Simultaneous bilateral aqueous misdirection following certolizumab therapy for rheumatoid arthritis

Aqueous misdirection syndrome is a rare, incompletely understood, sight-threatening eye condition that is difficult to diagnose and treat. We present a case of simultaneous bilateral aqueous misdirection following the administration of certolizumab in a 41-year-old women with rheumatoid arthritis and no known risk factors. To our knowledge, aqueous misdirection has not previously been associated with the use of tumour necrosis factor-alpha inhibitors.publishedVersio

Simultaneous bilateral aqueous misdirection following certolizumab therapy for rheumatoid arthritis

Aqueous misdirection syndrome is a rare, incompletely understood, sight-threatening eye condition that is difficult to diagnose and treat. We present a case of simultaneous bilateral aqueous misdirection following the administration of certolizumab in a 41-year-old women with rheumatoid arthritis and no known risk factors. To our knowledge, aqueous misdirection has not previously been associated with the use of tumour necrosis factor-alpha inhibitors

Paravascular microcirculation facilitates rapid lipid transport and astrocyte signaling in the brain

In the brain, a paravascular space exists between vascular cells and astroglial end-foot processes, creating a continuous sheath surrounding blood vessels. Using in vivo two-photon imaging we demonstrate that the paravascular circulation facilitates selective transport of small lipophilic molecules, rapid interstitial fluid movement and widespread glial calcium signaling. Depressurizing the paravascular system leads to unselective lipid diffusion, intracellular lipid accumulation and pathological signaling in astrocytes. As the central nervous system is devoid of lymphatic vessels, the paravascular space may serve as a lymphatic equivalent that represents a separate highway for the transport of lipids and signaling molecules

Novel inflammatory biomarkers in thyroid eye disease

Purpose: The aim of this study is to identify biochemical inflammatory markers predicting the presence or risk of developing thyroid eye disease (TED) in patients with Graves' disease (GD). Methods: Patients with GD (n = 100, 77 females) were included from the National Norwegian Registry of Organ-Specific Diseases. Serum samples were analysed for 92 different inflammatory biomarkers using the proximity extension assay. Biomarker levels were compared between groups of patients with and without TED and healthy subjects (HS) (n = 120). Results: TED was found in 36 of 100 GD patients. Significant (P < 0.05) differences in the levels of 52 inflammatory biomarkers were found when GD patients and HS were compared (42 elevated and 10 decreased). Out of the 42 elevated biomarkers, a significantly higher serum level of interleukin-6 (IL6) (P = 0.022) and macrophage colony-stimulating factor (CSF1) (P = 0.015) were found in patients with TED compared to patients without TED. Patients with severe TED also had significantly elevated levels of Fms-related tyrosine kinase 3 ligand (FLT3LG) (P = 0.009). Furthermore, fibroblast growth factor 21 (FGF21) was significantly increased (P = 0.008) in patients with GD who had no signs of TED at baseline but developed TED later. Conclusion: We demonstrate an immunologic fingerprint of GD, as serum levels of several inflammation-related proteins were elevated, while others were decreased. Distinctly increased levels of IL6, CSF1, FLT3LG, and FGF21 were observed in TED, suggesting that these inflammatory proteins could be important in the pathogenesis, and therefore potential new biomarkers for clinical use.publishedVersio