Excerpt from Hyperparathyroidism, Secondary

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The clinical manifestation includes bone and joint pain and limb deformities. The radiologic features of secondary hyperparathyroidism in the skeleton are similar to those of primary hyperparathyroidism.

Pathophysiology: In secondary hyperparathyroidism, pronounced hyperplasia of the chief cells of the parathyroid gland is often present. This hyperplasia usually affects all 4 glands, but 2 or even 3 may be spared. The cause of this asymmetric involvement is obscure. In exception cases, a true adenoma may develop. Histologically, islands of oxyphils are often present, and hyperplastic cells usually replace the fat.

The most common cause of secondary hyperparathyroidism is chronic renal disease, which is an occurrence in hemodialysis patients. Chronic hypocalcemia and secondary hyperparathyroidism may also occur in vitamin D deficiency, intestinal malabsorption syndromes with inadequate absorption of vitamin D and calcium, and pseudohypoparathyroidism. Other rare causes associated with secondary hyperparathyroidism include the long-term furosemide therapy in infants, the use of oral contraceptives, and idiopathic hypercalciuria.

In most cases, the sequence of events leading to the development of hypersecretion of parathormone is any long-standing osteomalacia. The most common cause is chronic renal insufficiency, such as that in renal polycystic disease or chronic pyelonephritis. Chronic renal insufficiency is accompanied by several biochemical abnormalities that include diminished urinary excretion of phosphate with consequent elevation of serum phosphate levels and elevation in the levels of the calcium-phosphate product. Serum calcium levels tend to be normal, but they may be marginally reduced. The alkaline phosphates are almost always elevated. The hyperphosphatemia and damaged renal parenchyma leads to a reduction of renal production of 1-a-(OH)₂ D3, or 1,25-dihydroxycholecalciferol (1,25-DHCC). Decreased intestinal absorption of vitamin D follows, which impairs mobilization of calcium from the bones due to PTH resistance.

Aluminum accumulates in patients undergoing long-term hemodialysis. This accumulation causes dementia and also prevents the mineralization of osteoid by means of an ill-understood mechanism. The bone changes that may occur with aluminum toxicity include osteopenia, fractures, and osteomalacia. An early sign of aluminum toxicity is periosteal new-bone formation along the shafts of long bones and at the pelvic inlet. Low or normal serum calcium levels usually indicate preexisting osteomalacia. A markedly elevated alkaline phosphatase level usually accompanies skeletal disease.

The most common presentation of renal osteodystrophy is a combination of osteomalacia, secondary hyperparathyroidism, and a varying degree of osteosclerosis. Several pathologic changes occur in association with renal osteodystrophy. These include lacunar bone resorption, fibrous replacement of the marrow following hemorrhage, necrosis, and brown tumors due to areas of intense osteoclastic activity. In children, the skeletal changes are typically those of rickets, which affect the epiphyseal plate, as demonstrated on undecalcified preparations.

Considerable speculation exists about to the cause of osteosclerosis that is so often encountered in secondary hyperparathyroidism. Two factors are implicated: (1) Excessive parathormone directly acts as an anabolic agent on the bone, causing osteosclerosis, and (2) a significant increase in the formation of woven bone contributes to the osteosclerotic a .....

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