Disease/disorder effects osteomalacia

Other chronic disorders cause osteomalacia. " " Phosphate depletion from low dietary intake, phosphate-binding antacids, and oncogenic osteomalacia (potentially phosphaturic effect) can cause osteomalacia. Hypophosphatasia is an inborn error of metabolism in which deficient activity of alkaline phosphatase causes impaired mineralization of bone matrix. Acidosis from renal dysfunction, distal renal tubular acidosis, hypergammaglobulinemic states (e.g., multiple myeloma), and drugs (e.g., chemotherapy) compromises bone mineralization. Renal tubular disorders secondary to Fanconi s syndrome, hereditary diseases (e.g., Wilson s disease, a defect in copper metabolism), acquired disease (e.g., myeloma), and toxins (e.g., lead) cause osteomalacia to varying degrees. Chronic wastage of phosphorus and/or calcium limits mineralization, which may be further compromised by acidosis and secondary hyperparathyroidism. 

Another potential long-term adverse effect of AED treatment is osteomalacia and osteoporosis. The bone disorders associated with AED use consist of a heterogeneous group of disorders. These include findings ranging from asymptomatic high-tumover disease. 

The majority of clinical applications of in vivo NAA have related to the determination of total-body and partial-body Ca to obtain invaluable clinical data on losses of calcium resulting from diseases such as osteoporosis, osteomalacia, and chronic renal diseases, as well as on the potential effect of drugs or therapy programs attempting to stem these losses (Krishnan 2000). Improvements in the technique, which mainly result in lower doses, allow applications to total-body Ca studies in population groups (ElKs et al. 2001). Other elements of clinical interest, such as Na, Cl, and I have been investigated in conjunction with various human diseases and disorders, while the clinical value of the measurement of major elements such as H, N, O, and P remains uncertain. Ellis (2000) recently reviewed the role of in vivo NAA among the in vivo methods for the measurement of human body composition. 

Probably the most notorious case of cadmium toxicity was the disorder known as Itai-Itai disease which occurred in Japan after World War II. This was essentially an osteomalacia associated with serious kidney damage and is discussed in Chapter 6.6.4. Changes in bones associated with cadmium toxicity have been described by Nicaud [44] and a specific effect is proteinuria caused by damage to kidney tubules [45-47]. Acute necrosis of the testes has also been reported [48] at relatively low doses of cadmium, although this effect does not seem to be a feature of chronic cadmium toxicity. Chronic bronchitis, hypertension and cardiovascular disease have also been reported as being associated with cadmium toxicity [49]. 

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