A 36yr old woman with a history of PCKD was referred for surgical treatment of hyperparathyroidism. She had a history of two prior failed kidney transplants following which she had been on dialysis for more than 10 years. She had a third renal transplant 10 years prior to this presentation which was still functional. At the time of her transplant, she had received OKT3 and was currently maintained on tacrolimus and prednisone. She had a long history of hyperparathyroidism. Six years prior to her transplant, she had a subtotal (3.5 glands) parathyroidectomy. The year of her transplant, she had another neck exploration with the removal of 8 nests of hypercellular parathyroid tissue.
At the time of this presentation, her PTH was 3,300 pg/ml despite treatment with cinacalcet. Her ionized calcium was normal (1.2 mmol/L) but she complained of poor concentration, fatigue and depression. Serum phosphorous and creatinine were normal. She had a normal sestamibi scan but an US revealed hyperplastic parathyroid tissue in her neck.
During the parathyroidectomy, frozen section revealed hypercellular parathyroid tissue that was removed. However, pre-op, intra-op and post-op PTH levels were elevated at >1700 pg/ml. Because of the persistently elevated PTH, it was considered a failed operation and calcium supplementation was not started post-op. However, within 3 hours of the operation, she developed perioral numbness, tetany and muscle spasms in her legs. Her ionized calcium was low (0.9 mmol/L) and her symptoms resolved after treatment with iv calcium. Her PTH remained elevated at 3000 pg/ml.
What is the reason for her acute hypocalcemia in this setting? Answer in the comments please.
At the time of this presentation, her PTH was 3,300 pg/ml despite treatment with cinacalcet. Her ionized calcium was normal (1.2 mmol/L) but she complained of poor concentration, fatigue and depression. Serum phosphorous and creatinine were normal. She had a normal sestamibi scan but an US revealed hyperplastic parathyroid tissue in her neck.
During the parathyroidectomy, frozen section revealed hypercellular parathyroid tissue that was removed. However, pre-op, intra-op and post-op PTH levels were elevated at >1700 pg/ml. Because of the persistently elevated PTH, it was considered a failed operation and calcium supplementation was not started post-op. However, within 3 hours of the operation, she developed perioral numbness, tetany and muscle spasms in her legs. Her ionized calcium was low (0.9 mmol/L) and her symptoms resolved after treatment with iv calcium. Her PTH remained elevated at 3000 pg/ml.
What is the reason for her acute hypocalcemia in this setting? Answer in the comments please.
Thanks Geroid for this very interesting case. Quite intriguing!
ReplyDeleteThis is a young female with multiple prior transplants and dialysis. Together with her history of parathyroid disease, she would have had a large burden of bone disease.
Do we know what her vitamin D levels are?
The drop in her calcium despite a persistently elevated PTH may be related to the relative drop in PTH causing "hungry bone syndrome". Release of calcitonin secondary to surgical manipulation may also have contributed to her transient hypocalcemia. It will be important to check her Mg level as well, as hypomagnesemia in this setting can contribute to hypocalcemia.
Another unlikely etiology that I would inquire about include receiving large volumes of blood products causing citrate toxicity.
I am very interested to know if there is an explanation for the transient drop and the subsequent rebound of PTH level. Also please let us know your considerations when giving IV Ca having in mind a possible rebound of levels.
vitamin D deficiency and accidental subtotal thyroidectomy with transient hypothryoidism.
ReplyDeleteOKT3 treatment can result in the production of human anti-mouse antibodies. These antibodies can interfere with any immunoassay and give spurious results
ReplyDeleteThe Fk506 is the culprit. It elevated the PTH level and lowered the serum calcium level.
ReplyDelete