Background Non-Helicobacter pylori species (NHPS) are newly emerging bacteria that naturally inhabit birds and mammals apart from humans and rarely cause diseases in humans. In recent years, a rise in the number of cases associated with NHPS infections in humans has been observed. Among them, infections with Helicobacter (H.) canis are sporadic and challenging to recognise clinically. To date, ten cases of H. canis infections in mainly immunocompromised humans have been reported in the literature. Transmission pathway is most likely zoonotic via the faecal-oral route during close contacts with dogs and cats or may result from a contaminated sheep milk intake. No clear guidelines for successful antibiotic regimen are known. Important additional risk factor for infection might be biologic agents and Janus kinase inhibitors (JAKi) used in the treatment of rheumatoid arthritis (RA) and other conditions. Herein we present the first case of H. canis bacteraemia in a RA patient treated with novel JAKi tofacitinib. Case presentation A 65-year-old female patient with RA and rituximab-induced hypogammaglobulinemia treated with tofacitinib, methotrexate, and methylprednisolone came to a planned visit in our outpatient rheumatology clinic. She presented with a history of back pain that significantly worsened 2 days before visit. She had numbness and tingling sensation in both legs and muscle weakness. Neurological examination was within a normal range. The patient was afebrile, had no chills, and was haemodynamically stable. She was in close contact with her pet dogs. Laboratory examination showed increased markers of inflammation. She was found to have H. canis bacteraemia with underlying multilevel degenerative lumbar spinal stenosis. Identification of H. canis was performed by MALDI-TOF MS and 16 S rRNA gene sequence analysis of isolate from subcultured positive aerobic blood culture bottles. Antimicrobial susceptibility testing showed low minimum inhibitory concentrations to amoxicillin-clavulanate, cefotaxime, ceftriaxone, meropenem, and gentamicin. She was treated with combined antibiotic regimen (ceftriaxone, doxycycline) for 14 days, which resulted in total remission of the infection. Conclusions Clinicians should recognise H. canis infection risk in patients with recent pet exposure and predisposing factors such as immunodeficiency disorders or diseases that demand immunosuppressive drug therapy. A minimum of two weeks of antibiotic therapy is suggested.

Rheumatoid arthritis (RA) is a chronic inflammatory disease, associated with increased mortality and morbidity due to the higher cardiovascular risk in these patients. Traditional risk factors are not the only answer for the accelerated atherosclerosis. In long term prospective study, we investigated the relationship between asymptomatic atherosclerosis and traditional risk factors as well as inflammatory markers in patients with RA and matched healthy controls. We studied the laboratory test results, the concentrations of inflammatory mediators, matrix metalloproteases (MMP) and inflammation markers in the total of 70 (60 at follow-up) premenopausal healthy women with RA and 40 (34 at follow-up) matched controls’. We used the B-mode ultrasound imaging of carotid arteries for detection of asymptomatic atherosclerosis. Correlation with different factors was evaluated. Statistically significant higher values of inflammatory markers such as selective adhesion molecules ICAM & VCAM, interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) and MMP-3 in patients` group were found in the follow-up study. More plaques were found in the patients’ group (42.4% vs. 12.9%; p=0.005), as compared with the controls’ group. The patients had also higher values of cIMT (p=0.001). Using bivariate regression analysis only VCAM was found as a prognostic factor for plaque occurrence (r= 0. 341, p=0.016), but not for cIMT (r= -0.130, p=0.327) in premenopausal female patients with RA after the follow-up. Therefore, the asymptomatic atherosclerosis is accelerated in premenopausal women with RA. The results of our follow-up study showed the association between the inflammation and accelerated atherosclerosis. Furthermore, VCAM was found to have statistically significant correlation with plaque occurrence in these patients.

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Background:Rheumatoid arthritis (RA) is chronic inflammatory disease, associated with increased mortality and morbidity due to higher cardiovascular risk in these patients.Objectives:Traditional risk factors are not the only answer for accelerated atherosclerosis. In long term prospective study, we investigated the relationship between asymptomatic atherosclerosis and traditional risk factors as well inflammatory markers in patients with RA and matched healthy controls.Methods:In 60 RA premenopausal women and 34 matched controls values of laboratory test results, concentrations of inflammatory mediators, matrix metalloproteases (MMP) and markers of inflammation were measured. Using B-mode ultrasonography carotid intima-media thickness (cIMT) and plaques occurrence (markers of asymptomatic atherosclerosis) at baseline and after 15 years of observation were defined in both groups. The differences in concentrations of inflammatory mediators, MMPs and markers of inflammation were compared. The relationship of inflammatory mediators and markers, MMPs and markers of asymptomatic atherosclerosis was examined using regression models.Results:After the follow up statistically significant higher values of inflammatory markers like selective adhesion molecules ICAM & VCAM, interleukin 6 (IL-6), tumour necrosis factor alpha (TN alpha) and MMP-3 in patient`s group was found. Among traditional risk factors only sedimentation rate and CRP levels were statistically higher in patient`s group. More plaques were found in patients’ group (12.9% vs. 42.4%; p=0.005), patients had also higher values of cIMT (p<0.0001). Using multiple linear regression analysis only VCAM was found as independent prognostic factor for plaques occurrence (p=0.016), but not for cIMT (p=0.314) in RA patients after the follow up.Conclusion:Asymptomatic atherosclerosis is accelerated in premenopausal women with RA patients. The results of our study showed the association between the inflammation and accelerated atherosclerosis, VCAM was found as independent risk factor for plaques occurrence in these patients.References:[1] Dalbeni A, et al. Traditional cardiovascular risk factors or inflammation: Which factors accelerate atherosclerosis in arthritis patients?. International J Cardial 2017; 236: 488-492.[2] Mahmoudi M, Aslani S and Jamshidi AR. New insights to the mechanisms underlying atherosclerosis in rheumatoid arthritis. International Journal of Rheumatic diseases 2017; 20: 287-297.[3] Johnson JL. Metalloproteinases in atherosclerosis. Eur J Pharmacol. 2017;816:93-106.[4] Agca R, Heslinga SC, Rollefstad S e tal. EULAR recommendations for cardiovascular disease risk management in patients with rheumatoid arthritis and other forms of inflammatory joint disorders: 2015/2016 update. Ann rheum Dis 2017; 76: 17-28.Disclosure of Interests:None declared