Coronal view CT of the sacrum after cement injection into bilateral sacral insufficiency fractures. Patient was able to ambulate with significantly less pain following the injections. Courtesy Dr. A. Brook.
Osteomalacia (OM) is a metabolic bone disease resulting from defective mineralization of bone that leads to the accumulation of unmineralized osteoid matrix. The disease most frequently affects elderly housebound sedentary people who are not exposed to sunlight and consume a diet deficient in vitamin D. OM is caused by biochemical disturbances of the calcium-phosphate metabolism, which may be caused by intestinal malabsorption, senile hypovitaminosis D, hypophosphatemia, chronic renal insufficiency, or various drugs that are used long term, including anticonvulsants, bisphosphonates, and nonabsorbable antacids. A high degree of awareness of this disease is required in order to include it in the differential diagnosis. The classical biochemical changes of OM consist of low calcium, low phosphorus, and an elevated bone-specific alkaline phosphatase. In many elderly patients, however, the values of these substances may remain normal. The presence of the disease can be confirmed with a bone biopsy. The serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D (calcitriol) may be decreased, and the parathyroid hormone may be elevated. The following paragraphs deal with OM due to hypovitaminosis D.
Quite often OM is identified rather late because it presents with vague nonspecific complaints that simulate other common conditions such as fibromyalgia, polymyalgia rheumatica, polymyositis, osteoporosis, and metastatic diseases.
The presenting symptoms include three p's: pain, polyarthral-gia, and proximal muscle weakness. Most patients present with pain of insidious onset. The pain may be progressive and involve the spine, rib cage, pelvis, and the limb girdles. Several areas may be painful and tender simultaneously, thus simulating fibromyalgia and other systemic diseases. Many patients complain of bilateral joint pain and diffuse muscle aches. Polyarthralgia with synovitis of the hands and feet may develop. Myopathy can result in proximal muscle weakness, especially of antigravity muscles such as the quadriceps. The weakness gradually evolves and brings about functional deficits. Initially the patients complain of fatigue. Later on they develop difficulties getting up from the seated position, stair climbing, and maintaining their balance, and they eventually suffer falls. In longstanding untreated patients bony deformities such as kyphosis, scoliosis, bowed legs, and protrusio acetabuli may develop.
Plain films may show diffuse demineralization with blurring of the bony trabeculae. Lucent sites appear in cortical bones, attesting to osteoid accumulation. These sites are oriented at a right angle to the cortex and are called pseudofractures or Looser's zones. Pseudofractures are not common. They may be seen in the pelvis, especially at the pubic rami and the bones of the extremities. Quite often they appear bilaterally and symmetrically. Calcified enthesopathies, fuzzy sacroiliac joints, and subchondral bone resorption of the symphysis pubis may be encountered as well. Occasionally sacral insufficiency fractures may occur. Their appearance on CT and MRI is not different from osteoporotic fractures (Figures 10-17 and 10-18).
Large doses of vitamin D or its derivatives (calcitriol or alfa-calcidol) can reverse the symptoms over time. Vitamin D-deficient patients should receive 2,000-3,000 IU of vitamin D per day for several months. Alternatively they may be treated with intramuscular injections of ergocalciferol, 50,000-100,000 IU per week for 1 month followed by one injection per month for the next five months. Daily calcium supplementation should be provided until the OM has resolved.
Vitamin D supplementation, however, can increase calcium and phosphate serum levels by enhancing intestinal absorption of these elements. Regular renal monitoring is important because progressive kidney calcification—nephrocalcinosis—may develop.
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