Endocrine Abstracts

A 54-year-old female presented with one week of weakness, fatigue, headache, worsening constipation, and general malaise. Background history included long-standing type 1 diabetes (glutamic acid decarboxylase positive), on continuous subcutaneous insulin infusion, proliferative diabetic retinopathy, end-stage diabetic nephropathy on haemodialysis and subclinical hypothyroidism. Tertiary hyperparathyroidism was diagnosed (adjusted calcium 2.82 mmol/l, phosphate 1.42 mmol/l, parathyroid hormone 62.6 pmol/l (RR 1.6–6.9)). Calcium level had been controlled prior to admission on Cinacalcet 90 mg and alfacalcidol 0.5micrograms daily. The patient deteriorated, becoming progressively drowsy with frequent hypoglycaemia, despite insulin downtitration. Calcium levels further increased. Etelcalcetide, pamidronate and denosumab were all implemented as treatment. However, worsening hypercalcaemia (corrected Calcium 3.78 mmol/l, ionised calcium 1.91 mmol/l) warranted transfer to the Intensive Care Unit for continuous veno-venous haemodialysis. Computed tomography of brain, thorax, abdomen and pelvis identified no cause for hypercalcaemia. Following positive parathyroid imaging, a three-gland parathyroidectomy with implantation of the 4th gland was undertaken on day 34 of admission for refractory hypercalcaemia. Histology was consistent with parathyroid hyperplasia. Postoperatively, episodes of fluctuating cognition, ongoing headaches, nausea, hypotension, and hypoglycaemia prompted Magnetic Resonance Imaging (MRI) of the brain (Gadolinium contrast contraindicated due to end-stage kidney disease). This revealed an enlarged pituitary gland extending into the suprasellar space, with thickening of the pituitary stalk, new from MRI two years prior. Visual field testing did not reveal hemianopia. Hypopituitarism was subsequently diagnosed: cortisol 32 nmol/l, adrenocorticotropic hormone 17 ng/l, TSH 0.02 miu/l, free T4 10.7 pmol/l on L-thyroxine 50 micrograms, estradiol <92 pmol/l, follicle stimulating hormone 1.8 IU/l, luteinizing hormone <0.5 IU/l. Intravenous hydrocortisone resulted in symptom resolution within days. Positron emission tomography showed no abnormal tracer uptake in the pituitary gland or elsewhere. IgG4 level was normal at 0.344 g/l. Cerebrospinal fluid and serum angiotensin converting enzyme levels were raised at 3.6 U/l (0.5–2) and 79 U/l (8–65) respectively. Quantiferon study was indeterminate. Following multidisciplinary conference discussion, surgery was felt not to be indicated. Pituitary biopsy was not undertaken. MRI eight months later showed pituitary gland normalisation. Adrenal insufficiency (AI) remains. This case highlights the importance of maintaining a high index of suspicion for unusual diagnoses when met with puzzling clinical scenarios. While limited by lack of contrast-enhanced MRI and absence of tissue diagnosis, we believe that the pituitary mass, hypopituitarism and hypercalcaemia were related to the same disease process, likely a hypophysitis, given its resolution on follow-up imaging. AI symptoms are non-specific, and AI remains an important diagnostic consideration.