96.6%; P < 0.001; 95% PI, 0 to 46.1 weeks). The mean delay from symptom onset to GCA diagnosis was 9 weeks, or longer when cranial symptoms were absent. Our research provides an evidence-based benchmark for diagnostic delay of GCA and supports the need for improved public awareness and fast-track diagnostic pathways.

Identification of axial spondyloarthritis (axSpA) remains challenging, frequently resulting in a diagnostic delay for patients. Current benchmarks of delay are usually reported as mean data, which are typically skewed and therefore may be overestimating delay. Our aim was to determine the extent of median delay patients’ experience in receiving a diagnosis of axSpA and examine whether specific factors are associated with the presence of such delay. We conducted a systematic review across five literature databases (from inception to November 2021), with studies reporting the average time period of diagnostic delay in patients with axSpA being included. Any additional information examining associations between specific factors and delay were also extracted. A narrative synthesis was used to report the median range of diagnostic delay experienced by patients with axSpA and summarise which factors have a role in the delay. From an initial 11,995 articles, 69 reported an average time period of diagnostic delay, with 25 of these providing a median delay from symptom onset to diagnosis. Across these studies, delay ranged from 0.67 to 8 years, with over three-quarters reporting a median of between 2 years and 6 years. A third of all studies reported median delay data ranging from just 2 to 2.3 years. Of seven variables reported with sufficient frequency to evaluate, only ‘gender’ and ‘family history of axSpA’ had sufficient concordant data to draw any conclusion on their role, neither influenced the extent of the delay. Despite improvements in recent decades, patients with axSpA frequently experience years of diagnostic delay and this remains an extensive worldwide problem. This is further compounded by a mixed picture of the disease, patient and healthcare-related factors influencing delay. Key points• Despite improvements in recent decades, patients with axSpA frequently experience years of diagnostic delay.• Median diagnostic delay typically ranges from 2 to 6 years globally.• Neither ‘gender’ nor ‘family history of axSpA’ influenced the extent of diagnostic delay experienced.• Diagnostic delay based on mean, rather than median, data influences the interpretation of the delay time period and consistently reports a longer delay period.

Background: The extent of diagnostic delay in inflammatory bowel disease (IBD) is incompletely understood. We aimed to understand the extent of diagnostic delay of IBD in adults and identify associations between patient or healthcare characteristics and length of delay. Methods: Articles were sourced from EMBASE, Medline and CINAHL from inception to April 2021. Inclusion criteria were adult cohorts (18 ≥ years old) reporting median time periods between onset of symptoms for Crohn’s disease (CD), ulcerative colitis (UC) or IBD (i.e. CD and UC together) and a final diagnosis (diagnostic delay). Narrative synthesis was used to examine the extent of diagnostic delay and characteristics associated with delay. Sensitivity analysis was applied by the removal of outliers. Results: Thirty-one articles reporting median diagnostic delay for IBD, CD or UC were included. After sensitivity analysis, the majority of IBD studies (7 of 8) reported a median delay of between 2 and 5.3 months. From the studies examining median delay in UC, three-quarters (12 of 16) reported a delay between 2 and 6 months. In contrast, three-quarters of the CD studies (17 of 23) reported a delay of between 2 and 12 months. No characteristic had been examined enough to understand their role in diagnostic delay in these populations. Conclusions: This systematic review provides robust insight into the extent of diagnostic delay in IBD and suggests further intervention is needed to reduce delay in CD particularly. Furthermore, our findings provide a benchmark value range for diagnostic delay, which such future work can be measured against.