Tophus size is associated with hallux valgus deformity in gout.

OBJECTIVE: Hallux valgus (HV) and gout are common pathologies of the first metatarsophalangeal joint (MTP1) leading to pain and deformation. In this study, we aimed to determine the correlation between tophus size and characteristics of HV in gouty patients. METHODS: In this case-control study, we included patients with gout (the presence of monosodium urate crystals in synovial fluid) and control patients with spondyloarthritis, without crystal disease disorders. Radiographic assessment and ultrasound (US) assessment were performed by two blinded operators. US features of gout (double contour [DC] sign and/or tophus) were collected. HV was defined by hallux abductus (HA) angle ≥20° and/or intermetatarsal angle (IM) ≥10°. Correlation between US findings and HV angles was estimated by Spearman correlation coefficient. RESULTS: We included 56 gouty patients (87.5% males, mean age of 63.9 ± 12.2 years) and 41 control patients (90% males, mean age of 59.0 ± 12.8 years). HV was more frequent in patients with gout than controls (62% vs 37%, P = .0007). Regardless of HV status, correlations were found between the size of US tophi and IM (r = .3381, P = .003) and HA angles (r = .2344, P = .043). CONCLUSIONS: Our results confirm a high prevalence of HV in gouty patients. We also observed a correlation between the size of the US tophus and the angles defining HV, which suggests a link between urate deposition load and HV. Early urate-lowering therapy for gout could limit the occurrence of HV.

Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias.

Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be a major source of channel dysfunction during cardiac arrhythmias. This has been well established with the discovery of mutations in the genes encoding several ion channels and ion channel partners during inherited cardiac arrhythmias. Fibrosis, altered myocyte contacts, and post-transcriptional protein changes are common factors that disorganize normal channel trafficking during acquired cardiac arrhythmias. Channel availability, described notably for hERG and KV1.5 channels, could be another potent arrhythmogenic mechanism. From this molecular knowledge on cardiac arrhythmias will emerge novel antiarrhythmic strategies.