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Biomedical subjects

H M Scott

Publications and source records attributed to H M Scott.

At least 55 records · Page 3Linked to original sources
PubMed1994

Critical leg ischaemia in New Zealand: economic cost of amputation versus intravenous iloprost.

The purpose of this study was to establish the incidence of surgical amputation for critical leg ischaemia in New Zealand, and estimate the hospital, prostheses and indirect costs of this intervention. The cost of amputations was then compared with the cost of treating such patients with iloprost. The study was retrospective. Individual patient records relating to 1991 for both public and private hospitals were analysed. Unit costs relevant to 1991 were applied to the volume data of patients and procedures to derive total costs. Costs were estimated on an incremental basis taking a societal perspective. Conservative estimates were obtained for hospital costs, prostheses and for production loss (loss of output or productivity). Total cost was $NZ15.9 million (hospital and prosthesis cost $NZ13.1 million, production loss $NZ2.8 million). The total quantified cost per amputation was $NZ23 038 (hospital and prosthesis cost $NZ19 020, production loss $NZ4017). 32% of patients requiring amputations were in the working age group. The theoretical avoidance of amputation by treatment with iloprost resulted in net savings of hospital and prosthetic costs of between $NZ6660 and $NZ8720 per patient. Amputation for critical leg ischaemia is costly and has a high mortality, but for iloprost treatment to be cost effective in a New Zealand hospital setting, patients must be targeted and a success rate of at least 55% achieved in avoidance of amputation and reduction of pain while at rest.

Amputation, Surgical↗
PubMed1993

Cost of coronary heart disease in New Zealand.

AIM: To conservatively estimate the costs of coronary heart disease from the perspective of New Zealand society. METHODS: A cross sectional or prevalence analysis (cases and associated costs in one year) was undertaken of the total annual cost of coronary heart disease. Estimates were made on an incremental basis of direct, indirect and intangible costs. Costs relate to 1989 volumes measured in March quarter 1992 dollars (net of goods and services tax). RESULTS: Cost estimates were in all instances conservative values. Direct medical costs amounted to $179 million and indirect costs were between $14 million and $24 million. Loss of life using the human capital approach ranged from $114 million to $264 million, but using the willingness to pay criteria, loss of life was $14,568 million. CONCLUSION: Because of the magnitude of the costs of coronary heart disease even small reductions in the incidence of coronary heart disease will produce substantial savings to society.

Absenteeism↗
PubMed1993

Astrocytic glucose-6-phosphatase and the permeability of brain microsomes to glucose 6-phosphate.

Cells from primary rat astrocyte cultures express a 36.5 kDa protein that cross-reacts with polyclonal antibodies to the catalytic subunit of rat hepatic glucose-6-phosphatase on Western blotting. Glucose-6-phosphate-hydrolysing activity of the order of 10 nmol/min per mg of total cellular protein can be demonstrated in cell homogenates. This activity shows latency, and is localized to the microsomal fraction. Kinetic analysis shows a Km of 15 mM and a Vmax. of 30 nmol/min per mg of microsomal protein in disrupted microsomes. Approx. 40% of the total phosphohydrolase activity is specific glucose-6-phosphatase, as judged by sensitivity to exposure to pH 5 at 37 degrees C. Previous reports that the brain microsomal glucose-6-phosphatase system does not distinguish glucose 6-phosphate and mannose 6-phosphate are confirmed in astrocyte microsomes. However, we demonstrate significant phosphomannose isomerase activity in brain microsomes, allowing for ready interconversion between mannose 6-phosphate and glucose 6-phosphate (Vmax. 15 nmol/min per mg of microsomal protein; apparent Km < 1 mM; pH optimum 5-6 for the two-step conversion). This finding invalidates the past inference from the failure of brain microsomes to distinguish mannose 6-phosphate and glucose 6-phosphate that the cerebral glucose-6-phosphatase system lacks a 'glucose 6-phosphate translocase' [Fishman and Karnovsky (1986) J. Neurochem. 46, 371-378]. Furthermore, light-scattering experiments confirm that a proportion of whole brain microsomes is readily permeable to glucose 6-phosphate.

Animals↗
PubMed1993

Roxithromycin versus cefaclor in lower respiratory tract infection: a general practice pharmacoeconomic study.

An economic evaluation comparing roxithromycin 150mg twice daily and cefaclor 250mg thrice daily in the treatment of lower respiratory tract infections (LRTI) was undertaken as part of a randomised clinical trial in New Zealand general practice. The observed statistically significant difference in adverse events, withdrawal rates and extra treatment courses in favour of roxithromycin in the clinical study was translated into medical cost savings. Treatment failures, withdrawals or adverse events resulted in additional costs for 11 of 120 (9%) patients receiving roxithromycin and 19 of 118 (16%) patients receiving cefaclor. In these cases (treatment failures, withdrawals, adverse effects) additional antibiotics and general practitioner visits were required 3 times more often and the cost of additional medication for treating failure or adverse effects was 3 times higher for patients treated with cefaclor than for patients receiving roxithromycin. The total direct medical cost per patient treated with roxithromycin was $NZ9.37 lower (on an incremental basis) than for patients treated with cefaclor, despite a higher drug acquisition cost. An estimate of $NZ656 000 per year in total savings in direct medical costs could be made in New Zealand if roxithromycin were to replace all cefaclor prescriptions in the treatment of LRTI.

