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A normal serum calcium level is 8 to 10 mg/dL. The diagnosis of hypercalcemia (ie, levels 10.5 mg/dL or greater) should be confirmed with an albumin-adjusted or ionized calcium level. The two most common causes of hypercalcemia are hyperparathyroidism and malignancy. Drugs, notably lithium and thiazide diuretics, also can cause hypercalcemia. Patients with severe or symptomatic hypercalcemia should be treated initially with hydration to decrease calcium levels. The evaluation should include a parathyroid hormone (PTH) level. If the PTH level is low, cancer is a likely cause, particularly multiple myeloma, breast cancer, or lymphoma. If the PTH level is normal or elevated, hyperparathyroidism is the likely cause. Symptomatic patients with hyperparathyroidism and patients with certain clinical markers should be considered for surgery. For patients with mild disease, monitoring is an option. Hypocalcemia often is caused by vitamin D deficiency. Symptomatic patients and patients with calcium levels less than 7.6 mg/dL should be treated with intravenous calcium gluconate; concomitant magnesium deficiency should be addressed. There is no evidence that routine calcium and vitamin D supplementation reduces the risk of fractures, but studies have shown that vitamin D supplementation does decrease the number of falls in older adults at risk., (Written permission from the American Academy of Family Physicians is required for reproduction of this material in whole or in part in any form or medium.)

The aim of this in vitro study was to evaluate the calcium and phosphorus concentrations in enamel surfaces before, during, and after treatment with in-office 35% hydrogen peroxide bleaching agents with 2% calcium gluconate (WCa) or without calcium gluconate (W). Twenty sound human third molars were divided into 2 groups of 10. The bleaching agents were applied to the tooth surfaces in accordance with the manufacturer's instructions: WCa, 40 minutes per day at 3 sessions with 7-day intervals; W, 3 × 15 minutes per day at 3 sessions with 7-day intervals. Enamel microbiopsies were performed prior to the bleaching treatment, immediately after each bleaching session (first, second, and third applications), and 7 and 14 days following the last bleaching treatment. The concentration levels of calcium and phosphorus in the microbiopsy specimens were recorded spectrophotometrically. There was a statistically significant decrease in the calcium concentration 7 days after the last bleaching treatment, but there was a recovery to baseline values at 14 days, regardless of the bleaching agent used (WCa and W). When W was used, there was no difference in the phosphorus concentration over time. The phosphorus concentration in the WCa group decreased after the third application, showing a significant difference from the W group at this time. However, an increase in the phosphorus concentration was observed in the posttreatment period, and no significant differences were observed between values at baseline and those at 14 days posttreatment. The in-office bleaching gel containing 2% calcium gluconate did not affect the calcium and phosphorus concentrations in enamel as compared to a calcium-free bleaching agent.

Polycalcium is a mixture of Polycan and calcium lactate-gluconate 1:9 (w/w) with demonstrated antiosteoporosis activity in vitro and in vivo studies. These studies were a 4-week open-label, single-center trial to evaluate the efficacy of oral Polycalcium on bone metabolism and safety. In total, 30 healthy women (range 40-60 years) were administered 400 mg of Polycalcium for 4 weeks. The primary efficacy parameter was urinary deoxypyridinoline (DPYR) levels, and serum osteocalcin (OSC), bone-specific alkaline phosphatase (BALP), urinary cross-linked C-telopeptide of type-1 collagen (CTx), urinary cross-linked N-telopeptide of type-1 collagen (NTx), calcium (Ca), and phosphorus (P) levels, which were evaluated for comparison before and after administration of Polycalcium. After 4 weeks of Polycalcium administration, 27 subjects completed the test plan. Three subjects withdrew their consent to participate. The values of blood OSC, BALP, serum Ca, and serum P from baseline to 4 weeks of treatment were changed by -28.44%, 14.37%, 6.11%, and 1.42%, respectively. Biomarkers of bone resorption: urinary DPYR, serum CTx, serum NTx, urinary Ca, and urinary P, at baseline after 4 weeks of treatment were changed by -13.40%, 6.67%, -5.13%, -22.43%, and -3.04%, respectively. Additionally, when considering the subjects' adverse effects and the results of the blood and urine tests over the 4-week trial period, the dose of 400  mg Polycalcium showed efficacy for improving bone metabolism and was well tolerated and safe. Polycalcium was apparently safe and efficacious.

