Objective Chronic inflammatory back pain (IBP) is frequently reported in axial SpA (axSpA) but also in the general population. We evaluated a recently proposed two-step referral system for early recognition of axSpA in primary care and compare it with other combinations of symptoms and SpA-related items. Methods Consecutive chronic back pain patients ≤45 years of age answered a questionnaire and were seen by a primary care physician who decided whether HLA-B27 needed to be determined. They were then referred to a rheumatologist who made the diagnosis. Generally sticking to the two-step system with HLA-B27 as an additional option, combinations with a sensitivity ≥90% and a likelihood ratio >4 were compared. Results A total of 326 patients were included, 46 of whom were diagnosed with axSpA (14.1%). The sensitivity of the strategy was 87%, the specificity was 56.8% and the positive and negative predictive values were 24.8% and 96.4%, respectively. A ‘good response to NSAIDs’, ‘morning stiffness >30 min’ and ‘elevated C-reactive protein’ performed best, with a sensitivity of 91%, specificity of 67%, positive predictive value of 31% and negative predictive value of 98%. On that basis, only three patients had to be seen by a rheumatologist to diagnose one. Conclusion The earlier proposed referral system worked well but was outperformed by other combinations with high sensitivity and better specificity, which deserve to be prospectively studied.

A B S T R A C TA subgroup of patients with gouty arthritis have a chronic recurring form that is particularly diffi cult to treat. Such patients experience repeated fl ares and often have abundant tophi. Many also have underlying comorbidities, such as renal impairment, cardiovascular disease, gastrointestinal disorders, obesity, and hypertension, which contraindicate the use of standard anti-infl ammatory medications. Five patients with diffi cult to treat gouty arthritis who were either candidates and/or treated with anti-IL therapy are described.

Skeletal muscle tissue (SKM) may be damaged due to mechanical, metabolic, and exertional causes. However, drug-induced myopathy is among the most frequent causes of muscle disease. The clinical picture of drug-induced myopathies may be highly variable. It may present as asymptomatic or mild myalgias, with or without muscle weakness, which are likely underreported. However, it may also appear as chronic myopathy with severe weakness and, rarely, even as massive rhabdomyolysis with acute kidney injury (AKI). Unfortunately, the available biomarkers for SKM injury do not fully meet the needs for satisfactory detection of drug-induced damage, both in clinical and research settings, mainly due to their low sensitivity and specificity. Therefore, the present study proposes a strategy for drug safety monitoring using the available biomarkers of SKM injury. Moreover, we will discuss mechanisms of drug-induced SKM injury, traditional laboratory testing for SKM injury, and novel skeletal myocyte biomarkers under investigation. This can be incredibly useful in both clinical practice and for de-challenge/re-challenge investigational trials where the risk of drug-induced SKM injury is present.