Silent Pituitary Infarction After Coronary Artery Bypass Grafting Procedure: Case Report and Review of Literature

Dany H. Zayour, MD; Sami T. Azar, MD


Endocr Pract. 2006;12(1):59-62. 

In This Article

Case Report

A 73-year-old woman was referred to our endocrinology unit for the evaluation of a high level of creatine kinase (CK) (526 U/L; normal range, 10 to 195) in association with generalized fatigue and weakness of 2 months' duration.

Ten months before this presentation, the patient had been admitted to the hospital for the management of unstable angina. Her previous medical history had been negative, except for atrial fibrillation managed medically with propafenone. At that time, results of thyroid function tests were normal. Coronary angiography revealed the presence of triple-vessel disease, and the patient underwent a coronary artery bypass grafting procedure. Except for an episode of intraoperative hypotension, during which the systolic blood pressure reached 80 mm Hg and stayed at that level for about 30 minutes, the intraoperative and postoperative course was uneventful, with normal electrolytes and kidney function. The patient had no headaches, no neuro-ophthalmologic symptoms, no focal neurologic deficits, and no fever. Since then, the interval history revealed no medical problems.

When the patient presented to our endocrinology unit, she complained of diffuse weakness and generalized fatigue, with no localizing symptoms. She also complained of constipation. There was no muscle pain, tenderness, or focal weakness. She had been taking simvastatin (10 mg daily) for 2 years, and the CK level was stable at 260 U/L. The patient had no history of recent intra-muscular injections. Physical examination showed a mildly "puffy" patient with stable vital signs and symmetrically delayed relaxation of deep tendon reflexes. The blood pressure was normal, and no orthostatic hypotension was noted. The thyroid gland was nonpalpable. There was some loss of pubic and axillary hair, according to the patient. The rest of the findings on physical examination were unremarkable. The differential diagnosis included, among other possible conditions, statin-induced myopathy and hypothyroidism.

Laboratory studies showed a normal blood cell count in conjunction with a borderline microcytic anemia. Blood urea nitrogen, serum creatinine, and liver enzymes were normal. Serum electrolytes were as follows: sodium, 141 mEq/L; potassium, 4.1 mEq/L; chloride, 109 mEq/L; and carbon dioxide, 24 mEq/L. The elevated CK level was of muscle origin. Electromyography and nerve conduction studies showed normal findings.

Simvastatin therapy was discontinued, and the patient underwent a battery of endocrinologic tests ( Table 1 ). A very low free thyroxine level in the presence of an inappropriately normal thyroid-stimulating hormone (thyrotropin) value raised the possibility of central hypothyroidism. The serum follicle-stimulating hormone concentration was also low in this postmenopausal woman. A random growth hormone (GH) level was <0.16 ng/mL, in association with a very low insulin-like growth factor-I (IGF-I) level. An 8 AM cortisol level was 1.3 µg/dL. In view of the normal level of thyrotropin, low free thyroxine, and low follicle-stimulating hormone, IGF-I, and cortisol, the possibility of panhypopituitarism precipitated by the coronary artery bypass surgical procedure was entertained, and the patient underwent dynamic endocrine testing ( Table 2 ). Included in these studies was an adrenocorticotropic hormone (ACTH) stimulation test, in which the patient received cosyntropin [ACTH[1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24]], 250 µg intravenously. The serum cortisol was 6.6 µg/dL and 9.6 µg/dL at 30 and 60 minutes, respectively, indicative of adrenal insufficiency. Thyrotropin-releasing hormone and gonadotropin-releasing hormone stimulation tests after adequate priming showed a blunt response ( Table 2 ). Magnetic resonance imaging (MRI) of the pituitary fossa showed an empty sella turcica, with a rim of enhancing pituitary tissue. There was no sellar enlargement. Glucocorticoid replacement therapy was then initiated. Subsequently, thyroxine replacement therapy was added, which yielded considerable improvement in the patient's clinical and biochemical conditions.