A 70-year-old Asian female with good functional capacity and independence in activities of daily living presented in 2012 with frontal headache of sudden onset, characterized as non-radiating, intermittent, with a pain scale of 10/10 and aggravated by movement and sneezing. The pain was temporarily relieved by paracetamol and other non-steroidal anti-inflammatory drugs. There were no associated symptoms of blurring of vision, diplopia, visual field cuts, anosmia, change in shoe size, galactorrhea, nausea and vomiting. Upon consult, cranial magnetic resonance imaging (MRI) showed an enhancing suprasellar mass measuring 1.3 cm x 1.3 cm x 1.4 cm indenting the optic chiasm, consistent with pituitary macroadenoma (Figures 1A and B). Further biochemical evaluation showed decreased LH and a normal baseline perimetry studies (Table 1).
Her other comorbidities were hypertension for more than 10 years, type 2 diabetes mellitus for 10 years and osteoporosis diagnosed one year ago. She had undergone right mastectomy for ductal carcinoma in situ 18 years ago, with no subsequent radiation or chemotherapy. Her menstrual history was unremarkable. She was nulligravid despite normal fertility work up and clomiphene intake for almost 3 years. She had also undergone cataract surgery and laparoscopic cholecystectomy. Her medications were sitagliptin, metformin, amlodipine, losartan, tamoxifen and ibandronic acid. She had no history of steroid use.
The clinical impression in 2012 was pituitary macroadenoma. The patient underwent transsphenoidal surgery with an unremarkable post-operative course. Post-operative cranial MRI showed interval resolution of the previously noted pituitary mass, with normal appearance of the pituitary gland including the optic chiasm and pituitary stalk (Figures 1C and 1D). Postoperative pituitary hormones showed normal results (Table 1).
The histologic features were consistent with chronic granulomatous inflammation with focal necrosis instead of a pituitary adenoma (Figure 2). Acid-fast bacilli and silver sethenamine stains showed negative results. Upon consult with another institution abroad, the diagnosis was non-caseating granulomatous inflammation involving the pituitary gland, with primary considerations of tuberculosis, giant cell granuloma (idiopathic granulomatous hypophysitis) or sarcoidosis. Mycobacterium tuberculosis PCR/nucleic acid amplification were also negative. There was no treatment rendered during that time. She was advised to have annual MRI for monitoring but the patient was lost to follow-up.
Interval history was unremarkable until five years after the surgery. The patient began to experience intermittent, non-radiating headache, with a pain scale of 3 to 10/10, temporarily relieved by paracetamol and tramadol. The persistence of her symptoms prompted consult with a Neurologist. Cranial MRI showed a 1.2 cm x 1.3 cm x 1.5 cm enhancing left sellar nodule (Figure 3). No visual field defects were noted on perimetry. Hormonal tests showed central hypothyroidism and hypogonadism (Table 2).
Surgical intervention was not advised at that time due to the high probability of recurrence and eventual impairment of pituitary function. As several case reports have shown that granulomatous hypophysitis may respond to steroid therapy, the patient was started on prednisone at 30 mg per day. Resolution of symptoms were noted after initiation of treatment. Prednisone was eventually tapered by 5 mg per day every 2 weeks. After attaining a dose of 5 mg per day for two weeks, it was then given at 3 times a week, twice a week, once a week, and then discontinued, with an interval of 2 weeks each. After 3 months of steroid therapy, cranial MRI showed complete resolution of the sellar mass (Figures 4A and 4B). During the course of treatment, the patient was clinically evaluated for the possible side effects of the steroid therapy and symptomatic hypothyroidism. Aside from the weight gain which completely resolved after treatment, there were no other adverse effects noted, particularly hypotension, uncontrolled hypertension, hypoglycemia, uncontrolled hyperglycemia, headache, body weakness, constipation and electrolyte imbalance. Upon reevaluation approximately 6 months post-treatment, cranial MRI showed no enhancing lesion in the pituitary gland (Figures 4C and 4D) and normal thyroid function (Table 2).
The patient remained asymptomatic during periodic monitoring. Biochemical tests done at one and a half years post-treatment showed complete resolution of central hypothyroidism (Table 2). The gonadotrophic hormones also showed improvement as compared to pretreatment results. Cranial MRI still showed absence of the pituitary mass.