The trade-off between equity and efficiency in population health gain: Making it real.

Two fundamental goals of health systems are to maximise overall population health gain (referred to as efficiency) and to minimise unfair health inequalities (equity). Often there is a trade-off in maximising efficiency vis a vis equity and the relative weight given to one goal over the other is acknowledged to be essentially a value judgement. Health systems necessarily make those value judgements but in making them would benefit from relevant and accurate opportunity cost information. Unfortunately the development of practical tools to measure equity-efficiency trade-offs has lagged theoretical advances in this area. We address this gap by presenting a practical technique to reveal opportunity costs of equity (and efficiency) gains in decentralised population-based health systems, applying stochastic data envelopment analysis to ethnic-specific life expectancy (LE) changes for 20 New Zealand (NZ) District Health Boards for the inter-census period 2006-2013, thereby deriving a notional health frontier from 10,000 Monte Carlo simulations. Four different ways to increase health equity emerge. These show that a trade-off between equity and efficiency does not always exist. In particular, improving both productive efficiency and allocative efficiency (up to its maximum) can also yield gains in equity through reductions in LE inequalities. However, in NZ's case, the opportunity cost (in sacrificed European life-years) of achieving gains in equity beyond the point of maximum productive and allocative efficiency is relatively high, even for quite small reductions in the LE gap between Maori and European populations. This high opportunity cost may explain why, despite governments' strong rhetorical commitment to equity, NZ's health gains have not strayed far from the path of maximising allocative efficiency. Nevertheless, this opportunity cost could be reduced significantly by measures which shift the health frontier outward, highlighting the importance of technical and organisational innovation as potential drivers of greater equity in health outcomes.

Increasing productivity, reducing cost and improving quality in elective surgery in New Zealand: the Waitemata District Health Board joint arthroplasty pilot.

BACKGROUND: In 2010, Waitemata District Health Board piloted a new model of care for total hip and knee arthroplasties. The pilot was incentive based and clinically led. The participating surgeons and anaesthetists were responsible for increasing surgical throughput. The pilot aimed to increase productivity, reduce cost and increase quality for patients. AIM: To compare costs and outcomes for elective hip and knee arthroplasties carried out at the pilot site (Waitakere Hospital) compared with the main District Health Board hospital site (North Shore Hospital (NSH)). METHODS: A retrospective matched cohort study of hip and knee replacements discharged between 1 July 2010 and 31 March 2011, comparing costs and outcomes at the pilot site compared with the NSH site. Only non-complex procedures were included, and routinely collected data were used. RESULTS: One hundred and seventy-seven hip replacements (77 NSH, 100 pilot) and 158 knee replacements (88 NSH, 70 pilot) were analysed. Total inpatient event costs were 12% and 17% lower for hip and knee replacements, respectively, at the pilot site compared with NSH. Significant reduction in operation length (39% hip, 36% knee) and length of stay (38% hip, 39% knee) were found in the pilot groups compared with NSH. CONCLUSION: Implementation of an innovative new model in a public hospital setting has produced significant increases in productivity and reduced overall costs. This model could potentially be used in other public healthcare settings for non-complex elective surgery.

High-level resistance to (-) enantiomeric 2'-deoxy-3'-thiacytidine in vitro is due to one amino acid substitution in the catalytic site of human immunodeficiency virus type 1 reverse transcriptase.

Passage of human immunodeficiency virus type 1 in the presence of increasing 2'-deoxy-3'-thiacytidine (3TC) concentrations results in high-level (> 100-fold) 3TC-resistant viruses. All 3TC-resistant viruses possess a substitution at the second codon (from a methionine into an isoleucine) at position 184 within the highly conserved motif (YMDD) of human immunodeficiency virus type 1 reverse transcriptase. 3TC-resistant viruses were cross-resistant to the (-) enantiomer of the fluorinated derivative of BCH-189 but remained susceptible to 2',3'-dideoxyinosine and 2',3'-dideoxycytidine. The susceptibilities of the 3TC-resistant viruses to the (+) enantiomers of BCH-189 and the fluorinated derivative of BCH-189 demonstrate an enantiomeric specificity for viruses selected under these conditions. Introduction of an isoleucine substitution at codon 184 into a background of two known 3'-azido-3'-deoxythymidine resistance mutations (amino acids 41 and 215) restored the susceptibility of this virus to 3'-azido-3'-deoxythymidine.

Cellular metabolism of (-) enantiomeric 2'-deoxy-3'-thiacytidine.

The metabolism of (-) enantiomeric 2'-deoxy-3'-thiacytidine (3TC) was examined in human immunodeficiency virus type 1 (HIV-1)-infected and mock-infected human cells. 3TC 5'-triphosphate levels accumulated comparably in HIV-1-infected and mock-infected phytohaemagglutinin-stimulated peripheral blood lymphocytes (PBL) and reached 40% or more of total intracellular 3TC metabolites after 4 hr. The rate of decay of 3TC triphosphate in HIV-1-infected and mock-infected PBL measured as a half-life (T1/2) ranged from 10.5 to 15.5 hr. 3TC did not significantly affect metabolism of deoxynucleotides in the U937 cell line, and was shown to be resistant to the action of human platelet pyrimidine nucleoside phosphorylase.

(-)-2'-deoxy-3'-thiacytidine is a potent, highly selective inhibitor of human immunodeficiency virus type 1 and type 2 replication in vitro.

The (-)-enantiomer of 2'-deoxy-3'-thiacytidine (3TC) was found to be a potent and selective inhibitor of human immunodeficiency virus types 1 (HIV-1) and 2 (HIV-2) in vitro. We determined its antiviral activity against a number of laboratory strains of HIV-1 and HIV-2 in a range of CD4-bearing lymphocyte cell lines (mean 50% inhibitory concentration [IC50] range, 4 nM to 0.67 microM). 3TC was also active against a range of HIV-1 strains in peripheral blood lymphocytes (mean IC50 range, 2.5 to 90 nM). The IC50 for cytotoxicity in seven lymphocyte cell cultures, including human peripheral blood lymphocytes, ranged from 0.5 to 6 mM. 3TC had no detectable antiviral activity against a range of other viruses or in cells chronically infected with HIV-1 or HIV-2. The effects of time of addition of the compound and varying the multiplicity of infection on the antiviral activity of 3TC were determined. The results showed that 3TC is a potent and selective inhibitor of HIV-1 and HIV-2 replication in vitro.