[Recent advances in gout: pathogenesis, diagnosis, comorbidities, treatment]. / Újdonságok köszvényben: patogenezis, társbetegségek, diagnosztika és terápia.

After a "silence" period for decades, a great body of new information has become available about the pathogenesis, diagnosis and treatment of gout. New data on purine metabolism and urate transporters have been published. It has become evident that gout is an autoinflammatory disease involving the inflammasome and interleukin-1. With respect to diagnosis, microscopic evaluation of the urate crystal is still the gold standard, however, sensitive imaging techniques (ultrasound, modern computed tomography methods) are able to visualize crystal deposition and tophus formation. Tophus size may also be monitored over time. We see a renaissance of non-pharmacological, lifestyle-related treatment modalities. Pharmacotherapy includes the resolution of attacks and urate-lowering maintenance therapy. In 2016, two recent series of recommendations have been published. Treat-to-target therapy aiming at urate levels ≤360 µmol/l is crucial. Urate-lowering therapy includes xanthine oxidase inhibitors (allopurinol, febuxostat). However, a number of novel compounds (urate transporter inhibitors, recombinant uricase, interleukin-1 inhibitors) are under development or before introduction to gout treatment. Comorbidites should be considered throughout the follow-up of gout patients. Orv Hetil. 2018; 159(40): 1625-1636.

Six-Month Follow-Up of Periodontal Condition in Rheumatoid Arthritis and Ankylosing Spondylitis Arthritis Patients Undergoing Anti-Tumour Necrosis Factor-α Therapy.

In our present study, we aimed to assess the effects of anti-TNF therapy on periodontal condition in a mixed cohort of patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Moreover, we wished to determine whether the baseline dental condition of these patients would affect response to biological therapy. A cohort of 24 arthritis patients was consecutively recruited before starting anti-TNFα therapy. After the dropout of six patients, we evaluated the dental status of 18 subjects at baseline and after 6 months of biological therapy. Clinical responder (R) and non-responder (NR) status was determined after 6 months of anti-TNF treatment. Plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD), PPDmax, clinical attachment loss (CAL), and CALmax were determined. During the 6-month treatment period, six patients (3 RA and 3 AS) terminated the study prematurely as they did not respond to treatment (NR). Therefore, 18 patients were included in the full analysis. There were no major differences in PI, BOP, PPD, PPD max, CAL, and CALmax, among R and NR patients. TNF inhibition resulted in increased GI (0.65 ± 0.34 vs. 0.88 ± 0.30; p < 0.05), as well as decreased PPDmax (4 ± 1.94 vs. 2.72 ± 1.36; p < 0.05) and CALmax (5.22 ± 2.56 vs. 2.72 ± 1.36; p < 0.05) after 6 months. Eight patients had incomplete canal fillings or dead pulps and/or apical periodontitis; six in the R and two in the NR group. In our present study, anti-TNF therapy seemed to worsen the extent of gingival inflammation (GI); however our results also do not support the reduction of mean CPD and CAL as reported by others.

Salivary citrullinated proteins in rheumatoid arthritis and associated periodontal disease.

Periodontal disease (PD) can be an important precipitating factor in the production of citrullinated proteins. Its importance is emphasized, but it is not the only way to produce citrullinated proteins. The aim of the current study was to determine the periodontal conditions and the salivary citrullinated protein content in patients with rheumatoid arthritis (RA) compared to healthy controls. We also wished to correlate citrullinated protein levels in the saliva and serum biomarkers with the periodontal status and temporomandibular joint (TMJ) involvement of patients with RA. Twenty-three patients with RA and 17 healthy controls participated the study. Saliva samples were taken: citrulline content of saliva was measured. Blood test results for patients with RA were collected. TMJ disorders were described. Cariological and periodontal indices were registered. Periodontal conditions and periodontal staging were also registered. Comparison of measured values between groups was performed. Intragroup correlation of patients' values was counted. The prevalence of TMJ complaints was significantly higher in the RA group (8/23) versus controls (1/17). The patients with RA had worse periodontal condition because more patients with RA had gingivitis with a significantly higher bleeding on probing (BOP) (RA: 22.4 ± 25.0%; controls: 6.36 ± 11.6%; p = 0.018). Gingival index (GI) was also significantly higher in the patients than in controls (RA: 0.68 ± 0.58; controls: 0.19 ± 0.38; p = 0.010). The citrullinated protein (relative) content of saliva did not differ significantly (p = 0.147) between patients with RA (1102.2 ± 530.8) and healthy controls (1873.1 ± 1594.9). In RA, the salivary anti-CCP levels positively correlated with PD staging (R = 0.464, p = 0.039) . Control subjects more commonly had healthy gingiva than RA patients. Moreover, in the control group more individuals had intact and reduced height periodontium than periodontitis compared to the RA group. There was no significant difference in the levels of salivary citrulline between patients with RA and controls, despite the significant differences in their periodontal status. Thus, salivary citrulline levels are not associated with RA disease severity.