Background: The authors conducted a study to evaluate tooth sensitivity (TS) and the bleaching effectiveness associated with use of a calcium-containing (CC) in-office bleaching gel., Methods: The authors used a 35 percent calcium-free (CF) hydrogen peroxide gel and a 35 percent CC hydrogen peroxide gel according to the manufacturer's instructions in 40 caries-free participants 18 years or older. They performed two bleaching sessions with a one-week interval between sessions. The authors registered the color at baseline and after the first and second bleaching sessions by using a shade guide and by gauging the participant's perception of TS as registered on a scale from 0 (none) to 4 (severe). The authors evaluated the bleaching effectiveness at each week's recall visit by means of the Friedman test, and they compared the groups at each assessment point by means of the Mann-Whitney test. They evaluated the percentage of participants with TS and the intensity of the TS by using the Fisher exact and Mann-Whitney tests., Results: Both groups demonstrated equivalent and significant tooth color enhancement compared with color values at baseline (P < .05), with an average bleaching of 7 to 8 shade guide units. Most of the participants from the CF group (80 percent) experienced sensitivity while undergoing the bleaching regimen, whereas only 40 percent of participants from the CC group reported experiencing TS (P = .02). The intensity of TS was significantly higher (P < .01) for the CF group during in-office dental bleaching., Conclusions: The CC 35 percent hydrogen peroxide gel reduced the TS during in-office dental bleaching without jeopardizing the bleaching effectiveness., Clinical Implications: The results of this study support the findings that a CC 35 percent hydrogen peroxide gel can reduce TS during in-office dental bleaching.

The antineoplastic efficacy of oxaliplatin, a widely used anticancer drug, is restricted by its adverse effects such as peripheral neuropathy. Infusing a combination of calcium gluconate and magnesium sulfate (Ca/Mg) suppresses the acute neurotoxic side effects of oxaliplatin, although the mechanism is unclear. To elucidate the molecular mechanisms of oxaliplatin-induced neurotoxicity and the effects of Ca/Mg against this toxicity, we examined the effect of Ca/Mg on oxaliplatin-induced inhibition of neurite outgrowth in PC12 cells, a commonly used neuronal cell model. Oxaliplatin and oxalate suppressed nerve growth factor (NGF)-induced neurite outgrowth and reduced the NGF-mediated increase in the intracellular calcium concentration [Ca(2+)](i). A calcium-chelating agent, BAPTA/AM, also exhibited similar inhibitory effects on neurite outgrowth and [Ca(2+)](i). The addition of Ca/Mg attenuated these inhibitions induced by oxaliplatin and oxalate. The NGF-induced upregulation of growth-associated protein-43 (GAP-43) was suppressed by oxaliplatin and oxalate. Oxaliplatin, but not oxalate, suppressed NGF-stimulated extracellular signal-regulated kinase activation, and this inhibition was not affected by Ca/Mg. Ca/Mg did not modify the oxaliplatin-induced loss of cell viability or apoptosis in PC12 or HCT-116 cells, a human colorectal cancer cell line. These results suggest that the inhibition of neurite outgrowth but not tumor cell death induced by oxaliplatin is partly associated with reductions in [Ca(2+)](i) and GAP-43 expression, and this inhibition was suppressed by the addition of Ca/Mg. Therefore, it may be assumed that Ca/Mg is useful for protecting against oxaliplatin-induced neurotoxicity without reducing the antitumor activity of oxaliplatin.

Background: Our recent data indicate that 21% of critically ill, adult, multiple-trauma patients receiving specialized nutrition support experience hypocalcemia. However, evidence-based methods for the treatment of moderate to severe acute hypocalcemia (ionized calcium concentration [iCa] <1 mmol/L) are lacking., Methods: The efficacy of an infusion of 4 g of calcium gluconate was evaluated in 20 critically ill, adult, multiple-trauma patients with moderate to severe hypocalcemia (iCa <1 mmol/L). The calcium gluconate was infused at a rate of 1 g/h in a small volume admixture. A serum iCa determination was obtained on the following day., Results: Calcium gluconate infusion significantly increased serum iCa from 0.90 +/- 0.08 mmol/L to 1.16 +/- 0.11 mmol/L (p < .001) on the following day. This dosage regimen was successful for achieving a serum iCa >1 mmol/L for 19 of 20 (95%) hypocalcemic patients and achieved a concentration >1.12 mmol/L in 14 (70%) of the patients. Two patients developed mild hypercalcemia (iCa of 1.34 mmol/L and 1.38 mmol/L) postinfusion., Conclusions: A short-term infusion of 4 g of intravenous (IV) calcium gluconate for the treatment of moderate to severe hypocalcemia appears to be a promising regimen for critically ill, adult, multiple-trauma patients.

