Hyperparathyroidism Adenoma

Primary hyperparathyroidism occurs as a result of hyperplasia or the occurrence of adenoma. Secondary hyperparathyroidism may result from renal failure because of the associated phosphate retention, resistance to the metabolic actions of PTH, or impaired vitamin D metabolism. The last-mentioned factor is primarily responsible for the development of osteomalacia. Muscle symptoms are much more common in patients with osteomalacia than in primary hyperparathyroidism. Muscle biopsy has revealed disseminated atrophy, sometimes confined to type 2 fibers, but in other cases involving both fiber types. Clinical features of osteomalacic myopathy are proximal limb weakness and associated bone pain the condition responds well to treatment with vitamin D. 

Ten patients who had taken lithium for less than 1 year and 13 who had taken it for more than 3 years were assessed for alterations in bone metabolism and parathyroid function (654). There were no differences in bone mineral density, serum calcium concentration, or PTH concentration, but both groups had increased bone turnover and the longterm group had nonsignificantly higher calcium and PTH concentrations (including one hyperparathyroid patient who had an adenoma excised). The authors conclusion that lithium therapy is not a risk factor for osteoporosis needs to be tempered by the small sample size, the case of adenoma, and the blood concentration trends. 

Awad SS, Miskulin J, Thompson N. Parathyroid adenomas versus four-gland hyperplasia as the cause of primary hyperparathyroidism in patients with prolonged lithium therapy World J Surg 2003 27 486-8. 

Lam P, Tsai S-J, Chou Y-C. Lithium associated hyperparathyroidism with adenoma a case report. Int Med J 2000 7 283-5. 

One female and one male patient had hyperparathyroidism with elevated serum alkaline phosphatase activities and extensive bone changes characteristic of generalized osteitis fibrosa cystica. In both instances, the serum acid phosphatase activity of the serum fell to normal values after removal of the parathyroid adenoma despite transitorily increased serum alkaline phosphatase activity. The fifth patient was a female with osteopetrosis involving the major part of the skeleton. The serum acid phosphatase was 8.7 K.A. units, the highest in the control series— yet the serum alkaline phosphatase was within normal limits. It would appear, therefore, that some patients with skeletal disease may have a slight but definitely elevated serum acid phosphatase activity, at least as determined by the Gutman method (GIO, G14), which cannot be explained by concurrent prostatic carcinoma or by a spillover of alkaline phosphatase activity to a pH of 5.0. 

Of 15 patients taking long-term lithium who had surgery for primary hyperparathyroidism, 14 had adenomas... 

Most cases of lithium-induced hyperparathyroidism are mild [43]. Both pre-existing parathyroid abnormalities which may have been unmasked by lithium therapy and de novo hypercalcemia and hyperparathyroidism have been documented [44]. Parathyroid hyperplasia [33%] and adenomas [67%] were reported in one series of hypercalcemic patients treated with lithium [45]. Bilateral neck exploration has been proposed as an appropriate management approach because of a relatively high frequency of multi-gland involvement. However, parathyroid resection should be limited to those with overt disease [46]. 

Primary hyperparathyroidism is characterized by excessive secretion of PTtI that results in hypercalcemia. It is most often due to a solitary adenoma (80% to 85% of cases), less frequently (about 15%) due to chief cell hyperplasia involving all glands, and rarely due to parathyroid carcinoma (<1%). 

Primary hyperparathyroidism results from hyperplasia, adenoma, or carcinoma of the parathyroid glands and from ectopic production of the hormone by squamous cell carcinoma of the lung or by adenocarcinoma of the kidney. In about 10% of hyperparathyroidism, hyperplasia or tumors of the parathyroid glands occur due to familial disorders known as multiple endocrine neoplasia (MEN). MEN syndromes consist of three subtypes (I, IIA, IIB) and are... 

