SFE2002 Poster Presentations Clinical case reports (21 abstracts)
1Diabetes and Endocrinology,Torbay Hospital,Torquay,UK; 2Diabetes and Endocrinology,Torbay Hospital,Torquay,UK; 3Diabetes and Endocrinology,Torbay Hospital,Torquay,UK; 4Department of Biochemistry,Torbay Hospital,Torquay,UK; 5Radiology Department,Torbay Hospital,Torquay,UK; 6Radiology Department,Torbay Hospital,Torquay,UK.
We present a patient with asymtomatic primary hyperparathyroidism who became normocalcaemic following spontaneous infarction of a parathyroid adenoma. He was referred by the General Practitioner following an episode of renal colic when he was found to have a raised adjusted serum calcium level of 3.07 millimols/litre (ref 2.10-2.70). Parathyroid hormone level was 33.2 picomols/litre (ref 1.3-7.6), confirming primary hyperparathyroidism. A SESTIMIBI scan revealed a parathyroid adenoma and he was referred for surgery. While on a waiting list to see the surgeon he developed sudden increase in the swelling in the left lower pole of thyroid gland. He also had minimal dysphagic symptoms. Serum calcium level performed by the General Practitioner had surprisingly returned to normal (2.04 millimols/litre) and he was referred to endocrine clinic once again for an early follow up. He remained asymtomatic and a repeat SESTIMIBI scan did not reveal any parathyroid adenoma, supporting the likelihood of spontaneous infarction in the parathyroid gland. Parathyroid hormone level returned to normal (4.1 picomols/litre). He is under regular follow up to ensure he remains normocalcaemic.
Though sub clinical infarction of abnormal parathyroid tissue is described in literature to occur relatively frequently, remission of primary hyperparathyroidism following spontaneous infarction is a rare occurrence. Regeneration of parathyroid adenoma may occur and hence regular follow up may be recommended.