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Vitamin D supplementation in primary hyperparathyroidism, not a bad idea?

Posted on: July 1, 2013   by  Brant Cebulla

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Research published in the journal Endocrine Connections suggests that vitamin D supplementation in the condition primary hyperparathyroidism might not be such a bad thing.

Primary hyperparathyroidism is a condition where your parathyroid glands have gone “haywire.” An adenoma – a word to describe a non-cancerous tumor – begins growing on your parathyroid, causing your glands to produce too much parathyroid hormone.

Parathyroid hormone (PTH) allows your body to pull calcium from your bones and tells your body to start making more activated vitamin D to absorb more calcium in the gut. This helps your body keep a narrow and healthy range of calcium in the blood. When calcium is just right in your blood, your PTH will lower and stop pulling calcium from your bones.

However, in primary hyperparathyroidism, no matter how much calcium you have in your blood, the parathyroid keeps producing and producing PTH, leading to chronically high PTH levels, high blood calcium (hypercalcemia), and if not treated, bone diseases like osteoporosis and osteomalacia.

Doctors who treat patients with primary hyperparathyroidism are sometimes reluctant to give these patients vitamin D. They worry that vitamin D might further cause blood calcium to rise and put the patient at even higher risk of hypercalcemia. Currently, due to a lack of research, there are no guidelines for how much vitamin D to administer or if to avoid completely for patients with primary hyperparathyroidism.

In this present study, Dr Ranganathan Rao of the University Hospitals Coventry and colleagues observed patients with primary hyperparathyroidism, if they were administered vitamin D and if that led to any adverse outcomes.

The researchers looked at records of patients who attended their clinic between 2003 and 2011. They found 40 patients had vitamin D levels below 20 ng/ml and elected not to have the adenoma removed (a common treatment for primary hyperparathyroidism).

Twenty-eight of the patients were put on vitamin D as part of the treatment plan, 12 were not. While the 28 patients were placed on a variety of vitamin D regimens, a common treatment out of these clinics is to take 40,000-50,000 IU of vitamin D3 once per month.

The researchers observed the patients’ records for a mean 17-18 months. Did they find any adverse outcomes in those who took vitamin D? Here’s what they found:

  • Mean baseline 25(OH)D levels were 12.8 ng/ml in the vitamin D group (13.2 ng/ml in the no-vitamin D group).
  • Over the varying observation periods of each patient, in the vitamin D group, the mean 25(OH)D level rose to 54.4 ng/ml.
  • In the vitamin D group, calcium did not rise, staying the same at a mean of 2.60 nmol/l over the course of the observation periods.
  • In the vitamin D group, PTH lowered in 89% of the patients, with a mean decrease of 21% (13.3 to 10.5 pmol/l).
  • In the vitamin D group, there were no adverse effects reported.
  • In the no-vitamin D group, PTH levels remained the same (15.8±2.7 vs 16.3 pmol/l).

The researchers concluded,

“In conclusion, long-term replacement of vitamin D deficiency with vitamin D in various commonly prescribed preparations effectively reduced circulating PTH levels. This approach may be helpful in patients with mild primary hyperparathyroidism and in patients who are not willing to undergo surgery or have medical contraindications.”

Are we ready to set new guidelines declaring that vitamin D supplementation is okay in patients with primary hyperparathyroidism? Not yet probably. The researchers call for a long-term randomized controlled trial to monitor the effects of vitamin D supplementation in patients with this condition. Also, one limitation of this study is that the researchers excluded patients that elected to have surgery for their condition. Thus, the patients studied likely had a more “mild” primary hyperparathyroidism compared to those excluded.

In the meantime, it looks like vitamin D supplementation shouldn’t necessarily be avoided in primary hyperparathyroidism, as long as the condition and supplementation regimen is closely monitored by a qualified health professional. The researchers close with the advice, “regular monitoring of calcium and 25(OH)D levels is advised” in patients with primary hyperparathyroidism.

Source

Rao RR et al. Prolonged treatment with vitamin D in postmenopausal women with primary hyperparathyroidism. Endocr Connect., 2012

5 Responses to Vitamin D supplementation in primary hyperparathyroidism, not a bad idea?

  1. Rita and Misty

    While many of us know that the obvious sign of primary hyperparathyroidism is hypercalcemia, few of us, perhaps, are familiar with the symptoms of this disease. These symptoms are often summarized as: “stones, bones, abdominal groans and psychiatric moans”.

    • “Stones” refers to kidney stones, nephrocalcinosis, and diabetes insipidus (polyuria and polydipsia). These can ultimately lead to renal failure.

    • “Bones” refers to bone-related complications. The classic bone disease in hyperparathyroidism is osteitis fibrosa cystica, which results in pain and sometimes pathological fractures. Other bone diseases associated with hyperparathyroidism are osteoporosis, osteomalacia, and arthritis.

    • “Abdominal groans” refers to gastrointestinal symptoms of constipation, indigestion, nausea and vomiting. Hypercalcemia can lead to peptic ulcers and acute pancreatitis. The peptic ulcers can be an effect of increased gastric acid secretion by hypercalcemia,[4] but may also be part of a multiple endocrine neoplasia type 1 syndrome of both hyperparathyroid neoplasia and a gastrinoma.

