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Thyroid disease
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
Graves’ ophthalmopathy can be disfiguring and can threaten sight. It becomes clinically apparent in approximately one-third of Graves’ patients. Its clinical course typically comprises an active phase lasting for up to 3 years involving increased tearing and ocular discomfort and proptosis, which may occasionally cause diplopia and even loss of vision. An inactive phase follows during which eye symptoms stabilise. More rarely, occurring in 1%–4% of Graves’ patients, thyroid dermopathy involving characteristically non-pitting pretibial swelling is evident. In some with dermopathy, acropachy, which resembles finger clubbing, is also evident.
Immunotherapy of Graves’ Eye Disease
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
N. R. Farid, G. Kahaly, J. Beyer
In 1984-1985, we carried out a controlled randomized prospective study in 40 patients with Graves’ ophthalmopathy.32-34 Half of the patients received decreasing doses of prednisone, and the other half received a comparable dose of prednisone, and in addition, cyclosporine. Steroid treatment was discontinued after 10 weeks in both groups. Cyclosporine therapy was continued over 12 months. Both subjective and objective parameters improved in both groups. The result was significantly better in the cyclosporine group, as reflected by a predefined activity score. At the end of prednisone therapy, there was a new increase of the score in the patient group treated with steroids only (see Figure 3). Before the beginning of therapy, the distribution of eye disease severity was comparable in the two groups. During therapy, the degree of severity of the disease had markedly declined in the cyclosporine group in favor of the milder grades (Figure 4). By contrast, there were no appreciable alterations in Graves’ ophthalmopathy grade after 6 months in the prednisone group.
The diagnostic evaluation and management of hyperthyroidism due to Graves’ disease, toxic nodules, and toxic multinodular goiter
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
The symptoms and signs of Graves’ ophthalmopathy are due to orbital inflammation, with the extraocular muscles and/or retro-orbital fibroblasts being the target of the autoimmune reaction (165–166). Glycosaminoglycans produced by fibroblasts responding to T-cell infiltration cause edema of the extraocular muscles, and further expansion of the retro-orbital tissues is due to increased orbital fat (168). Ultimately, fibrosis of the extraocular muscles can lead to diplopia, and severe enlargement of the muscles can cause an ischemic optic neuropathy due to compression of the optic nerve as it exits the apex of the orbit.
Assessment of subclinical left ventricular dysfunction with speckle-tracking echocardiography in hyperthyroid and euthyroid Graves’ disease and its correlation with serum TIMP-1
Published in Acta Cardiologica, 2021
Irfan Veysel Duzen, Suzan Tabur, Sadettin Ozturk, Mert Deniz Savcilioglu, Enes Alıc, Mustafa Yetisen, Sıddık Sanli, Huseyin Goksuluk, Ertan Vuruskan, Gokhan Altunbas, Fatma Yılmaz Coskun, Mehmet Kaplan, Seyithan Taysi, Murat Sucu
Hyperthyroidism causes systolic and diastolic dysfunction through its effects on heart rate, vascular resistance, oxidative stress and the renin–angiotensin system [11,12]. Consistently, impaired systolic and diastolic functions were observed in the current study in Graves’ patients with hyperthyroidism. However, amelioration of hyperthyroidism did not lead to a marked improvement in global strain values and serum TIMP-1 value remained elevated compared to the control group. This suggests that the autoimmune origin of Graves’ disease might be a determinant for its cardiovascular effects. As known, the most common non-thyroidal involvement of Graves’ disease is Graves’ ophthalmopathy [13]. While Graves’ ophthalmopathy clinically manifests in 5% of patients, ocular involvement is detected in more than 70% of patients by computed tomography (CT) and magnetic resonance imaging (MRI) [14]. TRAB positivity is present in clinically active cases but insulin-like growth factor and several unknown factors may have an impact on thyroid-related ophthalmopathy [15]. Thus, in a significant portion of patients with Graves’ disease, low-grade inflammation and autoimmunity prevail even after hyperthyroidism has been treated.
Reduced Retinal Microvascular Density Related to Activity Status and Serum Antibodies in Patients with Graves’ Ophthalmopathy
Published in Current Eye Research, 2020
Yufei Wu, Yunhai Tu, Lulu Bao, Chaoming Wu, Jingwei Zheng, Jianhua Wang, Fan Lu, Meixiao Shen, Qi Chen
Graves’ disease (GD) is an autoimmune disorder that results in the overproduction of thyroid hormones, resulting in changes in the vascular system, bone, and skin.1 The eyes may also be affected through a distinct, yet related, disease known as Graves’ ophthalmopathy (GO).2 The prevalence of GO in GD patients is relatively high, 34.7% to 46.7%.3 In GO patients, the immune system targets the area surrounding the eyes, and this may cause orbital inflammation that later manifests as chemosis, redness, orbital soft tissue swelling, eyelid retraction, lag exophthalmos, extraocular muscle involvement, corneal involvement, intraocular hypertension, as well as optic neuropathy.4–6 Dysthyroid optic neuropathy (DON) occurs in approximately 3% to 8% of GO patients and manifests as loss of visual acuity, visual field defects, dyschromatopsia, and optic disc edema.7–9
Smoking and environmental tobacco smoke exposure: implications in ocular disorders
Published in Cutaneous and Ocular Toxicology, 2023
Saeed Karimi, Hosein Nouri, Sahar Mahmoudinejad-Azar, Seyed-Hossein Abtahi
Graves’ ophthalmopathy (GO) is a rare ocular disease of autoimmune nature, mostly affecting patients with Graves’ disease (GD); its estimated incidence is 16/100 000 in women and 3/100 000 in men [48]. At the cellular level, local orbital inflammatory and autoimmune stimuli ignite excessive glycosaminoglycan production and fibroblast differentiation into mature adipocytes, leading to extraocular muscle swelling and adipogenesis. The consequent mechanical and anatomical effects include proptosis, diplopia, and compressive neuropathy [49]. The most prominent modifiable risk factor of GO among adults is smoking; it increases not only the risk of GO development but also its severity, activity, and resistance to treatment [50].