Biomedical subjects

R Fux

Publications and source records attributed to R Fux.

4 recordsLinked to original sources

PubMed2006

Multiple drug prescribing by general practitioners in a German region: Implications for drug interactions and patient safety.

OBJECTIVE: An increased number of drugs used by patients enhances the risk of potentially hazardous drug interactions. So far, no representative data are available about how common this problem is in German general practices. METHODS: We performed a retrospective analysis using a prescription database for a German region. The 50 general practitioners (out of 1,457) who wrote the most prescriptions during January to March 2003 were included. Data on 4,153 patients who were prescribed at least 10 drugs were analyzed for 92 predefined Drug Combinations Prone to Interact (DCPI) to a clinically relevant extent and possible contraindications. RESULTS: From 92 DCPIs, 71 occurred in the analyzed population between 1 and 275 times. The total number of DCPI cases was 1,295, which included 10% (n = 129) of contraindicated combinations. Among 4,153 analyzed patients, 822 patients (19.8%) were affected by at least 1 DCPI. In 268 patients (6.5%), multiple DCPIs occurred. The most frequently found drug pairs were digitalis/diuretics, digitalis/calcium channel blockers, and theophylline/quinolones. Among contraindicated combinations, tricyclic antidepressants, St. John's wort and antiarrhythmic drugs were most frequently involved. In about 1/3 of patients treated for chronic heart failure, pharmacotherapy appeared not to be guideline-adherent. CONCLUSION: Drug interactions, especially in polypharmacotherapy, represent a potential hazard which must be taken into account by the prescribing physician. Our study is the first to use a prescription database for the evaluation of drug prescriptions within a German region.

Databases, Factual↗

PubMed2005

Effect of acute hyperhomocysteinemia on methylation potential of erythrocytes and on DNA methylation of lymphocytes in healthy male volunteers.

Homocysteine is a precursor of S-adenosylmethionine (AdoMet) and a metabolite of S-adenosylhomocysteine (AdoHcy). The ratio of AdoMet to AdoHcy, defined as the methylation potential (MP), indicates the flow of methyl groups within the cells. Chronic elevations of total homocysteine (tHcy) in plasma correlate with increased AdoHcy concentrations, decreased MP, and impaired DNA methylation. However, the influence of acute hyperhomocysteinemia on MP is unknown. We induced acute hyperhomocysteinemia in 14 healthy volunteers by oral administration of l-homocysteine (65.1 micromol/kg body wt) in an open, randomized, placebo-controlled two-period crossover study. The kinetics of tHcy in blood and urine, MP in blood, and global DNA methylation in lymphocytes were studied systematically during 48 h. Plasma tHcy concentrations reached a peak at 34 +/- 11 min after an oral load with l-homocysteine and decreased with a half-life of 257 +/- 41 min (means +/- SD). Only 2.3% of the homocysteine dose were recovered in urine. AdoHcy concentrations and MP in whole blood and erythrocytes were not affected by the oral homocysteine load. Furthermore, global DNA methylation in lymphocytes did not change under these conditions. We found no difference between the genotypes of 5,10-methylenetetrahydrofolate reductase in response to the homocysteine load. However, AdoMet content in erythrocytes was significantly higher in the C677T carriers (CT; n = 7) compared with the CC genotype (n = 7). Although chronic elevation of tHcy has been shown to affect MP and DNA methylation, acute elevation of plasma tHcy above 20 micromol/l for 8 h is not sufficient to change MP and to induce DNA hypomethylation in lymphocytes.

Adult↗

PubMed2002

[Celecoxib].

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Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

Effect of urea and osmotic cell shrinkage on Ca2+ entry and contraction of vascular smooth muscle cells.

The present study was performed to elucidate the effects of urea on vascular smooth muscle cells (SMC). Addition of urea (20, 50, 100 mM) to physiological salt solution blunted the vasoconstrictory effect of phenylephrine (by 17, 25 and 30%, respectively) and of an increased extracellular K+ concentration (by 7, 14 and 19%, respectively) without affecting the basal tone of rabbit arterial rings. According to Fura-2 fluorescence in cultured SMC (A7r5), urea had no effect on basal intracellular calcium activity ([Ca2+]i), but significantly blunted the increase of [Ca2+]i following an increase of extracellular K+. Whole-cell patch-clamp studies revealed that the Ca2+ current through voltage-sensitive Ca2+ channels is significantly inhibited in the presence of urea. As evident from calcein fluorescence, addition of urea leads to sustained cell shrinkage. The effects of urea on vascular tone, [Ca2+]i activity, voltage-gated Ca2+ channels and cell volume are mimicked by addition of raffinose or NaCl. However, the cell shrinkage induced by urea is sustained, whereas the addition of equiosmolar NaCl is only transient and followed by a regulatory cell volume increase. Moreover, hypertonic NaCl increases, whereas urea decreases, the transcription of cell-volume-regulated kinase hsgk. In conclusion, urea leads to sustained shrinkage of vascular smooth muscle cells, which is followed by inhibition of voltage-gated Ca2+ channels, a decrease of [Ca2+]i and thus blunts the vasoconstrictory action of phenylephrine and increased extracellular K+ concentration.

Animals↗