    • Psychiatric moans” refers to effects on the central nervous system. Symptoms include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma.

    (BTW—I cannot take credit for knowing these symptoms. I referred to the much maligned Wikipedia for this data. As we all know, I’m not a physician nor am I a healthcare professional. I’m simply someone with an interest in health and well being—especially with respect to the master hormone: D).

    I do know a few people who suffer from this disease. It isn’t pleasant. It interferes with them living their lives to the fullest extent possible.

    Therefore, the choice of graphics for this article is very appropriate.

    Those suffering from this disease often must compartmentalize their lives according to how the illness impacts them from day-to-day.

    A compartmentalized life is no life to live, for sure!

    I was happy to read Brant’s closing statement: “…it looks like vitamin D supplementation shouldn’t necessarily be avoided in primary hyperparathyroidism, as long as the condition and supplementation regimen is closely monitored by a qualified health professional. “

    Optimal 25(OH)D levels are necessary, in my opinion, not only for bone health and protection from autoimmune diseases and (at least) 17 different types of cancer, but also for psychological and emotional health and well being.

    I choose to keep my 25(OH)D level at the higher end of the optimal range.

    Be well!!!
    Rita

  2. Davidclements

    I m an internist. I have not been willing to use Vitamin D for patients with very elevated calcium levels (for whom surgery is indicated). I have a number of patients with elevated PTH (Parathyroid hormone) but normal calcium. Sometimes this is so-called normocalcemic primary hyperparathyroid and sometimes it is hyperparathyroid secondary to Vitamin D deficiency or other cause. I routinely recommend achieving highish (50-80 ng/mL) levels of Vitamin D for those with elevated PTH, and note that sometimes the PTH appears to decrease after Vitamin D supplementation. Sorry to say, I can’t do a clinical trial, but would appreciate if someone would do this.

    Generally Vitamin D deficiency stimulates production of PTH. I have wondered whether Vitamin D deficiency might be one cause of Primary hyperparathyroidism. It seems plausible that a chronically stimulated parathyroid gland could begin to operate autonomously (ie, begin to ignore the blood calcium level, which normally regulates its activity, and produce PTH in an unregulated way). That is one theory of what causes so-called “tertiary hyperparathyroidism,” where parathyroid glands chronically stimulated by the metabolic consequences of renal disease begin to produce PTH autonomously.

  3. seriousgreta

    I think you need to stop thinking of vitamin D as a one part solution to everything!! Without all four nutrients working in concert, (K2, magnesium, vitamin D and calcium) bad things happen in bodies .. tumors grow and bones weaken and teeth get cavities … and on and on.

    I’ve had one of these under-diagnosed tumors and I believe that they are caused by vitamin D deficiency and exacerbated by deficiencies in magnesium and K2 Without a balance of these nutrients, women will keep forming these tumors with “no known cause”. GRRR!.

  4. Tom Weishaar

    With healthy people, it’s not plausible that doses anywhere near as low as 40 to 50 thousand IUs of vitamin D per MONTH (the equivalent of less than 2000 IUs per day) could raise vitamin levels to 54.4 ng/ml from 12.8 ng/ml. Something else is going on here to get that kind of response.

  5. IAW

    To: Tom W
    Good Catch! See below excerp from the study which I could access at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681316/

    Vitamin D replacement

    In agreement with the recent suggestions (5, 17), vitamin D-deficient patients with pHPT who are seen in the Endocrine Outpatient Clinics of the corresponding author and who show adjCa levels below 3mmol/l at baseline (18) are encouraged to increase the intake of vitamin D from natural sources and receive additional replacement with colecalciferol tablets 40000–50000 units (1000–1250μg) per month, dependent on the availability of the respective preparation in the hospital pharmacy. Doses are adapted/reduced according to biochemical response. In none of the patients were dose adjustments necessary because of increases in hypercalcaemia, but dose was reduced in four patients who showed increases in serum 25OHD above 200nmol/l. For clinical reasons (e.g. potential worsening of hypercalcaemia regardless of treatment with vitamin D; potential natural disease progression), all patients are prospectively observed with close monitoring of clinical symptoms and routinely performed blood tests. Patients who were seen in other clinics (n=29) were retrospectively identified. These patients were either treated with various vitamin D preparations (colecalciferol 20000 units (500μg), two tablets per month for up to 12 month; colecalciferol 50000 units (1250μg), one tablet per month for up to 12 month, up to colecalciferol 50000 units (1250μg) 1 tablet per week for up to 8 weeks; and i.m. injections of ergocalciferol, up to 300000 units (7500μg) as a single dose) and/or natural sources of vitamin D such as exposure to sun light, increased consumption of oily sea fish, e.g. salmon, mackerel and sardines, or fish oil supplements and/or no treatment with vitamin D was prescribed. Five of the patients were identified as having received a combination of calcium and vitamin D replacement preparation (containing colecalciferol 400 units (10μg) and calcium carbonate 2.5g daily), with three of them remaining vitamin D deficient during the observation period. This may be related to the relative small dose of vitamin D provided and/or to problems with long-term adherence with this medication. All patients were closely monitored for potential changes in adjCa levels.

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