Secondary Parathyroid Hyperplasia Research Articles

“Tertiary” hyperparathyroidism induced by osteomalacia resulting from phosphorus depletion

In the patient described clinical and chemical signs of osteomalacia developed as a result of phosphorus depletion caused by ingestion of excessive amounts of aluminum hydroxide. Symptoms disappeared and serum calcium and phosphorus levels were restored to normal by discontinuing these medications. Four years later hyperparathyroidism due to an autonomously functioning adenoma (“tertiary” hyperparathyroidism) developed. It is postulated that osteomalacia, with low serum calcium and phosphate concentrations, served as the stimulus for the development of secondary parathyroid hyperplasia and, in turn, to an autonomously functioning parathyroid adenoma.

The radiologist in diagnosis of nonendocrine endocrinology (tumors and humors).

Clinical endocrinological syndromes which arise from tumors of nonendocrine tissue are being recognized with increasing frequency (1, 2). The radiologist is often requested to assist in the diagnosis or treatment of this group of conditions which has been designated “tumors and humors,” or “humoral syndromes.” The patients are clinically recognized as having Cushing's syndrome, hypercalcemia-hypophosphatemia (hyperparathyroidism), hypoglycemia, and erythrocythemia. Less commonly the clinical picture may be hyponatremia (inappropriate antidiuretic hormone secretion (3)), hyperthyroidism (4), hyperserotonemia (5, 6), or precocious puberty (7), as well as one or another of a smaller group of conditions. A brief analysis of the four most frequent syndromes will be presented here to afford important information for the radiologist. The exact etiology and basic mechanism underlying the interrelationship of tumors and classical clinical manifestations of primary endocrine pathology have been the subject of much speculation (8). For instance, it has been suggested that massive metastasis to the liver might interfere with hormone catabolism or that metastasis to an endocrine gland migh stimulate excessive hormone formation. In most cases neither exists. Furthermore, it has been postulated that the endocrinopathy is present initially and that it is capable of stimulating carcinogenesis. Review of the cases, however, proves that in most instances this is not true. For example, there has never been a report of a cancer developing in a chronic case of Cushing's disease (9). Another consideration is that an unknown stimulus within the body is capable of producing both the endocrine disease and the malignant process, independent of each other, but this seems unlikely. Finally, it has been theorized that the tumor tissue itself may produce and secrete or leak the appropriate polypeptide responsible for the specific endocrine state. The recent developments in improved bioassay and immunologic technics have now demonstrated polypeptide hormone within the tumor tissue in most of the syndromes. It thus seems apparent that certain malignant tumors for reasons as yet unknown are capable of direct production of hormone or hormonelike substances. It is quite important to recognize and distinguish these situations from primary endocrine disease in view of marked differences in therapeutic approach. Hypercalcemia-Hypophosphatemia (Hyperparathyroidism) Hypercalcemia with hypophosphatemia is in most instances the result of excess parathormone production by parathyroid gland tissue. Hypercalcemia with a normal or elevated blood phosphorus level may be seen in a wide variety of states, such as Boeck's sarcoid, milk-alkali syndrome, excess vitamin D, Paget's disease, metastatic tumors to bone, including multiple myeloma, and in chronic renal failure with secondary parathyroid hyperplasia (10).

AUTONOMOUS SECONDARY (RENAL) PARATHYROID HYPERPLASIA.

SECONDARY parathyroid hyperplasia resulting from long standing renal insufficiency is a well described entity whose characteristics have been described by Castleman and Mallory1 and others.2 , 3 Moreover, clinical hyperparathyroidism due to such hyperplasia has been the subject of several reviews4 5 6 and case reports7 8 9 10 11 emphasizing the variety of complications that may ensue.However, despite suggestions that such secondarily stimulated hyperparathyroidism may become autonomous12 13 14 convincing data regarding such a possibility are not available, owing to the great excess of complexing anions in the blood that are an invariable consequence of significant uremia.The case reported below, therefore, is of considerable importance because it . . .

Brown tumor and secondary hyperparathyroidism.

SECONDARY hyperparathyroidism associated with chronic renal disease may simulate primary hyper-parathyroidism with secondary renal impairment in virtually every particular. An exception is the brown tumor, a relatively rare lesion, which has been considered to be almost specific for primary hyperpara-thyroidism and which to our knowledge has not previously been described as a manifestation of secondary parathyroid hyperplasia. Case Report A 22-year-old man was found to be hypertensive during a college entrance examination in January, 1962. He was asymptomatic. The past medical history revealed an operation for bladder-neck obstruction at the age of 3, but he had apparently been well since . . .

COMBINED PRIMARY AND SECONDARY HYPERPARATHYROIDISM: TWO CASE REPORTS AND A REVIEW

Excerpt Although the literature on hyperparathyroidism is extensive, there are few case reports of functioning parathyroid adenoma occurring simultaneously with secondary hyperplasia of the parathy...

Primary hypertrophy and hyperplasia of the parathyroid glands as a cause of hyperparathyroidism

Primary hyperplasia of the parathyroid glands is a distinct pathologic entity. Twenty-two cases have been collected from the literature; the morphologic and clinical aspects of these and four additional cases seen at the Mayo Clinic have been discussed. Primary hyperplasia must be differentiated from parathyroid adenoma composed of clear cells, from metastatic renal cell carcinoma to the thyroid and from secondary parathyroid hyperplasia. The question of hypertrophy versus hyperplasia has been discussed; evidence is given for assuming that both are present but that the latter predominates. The clinical implications of primary hyperplasia are discussed. In twenty-one of twenty-six patients primary hyperplasia was accompanied by primary hyperparathyroidism; it is probable that the condition always represents primary parathyroid hyperfunction.

Chronic renal disease, secondary parathyroid hyperplasia, decalcification of bone and metastatic calcification

Chronic renal disease, secondary parathyroid hyperplasia, decalcification of bone and metastatic calcification

HYPERPARATHYROIDISM WITH ADENOMA CAUSING RENAL FAILURE AND SECONDARY HYPERPARATHYROIDISM

It is well recognized that a serious form of renal disease may result from hyperparathyroidism.¹It is also well established that chronic renal insufficiency frequently is associated with secondary hyperplasia of the parathyroid glands.²On a priori grounds, therefore, one can reason that a paradoxic situation might exist wherein long-standing renal disease resulting from a parathyroid adenoma is so severe as to stimulate further overactivity of the other parathyroid glands. Actually this does occur. Johnson³reported a case in which removal of a parathyroid adenoma was followed by death from hypertension and uremia four years later, at which time the remaining parathyroid glands showed enlargement and hyperplasia. The following case report is submitted because it is the first to our knowledge in which secondary parathyroid hyperplasia has been proved to coexist with a parathyroid adenoma. <h3>REPORT OF CASE</h3> A. C., a former insurance salesman, aged 50, entered