No abstract available.
Humans ; Hypophosphatemia*

Hypophosphatemic osteomalacia is a rare form of metabolic bone disorder in neurofibromatosis type 1 (NF1). The exact disease mechanism of this disorder in NF1 is yet to be established. We present a 44-year-old female known to have NF1, who presents with debilitating bone pain, weakness and multiple fractures. Laboratory investigations showed persistent hypophosphatemia with renal phosphate wasting suggestive of hypophosphatemic osteomalacia. She also had concomitant vitamin D deficiency which contributed to the disease severity. Medical therapy with oral phosphate and vitamin D improved her symptoms without significant changes in fracture healing or phosphate levels.
Hypophosphatemia ; Osteomalacia ; FGF23 ; Vitamin D Deficiency

Oncogenic osteomalacia is a syndrome characterized by phosphaturia, hypophosphatemia, decreased 1,25-dihydroxyvitamin D level and specific signs and symptoms of osteomalacia. It is associated with the presence of neoplasm originated from mesenchyme. Until now, less than 100 cases of oncogenic osteomalacia have been reported. The pathophysiology of oncogenic osteomalacia has not been fully understood, but it has been suggested that a certain substance released by tumor may inhibit not only la-hydroxylase activity and reduce 1,25-dihydroxyvitamin D level in part, but directly inhibit reabsorption of phosphate. And then, reduced phosphaturia, hypophosphatemia and eventually osteomalacia develop. We report a case of osteosarcoma induced oncogenic osteomalacia detected by MRI in 59 year old woman.
Female ; Humans ; Hypophosphatemia ; Hypophosphatemia, Familial ; Magnetic Resonance Imaging* ; Mesoderm ; Middle Aged ; Osteomalacia* ; Osteosarcoma*

Tumour-induced osteomalacia (TIO) is a rare paraneoplastic syndrome, which is characterized by overproduction of FGF23 as a phosphaturic agent leading to chronic phosphaturia and hypophosphatemia, associated with inappropriately normal or low levels of vitamin D. We describe a rare case of a 57-year-old Indian female who presented with bone pains, muscle pains and lower limb weakness. On examination she was found to have hypophosphatemia. Our work up led to the identification of a FGF23 secreting parotid tumour. The tumour responsible for symptoms was a pleomorphic adenoma of the parotid gland. Its complete resection resulted in normalisation of patient's symptoms. Laboratory parameters and microsopic examination further revealed a mesenchymal tumour of mixed connective tissue type.

Human ; Female ; Middle Aged ; Adenoma, Pleomorphic ; Connective Tissue ; Hypophosphatemia ; Hypophosphatemia, Familial ; Lower Extremity ; Neoplasms, Connective Tissue ; Paraneoplastic Syndromes ; Parotid Gland ; Parotid Neoplasms ; Vitamin D ; Hypophosphatemia

Oncogenic osteomalacia is a rare paraneoplastic syndrome, characterized by hypophosphatemia, renal phosphate wasting, osteomalacia, and multiple insufficiency fractures, as a result of the tumor. A wide excision of the causative tumor is considered as the treatment of choice, following which, a dramatic recovery is expected. Authors report a case in which the symptoms and bone mineral density were dramatically recovered after an excision of the causative tumor around the tibialis posterior muscle in oncogenic osteomalacia.
Bone Density ; Fractures, Stress* ; Hypophosphatemia ; Osteomalacia* ; Paraneoplastic Syndromes

Adefovir dipivoxil is used antiviral agent in the treatment of chronic hepatitis B virus infection. This drug is recommended for patients infected with lamivudine-refractory hepatitis B. Many studies of low-dose adefovir have shown little evidence of renal tubular dysfunction. However, hypophosphatemic osteomalacia has recently been reported in patients treated with adefovir. We report three cases of low dose adefovir-induced hypophosphatemic osteomalacia with fractures. All three patients had been receiving adefovir due to lamivudine-refractory hepatitis B, presented multiple bone pain. The laboratory tests revealed hypophosphatemia and phosphaturia. Bone scintigraphy showed increased uptake in multiple lesions. They were diagnosed as adefovir induced hypophophatemic osteomalacia. Changing the antiviral agent and administration of calcitriol and phosphates improved hypophosphatemia and clinical symptoms. Patients with hepatitis B virus treated with adefovir should be monitored with the serum phosphate levels and presenting symptoms of diffuse bone pain, clinicians need to suspect this infrequent complication.
Calcitriol ; Hepatitis B ; Hepatitis B virus ; Hepatitis B, Chronic ; Hepatitis, Chronic ; Humans ; Hypophosphatemia ; Hypophosphatemia, Familial ; Osteomalacia ; Phosphates ; Radionuclide Imaging

