These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Influence of smoking on cotinine and caffeine plasma levels in patients with alcoholic liver cirrhosis.
    Author: Langmann P, Bienert A, Zilly M, Väth T, Richter E, Klinker H.
    Journal: Eur J Med Res; 2000 May 23; 5(5):217-21. PubMed ID: 10806124.
    Abstract:
    BACKGROUND: Retention of caffeine was observed in patients with alcoholic liver cirrhosis and impaired liver function. Cotinine, the major metabolite of nicotine, is transformed by microsomal N-oxidation to secondary metabolites. The aim of this study was to investigate if impaired liver function leads to a retention of cotinine in a similar way to caffeine retention. Furthermure the influence of smoking on cotinine and caffeine plasma levels was studied. METHODS: 91 smokers and 12 nonsmokers with alcoholic liver cirrhosis were subdivided according to their smoking habits. Cotinine plasma levels and fasting caffeine concentrations were measured by a gaschromatographic method. Concentrations of conjugated bile acids were measured by RIA. 10 healthy smokers and 11 nonsmokers were used as a control group. RESULTS: Mean plasma cotinine concentrations found in slight smokers (200 +/- 155 ng/ml), intermediate smokers (384 +/- 223 ng/ml) and heavy smokers (430 +/- 266 ng/ml) with alcoholic liver cirrhosis were significantly higher than in healthy, smoking volunteers with slight, intermediate, and heavy smoking (101 +/- 14; 274 +/- 112; 345 +/- 85 ng/ml) (p <0.01) respectively. In nonsmokers with alcoholic liver cirrhosis plasma cotinine (44 +/- 25 ng/ml) was significantly elevated compared to healthy nonsmokers (27 +/- 19 ng/ml) (p <0.01). - Fasting caffeine plasma levels in patients with alcoholic liver cirrhosis (4.00 +/- 5. 20 microg/ml) were significantly higher than in healthy volunteers (0.91 +/- 0.42 microg/ml) (p <0.01). A decrease of plasma levels was observed in correlation to the amount of smoking in patients with alcoholic cirrhosis (slight smokers: 7.67 +/- 8.54 microg/ml, intermediate smokers: 3.35 +/- 2.91 microg/ml and heavy smokers: 2. 48 +/- 2.68 microg/ml). Conjugated bile acids were elevated in patients with alcoholic liver cirrhosis to 32,56 +/- 38,24 mmol/l. CONCLUSIONS: Increased cotinine plasma levels in smokers and nonsmokers with alcoholic liver cirrhosis demonstrate a cotinine retention in patients with impaired liver function. The inducing effect of smoking is shown by a decrease of fasting caffeine plasma concentrations.
    [Abstract] [Full Text] [Related] [New Search]