Purpose: Oxaliplatin is active in colorectal cancer. Sensory neurotoxicity is its dose-limiting toxicity. It may come from an effect on neuronal voltage-gated Na channels, via the liberation one its metabolite, oxalate. We decided to use Ca and Mg as oxalate chelators., Experimental Design: A retrospective cohort of 161 patients treated with oxaliplatin + 5-fluorouracil and leucovorin for advanced colorectal cancer, with three regimens of oxaliplatin (85 mg/m(2)/2w, 100/2w, 130/3w) was identified. Ninety-six patients received infusions of Ca gluconate and Mg sulfate (1 g) before and after oxaliplatin (Ca/Mg group) and 65 did not., Results: Only 4% of patients withdrew for neurotoxicity in the Ca/Mg group versus 31% in the control group (P = 0.000003). The tumor response rate was similar in both groups. The percentage of patients with grade 3 distal paresthesia was lower in Ca/Mg group (7 versus 26%, P = 0.001). Acute symptoms such as distal and lingual paresthesia were much less frequent and severe (P = 10(-7)), and pseudolaryngospasm was never reported in Ca/Mg group. At the end of the treatment, 20% of patients in Ca/Mg group had neuropathy versus 45% (P = 0.003). Patients with grade 2 and 3 at the end of the treatment in the 85 mg/m(2) oxaliplatin group recovered significantly more rapidly from neuropathy than patients without Ca/Mg., Conclusions: Ca/Mg infusions seem to reduce incidence and intensity of acute oxaliplatin-induced symptoms and might delay cumulative neuropathy, especially in 85 mg/m(2) oxaliplatin dosage.

Background: ACD-A solution containing sodium citrate and citric acid is used as an anticoagulant agent during peripheral blood progenitor cell (PBPC) harvesting, and in rare cases can cause fatal citrate intoxication. The aim of this study was to establish effective methods for stabilizing ionized calcium (ICa) levels during PBPC harvesting., Study Design and Methods: ICa was measured during 46 apheresis procedures conducted in 26 patients. Four patients in four procedures were infused with calcium gluconate solution before PBPC harvesting; three patients in six procedures were infused with calcium gluconate when symptoms of citrate intoxication appeared; and four patients in five procedures received a continuous infusion. Five patients in five procedures took an isotonic sports drink containing calcium when hypocalcemic symptoms appeared. The ICa level, blood pressure, and pulse rate were measured., Results: ICa declined rapidly from the preapheresis level of 1.081(+/-0.092) mM to 0.937(+/-0.081) mM (13.3%, p < 0.0001) 10 minutes after the start of apheresis and continued to decline until the completion of the procedure. When patients received a continuous infusion of calcium during apheresis, ICa was relatively stabilized. ICa significantly rose (6.1 +/- 3.6%, p < 0.02) within 2 to 5 minutes after oral intake of an isotonic sports drink containing calcium and was maintained within normal range for 31 to 55 minutes., Conclusion: An isotonic sports drink containing calcium has a quick stabilizing and a longer maintenance effect on ICa. Thus, we recommend the intake of an isotonic sports drink containing calcium as the easiest and best method for preventing hypocalcemia during apheresis.

Objective: To determine whether supplemental i.v. calcium administration would attenuate or prevent gentamicin-induced acute renal failure, defined as an increase in serum creatinine concentration > or = 50% above baseline., Animals: 10 healthy pony mares., Procedure: Pony mares were randomly assigned to receive calcium at a dosage of 20 mg/kg of body weight or saline solution i.v., twice daily for 14 days. All pony mares received gentamicin at a dosage of 20 mg/kg i.v. every 8 hours for 14 days. Gentamicin pharmacokinetic, serum biochemical, and urinalysis data were measured every other day for the 14-day study period. Renal histologic examination was performed, and results were scored at the end of the 14-day period., Results: 4 of 5 mares not receiving calcium supplementation developed acute renal failure. Only 1 of the 5 mares receiving calcium supplementation developed acute renal failure. Over the course of the study, pony mares receiving calcium supplementation had significantly fewer changes in urinalysis variables, and significantly less microscopic renal damage., Conclusion: Daily i.v. administration of calcium attenuated gentamicin-induced acute renal failure., Clinical Relevance: Calcium supplementation may help diminish the risk of acute renal failure associated with aminoglycoside antibiotics.

