OBJECTIVE: To identify and quantify additional hidden costs associated with processing third party prescriptions. DESIGN/SETTING: Using time and motion techniques, the frequency of rejected third party prescriptions and the time involved to resolve those rejections were measured in one supermarket chain pharmacy and one independent pharmacy. From this information, additional costs attributed to processing third party prescriptions were calculated. RESULTS: In a market where almost 95% of all prescriptions are third party reimbursed, payers rejected 18.7% and 22.3% of the prescriptions submitted by the supermarket chain and independent pharmacies, respectively. Additional or hidden costs for rejected prescriptions averaged $1.10 at the supermarket chain pharmacy and $1.54 at the independent pharmacy, with the difference attributable to the higher level of pharmacy staff involvement in resolving rejections at the independent pharmacy. When additional costs for all third party prescriptions were calculated, the average additional cost per third party prescription dropped to $0.44 for the supermarket chain pharmacy and $0.61 for the independent pharmacy. CONCLUSION: Increasing pharmacist availability for pharmaceutical care requires decreasing time spent in the dispensing process, especially resolving third party problems. Systems analysis and time and motion techniques were effectively used to more accurately measure the time and costs associated with processing third party prescriptions. Actual costs found in this study were considerable, but significantly less than those reported previously in studies using estimates and surveys.

Costs and Cost Analysis↗

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Tissue manganese concentrations and antioxidant enzyme activities in rats given total parenteral nutrition with and without supplemental manganese.

BACKGROUND: Manganese is an essential but potentially toxic mineral. Parenteral administration of manganese via total parenteral nutrition (TPN) bypasses homeostatic mechanisms (intestinal absorption and presystemic hepatic elimination). Our objective in this study was to determine the effect of supplemental manganese in TPN solutions on manganese status in a rat model. METHODS: Male Sprague-Dawley rats underwent jugular catheterization and were given 61.0 +/- 0.4 g/d TPN solution providing 0.5 +/- 0.2 nmol manganese/g (Mn-; n = 6) or 16 +/- 3 nmol manganese/g (Mn+; n = 7) for 7 days. Reference rats (RF; n = 8) were fed a purified diet containing 1.3 mmol manganese/g. RESULTS: Liver manganese decreased in both TPN groups, but tibia, spleen, and pancreas manganese concentrations were greater in Mn+ rats than in Mn- or RF rats. Although no treatment differences were seen in heart or liver manganese superoxide dismutase activity, heart copper-zinc superoxide dismutase activity was lower in the Mn+ rats than in Mn- or RF rats (p < .05). Glutathione peroxidase activity was depressed in livers of both Mn- and Mn+ rats relative to RF rats (p < .0001), which was not due to selenium deficiency. CONCLUSIONS: Supplemental parenteral manganese is taken up to a greater extent by peripheral tissues than the liver. In this first report of antioxidant enzyme activities in animals maintained with TPN, we found that TPN as well as supplemental manganese can influence antioxidant enzyme activities. We conclude that it is generally unnecessary and potentially toxic to supplement TPN solutions with manganese during short-term usage.

Animals↗

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Sovereign immunity and tort claims.

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Hospitals, County↗

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Are hospitals liable for actions of physicians?

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Clinical Competence↗

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Liver tumorigenesis by Helicobacter hepaticus: considerations of mechanism.

A new animal model for the causation of liver tumors via a bacterial infection presented itself fortuitously in the form of a new species, Helicobacter hepaticus. This species of Helicobacter colonizes the hepatic bile canaliculi in susceptible strains of mice, resulting in hepatitis and hepatocellular and hepatocholangiolar adenomas and carcinomas. The mechanism by which this infection leads to cancer is unknown. Tests with Helicobacter hepaticus have revealed thus far that the bacteria do not secrete a mutagen which is capable of detection by the Ames Assay. Measurement of oxidatively damaged bases in the liver DNA of hepaticus infected mice have shown accumulation of 8-oxodeoxyguanosine with disease progression. Other promutagenic DNA lesions, 7-methylguanine and O6-methylguanine, indicative of nitrosation of endogenous amines by nitric oxide, were not detected. Analysis of carcinomas and adenomas taken from H. hepaticus infected A/JCr mice revealed no mutations in ras oncogenes or in exons 5-8 of the p53 gene. These preliminary results indicate that a non-genotoxic tumor promotion mechanism, possibly implemented by reactive oxygen species from the immune response, is more likely than a genotoxic mechanism.

Alkylation↗