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Results for “Hyperphosphatemia”

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PubMed1975

Complications and total care of a child with acute leukemia.

The complications which occur in a child with acute leukemia depend on the stage of the disease and the therapeutic regiman. Most children will present with some manifestation of marrow failure. An occasional child will have marked leukocytosis and disturbance of organ function due to massive leukemic infiltrates. Metabolic disturbances such as hyperuricemia and hyperphosphatemia-hypocalcemia may develop, expecially after therapy is initiated. The myelosuppression and immunosuppression due to drug toxicity may result in opportunistic infections. Other toxicities which can occur with a chemotherapeutic regimen are numerois and varied, and the physician must be cognizant of them in order to minimize damage. Therapy to the central nervous system, either for subclinical or clinical disease, has been associated with a variety of symptoms ranging from meningismus to paraplegia and death. To prevent the development of these complications, and to manage them effectively if they occur, the physician must be knowlegeable about their etiology, clinical and laboratory manifestations, and treatment.

Acute Disease↗

PubMed1984

Acute tumor lysis syndrome with metastatic medulloblastoma. A case report.

The acute tumor lysis syndrome occurs rarely in nonhematologic malignancies. This patient, a 34-year-old woman with metastatic medulloblastoma, was receiving palliative radiotherapy for a rapidly expanding abdominopelvic mass. After a total of 300 rad, the patient developed the biochemical hallmarks of the acute tumor lysis syndrome, hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. This was complicated by oliguria from hyperuricemic acute renal failure. The patient responded well to hydration, alkaline diuresis, phosphate and potassium binders, and allopurinol. The potential for acute tumor lysis syndrome should be anticipated when treating metastatic medulloblastoma.

Abdominal Neoplasms↗

PubMed1985

Multiple recurrences of acute tumor lysis syndrome in an indolent non-Hodgkin's lymphoma.

Acute tumor lysis syndrome (ATLS) is an entity consisting of combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia, and hypocalcemia and occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders with high tumor burdens. A patient is described with a diffuse intermediately differentiated lymphocytic lymphoma, considered by most an indolent B-cell non-Hodgkin's lymphoma, in whom developed multiple recurrences of ATLS after treatment when tumor regrowth occurred between cycles of therapy. The mitotic rate of this lymphoma was relatively high (30-80 mitoses/ten high-power fields). Lymph proliferative disorders with a high mitotic rate, and large tumor burden, regardless of histologic features, should be treated prophylactically against tumor lysis if regrowth between cycles occurs.

Acute Disease↗

PubMed1987

Fatal acute tumor lysis syndrome with metastatic breast carcinoma.

A 53-year-old woman presented with an extensively metastatic and rapidly growing breast adenocarcinoma, markedly elevated lactate dehydrogenase, and mildly elevated blood urea nitrogen. She received 5-fluorouracil, doxorubicin, and cyclophosphamide. Eighteen hours after chemotherapy she was noted to have hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and acute renal failure. She experienced cardiac arrest and died 72 hours after receiving chemotherapy. A postmortem liver biopsy revealed adenocarcinoma undergoing necrosis. This case represented the acute tumor lysis syndrome that occurred after chemotherapy of breast carcinoma. Patients with metastatic breast carcinoma and similar presentations should be considered for prophylactic therapy with allopurinol and hydration before chemotherapy.

Adenocarcinoma↗

PubMed1989

Tumor lysis syndrome in nonhematopoietic neoplasms.

A 57-year-old woman developed severe tumor lysis syndrome characterized by acute hyperuricemic nephropathy, hyperphosphatemia, hyperkalemia, and hypocalcemia after therapy with cyclophosphamide, methotrexate, and 5-fluorouracil for metastatic infiltrating ductal carcinoma of the breast involving the chest wall, lungs, pleurae, and liver. Similar metabolic derangements developed in a 58-year-old man after therapy with vinblastine and bleomycin for classical seminoma with widespread, bulky lymph node metastases. Both patients died of infection associated with granulocytopenia within 2 weeks after the initiation of chemotherapy despite significant improvement in the manifestations of tumor lysis syndrome. At autopsy, there was anatomic evidence of extensive tumor necrosis in each case. The pathogenesis of this problem in the present cases is discussed, and this unusual complication of the treatment of nonhematopoietic malignancies is reviewed.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2003

New syndrome of simplified gyral pattern, micromelia, dysmorphic features and early death.

