What information is obtained determining parathyroid hormone in the blood?
Dr. Renate Helda, endocrinologist
Parathyroid hormone (PTH) is one of the three major calcium metabolism – regulating hormones. It is produced by the epithelial cells (glandulae parathyreoidea), most often four, located on the posterior surface of the thyroidal gland. Blood circulating PTH using PTH receptor, located in the distal renal tubules (distal renal tubulosa) in a few minutes increases the calcium (Ca) and reduces tubular reabsorption of phosphates. PTH also increases the activity of osteoclasts and other bone cells, causing Ca bone loss within one to two hours. Prolonged exposure to PTH stimulates 1α-hydrolase activity in proximal renal tubule cells by promoting the production of active vitamin D, calcitriol (1.25(OH)2D) that regulates Ca reabsorption in the small intestine and Ca in the bones during days and weeks1.
These mechanisms correct Ca if its level is within the normal range, using feedback with a decrease in PTH and elevated calcitrol (1.25(OH)2D), which also reduces the transcription of the PTH gene.
Consequently, Ca homeostasis is primarily based on the ability of PTH to respond rapidly to changes in Ca, secondary, they are effector tissues – kidney canals, the bone system and small intestines that respond appropriately to circulating PTH and calcitriol (1.25(OH)2D) concentrations and, to a lesser extent, calcitonin levels.
What is the reduced PTH level?
In practice, the most common cause of reduced PTH or hyperparathyroidism is due to neck surgery (usually the thyroid or parathyroid surgery). Clinical hypoparathyroidism begins to manifest one or two days after surgery and can continue for many years. Such complications frequency depends on the extent of the operation, the surgeon’s experience and the operation target. Very rarely hypoparathyroidism may also occur as a complication in the treatment of radioactive iodine2.
Autoimmune epithelial defects can be both isolated and associated with some of the polygondal syndromes. Antibodies to the epithelial cells are found in up to 30% of patients with isolated hypoparathyroidism and 40% of patients with poliglantal desease3.
Another antibody target for hypoparathyroidism is calcium-sensitive receptors. In more than 50% of patients with first type polyglandular autoimune syndrome, these antibodies are positive. Maternal hyperparathyroidism may result in transient neoplastic hypoparathyroidism4. Maternal PTH pushes the child’s parietal activity, however, the postpartum effect will disappear rapidly with the release of material PTH.
PTH reduced secretion may also occur in some other cases, such as hypermalgemic and hypomagnesaemic cases, the latter including chronic alcoholics, as well as metastasis in the epithelia infiltration process, haemochromatis, iron accumulation due to multiple blood transfusion or sarcoidosis.
To confirm the diagnosis of hypoparathyroidism, it is also necessary to determine calcium in the blood (hypocalcaemia), then both normal and ionized calcium, phosphorus (hyperphosphatemia) may be lowered, whereas serum magnesium may be both elevated, normal and decreased. Decreased calcium may also result in ECG changes – prolonged QT intervals, bradycardia, or less frequent ST segment elevation. Ocular examination is also required as there is a possibility of cataract development due to chronic hypocalcaemia.
The patient should be referred to the endocrinologist. Aetiological treatment usually is not possible and calcium and vitamin D (calcitrol) preparations are used to prevent hypoglycaemia.
What is evidence of an elevated PTH?
Elevated levels of PTH in the blood may indicate to a number of abnormalities, the first of which is primary hyperparathyroidism.
Primary hyperparathyroidism is a condition characterized by a disturbance in PTH regulation when PTH concentration is inadequate for serum Ca level. The disease is more common in women (female to male ratio of 3 : 1) and the peak incidence is usually between the ages of 50 to 70 years. The prevalence in the population on average is one case per 1000 inhabitants. In 85% of cases, patients have a single benign glandular parathyroid adenoma. The normal parathyroid gland weighs up to 50 mg, but the adenoma is more often 2 to 20 times larger. 15% of patients may have multiple parathyroid adenomas of hyperplasia of all four epithelial cells. Parathyroid cancer occurs rarely – in approximately 0.5% of cases.
