Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 P56 | DOI: 10.1530/endoabs.35.P56

ECE2014 Poster Presentations Adrenal cortex (56 abstracts)

Takotsubo cardiomyopapthy and panhypopituitarism: case report

Ana Filipa Martins 1 , João Martin Martins 1, , Sónia do Vale 1, , Ana Raquel Gomes 1 & Rui Plácido 1

1Santa Maria’s Hospital, Lisbon, Portugal; 2Lisbon Medical School, Lisbon, Portugal.

Introduction: Takotsubo cardiomyopathy or stress-induced cardiomyopathy (SICM) is a rare condition. Even more rare cases associated with glucocorticoid deficiency have been described.

Case report: AAGM, a 74-year-old man was admitted to the inpatient Endocrine Department because of suspected panhypopituitarism. Six months before the diagnosis of SICM was established after an acute coronary syndrome episode with no lesions found in coronary angiography and after exclusion of variant angina. In the last year, fatigue, asthenia, adynamia, loss of muscular strength, decreased libido and loss of male hair pattern distribution were noted by the patient; however several hypertensive episodes were reported; these episodes had no triggering factor, had short duration (20–30 min) and spontaneous resolution. No concomitant headaches, visual impairment, palpitation, anxiety, pallor or sweating were noticed. Blood pressure was 100/60 mmHg on physical examination that also revealed yellowish skin color. Analytical evaluation diagnosed panhypopituitarism: TSH: 4.1 (Reference value (RV): 0.35–5.5 uU/ml); FT4: 0.5 (RV: 0.8–2 ng/dl); FSH: 2 (RV: 1.4–18.1 U/l); LH: 0.2 (RV: 1.5–9.3 U/l); TT: 14 (RV: 240–820 ng/dl); ACTH: 33 (RV: 0–46 pg/ml); cortisol: 2 (RV: 4.3–23 μg/dl); GH: 0.1 (RV<3 ng/ml); IGF-1: 32 (RV: 87–238 ng/ml). Combined pituitary testing confirmed this diagnosis. Pheochromocytoma/paragnaglioma was excluded by urinary metanephrines and normetanephrines measurement. Sellar CT scan was negative for any lesion.

Discussion and conclusion: Although SICM is a rare condition, toxicity of increased catecholamines to myocardium is well established. Few reports in the literature associate panhypopituitarism to SICM. More specifically, adrenal failure may be the link between these two identities, since glucocorticoids seem to protect myocardium against toxic catecholamine surge by maintaining membrane calcium transport function in the cardiac sarcoplasmic reticulum and maintaining phosphorylase activity and glyconeogenolysis in animal models, and therefore affecting myocardial contractility. It is tempting to speculate that panhpopituitarism may lead to compensatory hyperactivity of the sympathetic nervous system.

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