Abstract

46 year old patient was admitted as an emergency with vomiting, hypotension and serum cortisol of 0,940 μg/dl (26 nmol/l) indicative of adrenal failure. Despite previous history of panhypopituitarism he was found to be hyperthyroid [free T4 6.32 ng/dl (ref. range: 0.93–1.7), free T3 22.21 pg/ml (ref. range: 1.8–4.6)]. He was fit and well till the age of 45. Eight months prior to this hospitalisation he presented with diabetes insipidus and was found to have a large cystic tumour in the area of the pituitary gland. Surgery was only partially successful and histologically the tumour was diagnosed as craniopharyngioma. Endocrine assessment revealed deficiency in ACTH-cortisol, growth hormone, and gonadotropin, as well as low-normal free T4. On the day of his emergency admission he looked ill and dehydrated, though was fully conscious and cooperative. Heart rate was 120 beats/min (sinus rhythm), blood pressure 85/40 mm Hg. There were no obvious features of infection, but there was marked tremor and thyroid bruit. He received treatment with intravenous fluids and hydrocortisone. L-thyroxine was stopped. Administration of large dose of methimazole (60 mg/day) resulted in gradual decrease in free T4 and free T3 (to 1.76 ng/ml, and 5.92 pg/ml, respectively) over a 15-day period. The patient was found to have increased titre of antithyroperoxidase (anti-TPO) and anti-TSH receptor (anti-TSHR) antibodies [2300 IU/l (ref. range <40) and 3.6 IU/l (ref. range <1.0), respectively]. He was referred for radioactive iodine treatment. Iodine uptake scan performed prior to radioiodine administration confirmed uniformly increased iodine uptake consistent with Graves' disease.Our case illustrates coexistence of hypopituitarism and clinically significant autoimmune thyroid disease. The presence of hypopituitarism does not preclude the development of autoimmune thyrotoxicosis.

Highlights

  • Adrenal insufficiency of either a primary or secondary origin may culminate in a life-threatening adrenal crisis [1]

  • We present a case where a subject with known panhypopituitarism, including incipient secondary hypothyroidism, developed florid thyrotoxicosis that, in turn, contributed to an acute glucocorticoid deficiency

  • The most important factor is to recognise that such combination of two opposite conditions, i.e., thyrotoxicosis despite previous secondary hypothyroidism is possible

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Summary

Background

Adrenal insufficiency of either a primary or secondary origin may culminate in a life-threatening adrenal crisis [1]. Endocrine assessment completed after his discharge from neurosurgical department revealed deficiency in ACTH-cortisol and gonadotropin axes, as well as low-normal free T4 (Table 1) He was found to have low IGF-I indicative of growth hormone deficiency. He was commenced on hydrocortisone (20 mg in the morning+10 mg at noon), oral desmopressin (0.2 mg tds), fortnightly intramuscular testosterone and L-thyroxine (25 μg od) His clinical condition remained stable for about five months, i.e., till about 4 weeks prior to the emergency hospitalisation. He was found to have increased titre of antithyroperoxidase (anti-TPO) and anti-TSH receptor (anti-TSHR) antibodies [2300 IU/l

Discussion
Conclusion
Zgliczyński W
Findings
Bouillon R
Walse A
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