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PubMedDate not supplied

[Kinetics of sodium thiosulfate-35S fixation and effect of some sulfur compounds on iodine-131 fixation in ray thyroid gland].

In order to invalidate or confirm the affirmation that non antithyroid sulphide molecules alter the measure of the thyroid fixation rate of iodine 131 we undertook on the rat: on one hand a kinetic study of thyroid fixation of sodium thiosulfate labelled with sulphur 35, which showed a very low captation not exceeding 0,01% of injected radioactivity; on the other hand the study of the effects of some sulphide molecules on thyroid fixation of iodine 131 in the rat: sodium thiosulfate, association of sodium thiosulfate + metalloidal sulphur + methionine, carbutamide and dimethylsulfoxyde in various kinds of dose administration and periods. None of the products used in our work conditions produced a significant decrease of the fixation rate of iodine 131. In three different experimental protocols (sulfur association and dimethylsulfoxide), we showed a significant light increase of the fixation rate.

Animals↗

PubMed1984

Adsorption of sulfonylureas onto activated charcoal in vitro.

Adsorption of carbutamide, chlorpropamide, tolazamide, tolbutamide, glibenclamide (glyburide), and glipizide onto activated charcoal was compared in vitro using different charcoal-to-drug ratios. Maximal binding capacities of different sulfonylureas were 0.45-0.52 g/g of charcoal at pH 7.5. The affinity of the second generation derivatives, glibenclamide and glipizide, was considerably higher than that of the first generation derivatives. The affinity of sulfonylureas to charcoal was higher at pH 4.9 than at pH 7.5. Poor water solubility of sulfonylureas at pH 1 prevents the adequate testing in these conditions. Contrary to what has appeared previously, activated charcoal effectively adsorbs different sulfonylureas and can be used to possibly prevent their gastrointestinal absorption.

Adsorption↗

PubMed1978

A micromethod for the isolation of drugs from blood using amberlite XAD-2.

The extraction of drugs from small blood samples (1 ml or less) for subsequent quantitative determination is described. Isolation was carried out by adsorption of the drugs to Amberlite XAD-2 resin utilizing a batch procedure that enabled the simultaneous extraction of up to 200 samples in approx. 5 hours. A new desorption technique yielded extracts of high purity that could be used directly for gas chromatographic or radioimmunological determinations, even if hemolyzed or putrid blood was to be examined. The following 26 substances were quantitated after addition to postmortem blood speciments at concentrations of 1-10 microgram/ml: tilidine, diphenhydramine, dibenzepine, imipramine, chlorpromazine, amphetamine, pentazocine, phenacetin, methaqualone, meprobamate, parathion, diazepam, digoxin, beta-methyldigoxin, carbromal, glutethimide, amobarbital, pentobarbital, cyclobarbital, phenobarbital, diphenylhydantoin, carbutamide, tolbutamide, glycodiazin, tolazamide and chlorpropamide. Thereby recoveries of 60-100% could be achieved. The reproducibility of the procedure was satisfactory as demonstrated by coefficients of variation of 3.7-8%.

Humans↗

PubMed2000

Addition of low-dose rosiglitazone to sulphonylurea therapy improves glycaemic control in Type 2 diabetic patients.

AIMS: This study was designed to test the efficacy and safety of low-dose rosiglitazone, a potent, insulin-sensitizing thiazolidinedione, in combination with sulphonylurea in Type 2 diabetic patients. METHODS: For the intention-to-treat analysis, 574 patients (59% male, mean age 61 years) were available, randomized to receive 26 weeks of twice-daily placebo (n = 192), rosiglitazone 1 mg (n = 199) or rosiglitazone 2 mg (n = 183) in addition to existing sulphonylurea treatment with gliclazide (47.6% of patients), glibenclamide (41.8%) or glipizide (9.4%) (two patients were taking carbutamide or glimepiride). Change in haemoglobin A1c (HbA1c), fasting plasma glucose (FPG), fructosamine, insulin, C-peptide, albumin, and lipids were measured, and safety was evaluated. RESULTS: Mean baseline HbA1c was 9.2% and FPG was 11.4 mmol/l. Rosiglitazone at doses of 1 and 2 mg b.d. plus sulphonylurea produced significant decreases, compared with sulphonylurea plus placebo, in HbA1c (-0.59% and -1.03%, respectively; both P<0.0001) and FPG (1.35 mmol/l and 2.44 mmol/l, respectively; both P<0.0001). Both HDL-cholesterol and LDL-cholesterol increased and potentially beneficial decreases in non-esterified fatty acids and gamma glutamyl transpeptidase levels were seen in both rosiglitazone groups. The overall incidence of adverse experiences was similar in all three treatment groups, with no significant cardiac events, hypoglycaemia or hepatotoxicity. CONCLUSIONS: Overall, the combination of rosiglitazone and a sulphonylurea was safe, well tolerated and effective in patients with Type 2 diabetes.

