Journal of Pharmacy Technology

Renal allograft recipients are at increased risk of osteoporosis and fractures because of their multiple risk factors for reduced bone mineral density (BMD).

To retrospectively assess the risk factors that may predispose renal transplant recipients to reduced BMD.

Thirty-one consecutive renal allograft recipients who had their hip and spine BMD measured by dual energy X-ray absorptiometry were evaluated. Individual patient medical records were reviewed for risk factors including demographics, laboratory parameters, glucocorticoid use, medical history, physical activity, and gonadal status. Fisher's exact test and Kruskal-Wallis chi-square approximations were used to compare BMD groups (p < 0.05). Analysis of variance with a Bonferroni adjustment was used to compare differences between BMD groups (p = 0.01) Linear regression analysis was used to correlate BMD with clinical parameters.

A trend for younger patients (mean 43 y) to have osteoporosis and older patients (mean 54 y) to be osteopenic (p = 0.056) was seen. Higher body weight (p = 0.003) and higher creatinine clearance (p = 0.008) were associated with normal BMD results. Linear regression analysis showed a strong correlation between hip and spine BMD and creatinine clearance. Our data failed to show a statistical relationship between cumulative glucocorticoid dose or daily doses of greater than 7.5 mg and lower BMD. Neither male gender nor premenopausal status seemed to provide protection from reduced BMD.

These results suggest that all renal allograft recipients, regardless of age, gender, or hormonal status, may be at risk for the development of osteoporosis.

To review the contemporary management of dog bites with an emphasis on clinical presentation, wound care, microbiology, antimicrobial prophylaxis, and treatment.

The published literature was searched by use of MEDLINE (1990-December 2000) and bibliographic reviews of relevant textbooks and review articles.

Review articles, case reports, appropriate meta-analyses, and relevant textbook chapters dealing with mammalian bites and their management were evaluated. All pertinent information was synthesized and incorporated into the present review.

The incidence of serious and fatal dog bites has increased because of the acquisition of larger, more aggressive breeds. School-age children and young adults are at the highest risk. Most bites occur on the upper extremities, although head and neck bites are also common. The risk of infection is greatest for crush injuries, puncture wounds, and hand wounds. Infection tends to develop within 24–36 hours of the injury. Complications include osteomyelitis, septic arthritis, tenosynovitis, and septicemia. Most infections are polymicrobial and involve organisms isolated from the skin of the patient and the indigenous oral flora of the dog. Bites should be initially managed under accepted wound care protocols. Wound closure remains controversial and should be reserved for facial and head wounds. Immobilization and elevation are essential for therapeutic success. Prophylactic antibiotics should be reserved for bites at high risk for infection and the immunocompromised host. Whether for prophylaxis or treatment, empiric antimicrobial therapy should be directed against the most common bacteria: Pasteurella spp., streptococci, staphylococci, and anaerobes. Duration and route are dependent on the location and severity of the wound.

Dogs remain the major cause of mammalian bites in the US. It is important for clinicians to have an understanding of the contemporary management of dog bites. Good wound care is central to the prevention and treatment of complications. Appropriate antimicrobial therapy should be directed against both aerobic and anaerobic flora. Careful monitoring is imperative, and antibiotic changes should be made based on clinical response and, if appropriate, the results of culture and sensitivity reports.

To review the relevant literature concerning the biochemical mechanism(s) of valproic acid (VPA)-induced hyperammonemia in an attempt to present a unifying pathogenetic hypothesis.

The MEDLINE database (1966–July 2001) was searched for English-language articles and abstracts on VPA-induced hyperammonemia. References cited in relevant primary articles were also reviewed.

More than 150 original and review articles were evaluated, and the most relevant were selected.

Clinically significant hyperammonemia is a rare adverse effect of VPA therapy. The exact pathogenesis of VPA-induced hyperammonemia remains unclear, but is likely to involve a variety of contributing and possibly overlapping biochemical steps. These include VPA drug concentration, indirect inhibition of ureagenesis by valproyl coenzyme A (CoA), direct suppression of the urea cycle enzymes, depletion of mitochondrial acetyl CoA and decreased production of N-acetylglutamate, depletion of carnitine stores, and increased glutamate dehydrogenase activity.

Hyperammonemic encephalopathy is a rare, but clinically important, adverse effect of VPA therapy. The biochemical basis for this association remains unclear. Awareness of this adverse reaction by healthcare personnel is important in early recognition, treatment, and prevention.

To analyze and compare the pharmacokinetic parameters of a single daily dose (SDD) of gentamicin 5 mg/kg in adults with normal renal function who developed neutropenic fever during intensive non-nephrotoxic chemotherapy.

Ten patients received gentamicin in a 60-minute infusion and blood samples were drawn at 0, 0.5, 1, 2, 8, and 24 hours after the end of the infusion. Gentamicin concentrations were fitted to a noncompartment analysis (NCA) model and a 2-compartment open model for comparison.

The mean ± SD gentamicin concentrations were: maximum concentration at 0.5 hours, 15.7 ± 3.4 mg/L; at 1 hour, 12.3 ± 2.3 mg/L; at 2 hours, 8.3 ± 2.5 mg/L; and at 8 hours, 1.7 ± 1 mg/L. The minimum concentration at 24 hours was 0.27 ± 0.36 mg/L. No statistical differences were established between the mean AUC (63 ± 8.5 and 54.2 ± 9.9 mg/L · h; p = 0.5) and gentamicin clearance (101.0 ± 13.3 and 160.6 ± 27.3 mL/min; p = 0.065). Statistical differences were demonstrated between the mean elimination rate constant (p < 0.001), half-life (p < 0.001), and volume of distribution (p < 0.001), measured by the NCA and the 2-compartment models.

Based on our findings, the NCA method for kinetic analysis of gentamicin prescribed in high SDD can be applied only for AUC and gentamicin clearance calculations.