Etiology of Hyperplasia

The development of hyperplastic parathyroid glands in patients with renal failure is primarily due to hypocalcemia, although other factors, including low calcitriol or 1,25-hydroxy-vitamin D3, high phosphate levels, and local growth factors, are involved. The decrease in serum calcium levels results from a decrease in the enzyme la-hydroxylase in the kidney that converts 25-dihydroxy vitamin D3 to 1,25-dihydroxyvitamin D. Hyperphosphatemia in patients with renal failure decreases the activity of la-hydroxylase. The consequent decrease in 1,25-dihydroxy vitamin D results in decreased

Large parathyroid adenoma

Large parathyroid adenoma

FIGURE 53-2. CT scan of the mediastinum shows a large parathyroid adenoma in the right superior mediastinum. The patient is a 72-year-old man with persistent primary hyperparathyroidism after subtotal resection of three hypercellular parathyroid glands.

FOV:36x36 8.Oihk/2.Osp 20/06:06 256x192/2 HEX RC/St:SI/PG

FOV:36x36 8.Oihk/2.Osp 20/06:06 256x192/2 HEX RC/St:SI/PG

FIGURE 53-2. CT scan of the mediastinum shows a large parathyroid adenoma in the right superior mediastinum. The patient is a 72-year-old man with persistent primary hyperparathyroidism after subtotal resection of three hypercellular parathyroid glands.

Superior Parathyroid

Inferior thyroid artery

Recurrent nerve

FIGURE 53-1. The recurrent laryngeal nerve and its relationship to the parathyroid glands. (From Clark OH [ed], Endocrine Surgery of the Thyroid and Parathyroid Glands. St. Louis, CV Mosby, 1985.)

Inferior parathyroid

Superior Parathyroid

Inferior thyroid artery

Recurrent nerve

Inferior parathyroid

Right upper glarid

Right lower gland

Left lower gland

FIGURE 53-3. Common bean-shaped adenomatous hyperplasia and enlarged right upper and right and left lower hyperplastic parathyroid glands.

Right upper glarid

Right lower gland

Left lower gland

FIGURE 53-3. Common bean-shaped adenomatous hyperplasia and enlarged right upper and right and left lower hyperplastic parathyroid glands.

calcium absorption from the gastrointestinal tract and lower serum calcium levels. The parathyroid glands, therefore, compensate by increased secretion of parathyroid hormone (PTH). In general, the size of the hyperplastic glands in patients with secondary hyperplasia as documented by ultrasonography or surgery correlates with the degree of elevation of serum PTH levels.16

The cause of primary parathyroid hyperplasia or multiple abnormal parathyroid glands is less clearly understood. Certainly, patients with both multiple endocrine neoplasia (MEN) types 1 and 2 as well as those with familial non-MEN primary HPT have multiple abnormal parathyroid glands.17" 19 Patients with MEN 1 have had a chromosomal abnormality documented on chromosome 11,20 and patients with MEN 2A and MEN 2B have point mutations on RET protoonco-gene.21 Patients exposed to low-dose therapeutic radiation also are more likely to acquire parathyroid as well as thyroid neoplasms.22-23 Whether parathyroid hyperplasia occurs more often than in sporadic disease is unknown. Children given

Oval, bean-shaped, or spherical

Elongated Bilobated

Multilobated

Oval, bean-shaped, or spherical

FIGURE 53-4. Hypercellular parathyroid glands are usually oval or kidney shaped but occasionally are elongated, bilobated, or multilobated. (From Akerstrom G, Malmaeus J, Bergstrom R. Surgical anatomy of human parathyroid glands. Surgery 1984;95:14.)

FIGURE 53-5. Multilobed parathyroid gland (hyperplastic gland) in a 62-year-old woman with multiple endocrine neoplasia 1 and multiple abnormal parathyroid glands.

the diuretic furosemide (Lasix) experience parathyroid hyperplasia as the parathyroids enlarge to compensate for increased urinary calcium loss.24

Neonatal HPT has been documented to be caused by specific point mutations on chromosome 3.25'26 These patients have homozygous mutations, whereas patients with benign familial hypocalciuric hypercalcemia have heterozygous mutations at the same sites.25 26 Patients with neonatal HPT require total parathyroidectomy with autotransplantation and cryopreservation, whereas those with benign familial hypocalciuric hypercalcemia should be treated nonopera-tively because they do not appear to be adversely affected by the hypercalcemia, and virtually all patients experience recurrent hypercalcemia after parathyroidectomy.27

Studies have been performed to determine whether hyperplastic glands and parathyroid adenomas are monoclonal or polyclonal.28 30 Theoretically, the parathyroid adenoma originates from one cell because it is a neoplasm rather than a hyperplastic growth of normal parathyroid tissue. One study, however, showed that only 75% of adenomas are monoclonal.29 Hyperplasia theoretically originates from more than one cell. However, studies showed that in patients with MEN 1 large glands are monoclonal, whereas small glands are often polyclonal.31,32 Further studies are required to better clarify the mechanisms of parathyroid overgrowth.

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