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B General Measures
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For prevention and treatment of osteoporosis, the diet should be adequate in protein, total calories, calcium, and vitamin D Pharmacologic corticosteroid doses should be reduced or discontinued if possible Thiazides may be useful if hypercalciuria is present High-impact physical activity (eg, jogging) significantly increases bone density in men and women Stair-
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OSTEOMALACIA
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ESSENTIALS OF DIAGNOSIS
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Painful proximal muscle weakness (especially pelvic girdle); bone pain and tenderness
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found in 41% of these women; 35% in the United States and 125% in Italy Vitamin D deficiency is particularly common in the institutionalized elderly, with the incidence exceeding 60% in some groups not receiving vitamin D supplementation Deficiency of vitamin D may arise from insufficient sun exposure, malnutrition, or malabsorption (due to pancreatic insufficiency, cholestatic liver disease, sprue, inflammatory bowel disease, jejunoileal bypass, Billroth type II gastrectomy, etc) Cholestyramine binds bile acids necessary for vitamin D absorption Patients with severe nephrotic syndrome lose large amounts of vitamin D-binding protein in the urine, and osteomalacia may also develop Anticonvulsants (eg, phenytoin, carbamazepine, valproate, phenobarbital) inhibit the hepatic production of 25(OH)D and sometimes cause osteomalacia Phenytoin can also directly inhibit bone mineralization Serum levels of 1,25(OH)2D are usually normal Vitamin D dependent rickets type I is caused by a rare autosomal recessive defect in renal synthesis of 1,25(OH)2D It presents in childhood with rickets and alopecia; osteomalacia develops in adults with this condition unless treated with oral calcitriol in doses of 05 1 mcg daily Vitamin D dependent rickets type II (better known as hereditary 1,25[OH]2D-resistant rickets) is caused by a genetic defect in the 1,25(OH)2D receptor Adults respond variably to oral calcitriol in very large doses (2 6 mcg daily)
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Decreased bone density from defective mineralization Laboratory abnormalities may include increases in alkaline phosphatase, decreased 25-hydroxyvitamin D, or hypocalcemia, hypocalciuria, hypophosphatemia, secondary hyperparathyroidism Classic radiologic features may be present
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Defective mineralization of the growing skeleton in childhood causes permanent bone deformities (rickets) Defective skeletal mineralization in adults is known as osteomalacia It is caused by any condition that results in inadequate calcium or phosphate mineralization of bone osteoid
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Etiology (Table 26 12)
A Vitamin D Deficiency and Resistance
Vitamin D deficiency decreases the intestinal absorption of calcium and is the most common cause of osteomalacia Significant vitamin D deficiency (serum 25[OH]D < 50 nmol/L or < 20 ng/mL) was found in 243% of postmenopausal women from 25 countries in the MORE study The incidence varied: < 1% in Southeast Asia, 293% in the United States, and 36% in Italy Severe vitamin D deficiency (serum 25[OH]D < 25 nmol/L or < 10 ng/mL) was
B Deficient Calcium Intake
Table 26 12 Causes of osteomalacia
Vitamin disorders Decreased availability of vitamin D Insufficient sunlight exposure Nutritional deficiency of vitamin D Malabsorption Nephrotic syndrome Vitamin D dependent rickets type I Liver disease Chronic renal failure Kidney transplantation Phenytoin, carbamazepine, or barbiturate therapy Dietary calcium deficiency Phosphate deficiency Decreased intestinal absorption Nutritional deficiency of phosphorus Malabsorption Phosphate-binding antacid therapy Increased renal loss X-linked hypophosphatemic rickets Tumoral hypophosphatemic osteomalacia Association with other disorders, including paraproteinemias, glycogen storage diseases, neurofibromatosis, Wilson s disease, and Fanconi s syndrome Disorders of bone matrix Hypophosphatasia Fibrogenesis imperfecta Axial osteomalacia Inhibitors of mineralization Aluminum Bisphosphonates
Rickets and osteomalacia continue to be common problems in many tropical countries despite adequate exposure to sunlight A nutritional deficiency of calcium can occur in any severely malnourished patient Some degree of calcium deficiency is common in the elderly, since intestinal calcium absorption declines with age Ingestion of excessive wheat bran also causes calcium malabsorption
C Phosphate Deficiency
Phosphatonin is a circulating peptide that inhibits sodiumdependent phosphate transport in the renal tubule; high levels of this peptide cause excessive phosphaturia, resulting in hypophosphatemia X-linked hypophosphatemic rickets is associated with high levels of phosphatonin, probably caused by familial or sporadic mutations in PHEX endopeptidase, which fails to cleave phosphatonin Oncogenic osteomalacia is caused by excessive production of phosphatonin by a wide variety of soft tissue tumors (87% benign) Such tumors may be hard to find OctreoScan has been reported to detect many of these small tumors The condition is characterized by hypophosphatemia, excessive phosphaturia, reduced or normal serum 1,25(OH)2D concentrations, and osteomalacia Excessive renal phosphate losses are also seen in proximal renal tubular acidosis and Fanconi s syndrome Some cases of hyperphosphaturia are idiopathic Other causes of hypophosphatemic osteomalacia include poor nutrition, alcoholism, or chelation of phosphate in the gut by aluminum hydroxide antacids, calcium acetate (PhosLo), or sevelamer hydrochloride (Renagel)
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