|Lab Tests/Rule-Outs|| Test Electrolytes, Serum
| ||Calcium is the most closely controlled substance in the blood. The biologic variation of total calcium is approximately 2% and of the biologically active free (ionized, ionic) calcium only 1%. Thus, the monitoring of calcium in blood requires analytic procedures of high precision and accuracy. For patients with asymptomatic primary hyperparathyroidism, calcium monitoring involves the measurement of total calcium and free calcium.|
| ||Contrary to popular medical belief, calcium supplementation can be useful, even when calcuim levels are already too high in hyperparathyroidism. This high level of calcium is being maintained by taking calcium from your bones. Supplemental oral calcium helps prevent calcium being taken from your bones! In the mean time, one should be looking for a surgeon who specializes in this operation.|
The following study results indicate that calcium loading inhibits bone resorption in postmenopausal women with mild primary hyperparathyroidism.
Oral calcium loading is known to decrease parathyroid hormone levels in primary hyperparathyroidism. We have examined the effects of a calcium supplement on bone resorption in postmenopausal primary hyperparathyroidism. Fasting blood and urine samples were obtained in 12 postmenopausal women (median age 64 yr) with primary hyperparathyroidism associated with mild hypercalcemia (plasma calcium less than 3.00 mmol/l). Further samples were obtained 12 hours after a 1 g calcium supplement given at 2100 h. After calcium administration there were rises in plasma ionized calcium (p less than 0.02), plasma phosphate (p less than 0.05) and the renal tubular maximum reabsorption capacity for phosphate (p less than 0.01) and falls in parathyroid hormone (p less than 0.05) and the renal tubular maximum reabsorption capacity for calcium (p less than 0.05). The urinary calcium/creatinine increased (p less than 0.01) and the urinary hydroxyproline/creatinine (p less than 0.02) fell. [Horm-Metab-Res. 1994 Jan; 26(1): 39-42]
| ||Hyperparathyroidism can be cured with a routine operation which caries a success rate of about 95% and a complication rate of around 1% or less. Some centers are even performing minimal surgery for this disease which can be accomplished under local anesthesia on an outpatient basis. See www.parathyroid.com for additional excellent information about this condition and the importance of selecting an experienced surgeon.|
If you have mild hyperparathyroidism, you may not need any treatment, although your blood-calcium levels, kidney function and bone health will need to be regularly checked. When your kidneys or bones are affected, or you have bothersome symptoms, surgery may be the best option.
| ||Hyperparathyroidism is caused by a malfunction of the parathyroid glands in the neck, which regulate calcium in the blood by parathyroid hormone (PTH). The disease most often strikes women, particularly older women. It can cause fatigue, disorientation, and depression, and can also lead to bone loss, kidney stones, and even coma.|
A study published in the Journal of Clinical Endocrinology and Metabolism found an inverse relationship between the severity of the disease and patients' intake of vitamin D through diet and supplements. Such a link has long been suspected, but hadn't been shown until now, and the finding may affect the way some physicians treat the disease. Vitamin D hormone replacement reduces the production of PTH.
Dr. Rao says there is a myth among both doctors and patients that people with hyperthyroidism should avoid calcium and vitamin D, since they have too much calcium in their bloodstreams. But this is "biologically implausible," he says, and the myth only aggravates the situation.
Dr. De Papp echoes his concern. "The fear is if they take supplements, they will make their blood calcium go higher," de Papp says. "Although there is some truth to that, their blood calcium will be higher, it is at the expense of their bones, because if they don't take calcium supplements they are much more likely to � end up with nutritional osteoporosis from vitamin D and calcium deficiency on top of the primary hyperparathyroid bone disease that they may have. So they get bad bones for two reasons.
"If you restrict vitamin D, PTH levels go up, which stimulates bone loss, specifically cortical bone, which is in your wrist and your hip," she says. "Hip fractures are a tremendous cause of morbidity and mortality among postmenopausal women in this country."
"In other words, people with hyperparathyroidism need as much vitamin D and calcium, and perhaps more, than the general public," says Dr. Rao
Vitamin D -25 is suppressed and Vitamin D-1-25 is increased in patients with primary hyperparathyroidism in linear fashion as calcium levels increase, returning to normal within weeks of tumor removal. A protective mechanism is in play.
Overview: Vitamin D-25 is converted to Vitamin D-1-25 in patients with primary HPT in a linear fashion as calcium levels increase. Thus the vast majority of patients with primary HPT will have low Vit D-25 that normalizes by itself in most patients within several months.
Objective: Vitamin D-25 is often measured in patients with apparent primary HPT to rule out a possible secondary cause. This study was undertaken to examine if a relationship exists between Vit-D levels and parathyroid pathology in patients with elevated calcium levels.
Methods: A prospective, single institution study measured preoperative Vitamin D (25OH and 1-25OH) in 1,587 patients undergoing surgery for sporadic primary hyperparathyroidism (PHPT) over a 1-year period. All patients underwent curative parathyroidectomy with pathology noted. Patients were put on nominal doses of Vit-D postop contained within supplemental calcium tablets (Citracal+D; 250 IU cholecalciferol daily) for two months; none took additional Vit-D. Blood levels were measured at 1 and 2 months post-op.
Results: All patients had primary HPT with high serum calcium and PTH preop that normalized at all postop measures indicating cure. The average preop Vit-D25 was 25.8+10 ng/ml (range 4-65). 1039 patients (67%) had Vit-D25 levels below 30 ng/ml preop, while 594 patients (38%) had levels below 20 ng/ml preop (mean 14.6, range 4-19), No patient had high Vit-D25 preop. Vit-D25 levels decreased linearly as calcium levels increased such that 71% of those with levels above 12 mg/dl had Vit-D25 <20 (p<0.01, R=0.91).The levels of Vit-D1-25 were low in 0%, normal in 58.5%, and high in 41.5% (mean 56.2 + 14)(p<0.01). The findings at surgery were identical (p=0.98) for those with low vs. normal Vit-D25 (single adenoma=92%, double adenoma=6%, 4-gland hyperplasia=3%). 82% of patients with low preop Vit-D25 had increased levels at 1 month postop (mean 41.4+12, range 17-63, p<0.005), increasing to 91% at 2 months. All patients with normal Vit-D25 preop remained normal postop. 68% showed decreased Vit-D1-25 into the normal range (p<0.001) within 1 month of surgery.
Conclusion: Vit-D25 levels decrease in a linear fashion as calcium levels rise in patients with primary HPT. Overall, 38% will have Vit-D25 levels less than 20 ng/ml, increasing to 71% of those with calcium levels above 12mg/dl. Vit-D1-25 shows the opposite pattern suggesting a protective mechanism. The pathology found at surgery is identical in PHPT patients with low versus normal Vit-D25 indicating no causal relationship. Low Vit-D25 should not be interpreted as signaling secondary HPT in patients with elevated calcium levels. The vast majority of patients will normalize their low Vit-D25 and high Vit-D1-25 levels within 2 months of tumor removal.