Skeletal complications are frequently seen in prostate cancer, because the skeleton is the predilective site of metastases. These complications may respond successfully to androgen deprivation therapy, but the onset of hormone refractory status is associated with their reappearance and the resurgence in skeletal morbidity, mainly in the form of intractable bone pain (Coleman 1997; Pelger et al. 2001). A less frequent skeletal complication of prostate cancer is osteomalacia, which is resistant to various therapeutic manipulations and associated with invalidating generalized bony pain refractory to conventional analgesia. The most common pathophysiologic mechanism for osteomalacia is vitamin D deficiency, a relatively frequent finding in patients in a late stage of any malignancy. However, a severe form of osteomalacia associated with profound hypophosphatemia due to renal phosphate wasting has

24-hour urinary free cortisol/low dose dexamethasone suppression tests (DST) Plasma ACTH X 2

Fig. 14.2. Cushing's syndrome, diagnostic approach

Adrenal adenoma Adrenal carcinoma

CT Adrenal MRI Adrenal

Pituitary Adenoma Pituitary Hyperplasia


MRI pituitary High dose DST

Petrosal sinus venous sampling

Ectopic ACTH Producing tumor

> 2X normal been described in a number of malignancies, particularly those of mesenchymal origin. The tumor-secreted factor responsible for oncogenic hypophosphatemic osteomalacia has been identified as fibroblast growth factor 23 (FGF23) (Shimada et al. 2001). This hormonelike molecule has been recognized as playing an important role in the genesis of a number of disorders of phosphate homeostasis, having in common renal phosphate wasting and impaired mineralization of bone. Oncogenic hypophosphatemic osteomalacia presents clinically with fatigue, proximal myopathy (arthropa-thy, myalgia), bone pain (osteomalacia), metabolic en-cephalopathy (confusion, paraesthesia, seizures, coma) and gastrointestinal disturbances (anorexia, nausea, vomiting, gastric atony, ileus). It is characterized biochemically by increased urinary phosphate loss associated with low plasma phosphate and normal plasma calcium concentrations. In typical cases of oncogenic hypophosphatemic osteomalacia, low 1,25 dihydroxy-vitamin D concentrations are also observed, indicating a defect in the synthetic capacity of the renal one-alpha hydroxylase enzyme, which is normally stimulated by low serum phosphate concentrations. An analysis of 18 patients with metastatic prostate cancer treated with high-dose diethylstilbestrol diphosphate and 58 patients treated with doxorubicin, doxorubicin plus cis-platinum, doxorubicin plus diethylstilbestrol diphos-phate, or diethylstilbestrol diphosphate alone was conducted. A significant decrease in serum phosphate levels was seen only in patients treated with diethylstilbes-trol diphosphate. In conclusion, hypophosphatemia and possibly osteomalacia in metastatic prostate cancer may be related to estrogen therapy (Citrin et al. 1984).

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