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Purpose: To report a case of presumed fungal infection in a patient with JIA following prolong immunosuppression, and after initiation of adalimumab therapy. Method: Retrospective Chart Review. Result: A 20-year-old female, previously diagnosed with JIA, presented with a three-week history of blurred vision in her left eye. She had a long history of treatment with oral corticosteroids, sulfasalazine, and methotrexate, followed by tocilizumab injections and later etanercept. Recently, she was started on adalimumab injections. Fundus examination of the left eye demonstrated multifocal retinitis scattered throughout the fundus. Optical coherence tomography of the lesions showed hyperreflectivity in the inner retina with posterior shadowing and vitreous aggregates extending into the vitreous cavity. After her second adalimumab dose, she experienced blurred vision. Examination of the fundus revealed multifocal retinitis in the left eye, sparing the macula. After stopping immunomodulators and starting empirical antifungal therapy with oral fluconazole, her retinal lesions began to improve. A vitreous biopsy was performed, and intravitreal voriconazole was administered, but microbiological tests were negative. Nevertheless, her retinal lesions resolved almost completely with continued antifungal treatment. By the 6-week follow-up, her retinitis had fully resolved, maintaining excellent visual acuity. Conclusion: This case underscores the need for a high index of suspicion for infection in patients with long-term immunosuppression, highlighting the importance of early therapeutic intervention. [ABSTRACT FROM AUTHOR]

Background. Ankylosing spondylitis (AS) is a chronic inflammatory potentially debilitating disease predominantly affecting the axial skeleton. A few intermittently published studies and research have proved the existence of some not yet explained neurophysiologic abnormalities in patients with AS. Objectives. The aim of this study was to investigate the brainstem auditory evoked potentials and its relationship with clinical findings, laboratory tests and pharmacological therapy used in patients with AS. Material and method. Thirty-nine patients with AS were included in the study. The control group was composed of 50 healthy subjects. BAEP were recorded for all subjects. Patients were assessed by clinical specific tests, inflammatory laboratory tests, Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and type of pharmacological therapy. Results. The results have shown differences between the control group and the patients with AS in most of the wave latencies. Correlations Schober test, Ott index, chest expansion measurement and BASDAI were significant for some waves. CRP seems to be more valuable than ESR as a possible marker for neurologic subclinical involvement. Axial AS is more likely to be associated with BAEP abnormalities. There were also differences between the group with TNF alpha blockers therapy comparative with the group with other therapies. Conclusions. This study highlights some abnormalities of BAEP in patients with AS. Diagnosis of multiple sclerosis or demyelination due to administration of TNF alpha blockers should be excluded in medical practice. Collaboration between neurologists and rheumatologists should be considered in monitoring AS patients.

OBJECTIVE: We evaluated the incidence of and the main risk factors associated with cutaneous adverse events in patients with chronic inflammatory arthritis following anti-TNF-α therapy. METHODS: A total of 257 patients with active arthritis who were taking TNF-α blockers, including 158 patients with rheumatoid arthritis, 87 with ankylosing spondylitis and 12 with psoriatic arthritis, were enrolled in a 5-year prospective analysis. Patients with overlapping or other rheumatic diseases were excluded. Anthropometric, socioeconomic, demographic and clinical data were evaluated, including the Disease Activity Score-28, Bath Ankylosing Spondylitis Disease Activity Index and Psoriasis Area Severity Index. Skin conditions were evaluated by two dermatology experts, and in doubtful cases, skin lesion biopsies were performed. Associations between adverse cutaneous events and clinical, demographic and epidemiological variables were determined using the chi-square test, and logistic regression analyses were performed to identify risk factors. The significance level was set at p

Background. Ankylosing spondylitis (AS) is a chronic inflammatory potentially debilitating disease predominantly affecting the axial skeleton. A few intermittently published studies and research have proved the existence of some not yet explained neurophysiologic abnormalities in patients with AS. Objectives. The aim of this study was to investigate the brainstem auditory evoked potentials and its relation with clinical findings, laboratory tests and pharmacological therapy used in patients with AS. Material and method. Thirty-nine patients with AS were included in the study. The control group was composed of 50 healthy subjects. BAEP were recorded for all subjects. Patients were assessed by clinical specific tests, inflammatory laboratory tests, Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and type of pharmacological therapy. Results. The results have shown differences between the control group and the patients with AS in most of the wave latencies. Correlations Schober test, Ott index, chest expansion measurement and BASDAI were significant for some waves. CRP seems to be more valuable than ESR as a possible marker for neurologic subclinical involvement. Axial AS is more likely to be associated with BAEP abnormalities. There were also differences between the group with TNF alpha blockers therapy comparative with the group with other therapies. Conclusions. This study highlights some abnormalities of BAEP in patients with AS. Diagnosis of multiple sclerosis or demyelination due to administration of TNF alpha blockers should be excluded in medical practice. Collaboration between neurologists and rheumatologists should be considered in monitoring AS patients. [ABSTRACT FROM AUTHOR]

