Purpose The purpose of this study was to evaluate the utility of corneal confocal microscopy (CCM) in identifying small nerve fiber damage and immune cell activation in patients with systemic lupus erythematosus (SLE). Methods This cross-sectional comparative study included 39 consecutive patients with SLE and 30 healthy control participants. Central corneal sensitivity was assessed using a Cochet-Bonnet contact corneal esthesiometer and a laser scanning CCM (Heidelberg, Germany) was used to quantify corneal nerve fiber density (CNFD), nerve branch density (CNBD), nerve fiber length (CNFL), and Langerhans cell (LC) density. Results Age was comparable among patients with SLE (33.7 ± 12.7) and controls (35.0 ± 13.7 years, P = 0.670) and the median duration of disease was 3.0 years (2.0–10.0 years). CNBD ( P = 0.003) and CNFL ( P = 0.019) were lower and mature LC density ( P = 0.002) was higher, but corneal sensitivity ( P = 0.178) and CNFD ( P = 0.198) were comparable in patients with SLE compared with controls. The SELENA-SLEDAI score correlated with CNFD (ρ = −0.319, P = 0.048) and CNFL (ρ = −0.373, P = 0.019), and the total and immature LC densities correlated with CNBD (ρ = −0.319. P = 0.048, and ρ = −0.328, P = 0.041, respectively). Immature LC density was higher ( P = 0.025), but corneal sensitivity and nerve fiber parameters were comparable between patients with (33%) and without neuropsychiatric symptoms and SLE. Conclusions Corneal confocal microscopy identifies distal corneal nerve fiber loss and increased immune cell density in patients with SLE and corneal nerve loss was associated with disease activity. Translational Relevance Corneal confocal microscopy may enable the detection of subclinical corneal nerve loss and immune cell activation in SLE.

Background. Tumor necrosis factor antagonists (anti-TNF-α) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported, and literature data suggest a potential role of anti-TNF-α in the induction of demyelination. Case Presentation. In this series, we present three cases of demyelination after the use of anti-TNF-α agents. The first case involved a 21-year-old man with HLA-B27 negative peripheral spondylarthritis who had been taking adalimumab for 2 years. He developed headache, urinary incontinence, and bilateral lower extremity numbness that progressed to the middle of the trunk for 2 days. Magnetic resonance imaging (MRI) showed multiple hyperintense enhancement lesions in the left paramedian anterior pons consistent with multiple sclerosis (MS). The second case included a 17-year-old woman who was on 2 years of adalimumab treatment for juvenile idiopathic arthritis and chronic anterior uveitis and developed new-onset dizziness and tremors. The clinical examination showed signs of cerebellar dysfunction. MRI findings were consistent with multiple sclerosis. The third case was a 34-year-old male who was on 5 years of infliximab treatment for ankylosing spondylitis when he developed left hand numbness and weakness. Cerebrospinal fluid (CSF) analysis and MRI findings were consistent with demyelination. Discontinuation of tumor necrosis factor antagonists (anti-TNF-α) resulted in resolution of the symptoms with no recurrence in the first case, but there was evidence of recurrence in the other 2 cases, where one was managed with rituximab and the second one improved with pulse steroid therapy. Conclusion. Despite the small number of patients, our series adds to the growing body of evidence supporting a causal link between anti-TNF-α agents and demyelination. Thus, we can conclude that on suspicion of any neurological side effects, early discontinuation of the TNF-α blockers and requesting urgent MRI scan to confirm the diagnosis is of utmost importance.

Salmonella is a well-known cause of foodborne illness, commonly resulting in gastroenteritis, bacteremia, and focal infections. Salmonella septic arthritis is a rare entity with cases mostly prevalent in patients with sickle cell disease, immunocompromised state, and advanced age. Here, we present a case of Salmonella septic arthritis in a previously healthy young gentleman with no risk factors who presented with fever, skin rash, abdominal pain, and left hip pain. Initial laboratory findings showed high inflammatory markers and negative blood culture. MRI of the left hip joint showed effusion and features of inflammatory changes. The diagnosis was confirmed by joint aspirate culture growing Salmonella B. Furthermore, he underwent joint arthrotomy; pus was drained and treated with an antibiotic. Subsequently, the patient responded to treatment with marked clinical recovery.

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TNF blockers have revolutionized the management of immune-mediated inflammatory diseases. Despite their relatively safe profile, an increasing number of reported neurological adverse events suggest a role for TNF inhibitors in the induction of central and peripheral nervous system demyelination.