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Letters to the Editor |
-Glutamyltransferase and Vascular Disease
1 Departments of Clinical Biochemistry, and Vascular Surgery, (Vascular Disease Prevention Clinics), Royal Free and University, College Medical School, (University of London), Royal Free Hospital Campus, London NW3 2QG, United Kingdom
aAddress correspondence this author at: Department of Clinical Biochemistry, Royal Free and University College Medical School (University of London), Royal Free Hospital Campus, Pond Street, London NW3 2QG, United Kingdom. Fax 44-20-7830-2235; e-mail KHAILIDIS{at}aol.com.
To the Editor:
In their recent report, Whitfield et al. (1) suggest that serum 
-glutamyltransferase (GGT) may originate from atheromotous plaques. This interesting proposal can be further supported. There is evidence showing that human platelets may be a source of GGT (2)(3), but this contribution may be small (3). Therefore, increased platelet consumption at the site of these plaques may contribute to an increase in serum GGT activity.
In Table 1 of their report, the authors (1) do not consider serum bilirubin among the variables correlating with serum GGT activity. It may be interesting to assess that link because bilirubin concentrations may be lower in patients with vascular disease (4). Stronger evidence indicates that women and smokers have lower serum bilirubin even if they have vascular disease (4). The rationale is that bilirubin acts as an antioxidant and that its consumption is increased in smokers and patients with vascular disease (4)(5). A similar argument applies to serum albumin (4).
Finally, there is evidence that fibrates lower serum alkaline phosphatase activity as well as improving the lipid profile (6)(7). [Alkaline phosphatase is not considered in Table 1 of the Whitfield et al. report (1).] There is also evidence that serum GGT activity decreases in hypertriglyceridemic patients after treatment with a fibrate (6)(7). These changes thus may help toward a better understanding of the relationship between lipid variables and serum GGT activity or other liver function tests.
The elegant work of Whitfield et al. (1) may help develop new and easily accessible predictors/markers of vascular disease.
References
-glutamyltransferase activity and cardiovascular risk factors. Clin Chem 2002;48:1426-31.-Glutamyl transferase activity in human platelets: quantification of activity, isoenzyme characterization and potential clinical relevance. Platelets 1995;6:200-3.
-glutamyl transferase activity and the platelet count. Platelets 1997;8:333-5.[CrossRef][Web of Science][Medline]
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2 Royal Prince Alfred Hospital, Department of Biochemistry, Missenden Road, Camperdown, Sydney NSW 2050, Australia, Fax 61-2-9515-7931, E-mail john.whitfield{at}email.cs.nsw.gov.au
aAddress correspondence this author at: Department of Clinical Biochemistry, Royal Free and University College Medical School (University of London), Royal Free Hospital Campus, Pond Street, London NW3 2QG, United Kingdom. Fax 44-20-7830-2235; e-mail KHAILIDIS{at}aol.com.
To the Editor:
Krijgsman, Hamilton, and Mikhailidis make several points about possible mediators of the connection between serum -glutamyltransferase (GGT) activity and risk of cardiovascular disease.
The authors first suggest that serum GGT may in part come from platelets and that because platelet breakdown may be increased at the sites of atheromatous plaques, people with substantial atherosclerosis would have increased serum GGT of platelet origin. Such a mechanism is possible, but it seems to require a very substantial increase in platelet turnover at plaque sites to produce a detectable increase in GGT in the plasma. Furthermore, this would not explain the associations between GGT and obesity or the metabolic syndrome, or between GGT and the prospective risk of developing type 2 diabetes.
The authors also suggest a relationship between antioxidants in serum, including bilirubin and albumin, and GGT. Presumably this would be an inverse relationship, as "... consumption [of antioxidants] is increased in smokers and patients with vascular disease". We cannot currently provide information on bilirubin or albumin in our study population, but it is clear that the concentration of urate (the major antioxidant in plasma) is positively correlated with the GGT activity.
Finally, they cite evidence that serum GGT decreased in hypertriglyceridemic patients treated with fibrates. This would be consistent with a role for fatty liver in producing increased serum GGT and being associated with an increase in cardiovascular risk, and it offers a possible means of risk reduction. However, the mean decrease in GGT was small, alanine aminotransferase was unchanged, and aspartate aminotransferase actually increased. A short-term trial of fibrate treatment in patients with alcoholic fatty liver (1) failed to lower serum GGT (or aspartate aminotransferase or alanine aminotransferase) significantly, although serum triglycerides fell substantially. We do not know, at this stage, whether GGT would remain a significant cardiovascular risk factor if triglycerides and VLDL were lowered by treatment, but the published epidemiologic studies suggest that it would.
References
The following articles in journals at HighWire Press have cited this article:
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  M. J. Tutor-Crespo, J. Hermida, and J. C. Tutor Possible Induction of Cholinesterase in Epileptic Patients Treated With Anticonvulsant Drugs: Relationship With Lipoprotein Levels J. Clin. Pharmacol., September 1, 2004; 44(9): 974 - 980. [Abstract] [Full Text] [PDF]
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