Maintained hyperexcretion of thromboxane A2 metabolite in healthy young cigarette smokers: results from a prospective study in randomly sampled males with stable smoking habits

• Published in: Clinical physiology (Oxford) Vol. 13; no. 3; p. 257
• Main Authors: Wennmalm, A, Benthin, G, Granström, E F, Persson, L, Winell, S
• Format: Journal Article
• Language: English
• Published: England 01.05.1993
• Subjects: 6-Ketoprostaglandin F1 alpha - analogs & derivatives; 6-Ketoprostaglandin F1 alpha - blood; 6-Ketoprostaglandin F1 alpha - urine; Adult; Blood Platelets - metabolism; Epoprostenol - blood; Epoprostenol - urine; Humans; Male; Prospective Studies; Smoking - blood; Smoking - metabolism; Smoking Cessation; Sweden; Thromboxane A2 - blood; Thromboxane A2 - metabolism; Sweden
• ISSN: 0144-5979
• DOI: 10.1111/j.1475-097X.1993.tb00325.x

Although several studies have identified cigarette smoking as a factor increasing platelet formation of thromboxane A2 (TxA2), no prospective data on this issue have been presented in a defined population with stable smoking habits. Therefore, we analysed the relation between smoking habits and urinary excretion of the 2,3-dinor metabolites of thromboxane A2 (Tx-M) and prostacyclin (PGI-M) in 87 males, randomly sampled from a population of 18-19-year-old men, at two different occasions separated by 31-49 months. The daily cigarette consumption among the smokers was unchanged between the study occasions (11 vs. 11 cigarettes day-1), but 9 of 43 initial smokers had quit. None of the initial non-smokers had begun smoking. Tx-M was higher in the smokers than in the non-smokers and correlated with the daily cigarette consumption both at the initial (176 vs. 123 pg mg-1 creatinine; P = 0.01) and the second (214 vs. 164 pg mg-1; P = 0.002) study occasion. Those who had quit smoking since the initial study did not differ in Tx-M from the non-smokers at the second study occasion. Urinary PGI-M did not differ between cigarette smokers, non-smokers and quitters at either of the study occasions. We conclude that cigarette smoking elicits an increased formation of thromboxane A2, indicating platelet activation, that is stable during an observation period of up to 4 years. The increased platelet activity is reversible upon quitting.