Advances in the Management of Thyroid Eye Disease
For patients with mild TED, supportive care including ocular surface management offers substantial benefit. Selenium supplementation has also been examined for the treatment of mild, active TED. Selenium is a trace mineral and an essential nutrient for selenocysteine synthesis, which has antioxidant properties. In one study, patients with mild TED were given selenium (100 μg twice daily) and followed up for 6 months. They had a significant improvement in the clinical activity score versus placebo, with no adverse effects reported. Selenium has been linked to increased risk of type II Diabetes but only in doses exceeding 400 mcg/d. It is important to discuss these data with patients before initiating selenium therapy.
During the active phase of TED, corneal exposure can be severe, resulting in excruciating pain and loss of vision. Severe exposure must be recognized early, and steps must be taken early to ensure proper ocular surface lubrication and prevent vision-threatening sequelae. Options include artificial tears, ointments, gels, and topical cyclosporine. In addition, the clinician may use punctual plugging or cauterization. Surgical procedures such as tarsorrhaphies may also be necessary in cases of severe or vision-threatening corneal exposure.
Management of moderate to severe active TED may require systemic anti-inflammatory medications to mitigate the risk of vision loss. TED patients with reduction of visual acuity, visual field deficits, color deficits, or afferent pupillary defects are treated promptly with systemic corticosteroids, and some require emergent orbital decompression surgery for compressive optic neuropathy. Systemic corticosteroids may be administered orally or intravenously. Intravenous administration, although potentially less convenient, appears more efficacious and better tolerated. In a study by Macchia et al, 25 patients with TED were treated with twice weekly infusions of 1 g of methylprednisolone for 6 weeks and were compared with a group of 26 patients treated with oral prednisone at a dose of 60 to 80 mg/d, progressively reduced every 2 weeks for a total duration of 4 to 6 months. Both groups achieved the same level of improvement in signs and symptoms of orbital inflammation, but the intravenous group reported no significant side effects, whereas the oral treatment group reported typical side effects associated with oral steroid therapy. Radiation therapy (RT) has also been used as a treatment for active TED. The role of RT for the treatment of active TED, however, is controversial. It remains a viable option for patients who cannot tolerate systemic corticosteroid therapy. With a dose of 20 Gy in 10 fractions, 1 group has reported 96% stabilization of TED with RT, with complete resolution of symptoms in 46% of patients. In this study, most patients received concomitant therapy with corticosteroids. Reports of the effectiveness of orbital radiation in TED are quite variable. Orbital irradiation may provide a small incremental improvement of TED manifestations but given the paucity of published clinical validity, lack of mechanistic or pathogenic role, and unclear clinical indications, it is difficult to make the case for widespread implementation.
Corticosteroids or observation are the mainstay of therapy in active TED. Corticosteroids are powerful general immunosuppressive agents with well-characterized but potentially severe adverse effects. Significant research elucidating the pathogenesis of TED will hopefully fuel the development of targeted therapies.
Traditional Therapies for Active TED
For patients with mild TED, supportive care including ocular surface management offers substantial benefit. Selenium supplementation has also been examined for the treatment of mild, active TED. Selenium is a trace mineral and an essential nutrient for selenocysteine synthesis, which has antioxidant properties. In one study, patients with mild TED were given selenium (100 μg twice daily) and followed up for 6 months. They had a significant improvement in the clinical activity score versus placebo, with no adverse effects reported. Selenium has been linked to increased risk of type II Diabetes but only in doses exceeding 400 mcg/d. It is important to discuss these data with patients before initiating selenium therapy.
During the active phase of TED, corneal exposure can be severe, resulting in excruciating pain and loss of vision. Severe exposure must be recognized early, and steps must be taken early to ensure proper ocular surface lubrication and prevent vision-threatening sequelae. Options include artificial tears, ointments, gels, and topical cyclosporine. In addition, the clinician may use punctual plugging or cauterization. Surgical procedures such as tarsorrhaphies may also be necessary in cases of severe or vision-threatening corneal exposure.
Management of moderate to severe active TED may require systemic anti-inflammatory medications to mitigate the risk of vision loss. TED patients with reduction of visual acuity, visual field deficits, color deficits, or afferent pupillary defects are treated promptly with systemic corticosteroids, and some require emergent orbital decompression surgery for compressive optic neuropathy. Systemic corticosteroids may be administered orally or intravenously. Intravenous administration, although potentially less convenient, appears more efficacious and better tolerated. In a study by Macchia et al, 25 patients with TED were treated with twice weekly infusions of 1 g of methylprednisolone for 6 weeks and were compared with a group of 26 patients treated with oral prednisone at a dose of 60 to 80 mg/d, progressively reduced every 2 weeks for a total duration of 4 to 6 months. Both groups achieved the same level of improvement in signs and symptoms of orbital inflammation, but the intravenous group reported no significant side effects, whereas the oral treatment group reported typical side effects associated with oral steroid therapy. Radiation therapy (RT) has also been used as a treatment for active TED. The role of RT for the treatment of active TED, however, is controversial. It remains a viable option for patients who cannot tolerate systemic corticosteroid therapy. With a dose of 20 Gy in 10 fractions, 1 group has reported 96% stabilization of TED with RT, with complete resolution of symptoms in 46% of patients. In this study, most patients received concomitant therapy with corticosteroids. Reports of the effectiveness of orbital radiation in TED are quite variable. Orbital irradiation may provide a small incremental improvement of TED manifestations but given the paucity of published clinical validity, lack of mechanistic or pathogenic role, and unclear clinical indications, it is difficult to make the case for widespread implementation.
Corticosteroids or observation are the mainstay of therapy in active TED. Corticosteroids are powerful general immunosuppressive agents with well-characterized but potentially severe adverse effects. Significant research elucidating the pathogenesis of TED will hopefully fuel the development of targeted therapies.
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