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Case Reports
. 2021 Mar 17:22:101075.
doi: 10.1016/j.ajoc.2021.101075. eCollection 2021 Jun.

Teprotumumab for the treatment of mild compressive optic neuropathy in thyroid eye disease: A report of two cases

Carolina A Chiou  1 , Edith R Reshef  1 , Suzanne K Freitag  1
Affiliations
Case Reports

Teprotumumab for the treatment of mild compressive optic neuropathy in thyroid eye disease: A report of two cases

Carolina A Chiou et al. Am J Ophthalmol Case Rep. .

Abstract

Purpose: To report two cases of thyroid eye disease (TED) associated compressive optic neuropathy (CON) that resolved after treatment with teprotumumab.

Observation: Two patients presented with active TED resulting in mild CON with the typical corresponding visual field (VF) defects. Both patients were initiated on intravenous (IV) corticosteroid therapy but despite treatment had persistent VF defects. Both patients were then treated with teprotumumab and demonstrated marked clinical improvement and complete resolution of TED-CON VF defects early in their infusion course.

Conclusions and importance: These cases suggest that teprotumumab can be a rapid and effective treatment for TED-CON, and raises the question of whether it may be superior to IV corticosteroid therapy.

Keywords: Compressive optic neuropathy; Graves' disease; Teprotumumab; Thyroid eye disease; Visual field defect.

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Figures

Fig. 1
Fig. 1
Coronal computed tomography of the orbits without contrast demonstrated enlarged extraocular muscles, left greater than right, with apical crowding.
Fig. 2
Fig. 2
A, HVF 30-2 OS on initial visit showed a Stage 1a small inferior paracentral hemifield defect with MD = −0.83 dB. B, HVF 30-2 OS after IV solumedrol demonstrated a Stage 1b large inferior paracentral hemifield defect with MD = −3.70 dB. C, HVF 30-2 OS after teprotumumab demonstrated a full field with MD = +0.40 dB. HVF, Humphrey visual field; OS, left eye; MD, mean deviation.
Fig. 3
Fig. 3
Coronal computed tomography of the orbits without contrast demonstrated enlarged extraocular muscles bilaterally with more severe apical crowding on the right.
Fig. 4
Fig. 4
A, HVF 30-2 OD on initial visit showed a Stage 2a pattern with advancement of the inferior altitudinal defect above the horizontal midline into the superior temporal field with MD = −3.61 dB. B, HVF 30-2 OD after IV solumedrol demonstrated a Stage 1b inferior paracentral hemifield defect with MD = −2.80 dB. C, HVF 30-2 OD showed a full field with MD = −0.86 dB. HVF, Humphrey visual field; OD, right eye; MD, mean deviation.
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References

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