Linsitinib, an IGF-1R inhibitor, attenuates disease development and progression in a model of thyroid eye disease.

Introduction: Graves' disease (GD) is an autoimmune disorder caused by autoantibodies against the thyroid stimulating hormone receptor (TSHR) leading to overstimulation of the thyroid gland. Thyroid eye disease (TED) is the most common extra thyroidal manifestation of GD. Therapeutic options to treat TED are very limited and novel treatments need to be developed.

Influence of biological sex, age and smoking on Graves' orbitopathy - a ten-year tertiary referral center analysis.

Purpose: Severity of Graves' orbitopathy (GO) shows wide individual differences. For optimal treatment, it is important to be able to predict the natural course of the disease as accurate as possible to counteract with anti-inflammatory and surgical treatment. Therefore, we aimed to further elucidate the impact of sex, age and smoking on GO.

Macrophage-Orbital Fibroblast Interaction and Hypoxia Promote Inflammation and Adipogenesis in Graves' Orbitopathy.

The inflammatory eye disease Graves' orbitopathy (GO) is the main complication of autoimmune Graves' disease. In previous studies we have shown that hypoxia plays an important role for progression of GO. Hypoxia can maintain inflammation by attracting inflammatory cells such as macrophages (MQ).

An Early Wave of Macrophage Infiltration Intertwined with Antigen-Specific Proinflammatory T Cells and Browning of Adipose Tissue Characterizes the Onset of Orbital Inflammation in a Mouse Model of Graves' Orbitopathy.

Graves' orbitopathy (GO) is an autoimmune-driven manifestation of Graves' disease (GD) where pathogenic autoantibodies to the thyrotropin receptor (TSHR) activate orbital fibroblasts/preadipocytes in the orbital tissue to induce inflammation and extracellular matrix deposition. Since there are significant limitations to study immunological and proinflammatory mediator expression in early and during disease progression in GO patients, we used our experimental mouse model to elucidate early pathogenic processes. We have developed a robust mouse model of GD/GO induced by electroporation immunization of plasmid encoding human TSHR A-subunit, comprising multiple injections over a course of 15 weeks to fully recapitulate the orbital pathology.

Proposing a surgical algorithm for graduated orbital decompression in patients with Graves' orbitopathy.

Purpose: To determine the outcome after orbital decompression using a graduated technique, adapting the surgical technique according to individual patients' disease characteristics.

Methods: We retrospectively examined the postoperative outcome in patients treated with a graduated balanced orbital decompression regarding reduction of proptosis, new onset diplopia and improvement in visual function. 542 patients (1018 orbits) were treated between 2012 and 2020 and included in the study.

Modulating gut microbiota in a mouse model of Graves' orbitopathy and its impact on induced disease.

Background: Graves' disease (GD) is an autoimmune condition in which autoantibodies to the thyrotropin receptor (TSHR) cause hyperthyroidism. About 50% of GD patients also have Graves' orbitopathy (GO), an intractable disease in which expansion of the orbital contents causes diplopia, proptosis and even blindness. Murine models of GD/GO, developed in different centres, demonstrated significant variation in gut microbiota composition which correlated with TSHR-induced disease heterogeneity.

Risk Factors for New Onset Diplopia After Graduated Orbital Decompression.

Purpose: The aim of the study was to identify possible risk factors for new onset diplopia in 20° of primary position (NOD PP) after orbital decompression. A predisposition for NOD has been established for patients with pre-existing diplopia in secondary gaze; therefore, the authors focused on patients without preoperative diplopia.

Methods: Retrospective chart review of patients who underwent balanced orbital decompression between 2012 and 2019 due to Graves orbitopathy at the authors' institution.

Bony Orbital Decompression in Patients with High Myopia and Pseudoexophthalmos.

Introduction: High myopic eyes grow in length (> 0.35 mm/dpt) more than in height and width leading to a disturbing unilateral exophthalmos in patients with anisomyopia and - more rarely - a bilateral exophthalmos in high myopia affecting both eyes. Secondary consequences are sicca symptoms and painful eye mobility due to a large bulbus in a too small bony orbit.