Cases reported "Hypophosphatemia"

Filter by keywords:



Filtering documents. Please wait...

11/38. Malignant hypophosphathaemic bone disease.

    A case of crippling osteoporosis with muscular weakness, hypophosphatemia, hyperparathyroidism, defective skeletal calcification and cartilage destruction is reported. The patient, a male was observed from the age of 2 1/2 until his death at the age of 33 years. This bone/cartilage disease failed to respond to phosphate supplementation, parathyroidectomy and calcitriol. We believe this may represent a hitherto undescribed entity.
- - - - - - - - - -
ranking = 1
keywords = bone
(Clic here for more details about this article)

12/38. Recurrent malignant variant of phosphaturic mesenchymal tumor with oncogenic osteomalacia.

    Phosphaturic mesenchymal tumor is a rare neoplasm which causes osteomalacia or rickets. The tumor typically follows a benign clinical course. Even in the rare malignant cases, local recurrence and distant metastasis are uncommon. We report on an example of a malignant phosphaturic mesenchymal tumor which recurred several times over 16 years concurrently causing hypophosphatemia, bone pain, and osteomalacia. Following each surgery, symptoms and hypophosphatemia improved. The patient died of disease 17 years after the first surgery. Histologically, the initial tumor was composed of small spindle cells with clusters of giant cells, prominent blood vessels, poorly formed cartilaginous areas, and crystalline material. Cytological atypia was minimal. Following multiple recurrences, the tumor demonstrated areas of high-grade sarcoma exhibiting marked pleomorphism, numerous mitotic figures, and p53 overexpression. This case illustrates the potential lethality of incompletely removed phosphaturic mesenchymal tumors.
- - - - - - - - - -
ranking = 0.2
keywords = bone
(Clic here for more details about this article)

13/38. Hypophosphatemic rickets presenting as recurring pedal stress fractures in a middle-aged woman.

    Stress fractures frequently occur from overtraining. When stress fractures recur, underlying metabolic abnormalities should be ruled out. We report a middle-aged woman in whom such an evaluation demonstrated previously undiagnosed hypophosphatemic rickets after she presented with recurring stress fractures in her feet. Treatment with phosphate and calcitriol was associated with clinical improvement that would likely not have occurred without this intervention. Any patient with recurring stress fractures should be evaluated with several screening laboratory tests, metabolic bone x-rays, and a measurement of bone mineral density.
- - - - - - - - - -
ranking = 0.4
keywords = bone
(Clic here for more details about this article)

14/38. Hypophosphatemic rickets accompanying McCune-Albright syndrome: evidence that a humoral factor causes hypophosphatemia.

    McCune-Albright syndrome (MAS) is sometimes complicated by hypophosphatemia. However, it remains unclear whether a humoral factor is associated with the cause of hypophosphatemia. We isolated cells with mutations of the Gsalpha gene from fibrous bone dysplasia tissues of two MAS patients (MAS cells). severe combined immunodeficiency (SCID) mice were subjected to experiments using from one of these cells patients. Effects of conditioned media (CM) isolated from MAS cells (MAS-CM) on phosphate transport were investigated by using rat renal slices, the renal cell line OK-B, rat intestinal rings and the human intestinal cell line Caco-2. In addition, the effects of MAS-CM on human sodium-dependent phosphate transporter (NPT2) gene promoter activity expression were investigated in the renal cell line OK-B2400 and were compared with the effects of CM isolated from a patient with oncogenic hypophosphatemic osteomalacia (OHO). MAS cells caused significant hypophosphatemia (P < 0.05) and elevated serum alkaline phosphatase activity (P < 0.05) in SCID mice. The MAS-CM significantly inhibited phosphate uptake in everted intestinal rings (P < 0.01), whereas it had no effect on glucose uptake. The MAS-CM had no effect on either phosphate uptake in the kidney or NPT2 gene promoter activity. In contrast, the CM of the OHO patient significantly inhibited phosphate uptake and NPT2 gene promoter activity. These results indicate that the humoral factor derived from fibrous dysplasia cells of the MAS patient is different to that from OHO patients, because the humoral factor from the MAS patient inhibited phosphate transport not in the kidney but in the intestine.
- - - - - - - - - -
ranking = 0.2
keywords = bone
(Clic here for more details about this article)

15/38. Pseudo-(tumor-induced) rickets.

