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

Squamous cell carcinoma of the skin is a rare complication of hidradenitis suppurativa. We treated a case of hidradenitis-associated squamous cel carcinoma with metastases to the inguinal lymph nodes. Hypercalcemia also occurred, possibly in relation to the secretion of a hormonelike substance by the tumor. Chemotherapy with bleomycin sulfate, methotrexate sodium, and cisplatin led to tumor regression and control of the hypercalcemia.
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PMID:Hypercalcemia in association with cutaneous squamous cell carcinoma. Occurrence as a late complication of hidradenitis suppurativa. 397 41

The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.
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PMID:Endocrine regulation of calcium homeostasis during pregnancy. 636 Apr 69

Twelve dogs with lymphosarcoma and hypercalcemia were treated over a period of 36 months. Signs and laboratory findings were referable to hypercalcemia and azotemia. All dogs were staged, classified histologically, and given cytoreductive chemotherapy, using 5 drugs (vincristine sulfate, cytosine arabinoside, cyclophosphamide, L-asparaginase and prednisone). For azotemia, symptomatic therapy (0.9% NaCl solution and furosemide) was given. Seven dogs responded completely, with marked reduction of lymphadenopathy and return of serum calcium concentration to normal. Median duration of remission in this group was 48 days (range, 14 to 93), and median survival time was 112 days (range, 85 to 153). Five nonresponding dogs had less than 50% reduction in measurable tumor mass, although serum calcium concentration returned to normal. The median survival time for this group was 34 days (range, 23 to 68). Two of the nonresponders died from sepsis and another from disseminated intravascular coagulation. Response to therapy did not appear to be influenced by age, breed, sex, initial calcium concentration, degree of azotemia, or histologic classification.
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PMID:Chemotherapeutic responses in dogs with lymphosarcoma and hypercalcemia. 689 39

Sodium sulfate can be used to enhance the conjugation of phenolic drugs with sulfate and to treat hypercalcemia. It is thought that sulfate in is absorbed slowly and incompletely from the digestive tract. The purposes of this investigation were to determine the absorption of large amount of sodium sulfate (18.1 g as the decahydrate, equivalent to 8.0 g of the anhydrous salt) and to compare the bioavailability when this amount is administered orally to normal subjects as a single dose and as four equally divided hourly doses. The 72-hr urinary recovery of free sulfate following single and divided doses was 53.4 +/- 15.8 and 61.8 +/- 7.8%, respectively (mean +/- SD, n=5, p greater than 0.2). The single dose produced severe diarrhea while the divided doses caused only mild or no diarrhea. Thus, a large amount of sodium sulfate, when administered orally in divided doses over 3 hr, is well tolerated and is absorbed to a significant extent. Orally administered sodium sulfate may be useful for the early treatment of acetaminophen overdose.
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PMID:Absorption of orally administered sodium sulfate in humans. 726 5

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Bony fish use the glycoprotein hormone stanniocalcin (STC) to counteract hypercalcaemia. This is achieved through dual mechanisms involving gill calcium uptake inhibition and stimulation of renal inorganic phosphate reabsorption. Human STC (hSTC-1) shows considerable homology with both rat and mouse STC (mSTC) and their mRNA is expressed in a wide range of tissues. In fish, STC is produced by endocrine glands known as the corpuscles of Stannius but in mammals the widespread expression is suggestive of a paracrine rather than an endocrine role. In order to determine the distribution and strucutral characteristics of hSTC-1, the recombinant protein was expressed in bacteria, purified by metal-ion affinity chromatography, and a study was made of the likely epitopes for raising an antibody. This novel hSTC-1 antibody was used to test the purification protocol. Since the role of mammalian STC is largely unknown, the specific distribution of STC needed to be addressed. To test the specificity of the antibody, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)/Western blotting was undertaken in homogenised rat bladder, ovary and kidney.
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PMID:Expression and localisation of stanniocalcin 1 in rat bladder, kidney and ovary. 1045 Nov 17

Phosphate binders that contain aluminum or calcium are frequently prescribed to treat hyperphosphatemia in patients with end-stage renal disease (ESRD), but an accumulation of aluminum can lead to encephalopathy, aluminum-related bone disease (ARBD) such as osteomalacia, anaemia, and resistance to erythropoietin, and calcium accumulation can lead to hypercalcaemia. High phosphate concentrations are reduced in vitro and in vivo by a phosphate adsorption pill, which is synthesized by hydrolyzing ferrous sulfate in the presence of saccharides, to form an iron (III)-saccharide complex that is acid resistant and binds phosphate greater than iron (III) hydroxide alone. Under in vitro conditions, containing 3.26 mg P/dL, the iron (III)-sucrose complex showed the highest phosphate adsorption capacity at pH 2 with artificial gastric juice, 58.9 mg P/g binder. For the 7 day in vivo study, 0% (Group 1), 1% (Group 2), 4% (Group 3), and 8% (Group 4) iron (III)-sucrose complex was admixed into the rodent chow by weight and fed to 15 male Wistar rats. The weight and volume of the feces and urine, and the calcium, iron, and phosphorus excretions in the feces and urine samples were monitored for any signs of irregularity. Total urine outflow was collected during a 24-h period to determine the amount of phosphate recovered, which indicates the ability of the phosphate binder to reduce gastrointestinal phosphate absorption. The fecal iron excretion was significantly effected by the amount of binder ingested throughout the study for Group 2 (p < 0.001), Group 3 (p < 0.01), and Group 4 (p < 0.001). The urinary calcium excretion (mg/rat/24-h) significantly increased by the 7th day for Group 2 (p < 0.05) and Group 4 (p < 0.01) in comparison to the control. Finally, after 7 days, there was a significant drop in the urinary phosphorus levels (mg P/rat/24-h) in a dose dependent manner for Group 2: from 7.82 +/- 1.46 to 1.98 +/- 0.10 mg P/rat/24-h (102 mg P/dL/24-h; p < 0.05); Group 3: from 6.70 +/- 1.14 to 0.16 +/- 0.09 mg P/rat/24-h (6.0 mg P/dL/24-h; p < 0.01); and Group 4: from 8.25 +/- 0.67 to 0.04 +/- 0.01 mg P/rat/24-h (0.9 mg P/dL/24-h; p < 0.01). The results show that this new adsorbent might provide an alternative to conventional aluminum and calcium containing phosphate-binding agents for combating hyperphosphataemia.
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PMID:Oral phosphate binders: phosphate binding capacity of iron (III) hydroxide complexes containing saccharides and their effect on the urinary excretion of calcium and phosphate in rats. 1051 89

