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Background In the placebo (PBO)-controlled Phase III aSTRAEA study (ClinicalTrials.gov, NCT01860976) in psoriatic arthritis (PsA), abatacept (ABA) 125 mg SC weekly significantly increased the aCR20 response rate at Week 24 versus PBO (39.4% vs 22.3%, respectively; p Objectives To assess aBA safety up to 2 years in patients (pts) enrolled in aSTRAEA. Methods Pts with active PsA were randomised 1:1 to aBA or PBO for 24 weeks followed by 28 weeks’ open-label (OL) aBA (total time on study: 52 weeks); pts without ≥20% improvement in joint counts at Week 16 (early escape) were switched to OL aBA (total time on study: 44 weeks).1 Pts could subsequently receive OL aBA in a 52-week long-term extension (LTE; Year 2) for the collection of safety data. The proportions of pts in the cumulative aBA population (all pts who received ≥1 dose of aBA at any time in the study) with aEs (all aEs, serious aEs [SAEs], deaths, aEs leading to discontinuation), laboratory marked abnormalities and anti-ABA antibodies over the cumulative aBA period (date of first treatment dose to end of LTE) were recorded in 1-year and 6-month intervals. Results Overall, 398 pts were included in the analysis of the cumulative aBA period (213 received aBA from study Day 1; 185 completed initial randomisation to PBO and received aBA thereafter). Of these, 322 pts entered the LTE (initial randomisation: aBA, n=162; PBO, n=160) and continued to receive OL aBA beyond the 28-week OL period. Of 162 and 160 pts initially randomised to aBA and PBO, respectively, 19 (11.7%) and 21 (13.1%) pts discontinued aBA in the LTE. Median (range) number of aBA injections in the cumulative aBA period to end of LTE was 80 (1–133). Safety during the cumulative aBA period over 2 years is shown (Table 1); 6-month interval safety data will be available at time of presentation. In the LTE, there were 3 SAEs of infection (osteomyelitis, intervertebral discitis and cellulitis) and 3 pts discontinued due to infection (hepatitis a, Epstein-Barr virus, intervertebral discitis). No malignancies or deaths were reported, and no autoimmune events were reported as serious or led to aBA discontinuation during the LTE. AEs, SAEs and aEs of special interest occurred with a similar frequency regardless of concomitant MTX or prior TNF inhibitor (TNFi) use. The proportion of pts with anti-ABA antibodies during the cumulative aBA period was higher during the post-treatment period (≥22 days after last dose; 37.1% [91/245]) than in the on-treatment period (first treatment dose date to ≤21 days after last dose; 7.1% [28/392]). No apparent relationship between anti-ABA antibodies and efficacy in the on-treatment period or aEs suggestive of systemic immune reactions was seen. Conclusion Abatacept was well tolerated up to 2 years with no new safety signals during the LTE in this Phase III study in PsA. There was no impact of concomitant MTX use or prior TNFi exposure on the safety profile of abatacept. The occurrence of anti-abatacept antibodies had no impact on abatacept efficacy or safety. References [1] Mease PJ, et al. Ann Rheum Dis2017;76:1550–8. Acknowledgement Professional medical writing: andrea Plant, PhD, Caudex; funding: Bristol-Myers Squibb. Disclosure of interests Philip J Mease Grant/research support from: abbVie, amgen, BMS, Celgene, Janssen, Lilly, Novartis, Pfizer, SUN and UCB, Consultant for: abbVie, amgen, BMS, Galapagos, Gilead Sciences, inc., Janssen, Lilly, Novartis, Pfizer, SUN and UCB, Speakers bureau: abbVie, amgen, BMS, Celgene, Genentech, Janssen, Lilly, Novartis, Pfizer and UCB, alice B Gottlieb Grant/research support from: PI: incyte Corporation, Janssen-Ortho inc., Lilly ICOS LLC, Novartis, UCB, XBiotech, Consultant for: abbVie, Dermira, incyte Corporation, Lilly ICOS LLC, Novartis, Sun Pharmaceutical industries Ltd., avotres (unpaid), XBiotech (unpaid), Speakers bureau: abbVie, Eli Lilly and Company, Janssen Biotech; advisory board: Bristol-Myers Squibb, Celgene Corporation, Janssen Biotech, Janssen-Ortho inc., LEO Pharma, Novartis, UCB, Desiree van der Heijde Consultant for: abbVie, amgen, astellas, astraZeneca, Bristol-Myers Squibb, Boehringer ingelheim, Celgene, Daiichi, Eli-Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, Union Chimique Belge, Oliver FitzGerald: None declared, alyssa Johnsen Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Marleen Nys Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Subhashis Banerjee Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Harris a ahmad Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Dafna D Gladman Grant/research support from: abbVie, amgen, Celgene, Lilly, Novartis, Pfizer, and UCB, Consultant for: abbVie, amgen, BMS, Celgene, Galapagos, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB

