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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

We report a previously undescribed ultrastructural calcification of glomerular immune complex depositions in a patient with lupus nephritis. Such processes give rise to a distinctive ultrastructural calcified microspheriol in electron-dense immune deposits, and were associated with hypercalcemia and nephrocalcinosis. The cause of hypercalcemia in this patient was uncertain, but related to a granulomatous inflammation and abscess of the breast. Whereas ultrastructural microcalcification was associated with hypercalcemia, its distribution in the segmental glomerular lesions suggests that an inflammatory process was contributory. The clinical follow-up indicates that the microcalcifications of immune complexes have not affected the outcome of nephritis and renal function.
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PMID:Ultrastructural calcification of glomerular immune complexes. 883 67

A girl presented at the age of 8 months with idiopathic infantile hypercalcaemia complicated by hypercalciuria, nephrocalcinosis and failure to thrive. Her hypercalcaemia was partially corrected by prednisolone, but resolved with the addition of cellulose phosphate. Her height and weight showed significant improvement during the treatment period. Cellulose phosphate should be considered in the management of children with idiopathic infantile hypercalcaemia and nephrocalcinosis.
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PMID:Prednisolone and cellulose phosphate treatment in idiopathic infantile hypercalcaemia with nephrocalcinosis. 884 45

Multiple Endocrine Neoplasia type 1 (MEN 1) syndrome comprises tumors or hyperplasia of different glands, including parathyroid, pituitary, adrenal cortex and the gastroenteropancreatic system. The vast majority of MEN 1 are found in familial clusters, although a few cases are sporadic. Hypercalcemia and/or nephrocalcinosis are the first and most common clinical manifestation in familial MEN 1 syndrome, followed by islet cell tumors (especially those secreting gastrin or insulin) and pituitary dysfunction due to either functioning or non-functioning microadenomas. Genetic studies indicate that familial MEN 1 syndrome is inherited through a dominant gene with incomplete penetrance and variable expression. The diagnosis of MEN 1 syndrome is mainly based on the careful assessment of the clinical history, symptoms physical evaluation along with the assay of serum electrolytes (i.e., calcium, phosphorus, etc.) and hormonal substances (i.e., gastrin, insulin, pancreatic polypeptide, prolactin, adrenocorticotropic hormone, etc.). In addition, several provocative tests have been used to identify endocrine tumors (particularly those of the gastroenteropancreatic system) and imaging techniques play a crucial role for the diagnostic approach in MEN 1 syndrome. Even though in the long term, the prognosis of MEN 1 syndrome is unfavourable. Recently, however, many therapeutic strategies, including both surgical and pharmacological options, have been developed to reduce the size of the neoplasm and control symptoms associated with hormone oversecretion.
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PMID:[New etiopathogenic, clinical and therapeutic findings in multiple endocrine neoplasia type 1]. 892 87

The aim of the study was to characterize abnormalities of calcium-phosphate and vitamin D3 metabolism in children with a past history of "mild" Lightwood-type idiopathic infantile hypercalcaemia. Seventeen seemingly healthy children aged 2-12 years, with long-term idiopathic hypercalcaemic syndrome since infancy were studied. Two reference groups were also included (vitamin D3 intoxication/healthy and Williams groups). Despite a long-term milk-restricted diet and a restricted vitamin D3 intake, urinary calcium excretion in the study group was 0.117 +/- 0.07 mumol/kg per 24 h. Compared with the reference groups (0.047 +/- 0.029 and 0.067 +/- 0.06 mumol/kg per 24 h, P < 0.05), there was significant hypercalciuria in the children with idiopathic hypercalcaemia since infancy. Serum concentrations of 25-hydroxyvitamin D3 in the study group were also elevated compared with the reference groups (57.4 +/- 15.5 vs. 34.6 +/- 9.3 and 22.7 +/- 10.5 ng/ml). 1,25-Dihydroxyvitamin D3 levels were at the upper limit of normal (45.9 +/- 13.1 vs. 35.0 +/- 8.1 and 30.0 +/- 13.7 pg/ml). Non-progressive, clinically silent nephrocalcinosis was visible on ultrasound examinations. The disturbances of vitamin D3 and calcium-phosphate metabolism persistent in the normocalcaemic phase of idiopathic infantile hypercalcaemia may be a primary metabolic defect of the condition. The mechanisms leading to elevation of metabolites of 1,25-dihydroxy- and 25-hydroxyvitamin D3 and the relationship between this and persistent hypercalciuria and nephrocalcinosis need pathophysiological explanation.
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PMID:Persistent hypercalciuria and elevated 25-hydroxyvitamin D3 in children with infantile hypercalcaemia. 903 62

A 2-month-old child with infantile hypophosphatasia had hypercalcemia (3.49 mmol/L (14 mg/dl)), nephrocalcinosis, and diminished bone mineral content. Hypercalcemia was corrected with calcitonin. Hypercalciuria and bone demineralization abated with chlorothiazide. Hypercalcemia is hypothesized to be related to normal bone resorption in conjunction with impaired bone mineralization. Chlorothiazide may alleviate this impairment.
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PMID:Infantile hypophosphatasia: treatment options to control hypercalcemia, hypercalciuria, and chronic bone demineralization. 915 96

