[A case of Leber's hereditary optic neuropathy in a female patient with the recrudescence of hyperthyroidism].
BACKGROUND
Thyroid hormone increases oxygen consumption and regulates mitochondrial biogenesis. On the other hand, in Leber's hereditary optic neuropathy(LHON), retinal ganglion cells are exposed to the oxidative stress generated during the process of adenosine 5'-triphosphate (ATP) synthesis, eventually leading to a loss of vision. Although there is a possibility that the thyroid hormone may have a role in the development or the course of LHON, no case has been reported indicating a relation between them. We report a female case with LHON who also presented exacerbation of hyperthyroidism during the course of the disease.


METHODS
The patient was a thirty-nine-year-old woman who complained of bilateral loss of vision. Her corrected visual acuity was 0.2 in the right eye, and 0.1 in the left. Fundus examination showed characteristic findings of LHON in both eyes. The blood free thyroxin(FT4) level at that time was abnormally high. The diagnosis of LHON was confirmed by the presence of mitochondrial DNA mutation at the nucleotide position 11778. Her visual acuity improved after one month of FT4 normalization. A year later, her corrected visual acuity recovered to 0.9 in the right eye and 1.0 in the left.


CONCLUSIONS
Hyperthyroidism may be a trigger in the development of LHON.
Department of Ophthalmology, Kanagawa Children's Medical Center, Minami-ku, Yokohama 232-8555, Japan.
Yuri
Y
Kobayashi
Yoko
Y
Endo
Norihiko
N
Ito
Yasuhito
Y
Iijima
Nobuhisa
N
Mizuki
D000328:Adult; D005260:Female; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications*; D029242:Optic Atrophy, Hereditary, Leber / Q000503:physiopathology*; D012008:Recurrence