We report an 11 month-old infant with severe hypercalcemia associated with hyperlipidemia following bolus vitamin D administration. At the time of admission, serum concentration of calcium was 5.5 mmol/l (22 mg/dl); total cholesterol, high density lipoprotein cholesterol (HDL-C), very low density lipoprotein (VLDL), low density lipoprotein cholesterol (LDL-C), and triglyceride levels were respectively: 6.37 mmol/l (246 mg/dl), 0.77 mmol/l (30 mg/dl), 1.37 mmol/l (54 mg/dl), 4.1 mmol/l (162 mg/dl), 3 mmol/l (271 mg/dl). Physical examination revealed dehydration and irritability that was inappropriately mild according to the serum calcium level. On the 16th day of therapy that consisted of intravenous fluids with furosemide (sodium diuresis), steroid, calcitonin, magnesium sulfate, and phosphorus, serum calcium level declined below 3 mmol/l (12 mg/dl). The hyperlipidemia resolved gradually with a concomitant decline in serum calcium. This report is interesting in that hypercalcemia was associated with transient hyperlipidemia that disappeared with normocalcemia, which might suggest protection against hypercalcemic symptoms.
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PMID:Severe hypercalcemia of an infant due to vitamin D toxicity associated with hypercholesterolemia. 1151 34

The kidney plays an important role in the regulatory system for bone and mineral metabolism. In chronic kidney disease (CKD), various abnormalities, recently named CKD-mineral and bone disorder (CKD-MBD), may develop in this system. The optimal management of CKD-MBD should be achieved without increasing the risk of metastatic calcification, including that of blood vessels. Thus, it is quite important to identify severe cases of hyperparathyroidism refractory to medical therapy. The size of the parathyroid glands, serum levels of fibroblast growth factor (FGF)23, and, possibly, the overproduction of a novel form of parathyroid hormone (PTH), serve as useful markers for this purpose. Adynamic bone disease with low buffering capacity for calcium is another major cause of hypercalcemia in dialysis patients. Our recent studies suggest that indoxyl sulfate accumulated in uremic serum is responsible for the suppression of osteoblastic function. In order to maintain the bone quality in patients with CKD, bone changes due to aging, menopause, and malnutrition need to be considered by nephrolgists and non-nephrologists in collaboration.
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PMID:The kidney and bone metabolism: Nephrologists' point of view. 1707 34

Deficiency in 1alpha,25-dihydroxyvitamin D(3) (1,25D(3)) has been suggested as an important environmental factor for immuno-mediated disorders including inflammatory bowel diseases (IBD), comprising Crohn's disease and ulcerative colitis, both characterized by chronic intestinal inflammation. Administration of vitamin D receptor (VDR) agonists can ameliorate spontaneous and induced animal models of colitis, but hypercalcemia is a dose-limiting adverse event. Previous work in our laboratory has identified 1alpha,25(OH)(2)-16-ene-20-cyclopropyl-vitamin D(3) (BXL-62) as a potent anti-inflammatory VDR agonist with a low calcemic activity. In the present study, we confirm the marked anti-inflammatory properties of BXL-62 and show its capacity to induce VDR primary response genes, like CYP24A1 and CAMP, at lower concentrations than 1,25D(3), in PBMCs from IBD patients. Its higher anti-inflammatory potency compared to 1,25D(3) was demonstrated by the significantly more potent inhibition in PBMCs and in lymphocyte-enriched lamina propria mononuclear cells of the pro-inflammatory cytokines TNF-alpha, IL-12/23p40, IL-6 and IFN-gamma, both at mRNA and protein level. The therapeutic efficacy of intra-rectal administration of BXL-62 in experimental IBD is shown by its beneficial effects, significantly higher than 1,25D(3), to induce recovery of clinical symptoms of colitis at normocalcemic doses in mice undergoing dextran sodium sulfate-induced colitis. These results confirm the therapeutic efficacy of VDR agonists in experimental colitis, and suggest BXL-62 as a promising compound for IBD treatment.
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PMID:Efficacy of a potent and safe vitamin D receptor agonist for the treatment of inflammatory bowel disease. 2035 May 69


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