To gain some insights about the possible cumulative metabolic effect after a high-fibre meal, 6 subjects took two 80 g oral glucose loads, 4 h apart. Addition of 22.3 g guar to the first load decreased the rise in blood glucose and insulin after the second (guar-free) load by 50% (p less than 0.002) and 31% (p less than 0.02) respectively. This corresponded with decreased 3-hydroxybutyrate levels at the start of the glucose tolerance test after guar (by 20%, p less than 0.02). When no guar was added to the first glucose load, both 3-hydroxybutyrate and non-esterified fatty acids tended to rise before the second test. No significant effect was seen in the responses of the gut hormones, gastric inhibitory peptide and enteroglucagon. Spreading the intake of the first 80 g of glucose over the initial 4 h (2 subjects) similarly flattened the glycaemic but increased the insulin response. The effect of guar on carbohydrate and fat metabolism, therefore, lasts at least 4 h and may result in improved carbohydrate tolerance to subsequent guar-free meals.
the index is incomplete, and at present it probably provides only an underestimate of opiate use. One way in which the index might be modified to reflect more accurately the prevalence of all the serious forms of drug addiction would be to extend compulsory notification to include all self-injectors. Although this might have improved the accuracy of the index at the time of our survey (over 80% of addicts had injection marks), there is evidence that self-injection is becoming less common.14 This continuous, rapid change in the pattern of drug-taking behaviour makes any rigid system of notification, particularly one dependent on doctor-participation, unlikely to succeed in isolation as an epidemiological monitor, and it is in this context that the value of a survey such as ours in coroners' courts can be most easily appreciated. Repeated surveys not only in coroners' courts but in prisons, clinics, and accident and emergency departments would be a much more sensitive way to monitor drug misuse and its morbidity and mortality.Nevertheless Alcohol, 1959, 20, 261. 1 Gardner, R, Lancet, 1970, 2, 650. 12 Bransby, E R, Curley, G, and Kotulanska, M, Health Trends, 1973, 5, 17. 13 Pirrie, G D, British Journal of Addiction, 1977, 72, 365. 14 Rathod, N H, British Journal of Addiction, 1972, 67, 113. (Accepted 25 October 1978) Guar crispbread in the diabetic diet British Medical Journal, 1978, 2, 1744-1746 Summary and conclusions Nine diabetic patients who were receiving various treatments supplemented their normal home diets (two patients) or metabolic ward diets (seven patients) with guar crispbread for five days. Their mean urinary glucose excretion fell significantly by 38% during the last two days. A significant fall in fasting blood glucose concentration of 11±04 mmol/l (198± 72 mg/100 ml) was seen only in those who took guar after the control period. Over eight weeks' treatment insulin dosage was reduced by 21% in five patients, and home testing showed that glycosuria was reduced by 68% in six patients.
I . The influence of the dose and the form in which guar gum was given on the degree of 'flattening' of blood glucose curves was studied in five subjects using meals of bread and soup containing 5 or 10 g guargum. 2.When 5 g guar gum was added to bread the peak increase of blood glucose was reduced by 41 % (P < o.ooz), with 5 g guar in soup, the reduction was 54 % (P < 0.001) while a reduction of 68 % (P < 0.001) was seen with 10 g guar gum (5 g in bread and 5 g in soup). The corresponding reduction in insulin peak increases were 37 % (P < o a x ) , 50 % (P < 0.001) and 65 % (P < oaor) respectively.3. The difference between the two 5 g doses was not significant with respect to the reduction of the peak increases in blood glucose and serum insulin; however the difference between the 5 g dose in bread and the 10 g dose was significantly different (P < 0.02 for glucose, P < 0.01 for insulin). 4.The results indicate that as little as 5 g guar gum may reduce the glycaemia following a 45 g carbohydrate meal, but perhaps due to earlier and more complete mixing, guar gum is most effective when added to the liquid phase of the meal.
SHORT REPORTSSuspected anaphylactic reaction to Cremophor EL There have been several reports of anaphylactoid reactions to the intravenous anaesthetic drugs Althesin (alphaxalone and alphadolone) and propanidid (Epontol). ' The culprit in some of these reactions may have been Cremophor EL, a surfactant common to both drug formulations. Cremophor EL is produced by the epoxylation of castor oil and is actually a complex mixture of compounds. We report a case in which the clinical and laboratory evidence indicated that Cremophor EL was the cause of an anaphylactic (antibodymediated) response. Case reportAn otherwise fit 14-year-old girl had an ankle fracture reducLd on 15June 1979. The anaesthetic consisted of atropine 0-6 mg, Althesin 4 ml, nitrous oxide, oxygen, halothane, and trichloroethylene. The patient had never previously had a general anaesthetic. The operation was not entirely successful, and the patient presented again on 27 June for internal fixation. Anaesthesia was induced with propanidid injected into an antecubital vein. After the injection of about 20 mg the solution began to extravasate, and the injection was stopped. The anaesthetic was continued with nitrous oxide, oxygen, and halothane. The patient coughed and became cyanosed and then unconscious. Anaesthesia was discontinued. Peripheral vascular shutdown with absent radial pulses was noted; large arterial pulses were present. There was a pronounced expiratory wheeze. About 15 1 colloid (Haemaccel) and crystalloid (Hartmann's solution) was infused intravenously with dexamethasone and aminophylline. The patient's colour began to improve after about 20 minutes and she recovered consciousness. A salbutamol infusion was begun because she still had an expiratory wheeze. Some two hours after induction she was fully conscious with normal blood gas tensions while breathing room air. Blood was taken for complement and other plasma protein studies and also for haematological tests since she was bleeding extensively from venepuncture sites, suggesting an impaired haemostatic mechanism. Four days later she was given without incident an anaesthetic with no intravenous induction agents.Concentrations of fibrin degradation products were raised at both two hours (0-16 g/l) and 24 hours (0 04 g/l CommentThe patient had no history of allergy or atopy, although her father had had an allergic-type reaction to an injection of phenobarbitone many years previously. Nevertheless, she had a low plasma C4 q 4~..~~~~~~~~~~. concentration and an IgE concentration consistent with immunological hypersensitivity, and the interval between exposures to Cremophor EL was short. These three factors are said to predispose to an anaphylacteid response.' Evidence is steadily accumulating of the antigenicity of Cremophor EL, which is common to both Althesin and propanidid formulations. Although memory-mediated events after 'a second exposure to Althesin have been reported in man,2 Glen et al3 have shown that Cremophor EL alone can cause anaphylactic reactiorns when readministered t...
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