    An athletic 8-year-old boy developed severe muscle weakness over 2 years. At the age of 10 years, investigation for possible neuromuscular disease disclosed hypophosphatemia (1.8 mg/dl) and rickets. There was selective renal tubular wasting of inorganic phosphate (Pi) but no history of toxin exposure, familial bone or kidney disease, or biochemical evidence of vitamin d deficiency. urine amino acid quantitation was unremarkable. serum 1,25-dihydroxyvitamin D [1,25(OH)2D] concentration was in the lower half of the reference range. Our presumptive diagnosis was tumor-induced rickets; however, physical examination and bone scanning in search of a neoplasm were unrevealing. Soon after 1,25(OH)2D3 and Pi treatment began, muscle strength improved considerably. After 6 months of therapy, radiographic abnormalities were substantially better. During the next 6 years, physical examinations, a second bone scan, whole-body and nasal sinus magnetic resonance imaging, and octreotide scintigraphy were unremarkable. When his physes fused at the age of 16 years, assessment of his course showed excellent control of his rickets requiring decreasing doses of medication. Furthermore, fasting serum Pi levels and tubular maximum phosphorus/glomerular filtration (TmP/ GFR) values had increased steadily and normalized after 3 years of treatment. Accordingly, therapy was stopped. Seven months after stopping medication, he continues to feel completely well. fasting serum Pi levels, TmP/GFR, other biochemical parameters of bone and mineral homeostasis, creatinine clearance, and renal sonography are normal. Neither spontaneous or pharmacologic cure of tumor-induced rickets or osteomalacia nor a patient matching ours has been reported. His disorder, which we call pseudo-(tumor-induced) rickets, should be considered when investigation for oncogenic rickets or osteomalacia discloses no causal lesion. Consequently, prolonged medical therapy and futile searches for a neoplasm may be avoided.
- - - - - - - - - -
ranking = 0.8
keywords = bone
(Clic here for more details about this article)

16/38. Tertiary hyperparathyroidism after high-dose phosphate therapy in adult-onset hypophosphatemic osteomalacia.

    OBJECTIVE: To describe a case of adult-onset hypophosphatemic osteomalacia treated with orally administered phosphate and complicated by tertiary hyperparathyroidism. methods: We present pertinent clinical, radiologic, and laboratory details of the study patient for a period of more than 20 years and discuss the few reported cases of tertiary hyperparathyroidism attributable to prolonged phosphate therapy. RESULTS: A 49-year-old Jordanian man, who had been diagnosed at age 26 years as having sporadic adult-onset hypophosphatemic vitamin D-resistant osteomalacia, presented with severe right hip pain, severe osteopenia with lytic bone lesions, and hypercalcemia after prolonged oral treatment with phosphate and vitamin D. These clinical, radiologic, and biochemical findings, in conjunction with a very high serum parathyroid hormone level, indicated the diagnosis of tertiary hyperparathyroidism, which was substantiated histopathologically. CONCLUSION: physicians should be aware of the potential for development of tertiary hyperparathyroidism in patients receiving prolonged oral phosphate therapy.
- - - - - - - - - -
ranking = 0.2
keywords = bone
(Clic here for more details about this article)

17/38. Somatic mutations of the MEN1 gene and microsatellite instability in a case of tertiary hyperparathyroidism occurring during high phosphate therapy for acquired, hypophosphatemic osteomalacia.

    Somatic mutations of the MEN type 1 (MEN1) gene were recently shown to be responsible for tumorigenesis in 13-26% of sporadic, nonfamilial primary hyperparathyroidism. However, it is unknown whether these mutations are also involved in tumorigenesis of parathyroid glands occurring during high phosphate therapy for hypophosphatemic rickets or osteomalacia. A male patient with adult-onset, hypophosphatemic osteomalacia had been treated with 1alpha-OHD3 and oral phosphate for 13 yr when tertiary hyperparathyroidism developed. After total resection of four enlarged parathyroid glands and autotransplantation of a hyperplastic gland, the patient has continued to do well for the last 2 yr. sequence analysis of the coding exons of MEN1 gene revealed a 36-bp deletion with a 2-bp insertion (exon 2) in the right upper parathyroid gland accompanied with loss of heterozygosity at 11q13 locus and a heterozygous mutation of 2-bp deletion (AG) in exon 10 in the right lower gland, in which microsatellite instability was also found. No MEN1 gene mutation was detected in the other two hyperplastic parathyroid glands or in the peripheral blood. These findings indicate that MEN1 gene mutations contributed to tumorigenesis of the right upper parathyroid gland in this case of phosphate-induced tertiary hyperparathyroidism. Very recently a bone tumor was found in the right femoral neck, and the tumor (chondroblastoma) was resected.
- - - - - - - - - -
ranking = 0.2
keywords = bone
(Clic here for more details about this article)

18/38. Metabolic bone disease after chronic antacid administration in an infant.

