Lower Dose Prednisone Prevents Radioiodine-Associated Exacerbation of Initially Mild or Absent Graves’ Orbitopathy: A Retrospective Cohort Study

Lai, Adriana; Sassi, Lorenza; Compri, Emanuele; Marino, Franca; Sivelli, Paolo; Piantanida, Eliana; Tanda, Maria Laura; Bartalena, Luigi

doi:10.1210/jc.2009-2130

Cited by 114 publications

(63 citation statements)

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“…As 1989, it has been proposed that a short course of systemic corticosteroid treatment may prevent RAI-induced exacerbation of GO. Steroid prophylaxis has been carried out using very low doses of prednisone (0.2 mg/kg body weight), given 1 day after RAI therapy, and gradually tapered down and withdrawn after 6 weeks, which has been shown to be effective in a study in Italy (42) but not in a recent study on Japanese patients (43). Alternatively, methylprednisolone can be administered intravenously at the dose of 500 mg weekly for 2 weeks followed by another two weekly infusions of 250 mg (cumulative dose of 1.5 g) (40).…”

Section: Current Guidelines For Treatment Of Thyroid Dysfunction In Pmentioning

confidence: 99%

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THERAPY OF ENDOCRINE DISEASE: Endocrine dilemma: management of Graves’ orbitopathy

Campi

Vannucchi

Salvi

2016

European Journal of Endocrinology

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Management of Graves' orbitopathy (GO) must be based on the correct assessment of activity and severity of the disease. Activity is usually assessed with the Clinical Activity Score, whereas severity is classified according to a European Group On Graves' Orbitopathy (EUGOGO) consensus statement as mild, moderate-to-severe, and sight-threatening. Myopathic and chronic congestive forms are uncommon clinical presentations of GO. Restoration and maintenance of stable euthyroidism are recommended in the presence of GO. In moderate-to-severe disease, steroids have been widely employed and have shown to possess an anti-inflammatory activity, but about 20 -30% of patients are not responsive and present recurrence. Some novel immunosuppressors have already been employed in clinical studies and have shown interesting results, although the lack of randomized and controlled trials suggests caution for their use in clinical practice. Potential targets for therapy in GO are the thyroid-stimulating hormone and the insulin-like growth factor 1 receptor on the fibroblasts, inflammatory cytokines, B and T cells, and the PIK3/mTORC1 signaling cascades for adipogenesis. A recent open study has shown that tocilizumab, an anti-sIL-6R antibody, inactivates GO. Consistent reports on the efficacy of rituximab have recently been challenged by randomized controlled trials. As the main goal of treatment is the well-being of the patient, the therapeutic strategy should be addressed to better suit the patient needs, more than improving one or more biological parameters. The increasing availability of new therapies will expand the therapeutic options for GO patients and allow the clinician to really personalize the treatment to better suit the patients' personal needs.

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Section: Current Guidelines For Treatment Of Thyroid Dysfunction In Pmentioning

confidence: 99%

“…Several randomized clinical trials found a De novo occurrence or progression of GO after RAI treatment with or without steroid prophylaxis (39,40,41,42,43) Postablation hypothyroidism induces progression of GO (44,45) Stabilization of GO after total thyroid ablation (thyroidectomy followed by RAI treatment)…”

Section: Glucocorticoidsmentioning

confidence: 99%

THERAPY OF ENDOCRINE DISEASE: Endocrine dilemma: management of Graves’ orbitopathy

Campi

Vannucchi

Salvi

2016

European Journal of Endocrinology

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“…This detrimental effect is in most cases prevented by concomitant short-term treatment with low doses of oral glucococorticoids (steroid prophylaxis) [28,39,40]. In view of the above considerations and in the absence of well-designed (and extremely difficult to perform) RCTs, selection of the optimal thyroid treatment (antithyroid drugs, radioiodine, thyroidectomy, thyroidectomy followed by radioiodine treatment) in patients with GO is still a matter of argument and more an expert opinion than an evidence-based choice [36].…”

