A 44 year old woman presented in November 2000 with a two week history of headaches, vomiting and blurred vision. Past history consisted of type 2 diabetes and migraine. Initial investigation revealed hyponatraemia (sodium 114 mmol/l) and deranged liver biochemistry. ANA, anti dsDNA, cANCA, pANCA, anti Ro, La, RNP, Scl-70, Jo-1, smooth muscle and mitochondrial antibodies were negative. MRI revealed a 13x18x15mm pituitary mass elevating the optic chaism, without evidence of recent haemorrhage. Endocrine assessment indicated secondary hypothyroidism, growth hormone deficiency and variable gonadotrophin deficiency, but normal prolactin and cortisol reserve. In January 2001, prior to transnasal surgery, repeat MRI showed complete regression of the pituitary lesion. Despite no temporal relationship to pregnancy, a presumptive diagnosis of lymphocytic hypophysitis was made. Pituitary, adrenal, and ovarian antibodies were negative.
Subsequently she continued to require thyroxine replacement, but otherwise remained well with no significant headaches or visual disturbance. After failing to attend two outpatient visits, she was seen in June 2002, and was asymptomatic at that time. Surprisingly, further imaging in August 2002 showed the reappearance of a pituitary mass in contact with, but not compressing, the optic chiasm. The most likely diagnosis was then felt to be a pituitary tumour that previously underwent infarction and subsequently showed rapid re-growth. Surgery was considered, but a decision was made to re-scan four months later. Amazingly, on MRI scanning in January 2003 the pituitary mass had again completely involuted. Chest X-ray and serum ACE levels were normal, although ESR and CRP were marginally raised at 16 mm/hour (1-15) and 10 mg/l (0-5) respectively. MRI in July 2003 is unchanged from January 2003.
To our knowledge, there has been no reported case of a pituitary tumour that has grown and involuted spontaneously on two occasions.