Fanconi syndrome is a complex of renal tubular dysfunction defined by glycosuria without diabetes, generalized aminoaciduria, phosphaturia, bicarbonaturia, uric aciduria, and renal tubular acidosis. It is often associated with hypokalemia, hypophosphatemia, rickets and osteomalacia. We have experienced one case of Fanconi syndrome with chronic tubulointerstitial nephritis. The patient was a 4 year old and his chief complaints were polyuria, polydipsia, and poor weight gain. There were hyperchloremic metabolic acidosis, hypokalemia, glycosuria, generalized aminoaciduria and phosphaturia. We report a case of Fanconi syndrome with brief review of the literatures.
Acidosis ; Acidosis, Renal Tubular ; Child, Preschool ; Fanconi Syndrome* ; Glycosuria ; Humans ; Hypokalemia ; Hypophosphatemia ; Hypophosphatemia, Familial ; Nephritis, Interstitial ; Osteomalacia ; Polydipsia ; Polyuria ; Rickets ; Weight Gain

Refeeding syndrome refers to a life-threatening shift of electrolytes and fluid with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally, or parenterally. Clinical findings are fluid-balance abnormalities, abnormal glucose metabolism, hypophosphatemia, hypomagnesemia, hypokalemia and deficiencies of vitamin and trace element. Multiple organ systems including cardiac, respiratory, neurologic, renal, hematologic, and gastrointestinal can be affected. When recognized in a timely manner, these complications can be easily and successfully prevented and treated. Four factors appear fundamental: early identification of patients at risk, correction of abnormalities before refeeding, close monitoring during refeeding, and an appropriate feeding regimen.
Electrolytes ; Glucose ; Humans ; Hypokalemia ; Hypophosphatemia ; Metabolism ; Nutritional Support ; Refeeding Syndrome* ; Vitamins

Stress fractures typically result from repeated abnormal mechanical loading to the bones. In particular, multiple stress fractures may occur in patients with systemic disease, such as rheumatoid arthritis, osteoporosis, or osteoarthritis. Adefovir dipivoxil (ADV), a nucleotide analogue of adenosine monophosphate, very rarely causes severe hypophosphatemia when using a low dosage of 10 mg daily for treatment of chronic hepatitis B. To the best of our knowledge, in English literature, this is the first report of multiple stress fractures in a chronic hepatitis B patient who has been treated with a low dosage of ADV. We think it is important to consider that use of ADV in a patient with chronic hepatitis B could be a risk factor for stress fractures.
Adenosine Monophosphate ; Arthritis, Rheumatoid ; Fractures, Stress* ; Hepatitis B, Chronic* ; Humans ; Hypophosphatemia ; Osteoarthritis ; Osteoporosis ; Risk Factors

PURPOSE: Recent studies have suggested that renal phosphate leakage and the associated phosphaturia are significant underlying causes of calcium urolithiasis. The aims of this study were to assess whether phosphaturia relates to urinary metabolic abnormalities and recurrent stone formation. MATERIALS AND METHODS: A database of patient histories and urine chemistries was analyzed for 1,068 consecutive stone formers (SFs) and 106 normal controls. Urine values for phosphaturia that were higher than 95% of the normal control values were defined as indicating hyperphosphaturia, and the effect of phosphaturia on urinary metabolites and stone recurrence was determined. Of these patients, 247 patients (23.1%) who had been followed up for more than 36 months or had a recurrence of stones during follow-up (median, 46.0 months; range, 5-151) were included in the analyses for stone recurrence. RESULTS: Of the SFs, 19.9% (212/1,068) had increased urinary phosphate excretion. SFs with hyperphosphaturia had a greater urinary volume and higher levels of calcium, uric acid, oxalate, and citrate than did SFs with normophosphaturia. A multivariate Cox regression model, stratified by stone episodes, revealed that hyperphosphaturia was an independent predictor of recurrent stone formation in first-time SFs (hazard ratio [HR]: 2.122; 95% confidence interval [CI]: 1.100-4.097; p=0.025). No association was detected between hyperphosphaturia and recurrent stone formation in recurrent SFs. Kaplan-Meier curves showed identical results. CONCLUSIONS: This study demonstrates that hyperphosphaturia is closely associated with urinary metabolic abnormalities. Furthermore, hyperphosphaturia is a significant risk factor for stone recurrence in first-time SFs.
Calcium ; Citric Acid ; Follow-Up Studies ; Humans ; Hypophosphatemia, Familial ; Phosphates ; Recurrence ; Risk Factors ; Uric Acid ; Urolithiasis