Graves’ disease (GD), also called Basedow’s disease, owe the names respectively to the Irish physician Robert James Graves, who described the disease in 1835, and to Karl Adolph von Basedow, who reported the same clinical picture in Germany in 1840. Indeed, it was the Englishman Caleb Hillier Parry to firstly report a case of hyperthyroidism and goiter in 1786, but his report was not published until 1825. Earlier, in 1802, the Italian physician Giuseppe Flajani, described a disease characterized by the coexistence of palpitations and exophthalmos. Graves’ disease is an autoimmune, organ-specific, disorder sustained by auto-antibodies stimulating the thyroid-stimulating hormone (TSH) receptor (R). It is believed that the interaction between susceptible genes and environmental/endogen factors triggers the development of the disease. As a consequence of TSH-R improper stimulation, hyperthyroidism and goiter are the main clinical manifestations of the disease, accompanied, in the 25% of cases, by Graves’ orbitopathy (GO). GD is primarily diagnosed by demonstrating the presence of thyrotoxicosis and the pathognomonic TSH-R antibodies (TSH-RAb). In this manuscript we will refer to the disease as Graves’ disease.

Analysis of Graves’ disease from the origins to the recent historical evolution

Grace Coco;Eliana Piantanida;Daniela Gallo
;
Lorenzo Mortara
2021-01-01

Abstract

Graves’ disease (GD), also called Basedow’s disease, owe the names respectively to the Irish physician Robert James Graves, who described the disease in 1835, and to Karl Adolph von Basedow, who reported the same clinical picture in Germany in 1840. Indeed, it was the Englishman Caleb Hillier Parry to firstly report a case of hyperthyroidism and goiter in 1786, but his report was not published until 1825. Earlier, in 1802, the Italian physician Giuseppe Flajani, described a disease characterized by the coexistence of palpitations and exophthalmos. Graves’ disease is an autoimmune, organ-specific, disorder sustained by auto-antibodies stimulating the thyroid-stimulating hormone (TSH) receptor (R). It is believed that the interaction between susceptible genes and environmental/endogen factors triggers the development of the disease. As a consequence of TSH-R improper stimulation, hyperthyroidism and goiter are the main clinical manifestations of the disease, accompanied, in the 25% of cases, by Graves’ orbitopathy (GO). GD is primarily diagnosed by demonstrating the presence of thyrotoxicosis and the pathognomonic TSH-R antibodies (TSH-RAb). In this manuscript we will refer to the disease as Graves’ disease.
2021
2022
https://www.mattioli1885journals.com/index.php/MedHistor/article/view/12121
thyroid, Graves’ disease, autoimmunity, hyperthyroidism, ophthalmopathy, James Graves, Basedow disease
Coco, Grace; Gatti, Lucrezia; Piantanida, ELIANA ANGELA ROSA; Gallo, Daniela; Mortara, Lorenzo
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11383/2129714
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