Tissue calcification

Soft and hard acids and bases principle, 2, 1040 Soft-tissue calcification, 6,597 Sogrenite structure, 6, 849 Soils... 

High phosphate diets cause decreased Ca absorption, secondary hyperparathyroidism, accelerated bone resorption and soft tissue calcification in some animals, but not in normal humans. Although phosphates may decrease Ca absorption in man at very high (> 2000 mg/day) Ca intakes, they do not do so at more moderate Ca levels and enhance Ca absorption at very low levels (< 500 mg/day). Phosphates increase renal tubular reabsorption and net retention of Ca. At low Ca intakes, phosphates stimulate parathyroid hormone (PTH) secretion without causing net bone resorption. 

Calcium Metabolism, Bone Mineral Loss, and Soft Tissue Calcification in Rodents... 

Patients with advanced renal insufficiency (Ccr less than 30 mL/min) exhibit phosphate retention and some degree of hyperphosphatemia. The retention of phosphate plays a role in causing secondary hyperparathyroidism associated with osteodystrophy and soft-tissue calcification. Calcium acetate, when taken with meals, combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in the feces. 

Lactation It is not known whether these drugs are excreted in breast milk. Because zoledronic acid binds to bone long-term, do not administer to a nursing woman. Children Safety and efficacy for use in children have not been established. Children have been treated with etidronate at doses recommended for adults, to prevent heterotopic ossifications or soft tissue calcifications. 

Hypercalcaemia and soft-tissue calcification have been found in animals grazing on plants such as Cestrum diumum and Solanum malacoxylon, and attributed to the presence of a l,25-(OH)2D3-glycoside.453 The calcinogenic plant Trisetum flavescens causes severe calcification on ingestion, but the vitamin D3 species responsible has not been identified 454... 

Ho AM, Johnson MD, Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis. Science 289 265-70. 

Hypercalcemia (osteosclerosis or bone loss, and soft tissue calcification)... 

A detailed account of the biochemistry of the bisphosphonates has recently appeared elsewhere170). Briefly, the bis-phosphonates inhibit soft tissue calcification. Bis-phospho-nates, such as HEBP inhibit the mineralization of cartilage, bone and dentine. Prolonged administration of HEBP to man at oral doses of 10 mg-1 kg-1 for more than one month affects the mineralization of hard tissues. Slight changes in the substituents on the gemi-... 

Britton, W, M and Stokstad, E. L. R. (1970). Aorta and other soft tissue calcification in the magnesium-deficient rat- /. Nuir. 100,1501-1506. 

Okada J, Nomura M, Shirataka M, Kondo H. Prevalence of soft tissue calcifications in patients with SLE and effects of alfacarcidol. Lupus 1999 8(6) 456-61. 

Hypercalcemia occurs in horses with chronic renal failure and in a few neoplastic conditions. The clinical signs are usually those of the underlying pathophysiology but soft tissue calcification may occur. In experimental ponies, hypercalcemia induced ventricular fibrillation or cardiac arrest at ionized calcium concentrations of 18.2-40mg/dl (4.55-10.0 mmol/1) (Glazier et al 1979). Treatment for severe hypercalcemia (ionized... 

Hyperphosphatemia occurs without specific clinical signs in horses with strangulating intestinal lesions (Arden Stick 1988) and severe colitis (Svendsen et al 1979). The clinical findings reported in small animals include diarrhea, hypocalcemia, hypernatremia and an increased propensity to metastatic soft-tissue calcification. The treatment recommended in small animals includes i.v. fluids to correct any acidosis and promote renal phosphorus excretion and dextrose-containing fluids to promote translocation of phosphorus into cells (Macintire 1997). 

It appears that increased plasma phosphate concentrations are not directly toxic (Sutters et al 1996). Hypocalcemia and metastatic soft-tissue calcification caused by hyperphosphatemia result from the calcium/phosphate product exceeding that required for precipitation of calcium phosphate in the tissues (Macintire 1997, Sutters et al 1996). 

Parathyroid hormone (PTH) Primary hyperparathyroidism causes hypercalcemia, hypophosphatemia, and increased urinary cAMP hypoparathyroidism causes hypocalcemia and hyperphosphatemia, often with soft-tissue calcification and tetany and convulsions. Binds to cell-surface receptors and activates adenylate cyclase increases bone mineralization and activity of renal lot-hydroxylase in kidney, reabsorption of Ca " " increases and reabsorption of phosphate decreases. 

Vitamin D metabolites have been found in plants. En-teque Seca, a disease of cattle that graze on the plant Solanum glaucophyllum (malacoxalon) in South America, is characterized by calcinosis and soft-tissue calcification. Aqueous extracts of the leaves of this and other plants that have been used to treat uremic bone disease contain glycosides of l,25-(OH)2D. 

The cost beneflt ratio associated with more aggressive management of metabolic disorders (e.g., hyperphosphatemia and hypercalcemia) and sHPT has not been formally evaluated. If the associated complications such as vascular and soft tissue calcifications that may increase morbidity and hospitalizations can be significantly reduced, the additional medication costs may ultimately be of minimal consequence. 

The major effects of hyperphosphatemia are related to the development of hypocalcemia (caused by phosphate inhibition of renal la-hydroxylase) and its related consequences, as well as vascular and organ damage resulting from the deposition of calcium-phosphate crystals. Extravascular calcification can result in band keratopathy, red eye, pruritus, and periarticular calcification, especially in renal failure patients (see Chap. 44). In addition, soft-tissue calcifications in the conjunctiva, skin, heart, cornea, lung, gastric mucosa, and kidney have been observed, primarily in chronic renal failure patients." Hyperphosphatemia associated with chronic renal disease may result in renal osteodystrophy because of overproduction of parathyroid hormone. This condition is discussed in detail in Chap. 44. 

Parenteral phosphorus supplementation is associated with risks of hyperphosphatemia, metastatic soft tissue deposition of calcium-phosphate product, hypomagnesemia, hypocalcemia, and hyperkalemia or hypernatremia (caused by intravenous phosphorus salt) (Table 49-9). Inappropriate administration of large doses of parenteral phosphorus over relatively short time periods has resulted in symptomatic hypocalcemia and soft-tissue calcification. The rate of infusion and choice of initial dosage should therefore be based on severity of hypophosphatemia, presence of symptoms, and coexistent medical conditions. Patients should be closely monitored with frequent (every 6 hours) serum phosphorus determinations for 48 to 72 hours after starting intravenous therapy. It may be necessary to continue administration of intravenous phosphorus for several days in some patients, while other patients may be able to tolerate an... 

Johnson AR, Armstrong WD, Singer L. 1968. The incorporation and removal of large amounts of strontium by physiologic mechanisms in mineralized tissues. Calcif Tissue Res 2(3) 242-252. 

Jowsey J, Balasubramaniam P. 1972. Effect of phosphate supplements on soft-tissue calcification and bone turnover. Clin Sci 42 289-299. 

Shear stress induces larger amounts of elastin in cells and inhibits tissue calcification. Occludin, a transmembrane protein that forms tight junctions between cells, and is the main contributor to the blood-brain barrier (an obstacle to free passage of complex molecules into the central nervous system), is present in lesser amounts at high shear stress values (about 10% less at 20-30 dynes/cm ). 

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