Cefaclor↗
PubMed1993

Annual costs of benign prostatic hyperplasia in New Zealand.

Benign prostatic hyperplasia (BPH) has been regarded as part of the normal aging process in men and little attention has been focused on the cost of the disease in New Zealand. The purpose of this study was to estimate the direct and indirect costs of treating BPH in both the public and the private sectors in New Zealand. The costs of treatment were estimated from public and private hospital data on admissions for BPH, obtained from the New Zealand Department of Health, medical insurance reimbursement schedules, hospital ward costs at one centre, and urology and general practitioner consultation fees. The length of time spent off work, as a measure of indirect costs, during urological investigations or treatment was estimated from interviews with urologists. The annual 1991 total direct medical costs of treated BPH as primary diagnosis in New Zealand were estimated at $NZ16 million (the average of the end-month mid-point exchange rate for the first quarter of 1992 was $US0.5457 per $NZ1), and the costs of lost production plus loss of leisure time by patients was estimated at $NZ4 million (1992 dollars). Patients with a principal diagnosis of BPH stayed on average 8.9 days in a public hospital and 4.6 days in a private hospital. Based on the above costs, if the average length of stay of public hospital patients could be reduced to that of private hospital patients, then hospital ward costs for BPH could fall by 37% and the total direct medical costs by 21%. The most commonly performed surgical operation for BPH was transurethral prostatectomy (TURP). For operations performed in a public hospital, patients stayed on average 8.5 days, while patients whose operations were performed in private hospitals stayed 4.3 days. The mean age of these public hospital patients was 71 years compared with 67 years for those in private hospitals. A complication rate of 2.02% was recorded for TURP in public hospitals but audits (conducted by the researchers) in both public and private settings indicated that the complication rate was substantially under-recorded.

Aged↗
PubMed1992

Permeability of rat liver microsomal membrane to glucose 6-phosphate.

Light-scattering measurements of osmotically induced changes in the size of rat liver microsomal vesicles pre-equilibrated in a low-osmolality buffer revealed the following. (1) The increase in extravesicular osmolality by addition of glucose 6-phosphate or mannose 6-phosphate (25 mM each) caused a rapid shrinking of microsomal vesicles. After shrinkage, a rapid swelling phase (t1/2 approx. 22 s) was present with glucose 6-phosphate but absent with mannose 6-phosphate, indicating that the former had entered microsomal vesicles, but the latter had not. (2) Almost identical results were obtained in the absence of any glucose 6-phosphate hydrolysis, i.e. with microsomes pre-treated with 100 microM-vanadate. (3) The anion-channel blocker 4,4'-di-isothiocyanostilbene-2,2'-disulphonic acid (DIDS) suppressed the glucose 6-phosphate-induced swelling phase. (4) The swelling phase was more prolonged as the glucose 6-phosphate concentration increased (t1/2 = 16 +/- 3, 22 +/- 3 and 35 +/- 4 s with 25 mM, 37.5 mM- and 50 mM-glucose 6-phosphate respectively). The behaviour of glucose-6-phosphatase activity of intact and disrupted microsomes measured in the presence of high concentrations (less than 30 mM) of substrate also indicated the saturation of the glucose 6-phosphate permeation system by extravesicular concentrations of glucose 6-phosphate higher than 20-30 mM. Additional experiments showed that vanadate-treated microsomes pre-equilibrated with 0.1 mM- and 1.0 mM-glucose 6-phosphate (and [1-14C]glucose 6-phosphate as a tracer) rapidly (t1/2 less than 20 s) released [1-14C]glucose 6-phosphate when diluted in a glucose 6-phosphate-free medium. The efflux of [1-14C]glucose 6-phosphate was largely prevented by DIDS, allowing an evaluation of the intravesicular space of glucose 6-phosphate of approx. 1.0 microliter/mg of microsomal protein.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Analysis of human hepatic microsomal glucose-6-phosphatase in clinical conditions where the T2 pyrophosphate/phosphate transport protein is absent.

The availability of a rare set of human hepatic microsomes in which T2, a pyrophosphate/phosphate transport protein of the glucose-6-phosphatase system, has been shown immunologically to be completely absent, has permitted further characterization of multicomponent glucose-6-phosphatase (EC 3.1.3.9). Pyrophosphatase activity in intact microsomes was found to be totally absent, but was normal in disrupted microsomes. However, Pi did not accumulate within the lumen of the microsomes when glucose 6-phosphate was the substrate. This was not as predicted if there is only one transport protein in the endoplasmic reticulum capable of transporting Pi, produced by glucose-6-phosphatase, out of the lumen. The results suggest that the pyrophosphate/phosphate transport system of human hepatic endoplasmic reticulum must be more complex than previously thought, as it must comprise at least two protein components.

Adult↗
PubMed1991

Pentamidine activates T1 the hepatic microsomal glucose 6-phosphate transport protein of the glucose-6-phosphatase system.

The mechanism of activation of hepatic microsomal glucose-6-phosphatase (EC 3.1.3.9) in vitro by pentamidine has been investigated in both intact and fully disrupted microsomes. The major effect of pentamidine is a 4.7-fold reduction in the Km of glucose-6-phosphatase activity in intact diabetic rat liver microsomes. The site of action of pentamidine is T1 the hepatic microsomal glucose 6-phosphate transport protein. The activation of T1 by pentamidine may contribute to the disturbed blood glucose homeostasis seen in many patients after the administration of the drug pentamidine.

Animals↗