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Visual Field Defects and Pituitary Enlargement in Primary Hypothyroidism^*

KUNIHIRO YAMAMOTO, KOSHI SAITO, TAKAJI TAKAI, MAKOTO NAITO and SHO YOSHIDA

Department of Endocrinology and Metabolism, and Department of Ophthalmology (M.N.), Jichi Medical School Yakushiji 3311–1, Minamikawachi, Tochigi 329–04, Japan

Address requests for reprints to: Dr. Kunihiro Yamamoto, Department of Endocrinology and Metabolism, Jichi Medical School, Yakush-iji 3311–1, Minamikawachi, Tochigi 329–04, Japan.

In 14 patients with overt primary hypothyroidism, we examined visual fields by Goldmann's isopter perimetry. An unexpectedly high incidence (10 patients, 71.4%) of visual field defects was found. Two patients complained of visual failure, whereas 12 had no subjective symptoms. The extent of visual field change varied over a wide range, from early chiasmal compression to apparent bitemporal hemianopsia. The abnormality was characteristically restriction in the central visual field; peripheral vision was less often affected. The sella turcica was significantly enlarged in these patients as compared to controls. The volume of the sella turcica correlated significantly with both basal serum TSH and total pituitary reserve of TSH (r = 0.82, P < 0.001). There was no correlation between the extent of visual field change and the volume of the sella turcica or pituitary TSH reserve. Of 10 patients with visual field defects, 8 improved during 1–4 months of T₄ replacement. In 2 patients, however, the visual field defect deteriorated during replacement. The deterioration occured when serum TSH levels had decreased to about 50% and 20% of pretreatment values, respectively. The peak serum TSH after TRH stimulation was higher at the time of deterioration than before treatment. Visual fields became normal during treatment with an increased dose of T₄ (200 µg/day), when serum TSH was suppressed to an undetectable level. The paradoxical course of visual failure during T₄ replacement may be due to an imbalance between TSH synthesis in the pituitary and TSH release which may induce an increase in pituitary size. The data suggest that visual field defects and their deterioration are due to pituitary hyperplasia and are reversible with T₄ replacement. In order to rule out a pituitary tumor, hypothyroid patients with visual failure should be followed during T₄ replacement therapy.

^* Presented in part at the Second Asia and Oceania Thyroid Association Meeting, Tokyo, Japan, August 19–22, 1982.

Present address: Department of Ophthalmology, School of Medicine, Yogi 1–3–1, Naha, Okinawa 902, Japan.

Received September 9, 1982.

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