Primary hyperparathyroidism

Associated with elevated serum calcium, inappropriately normal or elevated parathyroid hormone levels.

Excess parathormone typically secreted by a single benign, parathyroid adenoma, acts directly indirectly on its target organs, the bone, kidney, and the G.I. tract.

Associated with low or low-normal serum phosphorus levels, high or high-normal 1-alpha,25-dihydroxyvitamin D concentrations and decreased renal tubular maximum for phosphate.

Parathyroid, hormone stimulates bone resorption and conversion of calcitiol to calcitriol which increases G.I. calcium absorption.

Parathormone, enhances kidney calcium resorption, exacerbating hypercalcemia.

Affects more than 100,000 patients a year in the U.S.

Reported in 0.1-0.3% of the population.

Occurs in 1:500 women over the age of 40 years, and 1:2000 men of any age.

Typical patients is a postmenopausal female with a mean age of 55 years.

Iincidence is 2-3 women per 1000 women and 1 per 1000 men.

Incidence declining since mid 1980’s despite an increase in the diagnosis due to automated chemistry tests.

Advanced cases are rare today.

Findings of persistent hypercalcemia and elevated PTH levels.

Approximately 10-20% of individuals with primary hyperparathyroidism will have normal parathyroid hormone levels.

With hypercalcemia, an PTH level of greater than 25 pg per mL is abnormal (10-65 pg/mL is normal).

Urine calcium can be low, normal, or elevated.

Nonparathyroid causes of hypercalcemia including malignancy, and thyrotoxicosis present with undetectable or suppressed PTH levels.

The major form of circulating parathyroid hormone is an 84 amino acid peptide.

Biotin supplements may impair PTH measurements, with low PTH LEVELS.

Distinguished from hypercalcemia of malignancy by the presence of low levels of PTH in the latter process.

Rare cases related to malignancy with high PTH levels can be seen in ectopic PTH secretion, coexisting primary hyperparathyroidism or PTH resistance.

Causes include: single solitary parathyroid adenoma 85% of cases, gland hyperplasia in 12%, double adenomas in 2% and parathyroid carcinoma in <1% of cases.

About 5% of cases or cause by familial syndromes.

In multiple endocrine neoplasia type I, benign tumors of the parathyroid of the first manifestation of the disease, followed by potentially malignant tumors of other parts of the body, such as the pancreas.

Prior to surgery an ultrsound plus four dimensionl CT scan are done to identify the adenoma.

About 6-8% of pateints with parathyroid diseae have a concomitant malignant thyroid tumor.

Most adenomas can be removed by minimally invasive parathyroidectomy.

Following surgical removal of an adenoma an immunochemiluminescent assay is used to determine whether the patient’s parathormone level has decreased: The half life of PTH, is 3 minutes, and a decreased level by 5 minutes confirmed by a 10 minute level verifies that the gland that was causing the hyperparathyroidism has been removed.

Following parathyroidectomy only 3% of patients experience a recurrence of a parathyroid tumor.

After parathyroidectomy for this disease 15% of patients show improvement in bone density 2-5 years after the procedure.

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