Hyperparathyroidism results from oversecretion of PTH. This condition leads to excessive bone turnover and demineralization and must be treated by removal of the parathyroid gland. The disorder is classified into primary, secondary, and tertiary hyperparathyroidism. Sporadic primary hyperparathyroidism is the third most common endocrine disorder, after diabetes and hyperthyroidism. It is most common in females older than 55 years of age and the leading cause is a single adenoma, which secretes the hormone constitu-tively, without regulation. Symptoms can include osteopenia and bone fractures, renal stones resulting from hypercalciuria, peptic ulcer disease, and pancreatitis. In milder cases, patients are asymptomatic or suffer only muscle weakness, fatigue, and/or depression. 

Til. Gill AJ, Clarkson A, Gimm O, et al. Loss of nuclear expression of parafibromin distinguishes parathyroid carcinomas and hyperparathyroidism-jaw tumor associated adenomas from sporadic parathyroid adenomas and hyperplasias. Am Surg Pathol. 2006 30 1140-1149. 

Very occasionally, patients are seen in whom hypercalcemia is apparently due to secondary hyperparathyroidism. This is in a sense a contradiction in terms, since the essence of secondary hyperparathyroidism is the continuous stimulation of the parathyroid glands by a reduced ionic calcium concentration. However, at least two such cases with steatorrhea have now been described (D4, El), and in each case a parathyroid adenoma was discovered. The implication is that parathyroid stimulation can in certain circumstances go on to adenoma formation this also occurs occasionally in prolonged renal failure (G5). 

MEN type I is characterized by hyperparathyroidism, together with pituitary and pancreatic tumours. Hyper-calcaemia caused by excess PTH. secretion is the dominant feature in this syn-drt)me. The most common pituitary tumour is a non-functioning chromophobe adenoma which, although it dws not secrete a hormone itself, may have effects on the secretion of other anterior pituitary hormones. The most common pancreatic tumour in MEN type 1 is an islet cell tumour secreting gastrin. The secretion of gastrin may lead to gastric ulceration. 

The most common cause of hypercalcemia in outpatients is primary hyperparathyroidism, due either to a single adenoma or diffuse hyperplasia. Primary hyperparathyroidism is often associated with significant hypophosphatemia due to PTH effects on renal phosphate reabsorption. The diagnosis is generally apparent from the elevated serum CcP associated with an inappropriately high PTH level. In contrast, secondary hyperparathyroidism is a disorder in which PTH levels are elevated in response to persistent threats to norrruil calcium homeostasis such as hyperphosphatemia from chronic renal disease. 

The ultimate therapeutic goal of managing hyperparathyroid hypercalcemia is returning blood PTH, calcium and phosphate levels to their normal range. In IPTH, when active bone, renal or 61 symptoms are present, surgery is the most effective treatment modality when the offending parathyroid adenoma can be identified. In MENl or hyperplasia, controversy exists as to whether total parathyroidectomy... 

The tumors of the parathyroid that can cause hyperparathyroidism are of four different histological varieties adenoma, wasserhelle cell hyperplasia, chief cell hyperplasia, and carcinoma (see Fig. 5-8). 

The most common cause of hyperparathyroidism is a single benign adenoma (80-90% of the cases). Adenomas develop in a single area of one of the parathyroids. After dissection, they appear as brown nodular masses, often browner than normal parathyroids. The weight of these tumors varies considerably— from not more than a normal parathyroid to as much as 100 g. Adenomas may be under the capsule of the thyroid gland or deeply embedded in the thyroid tissue. Histologically, the most typical characteristic of these tumors is the pleomorphism of the cell type. Oxyphil, chief, and clear cells all participate in the proliferative process. 

In rare cases, hyperparathyroidism results from multiple adenomas involving two, three, and even four... 

In six cases of hthium-associated hyperparathyroidism, four had parathyroid adenomas [67, 68 ]. The authors suggested that lithium can help uncover pre-existing parathyroid disease, although there does appear to be an increased incidence of multiglandular or multiadenomatous disease in patients taking lithium. Surgical treatment is often curative when adenomas are discovered. When hypercalcemia persists, cinacalcet, a calcimimetic can be used effectively. 

A disorder in which there are adenomas or hyperplasia occuring simultaneously in the pituitary, adrenals, pancreas, parathyroids or in any combination of these glands. The symptoms therefore include hyperparathyroidism, acromegaly, Cushing s syndrome, gastric ulceration (if the pancreatic cells produce... 

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