Secondary hyperparathyroidism is a situation in which the parathyroid glands are producing a large amount of parathyroid hormone (PTH) to compensate for another problem. One can easily measure parathyroid hormone levels, and there is a “normal” range, but the range is really meaningless unless one also knows the blood calcium level. PTH is designed to raise the blood calcium. If the calcium level is low, the PTH should be high, so a higher-than-normal level means that the parathyroid glands are doing their job properly. This is what’s called secondary hyperparathyroidism -- the PTH levels are high, but they should be high because there is something else causing the blood calcium level to be low and the PTH goes up to try to compensate.
There are many causes of secondary hyperparathyroidism, but by far the most common is some form of vitamin D deficiency. Severe deficiency of standard 25-hydroxy-vitamin D3 levels (lets call this 25-D), which is the form of vitamin D that is usually measured in the blood, will sometimes cause secondary hyperparathyroidism. Much more commonly, the problem results from an inability of the body to convert this form of vitamin D to the more active form, 1,25-dihydroxy-vitamin D3 (we’ll call this 1,25-D). Conversion of 25-D to 1,25-D takes place in the kidney and many people with kidney problems -- sometimes even with what appear to be mild kidney problems -- can’t properly convert vitamin D and will develop secondary hyperparathyroidism. This condition results in a low blood calcium, a low blood phosphorus, a form of bone disease called osteomalacia, which is similar to osteoporosis but is corrected by 1,25-D, and possibly muscle weakness. This problem is surprisingly common and is frequently not recognized. Treatment with an oral form of active 1,25-D is highly effective at correcting the problem. When the 1,25-D level rises, and when the blood calcium is restored to normal, the PTH levels will also fall back into the normal range.
