Osteitis fibrosa cystica

Osteitis fibrosa cystica Renal osteodystrophy Osteosclerosis Anticonvulsant treatment... 

ROD progresses insidiously for several years before the onset of symptoms such as bone pain and fractures. Skeletal complications include osteitis fibrosa cystica (high bone turnover), osteomalacia (low bone turnover) and adynamic bone disease. When ROD symptoms appear, the disease is not easily amenable to treatment. 

Anticonvulsant treatment Fibrogenes imperfecta ossium Osteitis fibrosa cystica Osteomalacia Osteoporosis Osteopenia Osteosclerosis Renal osteodystrophy Rickets... 

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. 

Renal osteodystrophy (ROD)—The condition resulting from sustained metabolic changes that occur with chronic kidney disease including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. The skeletal complications associated with ROD include osteitis fibrosa cystica (high bone turnover disease), osteomalacia (low bone turnover disease), adynamic bone disease, and mixed bone disorders. 

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. 

The clinical end product of the pathophysiological processes just described is usually osteitis fibrosa cystica. Skeletal raidography may show characteristic... 

Osteoporosis and osteitis fibrosa cystica Metastatic calcifications vi. Neurologic changes Secondary hyperparathyroidism a. Etiology... 

If hypercalcaemia is not detected early, the high circulating PTH causes a characteristic pattern of bone resorption, known as osteitis fibrosa cystica shown in Figure 3. As awareness of hyper-calcaemia has grown and detection methods have improved, such severe bone abnormalities are seen much less frequently. 

Although all cases of renal insufficiency may lead to moderate hyperplasia of the parathyroid associated with mild signs of demineralization of the skeleton, only in those cases in which slow and progressive destruction of the renal parenchyma occurs does renal osteitis fibrosa cystica generalisata (a disease resembling von Recklinghausen s disease) develop. In these advanced cases, metastatic calcification in soft tissue may also be found. Renal biopsy may prove useful in the differential diagnosis of primary and secondary hyperparathyroidism. 

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