Calcification in the brain due to hyperparathyroidism Pepper & Salt, classical X-Ray appearance of hyperparathyroidisim The gold standard of diagnosis is the PTH immunoassay. Once an elevated PTH has been confirmed, the goal of diagnosis is to determine whether the hyperparathyroidism is primary or secondary in origin by obtaining a serum calcium level: Serum calcium Phosphate ALP PTH Likely type ↑ ↓ ↑ ↑ Primary hyperparathyroidism ↓ ↑ ↑ ↑ Secondary hyperparathyroidism Tertiary hyperparathyroidism has a high PTH and high serum calcium. It is differentiated from primary hyperparathyroidism by a history of chronic kidney failure and secondary hyperparathyroidism. Hyperparathyroidism can<unk> hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Differential diagnosis Familial benign hypocalciuric hypercalcaemia can present with similar lab changes. In this condition, the calcium creatinine clearance ratio, however, is typically under 0.01. Blood tests Intact PTH In primary hyperparathyroidism, parathyroid hormone (PTH) levels are either elevated or "inappropriately normal" in the presence of elevated calcium. Typically, PTH levels vary greatly over time in the affected patient and (as with Ca and Ca++ levels) must be retested several times to see the pattern. The currently accepted test for PTH is intact PTH, which detects only relatively intact and biologically active PTH molecules. Older tests often detected other, inactive fragments. Even intact PTH may be inaccurate in patients with kidney dysfunction. Intact pth blood tests may be falsely low if biotin has been ingested in the previous few days prior to the blood test. Calcium levels In<unk>  of primary hyperparathyroidism or tertiary hyperparathyroidism, heightened PTH leads to increased serum calcium (hypercalcemia) due to: # increased bone resorption, allowing the flow of calcium from bone to blood # reduced kidney clearance of calcium # increased intestinal calcium absorption Serum phosphate In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased reabsorption of phosphate in the kidney tubules. However, this is only present in about 50% of<unk> . This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of kidney disease. Alkaline phosphatase Alkaline phosphatase levels are usually elevated in hyperparathyroidism. In primary hyperparathyroidism, levels may remain within the normal range, but this is inappropriately normal given the increased levels of plasma calcium. Nuclear medicine A technetium sestamibi scan is a procedure in nuclear medicine that identifies hyperparathyroidism (or parathyroid adenoma). It is used by surgeons to locate ectopic parathyroid adenomas, most commonly found in the anterior mediastinum. Classification Primary Parathyroid adenoma. Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves. The oversecretion of PTH is due to a parathyroid adenoma, parathyroid hyperplasia, or rarely, a parathyroid carcinoma. This disease is often characterized by the quartet stones, bones, groans, and psychiatric overtones referring to the presence of kidney stones, hypercalcemia, constipation, and peptic ulcers, as well as depression, respectively. In a minority of<unk> , this occurs as part of a multiple endocrine neoplasia (MEN) syndrome, either type 1 <unk>  by a mutation in the gene MEN1) or type 2a <unk>  by a mutation in the gene RET), which is also associated with the adrenal tumor pheochromcytoma. Other mutations that have been linked to parathyroid neoplasia include mutations in the genes HRPT2 and CASR. Patients with bipolar disorder who are receiving long-term lithium treatment are at increased risk for hyperparathyroidism. Elevated calcium levels are found in 15% to 20% of patients who have been taking lithium long-term. However, only a few of these patients have significantly elevated levels of parathyroid hormone and clinical symptoms of hyperparathyroidism. Lithium-associated hyperparathyroidism is usually<unk>  by a single parathyroid adenoma. Secondary Secondary hyperparathyroidism is due to physiological (i.e. appropriate) secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels). The most common<unk>  are vitamin D deficiency <unk>  by lack of sunlight, diet or malabsorption) and chronic kidney failure. Lack of vitamin D leads to reduced calcium absorption by the intestine leading to hypocalcemia and increased parathyroid hormone secretion. This increases bone resorption. In chronic kidney failure the problem is more specifically failure to convert vitamin D to its active form in the kidney. The bone disease in secondary hyperparathyroidism<unk>  by kidney failure is termed renal osteodystrophy. Tertiary Tertiary hyperparathyroidism is seen in those with long-term secondary hyperparathyroidism, which eventually leads to hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with end-stage kidney disease and is an autonomous activity.
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