    OBJECTIVE: To describe a case of hypophosphatemia and metabolic bone disease (MBD) due to aluminum-containing antacids. CASE SUMMARY: An 8-month-old white boy was brought to the emergency department due to irritability and pain with movement. Upon examination, the infant was irritable, unable to bear weight, had palpable clavicular bony lesions, point tenderness of the hips, and poor head control. The infant had lost several developmental milestones over the past 4 months (eg, ability to roll over) and had decreased appetite and minimal weight gain. Skeletal survey revealed multiple rib fractures, osteoporosis, and Ricketts. hypophosphatemia (2.3 mg/dL; normal 3.2-6.3) and an elevated serum aluminum level (14 microg/L, normal 0-9) were noted. Past medical history was positive for gastroesophageal reflux. He had been started on ranitidine and aluminum hydroxide (1/2 teaspoonful per 6-ounce bottle) at 2 months of age. The infant's formula contained elevated aluminum levels. Further investigation showed that 1/2 tablespoonful instead of 1/2 teaspoonful of antacid had been added to each 6-ounce formula bottle for the prior 6 months; only 1 month of antacid therapy had been recommended. An objective causality assessment revealed a probable adverse drug event. DISCUSSION: Phosphate-binding substances such as aluminum-containing antacids can bind large amounts of phosphorus, causing hypophosphatemia and MBD. CONCLUSIONS: We report this case to increase awareness of the risk of hypophosphatemia and MBD (likely aluminum related) with use of over-the-counter aluminum-containing antacids in pediatrics, as well as the hazards of prescribing doses in "spoonful" units.
- - - - - - - - - -
ranking = 1
keywords = bone
(Clic here for more details about this article)

19/38. Hypophosphaturic mesenchymal tumor of the ethmoid associated with oncogenic osteomalacia.

    Oncogenic osteomalacia is an uncommon syndrome characterized by bone pain, proximal muscle weakness, hypophosphatemia, hyperphosphaturia, and a low plasma concentration of 1,25-dihydroxy-vitamin D. The disease affects both sexes at around 40 years of age, although it can sometimes affect children and adolescents. Generally, the syndrome is associated with a tumor, usually benign, of mesenchymal origin and is resolved after removal of the tumor; this syndrome can sometimes be associated with malignant tumors. These tumors seem to be histologically heterogeneous and are generally localized in soft tissues and bone. In this article, a case of oncogenic osteomalacia associated with a hypophosphaturic mesenchymal tumor of the ethmoid is reported in a 24-year-old man. After surgical and radical removal of the tumor, the patient noted a decrease in the clinical symptoms and signs.
- - - - - - - - - -
ranking = 0.4
keywords = bone
(Clic here for more details about this article)

20/38. Bone densitometry in a patient with hypophosphatemic osteomalacia.

    A 60-year-old Caucasian woman with a 1-year history of pain at the ribs, spine, and pelvis consulted at our Institute in March 1999. She brought a bone densitometry performed using a Lunar DPX densitometer that showed bone mineral density (BMD) measurements in the osteoporotic range at both the lumbar spine and the femoral neck. As a child she had had bowed legs and had been treated with ultraviolet radiation. Results of the laboratory test performed at our institute showed normal total serum calcium, repeated low serum P levels, and a low renal phosphate threshold with elevated total and bone fraction of alkaline phosphatase with normal intact parathyroid hormone (PTH). A diagnosis of hypophosphatemic osteomalacia due to renal phosphate leak was made. She began treatment with neutral sodium phosphate at 1.5 g/day and calcitriol 0.5 microg/day. Her serum P levels normalized, and there was a progressive decrease in alkaline phosphatase levels. The densitometry showed a very rapid increase in BMD values with normalization at the lumbar spine after 10 months of treatment. This case shows the importance of bone densitometry in the follow-up of patients with suspected osteomalacia.
- - - - - - - - - -
ranking = 0.8
keywords = bone
(Clic here for more details about this article)
<- Previous || Next ->


Leave a message about 'Hypophosphatemia'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.