Calcium homeostasis in pregnant women receiving long-term magnesium sulfate therapy for preterm labor.

OBJECTIVES: The hypothesis of this study is that calcium homeostasis and bone mineralization are altered in pregnant women receiving long-term therapy with magnesium sulfate as compared with similar women not receiving magnesium sulfate to control preterm labor. STUDY DESIGN: Thirty-nine women between 24 and 32 weeks' gestation, matched for age, race, and duration of bed rest, were enrolled. Indices of calcium homeostasis in serum and urine were measured serially, and bone mineralization of the distal radius was measured at 1 and 11 weeks post partum. RESULTS: Magnesium therapy was administered for a mean duration of 26 +/- 14 days and a cumulative dose of 1405 +/- 963 gm. Serum concentrations of magnesium, phosphorus, and parathyroid hormone increased and those of calcium decreased from baseline values in the magnesium sulfate group and remained uniform throughout the 3-week investigation. The serum magnesium, phosphorus, parathyroid hormone, and calcium concentrations in the control group were unchanged during the study and differed significantly from those in the magnesium sulfate group (p < 0.001). Urinary output of magnesium, calcium, and copper was significantly greater in the magnesium sulfate group than in the control group throughout the study. Urinary losses of calcium in the magnesium sulfate group, approximately 800 to 900 mg/day, were substantial. Although radius bone density 1 week post partum did not differ between groups, the change in bone density from 1 to 11 weeks post partum was significantly lower in the magnesium sulfate group than in controls. CONCLUSIONS: These data suggest that calcium homeostasis is altered during and after long-term magnesium sulfate therapy. The marked, prolonged urinary calcium losses may affect maternal bone mineralization.     

Best evidence in anesthetic practice

Question  

In postoperative non-ventilated patients, what is the efficacy and harm of pharmacological interventions in treating postoperative shivering?     

Neomycin mimics the effects of high extracellular calcium concentrations on parathyroid function in dispersed bovine parathyroid cells.

We examined the effects of the polycationic antibiotic, neomycin, on the function of dispersed bovine parathyroid cells. Neomycin caused a reversible, dose-dependent inhibition of low calcium (Ca++)-stimulated PTH release, with half-maximal inhibition at 30 microM. Maximal inhibition (with 200 microM neomycin) was not additive with the suppressive effects of high (2 mM) Ca++. Neomycin also inhibited dopamine-stimulated cAMP accumulation by 90-98% at 100-200 microM, with a half-maximal effect at 40-50 microM. This action was reversible and was blocked by preincubating the cells overnight with 0.5 microgram/ml pertussis toxin. In addition to its suppressive effects on cAMP metabolism and PTH release, neomycin stimulated the accumulation of inositol phosphates and produced a transient increase in the cytosolic Ca++ concentration (Cai) in fura-2-loaded parathyroid cells. The neomycin-evoked spike in Cai persisted despite removal of extracellular Ca++, indicating that it arises from intracellular Ca++ stores. Exposure of cells to elevated magnesium (Mg++) concentrations elicited a similar spike in Cai but blocked the spike in Cai in response to subsequent addition of neomycin and vice versa. Thus, Mg++ and neomycin mobilize Ca++ from the same intracellular store(s). These results indicate that a polycation, neomycin, closely mimics the effects of polyvalent cations on parathyroid function, suggesting that both agents regulate parathyroid function via similar biochemical pathways.     

A comprehensive strategy for the evaluation and triage of the chest pain patient: A cost comparison study

BACKGROUND: Our objective was to determine the cost-effectiveness of a comprehensive, risk-based triage system, composed of multiple critical pathways, with the use of early myocardial perfusion imaging (MPI) in low-risk patients. We found previously that a chest pain evaluation system that uses MPI in low-risk patients was safe and effective, but the cost-effectiveness of this approach was not studied. METHODS AND RESULTS: We compared two groups. The Acute Cardiac Team (ACT) group (n = 874) was assigned prospectively to 1 of 4 risk levels by emergency department (ED) physicians. Level 1, 2, and 3 patients were admitted; level 4 patients were evaluated in the ED. Level 3 and 4 patients underwent ED MPI. The control group (n = 713) represented consecutive patients evaluated in the prior year according to standard care and assigned retrospectively to an ACT level based on the presenting electrocardiographic and clinical data. Record and hospital administrative data were assessed for clinical variables, outcomes, lengths of stay, and all expenses incurred within 30 days of the index visit. The baseline characteristics of the two groups were similar, including age, sex, myocardial infarction prevalence, and 30-day revascularization rates within each level or between the two groups. Mean costs per encounter were reduced for the ACT patients for each level, which was significant when all patients were compared ($5,030 +/- $7,081 vs $6,044 +/- $10,432, P =.02). Use of MPI in the low-risk patients was associated with reduced costs (level 3, $4,958 +/- $4,948 vs $5,051 +/- $7,036; level 4, $1,529 +/- $2,664 vs $1,794 +/- $6,854) and was associated with a significantly lower angiography rate and shorter length of stay. CONCLUSIONS: Implementation of a comprehensive strategy for chest pain evaluation and triage reduced overall costs for patients with chest pain on presentation. Acute MPI in the ED setting did not increase net cost.