It should be remembered that there is also secondary hyperparathyroidism. This condition is characterized by hypocalcaemia, hyperphosphatemia and corresponding elevated circulating PTH level. This situation can be caused by a chronic shortage of vitamin D on insufficient intake of Ca. This condition most often is associated with chronic kidney damage in the medical experience of developed countries. In this situation, damage to the renal tubule has led to phosphate retention, which is associated with damage to the vitamin D3 1α hydrolysis. The result is hypocalcaemia which is a strong incentive for PTH production and parathyroid cell proliferation. The effect is hyperplasia of all four epithelial cells. Autonomous PTH can also develop after prolonged uremia when hypocalcaemia and real bone disease develops. This state of hypocalcaemia is considered as tertiary hyperparathyroidism or refractory uremic hyperparathyroidism.
Returning to primary hyperparathyroidism, it is worth mentioning that today, in the 21st century, its clinic with a lot of weakness, kidney stones, nephrokalcinosis and advanced skeleton deformity has practically not been observed. The most commonly reported high levels of PTH are found in patients without any symptoms of elevated ca-routine in biochemical analysis Here immediately should be noted that, although hypercalcaemia most often binds to hyperparathyroidism, differential diagnosis should definitely exclude malignancy.
Differential diagnosis of hypoglycemia in adults5
|Malignant humoral hypercalcaemia (PTH-rP)
Bone metastases (especially lung an scalar cells)
|Less frequently||Vitamin D intoxication;
Benign Familiar hypocalciurial hypercalceamia;
Sarcoidosis and other granulomatosis disorders;
|Deficiency of calcium – sensitive receptors,
Linked to 1α hydroxylation
Linked to uraemeia
Use of thiazides;
So-called milk-alkaline or milk-alkali syndrome;
Immobilization at high Ca metabolism;
Recovery from renal canal damage;
Vitamin A intoxation;
|Growing children or adolescents, athletes, Paget’s disease, healing fractures
Rhabdomyolysis associated with 1α hydroxylation
Further action following the confirmation of primary diagnosis of hyperparathyroidism depends on its degree of aetiology and hypocalcaemia. All patients with Ca levels above 3.5 mmol/L or in patients with hypercalcaemia and Ca levels above 3.2 mmol/L require acute help6 (this will not be discussed in the article). In other cases, surgical resection of one or more enlarged epithelial cells should be considered as the main treatment method. However, this applies only to patients with high or moderately high Ca and hypercalcaemia symptoms. As mentioned in the National Institute of Health (NIH) recommendations7, only 27% of patients without symptoms and additional indications for surgical treatment during the 10-year follow-up period show the need for surgical intervention. This means that conservative treatment, monitoring blood levels of Ca and kidney function in most patients is a completely satisfactory form of healthcare8.
1Terry F. Davies Acase-based guide to clinical endocrinology Humana Press 2008:503-169
2Chandran M, Deftos LJ, Stuenkel CA, Haghighi P, Orloff LA. Thymic parathyroid carcinoma and postoperative hungry bone syndrome. Endocr.Pract. Mar- April 2003; 9 (2): 152-6 ( Medline)
3Maeda SS, Fortes EM, Oliveira UM, Borba VC, Lazaretti-Castro M. Hypoparathyroidism and pseudohypoparathyroidism. Arq Bras Endocrinol Metabol. Aug 2006;50(4):664-73. [Medline]
4Pieringer H, Hatzl-Griesenhofer M, Shebl O, Wiesinger-Eidenberger G, Maschek W, Biesenbach G.Hypocalcemic tetany in the newborn as a manifestation of unrecognized maternal primary hyperparathyroidism. Wien Klin Wochenschr. 2007;119(3-4):129-31. [Medline]
5Terry F. Davies Acase-based guide to clinical endocrinology Humana Press2008:503-173
6Terry F. Davies Acase-based guide to clinical endocrinology Humana Press2008:503-174
7NIH conference, Diagnosis and management of asymptomic primary hyperparathyroidism: consensus development conference statement. Ann Intern Med 1991;114:593-59
8Silverberg SJ, Shane E, Jacobs TP, Siris E, Bilezikian JP A10- yerar prospective study of primary hyperparathyroidism with or without parathyroid surgery. N Engl J Med 1999; 341:1249-1255