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

Systemic lupus erythematosus (SLE) is characterized by various symptoms and multi-organ involvement. Hypophosphatemia has been described in several diseases accompanied with systemic inflammation. However, hypophosphatemia has rarely been described in SLE patients, especially in those without nephritis. We report the case of a 13-year-old girl with SLE who developed hypophosphatemia without renal involvement. Her hypophosphatemia was caused by renal loss of phosphorus and persisted for 7 months. It improved as her complement levels increased. Therefore, hypophosphatemia may be related to disease activity in SLE patients.
Adolescent ; Complement System Proteins ; Female* ; Humans ; Hypophosphatemia* ; Inflammation ; Lupus Erythematosus, Systemic* ; Nephritis ; Phosphorus

Phosphate is an essential ion and plays a vital role in many physiological processes. Carpopedal spasm is known as a symptom of hypocalcemia, or rarely, hypomagnesemia. We present an unusual case of carpal spasm seen in a patient with hypophosphatemia. A fourteen year old boy was admitted with acute onset of both carpal spasm after vomiting and diarrhea. Biochemical investigation revealed only moderate hypophosphatemia without hypocalcemia. Other laboratory findings including hormone tests were normal. Carpal spasm improved with correction of hypophosphatemia. The phathophysiology of neurologic dysfunction related to hypophosphatemia is not clear yet. Careful observation of serum electrolytes including phosphate is necessary when the patient has neurologic symptoms.
Diarrhea ; Electrolytes ; Humans ; Hypocalcemia ; Hypophosphatemia* ; Male ; Neurologic Manifestations ; Physiological Processes ; Spasm* ; Vomiting