Here, we present a young male patient who was admitted with alveolar hemorrhage, arthritis and cutaneous lesions, who later developed bilateral orbital involvement and pyoderma gangrenosum ( PG). He also had pathergy test positivity. The patient was refractory to conventional immunosuppressive therapy. Therefore, multiple devastating PG lesions and disease activity in granulomatosis with polyangiitis ( GPA) were controlled with infliximab. Later, rituximab was used with success to prevent recurrence of symptoms. The relationship of PG with various autoimmune diseases is known; however, PG in GPA has been only rarely reported. Biologic agents might prove to be effective in GPA and PG patients who are refractory to standard immunosuppressive therapy. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the long-term efficacy of golimumab in patients with severe recalcitrant uveitis who had inadequate response to previous biologics. Methods: Retrospective study (13 patients with JIA, 4 with HLA-B27-associated uveitis). Indication for treatment was active uveitis despite biologics. Golimumab dosing was 50 mg monthly/subcutaneously. Main outcome measures: uveitis activity, visual acuity improvement, reduction of systemic therapy (corticosteroids/immunosuppressants), adverse events. Results: Of 17 patients (34 affected eyes), response to golimumab was seen in 14 patients; at last visit uveitis was inactive in 12 patients. Three patients were nonresponders. Mean follow-up time on golimumab was 21.9 months. Visual acuity remained stable in 26 eyes, improved in 7, and worsened in 1. Mean systemic prednisolone dose before and after golimumab was 12.5-3.5 mg/day. One patient developed pulmonary infection. Conclusions: Golimumab may be a promising new therapeutic option for severe uveitis patients who have not responded to other biologics. [ABSTRACT FROM AUTHOR]

There is a high co-morbidity between chronic inflammatory disorders and depression. Proinflammatory cytokines like TNF-α seem to play a central role in the pathogenesis of these disorders, and its neutralization provides a potent treatment for inflammatory disorders. Few studies showed that TNF-α blockers also caused an improvement in depressive symptoms associated with these chronic inflammatory disorders. To evaluate the effectiveness of TNF-α blockers on symptoms of ankylosing spondylitis (AS), depression, anxiety and quality of life, 9 AS patients resistant to classical therapy were enrolled and followed-up at 2nd and 6th weeks after a TNF-α blocker was started. Hamilton Depression and Anxiety Scales (HAM-D, HAM-A), Hospital Depression and Anxiety Questionnaire (HAD), Quality of Life Scale (SF36) and AS severity index (BASDAI) were applied to the patients at weeks 0, 2 and 6. ESR and CRP were evaluated to monitor biological disease activity. There was a significant reduction in HAM-D ( p = 0.00), HAM-A ( p = 0.00), HAD anxiety scores ( p = 0.02) and a significant improvement in SF36 physical function ( p = 0.00), physical role limitations ( p = 0.00), bodily pain ( p = 0.05), general health ( p = 0.01), vitality ( p = 0.03) and emotional role limitations ( p = 0.00) subscales, BASDAI scores ( p = 0.00), ESR ( p = 0.00) and CRP ( p = 0.00). Change in clinical disease activity (BASDAI) was not correlated with change in depression-anxiety scores, while change in biological disease activity (CRP) was correlated with change in depression-anxiety scores. TNFα blockers may have a potential antidepressant effect besides its anti-inflammatory effect that seems to be independent of its clinical effect. [ABSTRACT FROM AUTHOR]

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The aims of this study were to determine the association and potential mechanisms between TNF-antagonists and increased cardiovascular risk in rheumatoid arthritis (RA) patients. Three groups of RA patients were studied; ten treated with TNF-antagonists, 13 with methotrexate, and 14 were naïve to treatment. Mean age: 47.2 (SD 11.3), 52.3 (SD 16.6), and 51.2 (SD 13.3) years; mean disease duration 102 (SD 90.4), 72.9 (SD 67.3), and 71.3 (SD 87.1) months, and treatment duration 24.2 (SD 18.5), 34.7 (SD 32.2), and 0 months for each group. Clinical data: systolic and diastolic blood pressure and body mass index were assessed. Disease activity was determined by DAS-28 index. An ELISA assay for IL-6, sIL-6 R, IFN-gamma, TNF-alpha, sTNFRI, sTNFRII, IGF I, and adiponectin were performed. Fasting glucose, insulin, lipid profile, CRP, and ESR were also done. HOMA-IR and QUICKI indexes were calculated. Statistically significant differences observed between the TNF group and the other two groups were: TNF-alpha levels ( p, 0.0014), soluble TNF RII ( p, 0.0432), IFN-gamma ( p, 0.008), and DAS-28 <2.6 ( p, 0.033). Finding of elevated levels of sTNFRII and IFN-gamma in patients with RA on anti-TNF suggests that this therapy does not completely suppress the inflammatory process and may promote atherogenesis. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor (TNF)-alpha antagonists successfully modulate the pathogenesis of rheumatoid arthritis (RA). However, little is known about the effect of TNF-alpha blockade on the histology of chronic viral hepatitis. We describe the cases of two patients with RA, one with concurrent chronic hepatitis B virus and the other with hepatitis C virus infection who, as part of their evaluation, underwent liver biopsies while undergoing treatment with a TNF-alpha antagonist. [ABSTRACT FROM AUTHOR]