BackgroundsPatients who develop an active tuberculosis infection during tumor necrosis factor (TNF) inhibitor treatment typically discontinue TNF inhibitor and receive standard anti-tuberculosis treatment. However, there is currently insufficient information on patient outcomes following resumption of TNF inhibitor treatment during ongoing anti- tuberculosis treatment. Our study was designed to investigate the safety of resuming TNF inhibitors in ankylosing spondylitis (AS) patients who developed tuberculosis as a complication of the use of TNF inhibitors.MethodsThrough the nationwide registry of the Korean Society of Spondyloarthritis Research, 3929 AS patients who were prescribed TNF inhibitors were recruited between June 2003 and June 2014 at fourteen referral hospitals. Clinical information was analyzed about the patients who experienced tuberculosis after exposure to TNF inhibitors. The clinical features of resumers and non-resumers of TNF inhibitors were compared and the outcomes of tuberculosis were surveyed individually.FindingsFifty-six AS patients were treated for tuberculosis associated with TNF inhibitors. Among them, 23 patients resumed TNF inhibitors, and these patients were found to be exposed to TNF inhibitors for a longer period of time and experienced more frequent disease flare-up after discontinuation of TNF inhibitors compared with those who did not resume. Fifteen patients resumed TNF inhibitors during anti-tuberculosis treatment (early resumers) and 8 after completion of anti-tuberculosis treatment (late resumers). Median time to resuming TNF inhibitor from tuberculosis was 3.3 and 9.0 months in the early and late resumers, respectively. Tuberculosis was treated successfully in all resumers and did not relapse in any of them during follow-up (median 33.8 [IQR; 20.8–66.7] months).ConclusionsInstances of tuberculosis were treated successfully in our AS patients, even when given concomitantly with TNF inhibitors. We suggest that early resumption of TNF inhibitors in AS patients could be safe under effective coverage of tuberculosis.

Background Mean platelet volume (MPV) has been known to be a marker of platelet activity and influenced by inflammation.The correlations of MPV with disease activities were reported in several rheumatic diseases such as rheumatoid arthritis, ankylosing spondylitis, and psoriasis. However MPV is controversial as a marker of their disease activities. Furthermore, the association of MPV with disease activity in Behcet's disease (BD) is not determined yet. Objectives The aim of this study is to investigate the association of MPV with clinical manifestations and disease activity in BD. Methods We sequentially retrieved data on 193 patients with BD who visited to our rheumatic clinic from 1999 to 2013 by reviewing of medical records. BD was diagnosed according to International Criteria for BD. The data on demographics, clinical manifestations, and laboratory results including MPV, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were collected. Active BD was defined as it needed prednisolone of more than 0.5 mg/kg/day or to add immunosuppressive agents. Infection was demonstrated by culture or clinical improvement with antibiotic treatment. Statistical analysis was made by t-test and Pearson's correlation. A value of p<0.05 was considered as statistically significant. Results The ratio of female to male was 2:1 and the age of symptom onset was 32.2±11.1 years. The age at diagnosis of BD was 40.9±10.0 years and the follow-up duration was 4.7±3.8 years. Fifty-one patients (26.4%) had major organ involvements such as eye (17.6%), gastrointestinal (7.8%), vascular (4.7%) and nervous system (3.1%). MPV at diagnosis was 8.2±1.2 fl. MPV was not related with clinical manifestations, ESR and CRP. During follow-up, 79 patients had active BD and 12 patients had infections such as pulmonary tuberculosis and pyelonephritis. MPV in active BD (8.1±1.4 fl) was lower than that in inactive disease (8.9±1.3 fl; (p<0.0001). MPV significantly increased when the patients were infected (9.5±1.6 fl; p<0.0001) Conclusions MPV was not related with clinical manifestations of BD. However, there was an association of active BD with lower MPV and of infection with higher MPV. Thus, MPV level may be used as a marker of BD activity and to differentiate infection from active BD. References Are platelet volume indices of clinical use? A multidisciplinary review. Ann Med. 2012 Dec;44(8):805-16. Mean platelet volume in recurrent aphthous stomatitis and behcet disease. Angiology. 2014 Feb;65(2):161-5. Increased mean platelet volume in Behçet's disease with thrombotic tendency. Tohoku J Exp Med. 2010 Jun;221(2):119-23. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.5121

Objective: This study reported the effectiveness of Korean medicine for a patient with Type-1 diabetes mellitus after pancreatectomy with a compression fracture of the thoracic spine.Methods: A patient diagnosed with Type-1 diabetes mellitus after a pancreatectomy was treated with acupuncture, pharmacopuncture, <i>Gami-hwanggigyejiomul-tang</i> (modified Huangqi Guizhi Wuwu decotion), Jindang-won, etc. The conventional treatment was maintained using an insulin pump and insulin injection.Results: Blood glucose (FBS/PP2hrs), ESR and CRP decreased after one month of treatment.Conclusion: <i>Gami-hwanggigyejiomul-tang</i> and <i>Jindang-won</i> may be effective treatments for Type-1 diabetes mellitus. Further studies are needed to confirm the findings of this case.

Objective. To evaluate the effect of prophylactic therapy on gout flare during urate lowering treatment. Methods. We retrospectively examined the data derived from 59 patients who had been treated with allopurinol for more than six months after stopping prophylactic medication at our rheumatology clinic. Demographic data (age, sex, disease duration, tophi and comorbidity), clinical and laboratory features, including presence of gout flare during urate lowering treatment, dose of allopurinol, serum uric acid level and creatinine clearance at initiation and six months later, were collected. For the subgroup analysis, the same data were collected in 46 patients who had been followed up at one year after stopping prophylactic medication. Results. Twenty-eight patients among 59 (47.4%) had expe-rienced at least 1 gouty attack during urate lowering therapy. The mean duration of prophylactic medication was not different between the flare group (3.8 months) and the non-flare group (5.9 months, p=0.617). Six months later, the mean serum uric acid level was 6.3 mg/dL (6.1 mg/dL vs. 6.5 mg/dL). According to the duration of prophylactic treatment (＜6 months, ≥6 months), there were more frequent flares in the ＜6 months group than in the ≥6 months group (51.2% vs. 38.9% in the six month followup group, 70.6% vs. 50% in the one year follow-up group). Conclusion. Prophylactic medication for more than six months could be a favorable factor for the prevention of recurrent gout flare during urate lowering treatment.

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