Department of Psychiatry, University of Mainz, Untere Zahlbacherstr. 8, D-55131 Mainz, Germany
Received 21 July 2000; accepted 22 August 2000
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ABSTRACT |
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INTRODUCTION |
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Serum vitamin B12 levels, plasma cobalamin, total corrinoids and their analogues were found to be elevated in patients suffering from alcoholic cirrhosis (Airoldi et al., 1987). Lambert et al. (1997) found that the concentration of vitamin B12 bound to transcobalamins I and III was positively correlated with plasma aspartate aminotransferase (ASAT; rS = 0.53; P = 0.02) in alcoholic cirrhotic patients. In patients with alcoholic liver disease, vitamin B12 levels were found to range within normal limits, except for a group of cirrhotic patients where vitamin B12 levels were raised, so biochemical changes in blood vitamin B12 status may precede clinical manifestations of a cirrhotic process and may have prognostic value (Majumdar et al., 1982
). However, sex differences in the serum vitamin B12 levels have been described: in a study by Goldman et al. (1979), high vitamin B12 levels were as accurate an indicator of alcoholism in female patients as elevated alanine aminotransferase (ALAT), gamma-glutamyl transpeptidase (GGT) and mean corpuscular volume (MCV) values. In contrast, for males the vitamin B12 serum levels of alcoholics were not significantly different from non-alcoholics.
The markers GGT, MCV and carbohydrate-deficient transferrin (CDT) are clinically established markers of recent alcohol abuse (Sillanaukee, 1996). In this article, we report data of a sample of 80 male alcohol-dependent actively drinking patients consecutively admitted for detoxification at our department, where we investigated a possible relationship between vitamin B12 levels and CDT, MCV, as well as the the hepatic enzymes GGT, aspartate aminotransferase (ASAT), ALAT, and glutamate dehydrogenase (GLDH).
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METHODS |
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All parameters were measured using established routine techniques at the University's central laboratory. GGT, ASAT and ALAT levels were measured according to the International Federation of Clinical Chemistry (IFCC) methods for measurement of enzymes (Shaw et al., 1983; Bergmeyer et al., 1986a
,b
), GLDH according to the Optimierte Standard-Methode (Deutsche Gesellschaft für Klinische Chemie, 1974
). An automatic blood count including the determination of MCV was performed according to Weber (1992). CDT levels were determined using the CDTectTM method from Pharmacia, Sweden (Stibler et al., 1991
). Vitamin B12 levels were determined using the Chiron Diagnostics ACS:180TM assay (National Committee for Clinical Laboratory Standards, 1990
).
For every parameter, descriptive statistics (mean, SD, minimum and maximum) were calculated. For the analysis of the correlations between the parameters, Spearman's rank correlation coefficients (rS) were calculated using the SPSS statistical software package. This publication consists of anonymous data derived from the chart review, therefore it is in full accordance with the German regulatory laws (Landesgesetz für psychisch kranke Personen; PsychKG, from November 17, 1995; § 5 Abs. 1).
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RESULTS |
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Between CDT and vitamin B12, or between MCV and vitamin B12, no statistically significant correlation was found. The correlation coefficients are shown in Table 2.
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DISCUSSION |
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We would recommend determination of the elevation of methylmalonic acid and homocysteine as metabolites of vitamin B12 in urine or serum for diagnosis and confirmation of vitamin B12 deficiency. For the cobalamin-deficient patients, measuring serum metabolite concentrations has proved to be a highly sensitive test of deficiency and normal levels of both methylmalonic acid and total homocysteine are thought to rule out clinically significant cobalamin deficiency with virtual certainty (Savage et al., 1994).
Vitamin B12 values did not correlate with CDT, but did so with GGT. This may be due to the following. CDT and GGT reflect different patterns of drinking. For men, CDT levels appear to respond primarily to frequency of drinking, whereas GGT is influenced primarily by drinking intensity (Anton et al., 1998). Also CDT, as a more specific marker of alcoholism, is less influenced than GGT by associated liver disease (Rublo et al., 1997
). The mechanism of GGT and vitamin B12 elevation is assumed to be hepatocellular damage. In contrast, CDT elevation in alcohol-dependent patients is supposed to be due to decrease in hepatic sialyltransferase and increase in sialidase activities (Xin et al., 1995
).
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FOOTNOTES |
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REFERENCES |
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