Pituitary apoplexy in T3 thyrotoxicosis

Abstract

A 58-year-old male was brought to our emergency department because of acute onset of visual disturbances and headache. His past medical history revealed no specific illness. He was a nonsmoker. On history taking, we learned that the patient had experienced weight loss with decreased sexual activity for several months. On physical examination, beard and axillary hair were decreased. The thyroid gland was mildly enlarged on palpation. Examination of vital signs revealed a blood pressure of 120/60 mmHg, heart rate of 80/min, respiration rate of 18 breaths/min, and body temperature of 36.5 C. Radiologic examinations with brain computed tomography (CT) showed a mass in the pituitary gland. Laboratory tests revealed as follows: a serum sodium of 134 (135–150) mmol/L, serum glucose of 6.6 mmol/L, FSH of 0.9 (1.4–18.1) IU/L, LH of \0.07 (1.5–9.3) IU/L, testosterone of\0.01 (0.09–0.37) nmol/L, prolactin of 456.5 (78.3–691.3) pmol/L, IGF-1 of 9.0 (9.3–38.0) nmol/L, free T4 of 19.10 (11.5–22.7) pmol/L, TSH of \0.01 (0.55–4.78) mIU/L, and ACTH of 5.87 pmol/L. The random cortisol level was not measured before hydrocortisone was administered. Sellar magnetic resonance imaging (MRI) showed a 27 9 35 9 24 mm pituitary mass that was bulging into suprasellar area and contained a fluid–fluid level (Fig. 1a). Pituitary macroadenoma with hemorrhage was highly suspected. Standard ophthalmologic examination showed bilateral hemianopsia. Therefore, a high dose of hydrocortisone was administered intravenously immediately. However, neurosurgery was performed on this patient because of persistence of the visual field defect despite steroid treatment. Endonasal transsphenoidal surgery for pituitary adenoma was performed. The final pathologic diagnosis was pituitary adenoma originating from a gonadotrope. On the other hand, a diffuse goiter was detected on palpation and the free T4 level was in the high range of normal as described earlier. Therefore, we measured the free T3 level and thyroid autoantibody. Results revealed a free T3 of 9.7 (3.1–6.8) pmol/L, anti-TPO antibody of 600 (*34) IU/mL, and anti-TSH receptor antibody of 33.82 (*1.75) IU/L. Thyroid scan with pertechnetate revealed a diffuse toxic goiter that was compatible with primary hyperthyroidism (Fig. 1b). Therefore, antithyroid drug was started with physiologic replacement of hydrocortisone. Pituitary apoplexy is a life-threatening clinical syndrome characterized by sudden onset of headache, and visual impairment caused by the rapid enlargement of the pituitary adenoma usually due to hemorrhage. Various predisposing factors of pituitary apoplexy, such as systemic hypertension, alteration of intracranial pressure gradients, head trauma, pituitary irradiation, pregnancy, cerebral angiography, anticoagulation, dynamic study of pituitary gland, hemodialysis, and surgeries including cardiac surgery, have been reported. Among these factors, hypertension was the most common predisposing factor. It is also well known that thyroid dysfunction results in changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm disturbances [1]. Therefore, theoretically, it is possible that primary thyroid dysfunction causes pituitary apoplexy in patients with pituitary adenoma. However, clinically, the association between pituitary apoplexy and thyroid dysfunction has been unclear, and only one case of pituitary apoplexy caused by primary K. A. Lee T. S. Park H. S. Baek H. Y. Jin (&) Division of Endocrinology and Metabolism, Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk National University Hospital, Chonbuk National University Medical School, Chonbuk National University, Geonji Road #20, Deokjin-gu, Jeonju 561-712, South Korea e-mail: mdjinhy@jbnu.ac.kr