In the case of EaspAT-AC the correlation coefficient was only 0.76 and predicability coefficient 85%. This was because the colorimetric assay gave lesser coenzyme stimulated activity and lower AC values (Table 1). This bizarre effect was traced to the inhibition of the regenerated but not the native holoenzyme by the product oxaloacetate (OA)which accumulates in the colorimetric assays, but is removed in the enzyme coupled kinetic assays(Table1). At higher concentrations of OA, even the basal activity was inhibited. Inhibition of the enzyme activity by the product is know to occur in ping-pong type of enzyme reactions, characteristic of transaminases. However, selective inhibition of the regenerated but not the native enzyme by OA is surprising.
Interpretation of biochemical tests: biochemical-clinical-functional correlations
Guidelines for the interpretation of biochemical tests have been evolved on the basis of controlled depletion repletion type of experiments and/ or comparison of healthy well nourished populations with malnourished populations (3,4).The questions that have been raised are: is tissue saturation with vitamin necessary for good health? What is the level of biochemical lesion that an individual can tolerate without being ill? In the absence of a proper definition of good health, and of sensitive functional parameters to identify and quantitate the impact of subclinical malnutrition, it is difficult to answer the above questions. Till such time, the object of nutritionists should be to achieve tissue saturation provided this is possible with modest intakes of vitamins.
Clear-cut correlations between biochemical and clinical lesions of vitamin deficiency are not always observed. The main reasons for these are: a) in the development of a deficiency disease, biochemical changes precede clinical lesions. During recovery, biochemistry is corrected before pathology. Therefore in(ตาราง) cross-sectional surveys, individuals can be at different points in this spectrum; b) disease is a complex entity as indicated in the scheme; c) all biochemical tests do not change at the same rate during development of deficiency. And d) diseases and drugs may confound the picture as mentioned earlier. Thus, in surveys one can encounter many individuals with biochemical but not the clinical lesions (subclinical deficiency) and a few individuals with normal biochemistry despite the presence of clinical lesions.
In Hyderabad we see a very high incidence (over 80%) of biochemical riboflavin deficiency among the low income group adults and children. The incidence of riboflavin responsive mucocutaneous lesions of the mouth (angular stomatric, glossitis) is also very high (15-25%). Table2 gives the EGR – AC values in subjects with and without oral lesions in some of our (ตาราง) earlier studies (5-8). When the control and patient populations were drawn from the same socioeconomic background, the difference between the two groups even if significant was marginal (studies 3 and 4) ( 7, 8). The marked difference observed in our earlier studies (5, 6), was perhaps more a reflection where is a very high incidence of biochemical deficiency, all can be regarded to be at risk. Further discrimination between individuals with and without lesions may not be marked. After treatment with riboflavin there was significant biochemical and clinical improvement. Studies from Thailand and Yugoslavia reveal similar lack of clear-cut biochemical-clinical correlations in the case of oral lesions of B-vitamin deficiency (9, 10).
