Publications by authors named "I Velic"

Objective: We estimate the first monetary value of a health gain in Croatia to inform the debate about the appropriate "demand-side" cost-effectiveness thresholds in Croatia but also Central and Eastern Europe, where such debates are still uncommon. We test the empirical support for two equity considerations: age and severity operationalized as proportional shortfall (PS), and propose a pragmatic framework for combining equity considerations with the monetary value of health into a single threshold.

Methods: We used the contingent valuation method to elicit the willingness to pay per Quality-Adjusted Life Year (QALY) in Croatia, using a representative sample of the population (N = 1,500, online survey).

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Objective: We explored the monetary value of the end-of-life (EoL) health gains, that is, the value of a life-year (VOLY) gained at the end of a patient's life in Croatia. We tested whether the nature of the illness under valuation (cancer and/or rare disease) is a factor in the valuation of EoL-VOLYs. The aim was for our results to contribute to the health and longevity valuation literature and more particularly to the debate on the appropriate cost-effectiveness threshold for EoL treatments as well as to provide input into the debate on the justifiability of a cancer and/or a rare disease premium when evaluating therapies.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) can regress adenomas in patients with familial adenomatous polyposis (FAP), and the mechanism involves inhibition of cyclooxygenases (COX). Reactive intermediates formed during the arachidonic acid cascade, notably by COX-2, which is upregulated in polyps of FAP patients, may promote various stages of the polyp --> adenoma --> carcinoma sequence. Etheno-DNA adducts can be derived from reactive intermediates generated during arachidonic acid metabolism and lipid peroxidation.

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Promutagenic etheno (epsilon) adducts in DNA are generated through reactions of DNA bases with LPO products derived from endogenous sources or from exposure to several xenobiotics. The availability of sensitive methods has made it possible to detect three epsilon-adducts in vivo, namely epsilon dA, epsilon dC and N2,3-epsilon dG. One probable endogenous source for the formation of these adducts arises from LPO products such as trans-4-hydroxy-2-nonenal (HNE), resulting in highly variable background epsilon-adduct levels in tissues from unexposed humans and rodents.

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DNA adducts associated with oxidative stress are believed to involve the formation of endogenous reactive species generated by oxidative damage and lipid peroxidation. Although these adducts have been reported in several human tissues by different laboratories, a comparison of the levels of these adducts in the same tissue samples has not been carried out. In this study, we isolated DNA from the pancreas of 15 smokers and 15 non-smokers, and measured the levels of 1,N6-etheno(2'-deoxy)guanosine (edA), 3, N4-etheno(2'-deoxy)cytidine (edC), 8-oxo-2'-deoxyguanosine (8-oxo-dG), and pyrimido[1,2-alpha]purin-10(3H)-one (m1G).

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