Osteomalacia And Hypervitaminosis D: Clinical Manifestations, Diagnosis And Treatment
Osteomalacia denotes those disorders where mineralization of newly formed bone matrix (osteoid) is defective.
Etiology: Osteomalacia may be of two different types.
- Nutritional inadequacy of vitamin D
- Vitamin D-resistant osteomalacia. This occurs in the following conditions:
- In renal tubular defects which produce hypophosphatemia and chronic metabolic acidosis.
- Chronic administration of diphenylhydantoin which leads to excessive metabolism of vitamin D.
- After parathyroidectomy for osteitis fibrosa of hyperparathyroidism in which rapid formation of new bone outstrips bone resorption.
Osteomalacia In India
Looser’s zones In Osteomalacia
Codfish Vertebrae In Osteomalacia
Osteomalacia presents with vague pain which start as aches and pains insidiously, in the lumbar spine and thighs and spreading later to the arms and ribs. The pain is frequently felt over the bones themselves, and not at the joints. The pain is usually symmetrical and non-radiating and is accompanied by tenderness of involved bones. Proximal muscles are weak and there is difficulty in climbing up stairs and getting up from the squatting position. Occasionally, localized acute bone pain develops rapidly. These sites correspond to the development of pseudofractures. Classical radicular pain may develop due to compression fractures of the vertebra.
Physical signs include deformities, which may be missed if not specifically looked for. The usual deformities are triradiate pelvis and spinal kyphosis (due to action of gravity). Pathologic fractures due to weight bearing and avulsion of tendinous attachements may develop. Biochemical features resemble those of rickets.
Characteristic radiological features are the appearance of “pseudofractures” (Milkman’s lines and Looser’s zones). These are linear zones of decalcification which tend to be symmetrical and extend perpendicular to the cortex. The common sites are the pubic rami, ischium, the neck of the femur, the outer edge of the scapula, ribs and vertebrae. Occasionally, Looser’s zones may extend right across a long bone simulating complete fractures. They are called pseudofractures because the gap is bridges by uncalcified osteoid tissue. They do not reveal any discontibuity of bone clinically. The pseudofractures are caused by the decalcification along the course of the major arteries entering the bones especially in areas of muscular attachement, namely the adductor insertion on the pubic ramus and attachement of gluteal muscles to the trochanters of the femur.
Vertebral bones show compression and widening of intervertebral spaces to produce biconcave or “cod-fish” vertebrae.
However, in patients who develop osteomalacia secondary to renal tubular disorders or chronic renal failure, there is marked cortical thickening and increased density of trabeculae in spongy bone. The reason for this hyperosteosis is not clear. Despite the radiological appearances, the bone is abnormally brittle and prone to develop fractures.
Treatment: Nutritional osteomalacia responds well to daily administration of 2000 to 4000 IU of vitamin D (0.05 to 0.1 mg) for 6 to 12 weeks followed by maintenance doses of 200 to 400 IU daily. Adequate supplements of calcium are provided in the form of milk, 500 to 750 ml per day or calcium lactate tablets, 1g along with food.
Prolonged administration of massive doses of vitamin D results in vitamin D intoxication. This causes hypercalcemia. Symptoms include nausea, vomiting, constipation, drowsiness and signs of renal impairment. Metastatic calcification occurs in several tissues including the kidneys, lungs, gastric mucosa and blood vessels. Renal function may deteriorate before other signs of toxicity are manifest. Subjects receiving high doses of vitamin D should have regular monitoring of serum calcium and if it is above 2.6 mmol/liter (10.5 mg/dal), the intake of the vitamin should be stopped.
© 2014 Funom Theophilus Makama