285 Renal transplant recipients (RTR) are at increased risk of osteoporosis(OP) due to long-term glucocorticoid use and other risk factors. Glucocorticoid induced OP, unlike postmenopausal OP may be less influenced by gender or hormonal status. The objective of this study was to evaluate the risk factors for glucocorticoid induced OP at the hip and spine in RTR, with an emphasis on gender and menopausal status. The degree of OP was graded by the standard deviation (SD) in a patient's bone mineral density (BMD) compared to a normal adult's peak bone mass (T-score). The WHO defines OP and osteopenia in terms of T-scores of >2.5 SD and >1.5 SD below the mean respectively. Thirty-one consecutive renal transplant patients evaluated in the nephrology clinics at least six months post transplant received a BMD scan by dual energy x-ray absorptiometry between October and December 1997. A retrospective chart review was performed to assess the frequency of possible risk factors, including demographics, laboratory parameters, glucocorticoid history, medical history, physical activity and gonadal status. Fisher's exact test and Kruskal-Wallis Chi-square approximations were used to compare groups (p<0.05). The results (mean±SD) are summarized in thetable.As expected, higher body weight was a protective factor in the severity of glucocorticoid induced OP. However, neither gender nor menopausal status supplied an expected protective benefit. Our results suggest that all patients, regardless of age, gender or hormonal status should be considered as candidates for OP prevention.
To describe delayed peak lithium concentrations after an overdose of extended-release lithium tablets.A patient with borderline personality disorder and depression ingested extended-release lithium approximately 20.25 g along with other agents. At presentation, the lithium concentration was 1.4 mEq/L. Significant enteral intake was initiated 27 hours after presentation and the lithium concentration 5 hours later increased to 3.2 mEq/L. A second lithium peak concentration of 5.0 mEq/L was noted 40 hours after presentation. Two hemodialysis sessions lasting 4 hours each were performed along with administration of sodium polystyrene sulfonate in sorbitol 20% to enhance lithium elimination and decrease absorption. Eighty-eight hours after presentation, the lithium concentration had decreased to 1.5 mEq/L.Delayed and secondary peak lithium concentrations have been reported following an overdose with an extended-release product. Extended-release lithium may form an aggregate in the gastrointestinal tract and/or have delayed absorption secondary to coingested drugs. Toxicity may result if the patient begins enteral intake of drugs, fluids, or nutrition.Continued monitoring of lithium concentrations after an acute ingestion with an extended-release product are recommended until lithium concentrations are less than 1.5 mEq/L and there are no signs of toxicity, particularly once the patient begins significant enteral intake.
Background Ligand binding to the platelet membrane receptor glycoprotein (GP) IIb/IIIa, the final and obligatory step to platelet aggregation, can now be inhibited by pharmacological agents. This study was designed to evaluate the potential of lamifiban, a novel nonpeptide antagonist of GP IIb/IIIa, for the management of unstable angina. Methods and Results In a prospective, dose-ranging, double-blind study, 365 patients with unstable angina were randomized to an infusion of 1, 2, 4, or 5 μg/min of lamifiban or of placebo. Treatment was administered for 72 to 120 hours. Outcome events were measured during the infusion period and after 1 month. Concomitant aspirin was administered to all patients and heparin to 28% of patients. Lamifiban, all doses combined, reduced the risk of death, nonfatal myocardial infarction, or the need for an urgent revascularization during the infusion period from 8.1% to 3.3% ( P =.04). The rates were 2.5%, 4.9%, 3.3%, and 2.4% with increasing doses. At 1 month, death or nonfatal infarction occurred in 8.1% of patients with placebo and in 2.5% of patients with the two high doses ( P =.03). The highest dose of lamifiban additionally prevented the need for an urgent intervention. Lamifiban dose-dependently inhibited platelet aggregation. Bleeding times were significantly prolonged with platelet inhibition of >80%. Major (but neither life-threatening nor intracranial) bleedings occurred in 0.8% of patients with placebo and 2.9% with lamifiban. Conclusions The nonpeptide GP IIb/IIIa antagonist lamifiban protected patients with unstable angina from severe ischemic events during a 3- to 5-day infusion and reduced the incidence of death and infarction at 1 month, suggesting considerable promise for this new therapeutic approach.
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