Although numerous animal models for low back pain associated with intervertebral disk (IVD) degeneration have been proposed, insufficient data have been provided to make any conclusions regarding pain. Our aim in this study was to determine the reliability of complete Freund's adjuvant (CFA) injection into the rat spine as an animal model representing human discogenic pain.We studied IVD degenerative changes with pain development after a 10-microL CFA injection into the L5-6 IVD of adult rats using behavioral, histologic, and biochemical studies. Serial histologic changes were analyzed to detect degenerative changes. Expression of calcitonin gene-related peptide (CGRP), prostaglandin E (PGE), and inducible nitric oxide synthase (iNOS) were determined using immunohistochemistry or real-time polymerase chain reaction as support data for pain development. In addition, CGRP immunoreactivity (ir) at the IVD was considered indirect evidence of neural ingrowth into the IVD.There was a significant increase of the hindpaw withdrawal response in the CFA group until 7 wk postoperatively (P0.05). Histologic analyses revealed progressive degenerative changes of the disks without any damage in adjacent structures, including nerve roots. In the CGRP-ir staining study, the bilateral dorsal horns and IVD had positive ir after intradiscal CFA injection. CGRP mRNA expression was increased in the dorsal root ganglion (DRG) at 2 and 4 wk, whereas PGE and iNOS mRNAs were markedly increased at 2 wk. The increment of CGRP expression was higher in allodynic rats compared with nonallodynic rats.Intradiscal CFA injection led to chronic disk degeneration with allodynia, which was suggested by pain behavior and expression of pain-related mediators. The increment of CGRP, PGE, and iNOS also suggest pain-related signal processing between the IVD and the neural pathway in this animal model. This animal model may be useful for future research related to the pathophysiology and development of novel treatment for spine-related pain.

INTRODUCTION: Haemophilus influenzae is a common cause of bacterial meningitis in children and can cause upper respiratory tract infections in adults, but has yet to be reported solely involving intervertebral discitis. PRESENTATION OF CASE: A 67-year-old builder presenting with fever, myalgia and back pain is found to have intervertebral discitis (confirmed on MRI) caused by H. influenzae (identified on blood cultures). DISCUSSION: A nontypeable form of H. influenzae has not been reported causing discitis. We describe a case in a relatively fit individual who was treated successfully with antimicrobial treatment. A preceding upper respiratory tract infection is the presumed source of infection, predisposed by long-term low-dose steroid therapy. CONCLUSION: H. influenzae is a rare, but treatable cause of discitis.

We report a follow-up of 35 children, on average 17 years after they had intervertebral discitis. 15 patients still complained of backache. Flexion of the low back was normal in 32 patients, while extension was markedly restricted in 30. 26 patients had a block vertebra, and 28 patients had narrowing of the vertebral canal. Mode of treatment did not appear to affect the outcome.

Pseudomonas pickettii, a nonfermenting, gram-negative rod, is rarely pathogenic. Previous reports of infection with P. pickettii have largely involved direct contamination of supplies presumed to be sterile. We describe a case of vertebral osteomyelitis and intervertebral discitis caused by P. pickettii in a debilitated patient. The aggressive nature of this infection demonstrates that P. pickettii may be a more invasive organism than previously noted, particularly in hosts with weakened immunity secondary to underlying disease.

Discitis (with intervertebral disc destruction), found pathologically in the thoracic region of 8 out of 114 rheumatoid patients, is shown to derive and spread from primary rheumatoid involvement of the costovertebral joints. Erosion and destruction of bone may occur, followed by healing, visible radiologically as disc narrowing and posterolateral bony sclerosis and sometimes with ankylosis. There are few clinical symptoms, since most of these patients have limited locomotor function.

In 29 children wih symptoms and signs as well as laboratory and radiographic findings consistent with intervertebral discitis, the syndrome appeared to be a manifestation of both infectious and noninfectious inflammatory processes. When systemic sepsis is present, antibiotic therapy is indicated. In the absence of fever and leukocytosis, plaster cast immobilization should suffice. Craig needle aspiration and/or open biopsy are not routinely required, but should be reserved for those patients who fail to respond to routine treatment in whom tuberculosis is suspected.