Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 41 EP253 | DOI: 10.1530/endoabs.41.EP253

ECE2016 Eposter Presentations Clinical case reports - Pituitary/Adrenal (81 abstracts)

Adrenal insufficiency precipitated by Graves’ hyperthyroidism in a patient on megestrol acetate treatment

Carolina García-Figueras Mateos , Manuel Cayón Blanco & Alberto Terrón Pernía


Hospital SAS Jerez de la Frontera, Jerez de la Frontera, Spain.


Introduction: Megestrol acetate (MA) is commonly used to promote weight gain in patients with HIV infection. Adrenal insufficiency (AI) has been reported as an adverse effect of MA but this association is not frequently recognized in clinical practice and only few cases develop symptoms of AI. We describe a case of symptomatic AI precipitated by Graves’ hyperthyroidism in a HIV patient on long-term MA treatment.

Case report: A 44-year-old man with HIV-infection, followed in Infectious Diseases Unit since 1999, was admitted at hospital by weight loss, tremor and tachycardia. Thyroid function study revealed autoimmune hyperthyroidism (TSH: 0.01 μUI/ml; FT4: 4.88 ng/dl and positive TSH receptor antibody). Therapy with methimazole was started. He was taking 240 mg of MA daily irregularly for more than 11 years and discontinued MA for long time periods, but he never developed symptoms of AI. One month after discharge, he developed diarrhoea, abdominal pain, hypotension and asthenia. Laboratory analysis found hyponatremia and hyperkalemia and thyroid function still remained uncontrolled (elevated FT4 and undetectable TSH). Serum cortisol was 1.1 μg/dl and after cosyntropin stimulation, were 7.6 and 10.7 μg/dl at 30′ and 60′, respectively. The adrenocorticotropic hormone level was <5 pg/ml (normal, 5–50 pg/ml) and adrenal antibodies were negative. MA was discontinued and steroid replacement was initiated. The symptoms disappeared and the patient improved progressively. During follow-up, corticoids dose was progressively decreased to discontinuation, and radioactive iodine was prescribed to control hyperthyroidism. One year later, cortisol and ACTH levels were normal without need for corticoids.

Conclusions: To the best of our knowledge, it has not been reported that Graves’ hyperthyroidism causes a symptomatic AI in patients with unrecognized or subclinical adrenocortical disease associated with MA treatment. Clinicians should be alert to the possibility of development of AI in patients taking MA, particularly if a stress situation is present.

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