We report two sisters with a new syndrome of simplified gyral pattern, normal head circumference at birth but with subsequent development of microcephaly, intractable seizures, and early death. Dysmorphic features included coarse face, hypertrichosis, short nose, paranasal widening, long philtrum, short neck, upper limb micromelia, single transverse palmar lines, and clasp thumbs. The proband had repeated convulsions from shortly after birth and she required continuous artificial ventilation. Neurological examination showed absent sucking, rooting, Moro and grasping reflexes. MRI revealed a diffuse simplified gyral pattern with apparent agyria over the frontal lobes. Biochemical screening gave normal results. Her older sister had bilateral renal pelvic dilatation on prenatal ultrasound. She also developed severe convulsions on the first day of life, and she had to be artificially ventilated for 38 days. She had severe developmental retardation and neurological examination showed absence of spontaneous movements and Moro reflex, weak sucking reflex, and hypertonicity. CT scan of the brain showed a simplified gyral pattern. At 3 months, she developed hypocalcemia and hyperphosphatemia with normal levels of vitamin D and alkaline phosphatase, and parathyroid hormone level was low. Other biochemical tests gave normal results. She died at 5 months due to a massive aspiration event. Based on the unique clinical and radiological features found in our patients, we propose that this is a new syndrome.

Brain Diseases↗

PubMed1987

The effect of 1 alpha-hydroxyvitamin D3 on the mineralization defect in disodium etidronate-treated Paget's disease--a double-blind randomized clinical study.

A double-blind randomized study of 29 patients with symptomatic Paget's disease was conducted comparing the clinical, biochemical, and histomorphometric responses to 3-month treatment with placebo (10 patients), low-dose disodium etidronate (EHDP) (5-7 mg/kg/day) (10 patients), and low-dose EHDP plus 1 alpha-hydroxyvitamin D3 (1 alpha D3) 0.5 mcg daily (9 patients). In placebo-treated patients no significant changes were observed in symptoms, biochemistry, or bone histomorphometry. Histologically apparent mineralization defects developed after 3 months of therapy in 90% of patients in the EHDP group, compared with 45% of patients in the EHDP/1 alpha D3 group. In 19% of the patients treated with active medication, the mineralization defects in pagetic bone were accompanied by histological evidence of continued osteoclastic resorption. The development of mineralization defects was not related to serum levels of vitamin D metabolites, alkaline phosphatase, or intestinal calcium absorption but did correlate with the occurrence of hyperphosphatemia during treatment, which was most marked in patients treated with EHDP alone. Although mineralization defects were less frequent in the EHDP/1 alpha D3 group, these patients also responded less well symptomatically, thus limiting the potential usefulness of this drug combination in Paget's disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

PubMed1993

Pseudohypoparathyroidism with osteitis fibrosa cystica: direct demonstration of skeletal responsiveness to parathyroid hormone in cells cultured from bone.

A young girl had tibial osteotomies at age 14 for genu valgum and then had recurrent tibial cysts over a number of years. Hypocalcemia and hyperphosphatemia were first noted at age 21. The diagnosis of pseudohypoparathyroidism was made at age 28, when elevated plasma PTH was detected. Clinical and biochemical features, including a PTH response test and assay of RBC Gs, established the diagnosis of pseudohypoparathyroidism type 1b. Failure to suppress plasma PTH with vitamin D therapy led to an exacerbation of her cystic bone disease; there were widespread lytic lesions radiologically, most of which took up [99mTc]diphosphonate on bone scan. Microradioscopy revealed evidence of resorption of phalangeal tufts. Bone biopsy showed osteitis fibrosa cystica. During an orthopedic procedure, trabecular bone fragments were taken from her right humerus, and bone-derived cells cultured using an explant technique. The cultured cells were osteoblast-like in morphology, fully responsive to PTH, cholera toxin, forskolin, and PGE1 in vitro, and had an alkaline phosphatase and osteocalcin response to 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Following this examination of skeletal responsiveness, attempts were made to suppress the elevated plasma PTH levels and symptomatic bone disease by optimizing therapy with oral 1,25-(OH)2D3. When bone pain associated with the cystic bone disease failed to resolve, the patient underwent total parathyroidectomy, following which the bone pain gradually resolved. This is the first direct demonstration of PTH responsiveness in cultured bone cells in the syndrome of pseudohypoparathyroidism with osteitis fibrosa cystica.

