Mechanism of Grave's Opthalmopathy

Hendrian Dwikoloso Soebagjo (2018) Mechanism of Grave's Opthalmopathy. In: Proceeding 43rd Annual Scientific Meeting of Indonesian Ophthalmologist Association. Persatuan Dokter Ahli Mata Indonesia, Padang, pp. 595-600.

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Grave's opthalmopathy (GO) also known as Thyroid Associated Orbitopathy is an extra-thyroidal manifestation of autoimmune inflammatory disorder of the orbit and periorbital tissues. The occurrence of orbitopathy is the most difficult disorder to deal with, although the thyroid hormone abnormalities that often accompany this disease have been treated optimally. Grave's disease is very potential to threaten the eye that causes impaired visual function and reduce the quality of life of patients. Grave's ophthalmopathy (GO) is an autoimmune disease characterized by follicular enlargement of the follicle of the thyroid gland because of dysregulation of thyroid hormone synthesis. Increased circulation of thyroid hormones causes clinical symptoms and signs of hyperthyroidism. TSH binds to the follicular cell receptor together with the thyroid gland stimulates the synthesis and secretion of the thyroid hormone. T-lymphocytes experience stimulation of antigens in the thyroid gland and stimulate B-lymphocytes to synthesize antibodies against these antigens. The synthesized antibodies will react with TSH receptors in the thyroid cell membrane, thereby stimulating the growth and function of thyroid cells (known as TSH-R antibody). There are 3 predisposing factors that result in the emergence of GO namely genetic factors, enviromental, and hormonal factors. Indeed, GO appears as an autoimmune process in the body. Hypersensitivity reactions that act as Type II (Antibody Mediated Toxicity/Cytotoxic Reaction) and Type V (Stimulatory Hypersensitivity). The reaction to the autoimmune process results in the organ specific target reacting (organ specific autoimmune reaction). This process causes some specific changes, namely the emergence of inflammation and adipogenesis process runs, then leads to histopathologic changes that increase the volume of extraocular muscles (hypertrophy) and subsequent fibrosis resulting in tissue retraction of orbital tissue. IN the inflammatory process, T-cells secrete various inflammatory cytokines as TNF-α, IL-Iβ and leukoregulin which will activate the inflammatory pathway thriugh transcription of the NF-Kβ inflammatory factor in the nucleus. The orbital process of adipogenesis is influenced by the role of antibody anti thyrotropin receptors in the orbital tissues and also induced by the Peroxisome proliferator activated receptor gamma (PPAR-γ) by T-cells to activate the formation of fibroblasts, producing GAG including hyaluronic acid and proliferation, differentiation and accumulation of fat in orbital tissues. The histopathological changes that occur in GO that cause increased volumes of extraocular muscle (hypertrophy) are associated with increased production of hyaluronic acid which is a class of glycosaminoglycans (GAG) and has a hydrophilic property which has the ability to bind large amounts of water to its hydroxyl group secreted by fibroblast orbital network. The nature of these hyaluronic acids causes interstitialedema and the influence of inflammatory cell cells to cause swelling of various tissues in the orbit and extraocular muscle dysfunction in GO. The increased volume of connective tissue and the occurrence of impaired movement of the extraocular muscle (retraction) muscle results from the stimulation of fibroblast to induce clinical manifestations of orbitopathy. Increased volumes covering a wide range of orbital tissues, causing secondary elevations of intraorbital pressure, can lead to more retention than orbital tissue. At a further stage, the muscle cells becomes hypertrophy accompanied by lymphocyte infiltration and may eventually become artrophy or fibrotic.

Item Type: Book Section
Uncontrolled Keywords: Grave's ophthalmopathy, mechanism, thyroid, orbitopathy
Subjects: R Medicine > R Medicine (General)
R Medicine > RE Ophthalmology
Divisions: 01. Fakultas Kedokteran > Ilmu Penyakit Mata
Hendrian Dwikoloso SoebagjoNIDN8860900016
Depositing User: hanif kurniawan
Date Deposited: 18 Nov 2019 01:15
Last Modified: 12 Mar 2020 06:38
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