Osteomalacia as a Result of Vitamin D Deficiency

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Historical perspective and scope of the problem

The first description of osteomalacia was by Gustav Pommer, a German pathologist, in the late nineteenth century who discussed the histologic differences between osteomalacia, osteoporosis, and osteitis fibrosa.1 One of the earliest reports of osteomalacia studied by tetracycline-based bone histomorphometry of the ribs was reported from Henry Ford Hospital in 1966.2 Based on current concepts of bone remodeling, Pommer's observations can be restated as replacement of resorbed bone by the same

Clinical manifestations of osteomalacia

Osteomalacia in its classic form manifests with a constellation of symptoms and signs that can be collectively referred to as osteomalcic syndrome. Some symptoms are vague and nonspecific and can easily escape the attention of the clinician, whereas others are highly specific and often diagnostic. Between these 2 extremes a patient may present with a combination of symptoms and signs. Therefore, a high degree of suspicion in the right clinical context is necessary to diagnose osteomalacia

Radiological features of osteomalacia

Many structural and pathologic changes in bone can be detected on radiograph examination and are the result of increased PTH secretion or of impaired matrix mineralization (Fig. 3, Fig. 4, Fig. 5, Fig. 6). Secondary hyperparathyroidism, an inevitable consequence of vitamin D depletion, leads to thinning of cortical bone. Increased cortical porosity is manifested as cortical striations in the metacarpals and phalanges on high-resolution radiographs of the hands. Rarely, generalized osteitis

Skeletal fractures

Several types of fractures occur in patients with osteomalacia with the pseudofractures that can progress to a complete fracture, usually in the subtronchanteric region of the femur or metatarsals, the greatest load-bearing bones. Rib fractures also occur commonly. When osteomalacia begins in childhood, the adult bones tend to be soft rather than brittle. Conversely, when osteomalacia begins later in adult life, the usual type fractures are more common. Spontaneous fractures of the sternum in

Biochemical changes in osteomalacia

In its classic presentation, hypocalcemia, hypophosphatemia, and increased serum alkaline phosphatase level are the classic biochemical triad of osteomalacia,1, 8 but increased serum alkaline phosphatase level is the most frequent and the earliest biochemical manifestation.8 As the vitamin D depletion advances, so does PTH hypersecretion leading to increased bone remodeling, endocortical bone resorption, and cortical thinning, which collectively results in irreversible cortical bone loss and

Diagnostic approach to osteomalacia

In the right clinical setting, a careful history and physical examination and a high degree of suspicion should facilitate the diagnosis of osteomalacia. However, despite many advances in biochemical measurements none of them are specific and most have moderate to low sensitivity. A reduced serum calcium × phosphate product and high alkaline phosphatase level in the presence of low 25-hydroxyvitamin D and high PTH makes the diagnosis of osteomalacia highly likely. On the other hand, a low serum

Treatment of osteomalacia

Depending on the urgency with which vitamin D replenishment is needed, several dose regimens can be used.19 Although each has some advantages the authors routinely prescribe ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) 50,000 IU (1.25 mg) once a week for 8 weeks followed by dose adjustments based on serum 25-hydroxyvitamin D and PTH levels. In our experience, there are no distinct differences between the vitamin D preparations except perhaps a shorter half-life of vitamin D2 and

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This article originally appeared in Endocrinology and Metabolism Clinics of North America Volume 39, Issue 2, June 2010.

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