A 58-year-old man initially had a three-month history of persistent severe headache, lethargy and decline in sexual function with no visual and neurological deficit. There were no drenching night sweats, unexplained weight loss, fever, abdominal discomfort, swelling on the neck, axilla or groin, arthralgia and joint swelling, myalgia or myositis, shortness of breath or cough. His past medical history was unremarkable with no history of autoimmune disorders or endocrinopathy. The baseline early morning serum cortisol level was low (<22 nmol/L) (N: 68-469) with a normal serum adrenocortical hormone (ACTH) level of 5.0 pg/mL (N: 0-46.0). Despite the subnormal serum luteinizing hormone (LH) 0.9 IU/L (N: 2.0-12.0) and the follicle stimulating hormone (FSH) of 1.9 IU/L (N: 1.5-14.0) at the lower limit of normal, the corresponding serum testosterone level of 1.71 nmol/L (N: 9.9-52.4) was also low. In addition, the low level of serum TSH (0.86 uIU/L) (N: 032-5.0) response was inappropriate to the low serum free thyroxine (T4) level of 9.26 pmol/L (N: 9.10-23.80). There was also a low growth hormone (GH) level of <0.15 mIU/L (N: 0.16-16.0) with normal prolactin level of 2.04 ug/L (N: 1.61-18.77) at presentation. Formal perimetry showed no visual field deficit. There was no diabetes insipidus. Anti-thyroid peroxidase (TPO) antibodies level was not raised at 20.4 IU/mL (N: 0-35). The full blood picture did not show any histiocytes. Chest X-ray also showed no mediastinal enlargement, pulmonary infiltrates or hilar lymphadenopathy in both the lung fields. However, serum angiotensin-converting enzyme was not sent as there was no suggestion of sarcoidosis from our clinical assessment. Moreover, this assay was not available in our institution, and the patient could not afford the additional cost of sending to another laboratory with the facilities.
Initial magnetic resonance imaging (MRI) demonstrated a 20 mm by 14 mm by 10 mm non-homogenous mass occupying the pituitary fossa. This enlarged pituitary mass (white arrow in A) is associated with suprasellar extension (Figure 1). There is a T1 hyperintense rim around the wall of the mass, with some more amorphous hyperintensities at a dependent location within the lesion core. These T1 hyperintensities could represent either methemoglobin or proteinaceous content. Polypoidal T1 hypointensity within the sphenoid sinus anteriorly (white arrowhead in A), which enhanced post-gadolinium (not shown), is attributed to reactive inflammation. No appreciable enhancement of this mass was detected, nor was there evidence for a thickened pituitary infundibulum or hypothalamus. This initial MRI features of the enlarged pituitary, no thickening of pituitary infundibulum or hypothalamus, the negative clinical screening test for autoantibodies, sarcoidosis, tuberculosis, lymphoproliferative disorders and other granulomatous lesions suggested a macroadenoma.
Correction of the hormonal deficit was the priority as our patient did not have compression of the optic nerve leading to visual field deficit. A physiological dose of hydrocortisone (10 mg am and 5 mg at noon) and oral levothyroxine of 75 mcg daily were commenced. Intramuscular testosterone 250 mg every three weeks was also initiated. His symptoms improved with the hormonal replacement therapy, which correlated with the improvement in his repeated hormonal profile. After the hormonal treatments for more than six months, the free T4 level improved to 16.72 pmol/L with only a minimal decline in the serum TSH level (0.27 uIU/L) and an improvement in serum testosterone of 49.8 nmol/L. His early morning serum cortisol level remained at <0.22 nmol/L. During this interval period, he denied any symptoms, such as syncope and severe headache, nor there was a new hormonal deficit to suggest pituitary apoplexy.
An MRI of the pituitary was repeated seven months following clinical improvement with hormone replacement therapy. Despite the absence of visual field deficit, reassessment of the size of pituitary mass is important for the determination of the subsequent treatment course. This follow-up MRI showed a drastic regression of the pituitary mass (Figure 2). While the T1 hyperintense "bright spot" of the posterior pituitary is appreciated (white arrowhead in A), much of the anterior pituitary appears to be flattened against the seller floor (white arrow in A). The optic chiasm prolapsed directly and inferiorly into the sella from its normal suprasellar location (black arrow in B), possibly reflecting traction due to post-inflammatory fibrotic process. Predominantly cerebrospinal fluid-filled pituitary fossa and the resolution of the inflammatory changes within the sphenoid sinus is also noted. A third MRI six months later revealed similar features of an empty sella. Formal perimetry assessments on both follow-up assessments did not show any visual field deficit.