Section: Preventionmentioning

confidence: 99%

Graves' Orbitopathy: Imperfect Treatments for a Rare Disease

Bartalena

2013

Eur Thyroid J

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Graves' orbitopathy (GO) is the most frequent and invalidating extrathyroidal expression of Graves' disease. Its incidence and prevalence are, however, low. About three quarters of Graves' patients have no GO at diagnosis, and moderate-to-severe and severe forms represent no more that 5-6% of cases. Progression to severe forms occurs rarely, but it may be caused by risk factors, the most important being smoking and poor control of thyroid dysfunction. Lot of progress has been recently achieved in the understanding of GO pathogenesis, while the disease remains a therapeutic challenge and dilemma. Common treatments for moderate-to-severe and active forms of GO (glucocorticoids and orbital radiotherapy) frequently provide incomplete responses and may be followed by relapse or progression of GO. After the disease has been inactivated by medical treatment, many patients need rehabilitative surgery for residual manifestations (orbital decompression for exophthalmos, squint surgery for extraocular muscle dysfunction, eyelid surgery for eyelid malposition). Novel pharmacological treatments are on the horizon and might target pathogenetic mechanisms of the disease better than glucocorticoids. Clinical evidence concerning their efficacy and safety is presently lacking.

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“…Un metaná-lisis 29 , que incluye pacientes adolescentes, mostró que el radioyodo tiene un efecto adverso sobre la OG en 15-20% de los casos, no obstante este riesgo puede disminuirse con el uso de glucocorticoides profilácticos 30 . El mecanismo por el cual esto ocurre es probablemente una exacerbación de la respuesta autoinmune, debido a la liberación brusca de antígenos, secundaria a la acción citolítica del radioyodo en las células foliculares del tiroides.…”

Section: Radioyodounclassified

Orbitopatía de Graves en pediatría

2015

Rev. méd. Chile

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Graves' orbitopathy in pediatrics Graves' orbitopathy (GO) is rare in pediatric patients, however is the most common extrathyroid manifestation of Graves' disease (GD) camendoza@uc.cl caromendozafuentes@gmail.com E l hipertiroidismo autoinmune es la causa más común de tirotoxicosis en niños y adolescentes. La incidencia reportada en Europa es de 0,8/100.000 niños/año, con una relación por sexo femenino: masculino de 3-5:1 1 . La Orbitopatía de Graves (OG) es la manifestación extratiroidea más frecuente de la enfermedad de Graves (EG) y se presenta en 30-67% de los pacientes. Es una patología poco frecuente en pediatría y el riesgo de desarrollarla aumenta con la edad 2 . Al comparar por grupos etarios se observa una frecuencia de 31,8% en pacientes menores de 11 años versus 68,2% en adolescentes (11-18 años) 3 .La OG es una enfermedad inflamatoria autoinmune. Se asocia a hipertiroidismo autoinmune en 80-90% de los casos, 3-4% de los casos se presenta en pacientes con tiroiditis de Hashimoto y 5-10% en pacientes eutiroideos 4 . El 80% de los casos de OG se presenta dentro de los primeros 18 meses desde que se diagnostica la enfermedad tiroidea, sin embargo, se puede desarrollar antes o después de la aparición del hipertiroidismo 5 . FisiopatologíaLa patogenia de la OG está determinada por una infiltración perivascular difusa de linfocitos T CD4+, CD8+, linfocitos B, células plasmáticas y macrófagos; estas células liberan citoquinas inflamatorias y prostaglandinas las que inducen remodelación del tejido conectivo, lo que asociado a una infiltración de glicosaminoglicanos producen un aumento de volumen de los músculos extraoculares (MExO) y del tejido adiposo orbitario 6-7 . Fibroblasto orbitario (FO): la célula dianaActualmente se reconoce a los FO como las células diana en la OG 7-8 . Estudios sugieren que los linfocitos T CD8+ actuarían reconociendo a los FO y estimulando su proliferación vía complejo mayor de histocompatibilidad clase II. A diferencia de las células de los MExO, los FO expresan antígeno leucocitario humano (HLA-DR), los que actuarían como células presentadoras de antígenos 9 .

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Lower Dose Prednisone Prevents Radioiodine-Associated Exacerbation of Initially Mild or Absent Graves’ Orbitopathy: A Retrospective Cohort Study

Abstract: Lower doses of oral prednisone (about 0.2 mg/kg bw) are as effective as previously reported doses (0.3-0.5 mg/kg bw). A shorter treatment period (6 wk) is probably sufficient. The increase in bw is less using lower doses of prednisone.

Cited by 114 publications

References 18 publications

THERAPY OF ENDOCRINE DISEASE: Endocrine dilemma: management of Graves’ orbitopathy

THERAPY OF ENDOCRINE DISEASE: Endocrine dilemma: management of Graves’ orbitopathy

Graves' Orbitopathy: Imperfect Treatments for a Rare Disease

Orbitopatía de Graves en pediatría

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