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D Stoffel

Publications and source records attributed to D Stoffel.

6 recordsLinked to original sources

Effect of future costs on cost-effectiveness of medical interventions among young adults: the example of intensive therapy for type 1 diabetes mellitus.

OBJECTIVES: Recent research based on a lifetime utility maximization model has suggested that cost-effectiveness analyses should account for all future costs, including medical costs for related and unrelated illnesses and nonmedical costs. This work has also shown that analyses that omit future costs are biased to favor interventions among the elderly that extend life over interventions that improve quality of life. However, the effect of including future costs on the cost-effectiveness of interventions among the young has not been studied. This article examines the effect of including future costs on the cost-effectiveness of intensive therapy for type 1 diabetes mellitus among young adults. METHODS: By modifying a cost-effectiveness model based on the Diabetes Control and Complications Trial to include future costs, the effect of including future costs on the cost-effectiveness of intensive therapy for type 1 diabetes mellitus among young adults was examined. Future costs added to the model included future costs for medical expenditures for illnesses unrelated to diabetes and future nonmedical expenditures net of earnings. RESULTS: Intensive therapy among young adults led to approximately equal increases in the expected number of years lived before age 65, when people generally produce more than they consume, and after age 65, when the opposite tends to hold. Because the discounted value of savings due to lower mortality before age 65 exceeded the discounted value of later increases in costs due to lower mortality after age 65, accounting for future costs decreased the cost-effectiveness ratio from $22,576 to $9,626 per quality-adjusted life-year. CONCLUSIONS: The inclusion of future costs can significantly improve the cost-effectiveness of interventions that decrease mortality among young adults. The common practice of excluding future costs may bias cost-effectiveness analyses against such interventions.

Adolescent↗

P2-purinoceptors on postganglionic sympathetic neurones.

1. Postganglionic sympathetic neurones possess both excitatory and inhibitory P2-purinoceptors. 2. The mechanisms of action of excitatory P2-purinoceptors have recently been studied on cultured sympathetic neurones of the rat. The receptors mediate fast increases in intracellular Ca2+ levels and a release of noradrenaline. They are likely to belong to the neuronal types of P2X-purinoceptors and to be located on the sympathetic nerve cell bodies or their dendrites. 3. Inhibitory P2-purinoceptors have been shown to operate at sympathetic axon terminals in isolated tissues. Adenine nucleotides decreased the stimulation-evoked release of noradrenaline by activation of these receptors. The receptors are likely to belong to the group of G-protein-coupled P2Y-purinoceptors. They mediate a negative feedback in which co-transmitter ATP inhibits subsequent sympathetic transmitter release.

Action Potentials↗

P2-purinoceptor-mediated inhibition of noradrenaline release in rat atria.

1. We looked for P2-purinoceptors modulating noradrenaline release in rat heart atria. Segments of the atria were preincubated with [3H]-noradrenaline and then superfused with medium containing desipramine (1 microM) and yohimbine (1 microM) and stimulated electrically, by 30 pulses/1 Hz unless stated otherwise. 2. The adenosine A1-receptor agonist, N6-cyclopentyl-adenosine (CPA; EC50 9.7 nM) and the nucleotides, ATP (EC50 6.6 microM) and adenosine-5'-O-(3-thiotriphosphate) (ATP gamma S; EC50 4.8 microM), decreased the evoked overflow of tritium. The adenosine A2a-agonist, 2-p-(2-carbonylethyl)-phenethylamino-5'-N-ethylcarboxamido-a denosine (CGS-21680; 0.03-0.3 microM) and the P2x-purinoceptor agonist beta, gamma-methylene-L-ATP (30 microM) caused no change. 3. The concentration-response curve of CPA was shifted to the right by the adenosine A1-receptor antagonist, 8-cyclopentyl-1,3-dipropyl-xanthine (DPCPX; 3 nM; apparent pKB value 9.7) but hardly affected by the P2-purinoceptor antagonist, cibacron blue 3GA (30 microM). In contrast, the concentration-response curves of ATP and ATP gamma S were shifted to the right by DPCPX (3 nM; apparent pKB values 9.3 and 9.4, respectively) as well as by cibacron blue 3GA (30 microM; apparent pKB values 5.0 and 5.1, respectively). Combined administration of DPCPX and cibacron blue 3GA caused a much greater shift of the concentration-response curve of ATP than either antagonist alone. The concentration-response curve of ATP was not changed by indomethacin, atropine or the 5'-nucleotidase blocker alpha, beta-methylene-ADP. 4. Cibacron blue 3GA (30 microM) increased the evoked overflow of tritium by about 70%. The increase was smaller when the slices were stimulated by 9 pulses/O00 Hz instead of 30 pulses/I Hz.5. The results indicate that the postganglionic sympathetic axons in rat atria possess P2-purinoceptors in addition to the known adenosine Al-receptor. Both mediate inhibition of noradrenaline release. Some adenine nucleotides such as ATP and ATP gamma S act at both receptors. The presynaptic P2-purinoceptor seems to be activated by an endogenous ligand, presumably ATP, under the condition of these experiments. This is the first evidence for presynaptic P2-purinoceptors at cardiac postganglionic sympathetic axons.

Adenosine↗

[Liver injuries].

Mortality in blunt hepatic trauma is still high, death being most frequently caused by hemorrhage. Associated injuries are present in nearly all cases. A variety of possible surgical procedures allow treatment tailored to fit the individual situation. Even the sophisticated intensive care required by the frequent posttraumatic complications is not a substitute for adequate surgery.

Abdominal Injuries↗

Polyvalent immunoglobulins for prophylaxis of bacterial infections in patients following multiple trauma. A randomized, placebo-controlled study.

One hundred and fifty severely injured patients requiring long-term artificial ventilation were evaluated in a prospective, randomized, double blind study comparing the prophylactic effect of an intravenous immunoglobulin (Sandoglobulin; IGIV) against nosocomial infections with a placebo preparation. The groups were comparable in age, sex, injury pattern, and severity of the trauma. Seventy-six patients received 12 g of Sandoglobulin as a 3% solution on day 0, day 5 and day 12, i.e. a total of 36 g. Sandoglobulin significantly reduced the incidence of pneumonia (28 cases in the IGIV group, 43 cases in the placebo group, p = 0.0111). This resulted in a reduced therapeutic use of antibiotics. For the occurrence of sepsis (IGIV: 14 cases; placebo 19 cases) and other infections (IGIV: 11 cases; placebo: 10 cases) no significant differences were found. No side effects of the administration of IGIV were observed. IGIV prophylaxis neither reduced the overall death rate nor those deaths caused by infection. On day 5 after administration of the first 12 g of IGIV, the IgG serum concentrations were significantly higher in the Sandoglobulin group (8.41 +/- 1.96 mg/ml and 7.42 +/- 2.25 mg/ml respectively, p less than 0.001) whereas later serum samples showed no significant differences.

Adolescent↗