Acute aortic dissection in a patient with untreated hypopituitarism
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LETTER TO THE EDITOR
Acute aortic dissection in a patient with untreated hypopituitarism Kyung Ae Lee • Hong Sun Baek • Tae Sun Park Heung Yong Jin
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Received: 29 March 2013 / Accepted: 15 April 2013 Ó Springer Science+Business Media New York 2013
To the Editor, A 53-year-old man was brought to our emergency department with a chief complaint of chest pain. The patient had a past history of drinking alcohol 60–120 g every other day and smoking a pack of cigarettes a day for 20 years. The patient had weakness, poor appetite, and decreased sexual activity over the several years. But the patient did not receive a health check-up for these symptoms. On arrival, vital signs were—blood pressure 100/60 mmHg, pulse rate 82/min, respiration rate 22/min, and body temperature 36.9 °C. On chest radiography, the patient had a cardiomegaly and an anterior mediastinal widening. The patient therefore received a transthoracic echocardiography and a chest computed tomography (CT). An echocardiography showed a large amount of pericardial effusion with hemodynamic significance but preserved systolic function. Moreover, the patient also had an abnormal structure that is indicative of the suspected intimal flap. A CT scan demonstrated acute aortic dissection (AAD) of Stanford type A (Fig. 1). The patient was admitted at an intensive care unit and underwent pericardiocentesis. Vital signs were stable and follow-up CT revealed stable aortic dissection. Therefore, medical treatment was maintained without emergent vascular surgery. But the patient had a persistent presence of low blood pressure and hyponatremia. Initial
K. A. Lee H. S. Baek T. S. Park H. Y. Jin (&) Division of Endocrinology and Metabolism, Department of Internal Medicine, Research Institute of Clinical Medicine of Chonbuk National University-Chonbuk National University Hospital, Geonji Road #20, Deokjin-gu, Jeonju 561–712, South Korea e-mail: [email protected] K. A. Lee e-mail: [email protected]
laboratory examinations showed serum electrolytes (Na–K–Cl) were 129(135–50)–4.3(3.5–5.5)–98(91–110) mmol/L, respectively. In addition, serum and urine osmolality were 264 mOsm/kg and 511 mOsm/kg, respectively. For the evaluation of euvolemic hypotonic hyponatremia, the patient was tested for thyroid function and serum cortisol levels. This showed results: free T4 7.39 (11.5– 22.7) pmol/L, TSH 0.64 (0.55–4.78) mIU/L, baseline serum cortisol 41.4 ([193) nmol/L, and baseline ACTH 4.1 (2.2–19.8) pmol/L. Based on these findings, the patient was tentatively diagnosed with central hypothyroidism and secondary adrenocortical insufficiency. To confirm the diagnosis, we performed further hormone studies. This showed the results: serum prolactin 474.8 (175.7–660.8) pmol/L, IGF-1 \3.3(11.8–47.2) nmol/L, FSH 1.4 IU/L, LH 0.5 IU/L, and testosterone 0.2 (8.7–36.8) nmol/L. Cortisol responses to intravenous injection of synthetic ACTH (250 lg) were baseline cortisol 41.4 nmol/L, 30 min cortisol 309 nmol/L, and 60 min cortisol 375.2 ([500) nmol/L. The patient denied any visual symptoms
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