Patellofemoral joint arthroplasty: patient selection,surgical technique and outcomes

Isolated patellofemoral arthritis is an increasingly recognized entity, and is usually associated with previous patellofemoral dysplasia or instability. Patellofemoral arthroplasty (PFA) has evolved significantly in recent years, both in terms of implant design and importantly in the understanding of appropriate patient selection. This review outlines the indications and investigations for PFA, provides a brief history of the development of contemporary implants, and presents the clinical outcomes for the prostheses most commonly used in the UK. In addition, it provides a detailed surgical technique for implantation of an onlay implant, with tips on how to optimize patellofemoral biomechanics and thus achieve a consistently good outcome.     

Serum monitoring of antipsychotic drug levels during concomitant administration of sertraline and antipsychotic medication.

OBJECTIVE: To assess whether pharmacokinetic drug interactions occur when sertraline is added to antipsychotic medications. METHOD: Forty-eight patients with remitted DSM-IV schizophrenia and comorbid major depression were randomized to placebo for 6 weeks or sertraline 50 mg for 4 weeks followed by sertraline 50 mg to 100 mg for 2 weeks for nonresponders. Treatment with the patients' usual antipsychotic continued. Weekly clinical outcome assessments occurred for 6 weeks, and serum samples for drug monitoring were collected at Weeks 1, 5, and 6. Serum concentrations of sertraline and antipsychotics were measured with standard assays. RESULTS: In both placebo- and sertraline-treated groups, most patients displayed minor fluctuations in antipsychotic serum levels over 6 weeks. There was no clinical evidence of drug interactions in the sertraline-treated group. CONCLUSIONS: Clinically significant adverse effects did not occur despite variable antipsychotic serum levels with or without sertraline. Concern about pharmacokinetic interactions should not deter the use of sertraline for depression in individuals with schizophrenia.     

In vivo determination of body fat by measuring total body carbon

Total body carbon (TBC) is measured in vivo by neutron inelastic scattering. The fast neutrons needed for the irradiation are produced by a miniature deuterium-tritium (D-T) neutron generator. Body fat and protein are the main contributors to TBC. Bone ash and carbohydrates contribute less than 3%. Fat is calculated from TBC after the subtraction of the carbon contributions from protein, bone, and glycogen. The technique was applied to 14 normal volunteers (8 females, 6 males) aged 24-94 y who underwent neutron inelastic scattering and neutron activation measurements for body carbon, nitrogen, and calcium. The initial results agree with other techniques. Unlike models that evaluate body fat by subtracting lean body mass from body weight, the TBC technique is not sensitive to assumptions on the composition of lean body; therefore, it is appropriate for studies of adults of any age and health condition.     

Increased hepatic efflux of glutathione after chronic ethanol feeding

Chronic ethanol feeding increases hepatotoxicity of drugs, such as acetaminophen, which form electrophilic metabolites. Availability of glutathione (GSH) is important in preventing liver damage from reactive metabolites. Chronic ethanol feeding has been reported to increase turnover of hepatic GSH in rats. The results of the present study show that the total hepatic efflux of GSH was increased from 5.95 +/- 0.42 nmoles/min/g liver (control) to 9.96 +/- 0.57 nmoles/min/g (P less than 0.001) in isolated perfused livers from rats 24 hr after withdrawal from chronic ethanol feeding. The increase in total efflux of GSH was due to a significant increase in sinusoidal GSH efflux from 4.76 +/- 0.49 nmoles/min/g liver in control rats to 9.07 +/- 0.47 nmoles/min/g (P less than 0.001) in ethanol-fed rats, while biliary efflux decreased slightly, 1.20 +/- 0.11 (control) vs 0.89 +/- 0.31 (ethanol). The increase in cellular efflux of GSH was similar in magnitude to the increase in hepatic GSH turnover that we reported previously. Biliary GSSG was similar in both groups of animals. Hepatic GGT activity was increased slightly, but not significantly, whereas renal GGT activity was similar in ethanol-fed rats. Hepatic GSH and GSSG levels were also similar. The increase in turnover of hepatic GSH in rats withdrawn from chronic ethanol feeding was most likely due to increased cellular efflux of GSH. This finding suggests that chronic ethanol feeding may increase cellular requirements for GSH, although the mechanism remains unknown. This alteration in GSH turnover may have important consequences for detoxification of xenobiotics or their metabolites by the liver.