Treatment for X-linked hypophosphatemia (XLH; vitamin D metabolites and phosphate salts) may result in hypercalcemia, hypercalciuria, nephrocalcinosis, and hyperparathyroidism. Cardiovascular abnormalities occur in association with these complications, but have not been reported in XLH. We hypothesized that such abnormalities may occur in XLH and evaluated cardiovascular status in 13 patients with this disease. All patients were asymptomatic and had normal cardiovascular physical examinations and Holter studies. Serum calcium and creatinine clearance were normal in all. However, all patients had mild to moderate nephrocalcinosis. Left ventricular hypertrophy was diagnosed by electrocardiogram in three and by ultrasonography in seven children. Baseline blood pressure (BP) was normal (mean +/- SD, 116 +/- 15/74 +/- 6 mm Hg). During exercise stress testing, systolic BP increased in all patients, but the maximal systolic pressure was less than that in healthy age- and sex-matched controls (156 +/- 20 vs. 175 +/- 23; P = 0.002, by t test). An abnormal increase in diastolic BP occurred at all levels of work load in XLH patients; their peak exercise diastolic BP was 91 +/- 12 vs. 72 +/- 6 mm Hg in controls (P < 0.0001, by t test). Whether these abnormal findings are primary defects in XLH or represent complications of treatment is unclear. Patients with XLH should be monitored closely for the development of hypertension and left ventricular hypertrophy. Investigation of the mechanisms involved and establishment of therapeutic guidelines are indicated.
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PMID:Cardiovascular abnormalities in patients with X-linked hypophosphatemia. 925 16

To improve the growth failure, bowed legs, and biochemical and radiological abnormalities in patients with X-linked hypophosphatemic vitamin D resistant rickets (XLH), combined therapy of phosphate and calcitriol is the best therapeutic approach at present. However, the complications involving combined therapy, such as hypercalcemia, nephrocalcinosis and hyperparathyroidism, are not fully solved. To achieve better control, new therapeutic approaches have been reported recently, for example, growth hormone (GH) or new vitamin D analogs. GH improved linear growth, decreased phosphate reabsorption and increased 1-alpha-hydroxylase activity. Furthermore, 24R,25-dihydroxyvitamin D3 (24,25) improved the bone lesions in hypophosphatemic (Hyp) mice, and also in XLH, without the adverse effects such as hypercalcemia or hypercalciuria compared with 1,25-dihydroxyvitamin D3. These new approaches should be considered for the treatment of patients with XLH.
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PMID:Medical management and complications of X-linked hypophosphatemic vitamin D resistant rickets. 931 1

Nephrocalcinosis (NC) detected by ultrasound is a recognized abnormality for some patients with X-linked hypophosphatemia (XLH) who received vitamin D2 and inorganic phosphate therapy, but is commonly observed in XLH patients treated with 1,25-dihydroxyvitamin D3 and inorganic phosphate supplementation. Nevertheless, long-term follow-up of kidney function in XLH patients with NC detected ultrasonographically has not been reported. We investigated two women with XLH, ages 31 (patient 1) and 39 (patient 2) years, each of whom had suffered at least one documented episode of vitamin D2-induced hypercalcemia and renal azotemia during childhood. Patient 2 had also been treated with inorganic phosphate. No medications for XLH had been taken during adulthood. Renal ultrasonography at our institution demonstrated marked bilateral medullary NC in both women. No other explanation was found for their NC that apparently occurred several decades earlier from medical therapy for XLH. Detailed studies (including creatinine clearance, beta2-microglobulin excretion, and fasting urinary osmolality and acidification) revealed no impairment of kidney function in either patient. Our findings indicate that subradiographic medullary NC acquired during medical therapy for XLH may persist for decades, but with no adverse renal sequelae. Definitive (long-term) assessment of kidney function in the XLH population with NC, however, will be necessary to fully understand the risk of current medical treatment for this most common heritable form of rickets.
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PMID:X-linked hypophosphatemia: normal renal function despite medullary nephrocalcinosis 25 years after transient vitamin D2-induced renal azotemia. 943 Feb 41

Although primary hyperparathyroidism has rarely been described in pediatric patients, prompt diagnosis can avoid severe CNS and metabolic consequences. The aim of this paper is to report a 6 year-old girl whose first symptoms began at eight days of age with cyanosis, hypotonia, and upward gaze deviation. At 4 months, she was admitted due to neurologic disorders and recurrent infection, but the definite diagnosis was made only six years later. Her serum calcium levels are among the highest ever reported in the medical literature, reaching 25.5 mg/dl (6.36 mmol/l). Hypercalcemia, very high levels of parathormone (1550 ng/l--normal range 10-65) and bone deformities posed no problem to diagnosis when she first came to our attention. Nephrocalcinosis and impaired renal function were detected and this child had to be treated with diuretics (furosemide) and hydration that were able to lower her serum calcium levels. Imaging studies including 99mTc-sestamibi scan were not diagnostic. At surgery, the four parathyroid glands were mildly enlarged, with primary hyperplasia. The four glands were removed, cryopreserved, and 14 fragments (1 mm each) were autotransplanted to the braquioradial muscle of the left forearm. After a first phase of hypocalcemia (hungry-bone syndrome), treated with calcium and calcitriol, the calcium levels stabilized. The question is whether she will experience some degree of recovery from her neurological problems, since her severely high calcium levels have been maintained for such a long time.
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PMID:Primary hyperparathyroidism in children: patient report and review of the literature. 964 34


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