Objective: To investigate the mechanism of hemorrhagic tendency after phosphorus poisoning., Methods: 45% phosphoric acid and 20 mg/cm2 phosphorus were used to produce burn injury in rabbits. The total content of phosphorus remaining on the wound and 7-day mortality were similar in both groups., Results: The results showed that plasma free calcium contents were significantly lower in both phosphorus groups than healthy and thermal burn controls (0.80 vs 1.40 mol/l, P < 0.01). The free calcium content of platelet was lowered to 116-140 nmol/l, which was significantly lower than that of healthy control (285 nmol/l) and thermal injury group (480-504 nmol/l). Concomitantly, the platelet aggregation rate was lowered to 1.29% and 10.78% in phosphoric acid group and phosphorus group, respectively, while it was 67.01% in healthy control and 82.1%-84.9% in thermal injury group; the difference was statistically significant., Conclusion: Calcium therapy brought back intracellular and extracellular free calcium contents to normal in phosphorus burn group. Also platelet aggregation rate approached normal level after calcium therapy. The results suggest that the bleeding tendency after phosphorus burn is due to combination of phosphorus with intracellular and extracellular calcium of platelets, thus inhibiting aggregation of platelets.

A 5-year-old child suffering from familial idiopathic hyperphosphatasia (FIH) was treated by: (1) intravenous infusion of pamidronate (APD) (3 h) (0.75 mg/kg/day) for 5 days; and (2) oral administration of APD (8 mg/kg/day) for 1 year, in association with calcium (1 g/day) as calcium gluconate. A decrease of both serum calcium and phosphate, and a slight PTH increase were observed immediately after the IV treatment; serum alkaline phosphatase did not change, but a marked and rapid decline in the hydroxyprolinuria was observed: basal 659 +/- 207 during IV treatment 169 +/- 59 (mean +/- SD mg/24 h, P < 0.005). At the end of one year of oral APD treatment clinical and radiological findings showed a remarkable improvement. Serum calcium, phosphate and PTH returned to the initial values. Plasma alkaline phosphatase levels showed a 70% decrease: basal 1370 IU/l, 1 year 410 IU/l whereas the hydroxyprolinuria values were similar to those determined at the end of the intravenous treatment (212 +/- 13 mg/24 h), but still significantly lower than the basal levels (P < 0.01). No side-effects were observed. APD appears to be a promising treatment for patients with FIH.

Packed cell volume, total plasma protein, serum sodium, potassium, and ionized Ca2+ concentrations, and blood pH were determined at the time of admission and following surgery in 147 horses with acute abdominal crisis. Horses were allotted to 3 categories on the basis of the surgical lesion: (1) nonstrangulating obstruction of the ascending or descending colon (category A, n = 76), (2) strangulating and nonstrangulating infarction of the cecum or ascending colon (category B, n = 37), and (3) strangulating and nonstrangulating infarction of the small intestine (category C, n = 25). Horses with low serum ionized Ca2+ concentration following surgery were given 23% calcium gluconate (100 to 300 ml) IV to effect, and ionized Ca2+ concentration was determined following treatment. The serum ionized Ca2+ concentrations of horses in categories A, B, and C before and after surgery were lower than our normal laboratory reference range. Prior to surgery, serum ionized Ca2+ concentration measured from horses in category B and C was lower than that in horses in category A. There was no difference in ionized Ca2+ concentration in serum samples obtained before surgery in horses from category B and C, and in serum samples obtained following surgery. There was a decrease in ionized Ca2+ concentration during surgery in horses in category A. There was no change between preoperative and postoperative ionized Ca2+ concentration in the samples obtained from horses in category B and C. After calcium gluconate administration, all horses with low serum ionized Ca2+ after surgery had concentrations within our normal range. Measurement of serum ionized Ca2+ in horses with an acute abdominal crisis is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)

