BAY m1099 (a 1-deoxynojirimycin derivative) is a glucose analogue which is an alpha-glucosidase inhibitor. Its effects on post-prandial blood glucose and insulin levels was compared with a placebo in 12 healthy male volunteers (6 Blacks and 6 Whites). It produced a similar, significant depression of post-prandial blood glucose and insulin levels when the groups were assessed separately and when the data were pooled. Although blood insulin levels in Whites were higher than in Blacks, as previously reported, the difference was not statistically significant and did not appear to influence the response to the drug. BAY 1099 produced no objective or subjective untoward effects and appears to warrant further investigation as an adjuvant to dietary control of diabetes mellitus.
Whether these differences have a role in the causation of an idiopathic hydrocele is, at this stage, speculative. A similar study on a larger scale would probably be more conclusive.
Epilepsy is a common disorder and requires long-term drug treatment. Epileptics on anticonvulsant therapy have often been reported to have a depressed immune system, especially an IgA deficiency. An association with clinical manifestations has not yet been clearly explored. So far investigations have been performed in Whites only. The objectives of this study were to assess if there is a racial difference in the immune response to anticonvulsants between Blacks and Whites and to establish the clinical significance of the IgA deficiency. Our results showed normal IgA values in Black and White epileptics on anticonvulsant therapy. This implies, at least at the present stage, that patients do not require immunological monitoring or protective measurements. Further studies including the determination of secretory IgA might help to explain the discrepancy between our findings and the literature and should provide deeper insight into the correlation between potential immune disturbances and clinical implications.
Disturbances in IgA have often been reported in white epileptics on anticonvulsant therapy. The clinical significance of these disorders is of interest as this aspect does not appear to have been sufficiently explored. In a previous study neither African nor Caucasian epileptics on treatment showed a deficiency of serum IgA. Since secretory IgA is the main defence factor in protecting mucosal surfaces, the object of the present study was simultaneously to determine serum and salivary IgA in suitable subjects and to monitor related clinical events. A similar elevation of salivary IgA level was found in Black and White epileptics on treatment. Clinical events were rare and were not related either to serum or secretory IgA concentrations. It is concluded that at present epileptics do not seem to require special immunological or clinical monitoring.
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