Primary hyperparathyroidism (PHPT) causes elevated blood calcium levels (hypercalcemia) through the excessive secretion of parathyroid hormone (PTH), usually from a benign tumor of the parathyroid glands.
It is three times as common in women as men. It is suspected when blood calcium levels are high and often confirmed when serum parathyroid hormone (PTH) is elevated as well. The signs and symptoms of PHPT are those of hypercalcemia. They are classically summarized by the mnemonic “stones, bones, abdominal groans and psychiatric moans.”
“Stones” refers to kidney stones. “Bones” refers to bone-related complications. “Abdominal groans” refers to gastrointestinal symptoms of constipation, indigestion, nausea and vomiting. “Psychiatric moans” refers to tiredness, fatigue, depression, memory loss, psychosis, and even coma.
PHPT is one of the few diseases in which doctors have said vitamin D should not be used, as it might raise blood calcium levels even higher. Recently, Dr Diana Wagner and colleagues of the University of Rochester Medical Center wanted to see if vitamin D was a problem or was it safe to use in patients with PHPT.
The authors point out that vitamin D deficiency occurs very frequently in patients with PHPT and is associated with a more severe form of disease. One study from France reported an incidence of vitamin D deficiency of almost 100% in PHPT patients. Patients with vitamin D deficiency and PHPT have higher PTH levels, alkaline phosphatase and urinary calcium levels, larger parathyroid tumors and more bone problems than PHPT patients with higher vitamin D levels.
The authors studied 35 patients diagnosed with PHPT and vitamin D deficiency who were either treated with 1,000-2,000 IU of vitamin D daily or 50,000 IU/week for an average of 5 months. In the 50,000 IU/week group, the 25(OH)D increased significantly from 15 ng/ml to 42 ng/ml and increased from 22 ng/ml to 33 ng/ml in patients treated with 1,000-2,000 IU of vitamin D daily. Six of the 35 patients did not reach 30 ng/ml, irrespective of their treatment groups.
The blood calcium remained stable in the 50,000 IU/week group but actually decreased mildly in 1,000-2000 IU/day group [10.76 to 10.11 mg/dl (p=0.0007)]. Neither treatment changed PTH levels or kidney function tests. No new case of kidney stones developed during vitamin D replacement. Five patients had history of kidney stones, 2 of them with multiple episodes. None of those 5 patients developed recurrent kidney stones regardless of their treatment group.
The authors concluded,
“Our retrospective study demonstrated that patients with primary hyperparathyroidism and concurrent vitamin D deficiency can be effectively treated with either vitamin D 50,000 IU once per week or 1,000-2,000 IU once per day. Either treatment does not cause hypercalcemia to dangerous levels and therefore can be considered for routine practice.”
The usual tumors seen in PHPT are adenomas, not cancers. Glandular adenomas are usually concentrated cells all working overtime to make whatever hormone the involved gland makes. As vitamin D deficiency forces the parathyroid gland to tonically secrete more PTH hormone, I have always wondered if long-standing severe vitamin D deficiency actually causes some cases of PHPT. However, if that were true, then vitamin D treatment should lower PTH levels, and that was not seen in this study but has been seen in other studies with vitamin D treatment of PHPT.
Grey A, Lucas J, Horne A, Gamble G, Davidson JS, Reid IR. Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency. J Clin Endocrinol Metab. 2005 Apr;90(4):2122-6.
Grubbs EG, Rafeeq S, Jimenez C, Feng L, Lee JE, Evans DB, Perrier ND. Preoperative vitamin D replacement therapy in primary hyperparathyroidism: safe and beneficial? Surgery. 2008 Dec;144(6):852-8; discussion 858-9.