Eleven Nigerian children with clinically and radiologically proven rickets were assessed biochemically. The children had low or low normal concentrations of total and corrected calcium, and elevated plasma alkaline phosphatase (ALP) activity, but normal plasma phosphate concentrations. Their serum 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations were not significantly different from those in controls, but the ratio of 1,25-(OH)2D to 25-OHD was significantly greater than that in controls. Parathyroid hormone (PTH) concentrations were greater in rachitic children, and there was a significant correlation between 1,25-(OH)2D and PTH concentrations. Osteocalcin concentrations in rachitic children were not significantly different from those in controls, but they were markedly elevated in the three patients with the highest 1,25-(OH)2D and PTH concentrations. One child, from whom a sample of bone (from a corrective osteotomy) was available for histological examination, showed markedly thickened osteoid seams, characteristic of rickets. All the rachitic children had a calcium intake of less than 150 mg daily. Treatment of these rachitic children with calcium gluconate (1 g/d) led to clinical, radiological, and biochemical healing of rickets. We conclude that rickets in Nigerian children is not due to vitamin D deficiency, but to a lack of calcium. This observation has implications regarding the pathogenesis, treatment, and prevention of rickets/osteomalacia in Nigeria and possibly other African and tropical countries.

Calcium is important in the maintenance of arterial smooth muscle function and its alteration from normal may predispose to atherogenesis and hypertension. Slow channel inhibitors such as nifedipine and calcium salts have been used separately to modulate arterial calcium in patients with hypertension. This study included 41 patients with essential hypertension, of whom 29 responded to calcium gluconate therapy (9.8/6.3 mmHg) and the remaining 12 (group B) showed either no response or a rise in blood pressure. Combined administration of calcium and nifedipine in responders (29 cases, group A) in a single-blind, placebo-controlled manner showed a further substantial decrease (9.6/3.2 mmHg) in pressure compared with pressures during placebo administration in both short- as well as long-term administration in group B patients. Although it is difficult to predict the positive role of calcium in hypertension, non-obese females with increased salt intake show a greater response to calcium therapy. It is possible that calcium salts plus calcium blocker therapy can further reduce the blood pressure in a particular subset of hypertensives. However, this needs further confirmation in a larger study.

Two patients with long-standing hyperparathyroidism due to a parathyroid adenoma are described. Both had severe osteitis fibrosa cystica and a proximal myopathy. Both were treated with alfacalcidol (2 micrograms/day) prior to and following parathyroidectomy, and infused with calcium gluconate following the operation. Plasma total and ionized calcium and magnesium concentrations were maintained within the normal range. However, both developed tetany in the postoperative period in spite of normal ionized calcium and magnesium concentrations. Tetany continued for 4 weeks in one patient and for longer in the other. Prolonged hypercalcaemia may result in a state of neuromuscular excitability following parathyroidectomy even at high normal concentrations of ionized calcium.

The antiulcer effect of verapamil, and its relationship to stomach calcium levels, were examined in rats restrained at 4 degrees C (stress). Stress for 2 hr significantly increased muscle calcium and induced mucosal ulceration in the gastric glandular segment; calcium concentrations in the glandular mucosa and serum were unaffected. Verapamil or calcium gluconate given 30 min before stress prevented the rise in gastric muscle calcium, and attenuated ulcer severity. Bis(beta-aminoethylether)-NNN'N'-tetra-acetic acid (EGTA) pretreatment, however, further elevated stomach muscle calcium and markedly worsened lesion formation. These findings suggest that increased stomach muscle calcium could be a causal factor in stress-induced gastric glandular ulceration.

Various preparations of calcium are recommended for use in treatment of cardiac arrest and advantages are claimed for one preparation over another because of increased availability of the calcium to the heart. Ionised calcium levels in human blood have been assayed following the addition of calcium increments by use of the calcium electrode. The results showed no difference between calcium chloride and calcium gluconate.

The absorption of calcium pidolate is studied in 10 females suffering from osteoporosis by oral overload compared to the results of the glucono-lactate-carbonate. 405 mq of Ca pidolate produced a higher excretion of calcium by urine and an increase of Ca levels in blood than that produced by 1000 mq of Ca glucono-lactate-carbonate. The tolerance and the lack of side effects were the common feature in both salts. There were no effects on parathyroid glands nor bone resorption. We concluded that calcium pidolate is a safe and efficient treatment for osteoporosis because of easy absorption, which is very helpful in maintaining the calcium balance.