Adenylyl Cyclases↗

PubMed1984

Adsorption of phosphate by aluminum hydroxycarbonate.

Phosphate is specifically adsorbed by aluminum hydroxycarbonate by anion ligand exchange. IR analysis indicated that phosphate exchanged with specifically adsorbed carbonate. Adsorption is favored by low pH and is inversely related to particle size. Adsorption of phosphate decreases the rate of acid neutralization of aluminum hydroxycarbonate. The results are applied to the treatment of hyperphosphatemia and hypophosphatemia.

Adsorption↗

PubMed1995

Effect of various vitamin D metabolites on serum calcium and inorganic phosphate in the freshwater snake Natrix piscator.

Vitamin D3 (650 pmol and 6.50 nmol/100 g body wt), 25-hydroxyvitamin D (650 pmol and 6.50 nmol/100 g body wt), and 1,25-dihydroxyvitamin D (65 pmol and 650 pmol/100 g body wt) were administered daily to the freshwater snake Natrix piscator for 15 days. Both serum calcium and inorganic phosphate levels were increased significantly in all of the treated groups. This is the first report of hypercalcemia and hyperphosphatemia in reptiles induced by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D.

Animals↗

PubMed1993

Acute tumor lysis syndrome with squamous cell carcinoma of the vulva.

Acute tumor lysis syndrome (ATLS) is a rare metabolic complication in nonhematologic malignancies. We report a unique case of extensive regionally recurrent squamous cell carcinoma of the vulva who developed a picture compatible with ATLS 36 hr after the initiation of palliative chemotherapy. The patient suffered acute renal failure with hyperuricemia, hyperphosphatemia, and hypocalcemia as well as a picture suggestive of congestive heart failure. The patient responded well to adequate hydration, alkaline diuresis, and allopurinol. The potential for ATLS should be anticipated when treating metastatic or locally advanced squamous cell carcinoma of the vulva with chemotherapy.

Aged↗

PubMed1988

Characterization of a mouse model of chronic uremia.

A mouse model of renal failure, which is induced by the sequential electrocoagulation of the right renal cortex and left nephrectomy, was examined for the capacity to reproduce the characteristics of chronic uremia. Assessment was conducted six weeks after the second surgical procedure in 13 week old female C57BL/6 inbred mice with renal failure and in normal and sham-operated controls. The surgery, which was well tolerated, was free of local and systemic signs of inflammation or infection. Growth was significantly delayed in all animals post surgery however renal failure mice presented the most severe growth retardation. Biochemical analysis of plasma revealed multiple abnormalities with commensurate elevations of urea and creatinine. In addition to the expected hyperphosphatemia, hyperkalemia and acidosis, a significant increase in cholesterol was present. Furthermore, in contrast to controls, renal failure mice produced large volumes of urine which contained significant levels of protein. Renal failure mice presented profound hematological changes in the red cell series in which anemia was evident. Changes in plasma biochemistry and in bone histology revealed the presence of severe secondary hyperparathyroidism. It was therefore concluded that the described mouse model of chronic renal failure presented characteristics consistent with those observed clinically in end-stage renal disease.

Animals↗

PubMed1977

Fetal development in experimental uremia.

Uremic women on hemodialysis with metabolic bone disease (hyperparathyroidism, osteomalacia resulting from defective vitamin D metabolism) and anemia (erythropoietin deficiency) are known to give birth to infants without bone disease or anemia. Therefore, skeletal development (enchondral and desmal bone formation) and hepatic erythropoiesis were evaluated in fetuses of uremic rats. These fetuses failed to show defective mineralisation or evidence of bone disease. Bolus injection of high doses of exogenous PTH into the maternal or fetal organism did not affect fetal bone histology. In addition, no apparent defect of bone mineralisation or bone formation was found in fetuses of ricketic rats. Normal mineralisation in the offspring of uremic rats may be explained by fetal hyperphosphatemia and/or insensitivity of fetal (woven) bone mineralisation to vitamin D. Absence of fetal anemia (normal hematocrits, normal density of hematopoietic cells in the liver) in the presence of maternal anemia is presumably due to the insensitivity of fetal erythropoiesis to erythropoietin.

