Biomedical subjects
Publications and source records attributed to G N Foukaridis.
A water extract of the bulb of the plant Urginea sanguinea Schinz = (Urginea burkei Bak) (Liliaceae) is used by the black people mainly as a 'blood purifier'. Patients admitted at the Ga-Rankuwa Hospital with Urginea sanguinea poisoning had clinical symptoms effecting any of the following systems: GIT, urinary, CNS or the splanchnic.
A large percentage of acute poisonings in black South Africans is due to traditional medicines and plants. The combination of isocratic high performance liquid chromatography (HPLC) with on line UV spectrum detection via a diode array configuration has been applied to the detection and identification of traditional medicines (and plants) in poisoned patients. Four standard isocratic systems are used. Combination of the retention times in the HPLC chromatogram and a comparison of the full spectra between 190-600 nm of the peaks obtained from extracted patient samples (urine or blood) with that of traditional medicine extracts (collected and stored in a reference data file) makes reliable identification possible. Such information could improve the quality of data accumulation and therapeutic strategies.
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Poor compliance with drug therapy is an important cause of therapeutic failure. Sixty-eight black patients with non-insulin-dependent diabetes mellitus receiving oral hypoglycaemic agents were interviewed and various factors, such as age, sex, degree of control and type of therapy, were recorded by means of a questionnaire. Compliance was determined by qualitatively assessing urine for the presence of the drugs. An alarmingly high incidence of non-compliance of 65% was found, which could still be an under-estimation because of the long half-life of one of the drugs involved--chlorpropamide. Although interesting trends were noted, no statistically significant differences between compliant and non-compliant patients were found. In the light of the high incidence of non-compliance, a larger and more detailed study seems to be warranted to identify problem areas and to plan appropriate interventions.
Although current immunoassay kits for digoxin supposedly have antibodies of high specificity, serum digoxin levels in patients taking spironolactone suggest that spironolactone interferes with the determination. In vitro determinations of digoxin performed on blank serum spiked with spironolactone and its metabolite canrenone showed that contrary to the belief gained from reading the manuals of some diagnostic immunoassay kits, spironolactone significantly influences digoxin determinations.
1. Alpha-glucosidase inhibitors such as miglitol and acarbose lower blood glucose after a starch load in healthy volunteers and diabetic patients by interfering with the conversion of disaccharide to monosaccharide in the gastrointestinal tract. 2. The effect of placebo, 100 mg miglitol and 100 mg acarbose given 30 min prior to a 75 g oral glucose load was investigated in nine healthy Caucasian volunteers. 3. Miglitol produced a statistically significant fall in post-peak blood glucose levels when compared with placebo and acarbose. Serum insulin did not change significantly. 4. As miglitol is well absorbed and acarbose is not, it is suggested that miglitol has a systemic hypoglycaemic effect, probably related to its close structural similarity to glucose, which warrants further investigation.
Miglitol is an alpha-glucosidase inhibitor which lowers blood glucose and insulin concentrations in healthy volunteers after a starch meal. It also lowers blood glucose concentrations after a starch meal in patients with non-insulin-dependent diabetes mellitus, but under these circumstances insulin is unaffected. We have studied the effect of miglitol after a glucose load in six healthy male volunteers. Although one would expect an alpha-glucosidase inhibitor to have no effect on blood glucose concentrations after a glucose load, miglitol produced a significant decrease in blood glucose concentrations after the absorption peak. This could be due to enhancement of insulin effects or to depression of anti-insulin factors.