Management of Hypercalcemic Hyperparathyroidism


I have a puzzling hypercalcemia case which I have not been able to solve. This is her story below - also please find attached a spread sheet with all her bone metabolic parameters over the past 2 years. It is my impression that she has primary hyperparathyroidism with PTH now 18-20. PTH should be suppressed however given her degree of hypercalcemia.

The patient has now had significant bone loss (3 % in spine) and is getting more and more symptomatic with hypercalciuria.

51-year-old female with presumed primary hyperparathyroidism (PTH 59, Ca 10.8)- s/p neck exploration and removal of the right upper parathyroid gland in 2008 , which per pathology report measured 7 mm. No intraoperative PTH drop.

Since her surgery her calcium levels have been between 10.1 with a iPTH of 25, and 11.0, iPTH 51, albumin of 4.9. Hypercalciuria between 413 to 508 mg in 24 hours (2008- mid 2009). 25-OH D level have always been greater than 32.

Calcium levels have been rising since please see spreadsheet - PTH levels have been coming down- but never suppressed. I considered granulomatous disease (when one PTH came back as low as 12 ) and evaluated the patient further. 1,25 dihydroxy vitamin D 44 pg/ml, ACE level 6 U/l, normal serum and urine protein electrophoresis, PTH related peptide 14, calcium 11.2, albumin 4.8, ionized calcium 5.8, iPTH 47. The case was discussed with Michael Hollick ( I used to be a fellow at BUMC) who recommended prednisone 10 mg for one week to see if her calcium comes down. Calcium measurements were unchanged after 10 mg of prednisone for one week. I then sent the patient for a venous neck localization study, which did not identify any clear cut PTH elevation, but localization mainly performed on the left side of the neck as the right thyroidal vein was not clearly identified ( difficult postop neck!)

The patient had a repeat dual isotope, dual phase subtraction 99 technetium/I 123 sestamibi scan which identified mild increased activity at 15 minutes on right inferior pole on subtraction imaging. Neck ultrasound in 1/2010 showed two hypoechoic lesions inferior to the right thyroid lobe. The more superior lesion was hypoechoic, measured 5.8 x 3.0 x 4.1 cm, was difficult to compress, did not have a central fatty hilum, but a small pole artery. The inferior lesion was hypoechoic, measured 4.9 x 3.7 x 6.1 mm, was difficult to compress, did not have a central fatty hilum and also appeared to have a pole artery. These two lesions look like 2 small parathyroid adenomas in the classical position. I was planning on doing a PTH washout,but was hesitant as lesions are small, neck is scarred and patient a little worried.

The patient feels unchanged, with extreme fatigue, polyuria and polydipsia. She denies any fractures, bone aches or bone pain. She takes calcium 2000 units daily along with 2000 units of cholecalciferol . The patient is very frustrated because she does not know what to do. She's was considering consulting Dr. Norman in Florida who would charge her $2500 for consultation, however does not have the money to go ahead.

Bone density in June 2009 in the osteopenic range, with nonsignificant changes from 2006 to 2002. BMD in 2010 with 3.5 % decrease in spine, normal value in 1/3 radius

12/09 : PTH 45, calcium 10.8, albumin 4.6 (corrected calcium 10.4) 25-OH D 66, urine n-Tx 35

1/10 : PTH 37, Ca 11.1, Alb 4.5, corrected calcium 10.7. Ionized calcium 6.0.

4/10: PTH 29, albumin 4.2, calcium 9.6, ionized calcium 5.7, 25OH-D level wrr.

please see attached sheet for all labs

Can you please help me with this case.. Am I correct thinking that her PTH is inappropriately normal for her hypercalcemia ( upper end of ref range for 40-50 year old more around 40-50 pg/ and not 65 pg/ml as given by lab? What else should I do?.Claudia Panzer, M.D.


-: Dr. DeGroot asked me to respond to your request as I have extensive experience with primary hyperparathyroidism. I assume the parathyroid gland which was removed was abnormal and that the patient has parathyroid hyperplasia. About 10% of our surgically proven hyperparathyroid patients have a normal serum PTH, as low as 20 pg/ml. I don't know why your patient had 18 and 14 pg/ml levels recently. Possibly magnesium deficiency could do this. Assuming further PTH levels are not fully suppressed the patient could be treated either with cinecalcet 30 mg every 12 hours or with surgery by a very experienced parathyroid surgeon. At least 2 other glands will need to be removed and intraoperative PTH would be desirable to decide the adequacy of the surgery. If the patient is presently symptomatic it would be worthwhile to start her on cinecalcet to see if she feels better. It lowers serum calcium immediately. Unfortunately it would have to be used off-label but I usually can persuade insurance companies to approve its use. I hope this is helpful. Frederick R. Singer, M.D.

Hypercalcemia- Vitamin D Deficiency in Possible Hyperparathyroidism


I have 66 year old lady with PHM Diabetes type II, obesity and hypertension. Referred by her GP with corrected Calcium mildly high at 2.68nmol/l (2.2-2.6), phosphate 1.07nmol/L , ALP normal PTH 6.2(1.1-6.9) as query hyperparathyroidism. Patient is completely asymptomatic and no weight loss.

No medication causing hypercalcemia. 24 hour urine for Cacium was non detectable 0.00 and Ca/Creatinine was 0.0. Vitamine D was defient at D2 <1.3 nmom/L D316.3 nmol/L.

U/S parathyroid showed thyroid nodule but no parathyroind nodule .

My question is is this primary hyperparathyroidims or secondary to vitamin D defiency ? how would i confirm this ? and would i have to treat with Vitamin D replacement despite teh hypercalcemia ?

Appreciate your help. Dr Yahya Mahgoub


As the urinary calcium is very low, the diagnosis of FHH (Familial Hypocalciuric Hypercalcemic) should be considered. Conclusively diagnosed only by genetic testing, FHH may be diagnosed clinically if there is also a strong (autosomal dominant) family history of hypercalcemia. The vitamin D deficiency should be treated cautiously to avoid further increase in serum calcium. Primary hyperparathyroidism is still possible if the very low urinary calcium can not be confirmed; the absence of creatinine in the urine makes the test suspect. Secondary hyperparathyroidism is inconsistent with an elevated serum calcium, and there is no information regarding renal function. To be diagnostically useful, the serum phosphate must be done in the fasting state. Bone DXA would also be useful, and a 1, 25 dihydroxyvitamin D-mediated cause of hypercalcemia needs to be ruled out. Leonard J Deftos, MD