Animals↗

PubMed1979

Pseudohypoparathyroidism type II and anticonvulsant rickets.

A patient treated with anticonvulsants showed hypocalcemia and hyperphosphatemia in association with increased serum parathyroid hormone, reduced serum 25-hydroxy D3, diminished response in phosphorus excretion to exogenous parathyroid hormone and normal response in cyclic AMP excretion. Oral administration of Vitamin D3 resulted in normalization of serum 25-hydroxy D3, calcium, and phosphorus. At this stage, phosphorus excretion after parathyroid hormone returned to normal. These findings suggest that the patient had pseudohypoparathyroidism type II with anti-convulsant medication as a complicating factor.

Adolescent↗

PubMed1987

Long-term suppression of hyperparathyroidism by phosphate binders in uremic children.

Forty-five children with stable chronic renal failure, not on dialysis, were treated conservatively with a regimen of mild dietary phosphate restriction and high-dose phosphate binders for up to 5 years. Both aluminum hydroxide and calcium carbonate were used initially, but almost all patients were taking calcium carbonate towards the end of the period. Serum immunoreactive parathyroid hormone concentrations were significantly decreased and were within the normal range after 1 year and remained normal during treatment. There was no significant change in renal function over the same treatment period. We conclude that calcium carbonate should be used as the phosphate binder of choice in the long-term suppression of hyperphosphatemia and hyperparathyroidism in uremic children.

Adolescent↗

PubMed1996

Calcitriol administration in end-stage renal disease: intravenous or oral?

1,25-Dihydroxyvitamin D deficiency plays an important role in the pathogenesis of secondary hyperparathyroidism, and adequate replacement of this hormone is considered essential to normalize parathyroid gland function and restore bone homeostasis in patients with advanced renal failure. Although initial uncontrolled clinical trials suggested the superiority of intravenous calcitriol treatment, more recent controlled investigations show that different routes (oral versus intravenous), frequency (daily versus intermittent), and dosing (physiological versus pharmacological) of calcitriol administration are clinically equivalent. Overall, the response to calcitriol treatment depends more on the severity of secondary hyperparathyroidism and the presence of confounding variables, such as hyperphosphatemia and acquired abnormalities of parathyroid cell function, than the method of calcitriol administration.

Administration, Oral↗

PubMed1996

Abnormal skeletal response to parathyroid hormone and the expression of its receptor in chronic uremia.

Chronic renal failure is characterized by a resistance to the hypercalcemic action of parathyroid hormone (PTH). This resistance probably involves several mechanisms, including a disturbance of vitamin D metabolism, a desensitization of the skeleton by high PTH levels, hyperphosphatemia, uremic toxins, and acidosis. We have explored the possibility that a downregulation of the recently cloned PTH/PTHrp receptor might also be involved. We found a marked decrease in the expression of the receptor mRNA in the kidney and the bone of uremic rats; other authors have found a decrease in the heart and the liver. The reduced expression in the kidney was accompanied by a diminished stimulability of renal adenylate cyclase activity, suggestive of a functional depression of the hormonal response in this target tissue. It is probable that the downregulation of the PTH/PTHrp receptor plays an important role in the skeletal resistance to the calcemic effect of PTII in chronic renal failure.

Animals↗

PubMedDate not supplied

Phase II trial of carbetimer in metastatic melanoma.

A phase II study of the synthetic polyelectrolyte Carbetimer 6500 mg/m2 i.v. daily for five days every 21-day cycle was conducted in patients with metastatic melanoma. No responses were seen in 18 evaluable patients. Two patients had stable disease for five months. Toxicity was generally manageable and included mild hyperphosphatemia, mild proteinuria, fatigue, pain at the injection site, and nausea. Carbetimer is inactive in metastatic melanoma at this dose and schedule.

Adult↗