[Hypothyreoidism with thyroglobulin antibodies during corticoid replacement in a 54-year-old man with isolated ACTH deficiency]
Hypothyroidism with thyroglobulin antibodies during corticoid replacement in a 54-year-old man with isolated ACTH deficiency. HISTORY AND ADMISSION FINDINGS: A 54-year-old previously healthy man was admitted because of fatigue, tiredness, diarrhoea and weight loss for the last 3 years. Physical examination revealed dry but normally pigmented skin and markedly reduced Achilles reflex bilaterally. INVESTIGATIONS: Erythrocyte sedimentation rate was slightly elevated at 32 mm/h, C-reactive protein was normal. Both haemoglobin (12.4 mg/dl) and the corpuscular indices were normal, as were serum electrolytes, and sodium bicarbonate. But basal levels of thyroid stimulating hormone (TSH, 8.5 mU/ml) was markedly elevated, while free peripheral triiodothyronine (3.2pg/ml) was normal and free thyroxine (fT4) at 0.7 ng/d was slightly reduced. Thyroid ultrasound was normal. Test for antinuclear antibodies was slightly positive, but double-strand DNA was not demonstrated. Antithyroglobulin antibodies were slightly raised to 1012 IU/ml (normal <350). The basic level of ACTH was repeatedly below detection, as were plasma cortisol and cortisol excretion in 24-hour urine. Nuclear magnetic imaging was normal. Failure to stimulate corticol synthesis in the short ACTH test and by CRH indicated an isolated ACTH deficiency at the level of the anterior pituitary, while other hypophyseal functions were unaffected. TREATMENT AND COURSE: The patient"s condition rapidly improved on replacement with hydrocortisone, 30 mg/d, and thyroxine, 100 mg/d. No thyroglobulin antibodies or antinuclear antibodies were demonstrable after 6 months. Thyroxine was discontinued after 15 months. Frequent monitoring of thyroid function over the next 2 years always indicated a euthyroid state. CONCLUSION: Subnormal concentration of peripheral thyroid hormone combined with elevated TSH levels can, in the presence of hypercorticolism, be due to reversible abnormal thyroid function.
Keuneke
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Medizinische Poliklinik (Direktor: Prof. Dr. Detlef Schlöndorff), Ludwig-Maximilian-Universität, München.
Schlöndorff
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