Adult↗

PubMed1957

The action of hypoglycaemic sulphonylureas on carbohydrate metabolism in the fasted rat.

Tolbutamide and carbutamide given orally to fasted rats cause a rise in the liver glycogen content 1(1/2) to 3(1/2) hr. after administration of the drugs. Glycogen accumulates preferentially in the right lobe. Subcutaneously injected tolbutamide has the same effect. Both sulphonylureas cause inhibition of glucose-6-phosphatase activity of rat liver homogenates in vitro, but at drug concentrations comparable with those found in plasma of treated patients the degree of inhibition is less than 10%. Livers from treated rats show normal glucose-6-phosphatase activity. The glucose uptake of the isolated rat diaphragm is unaffected by the sulphonylureas added in vitro. Diaphragms from treated rats show normal glucose uptake in the presence or absence of insulin. The inferences to be drawn from these results are discussed in the light of previous work. It is concluded that the sulphonylureas exert hypoglycaemic action by inhibiting glycogenolysis and it is suggested that they might do so by inhibiting release of glucagon from the pancreas.

Animals↗

PubMed1977

Effect of sulfonylureas on triglyceride metabolism in the rat liver: possible role of the lysosomes in hepatic lipolysis.

It has been suggested previously that chlorpropamide and other hypoglycemic sulfonylureas interfere with hepatic triglyceride breakdown. Since ketogenesis from endogenous hepatic lipid stores is a measure of hepatic triglyceride hydrolysis, ketogenesis derived from endogenous lipids as well as ketogenesis derived from exogenously added isotopic oleate was determined in isolated hepatocytes from fasted rats in an attempt to identify the nature of the direct effects of sulfonylureas on hepatic lipid metabolism. Ketogenesis from endogenous lipids was inhibited by 1 mM chlorpropamide, while ketone production from exogenous oleate did not change. The effect of chlorpropamide on hepatic triglyceride metabolism was further studied in the isolated perfused liver of normal rats in the presence of a continuous [3H]oleate infusion and in isolated liver cells incubated in the presence of [3H]oleate. In liver perfusion experiments, 1 mM chlorpropamide enhanced the incorporation of tritium into triglycerides (but not other lipid classes) and increased both liver triglyceride content and triglyceride secretion. Using isolated cells similar effects could be demonstrated at 0.5 mM chlorpropamide. Chlorpropamide, tolbutamide, and carbutamide, all of which inhibited endogenous ketogenesis in isolated liver cells, also inhibited lysosomal triglyceride lipase activity in rat liver homogenates. The drugs were not inhibitory towards alkaline lipase activity. Demethylglycodiazin (2-benzolsulfonamid--5-(beta-hydroxyethoxy)-pyrimidin), which did not inhibit endogenous ketogenesis in isolated liver cells, did not affect lysosomal lipase activity. The lysosomotropic drug chloroquine was markedly antiketogenic when tested in liver cells. The reduction in endogenous ketogenesis, the enhanced accumulation of liver triglycerides, and the stimulation of hepatic triglyceride output by chlorpropamide are ascribed to an interference of the drug with hepatic triglyceride breakdown. The present results also suggest that the lysosomes play a significant role in hepatic lipolysis.

Animals↗

PubMed1977

Tolbutamide-induced hemolytic anemia.

A 67-year-old female diabetic is presented who developed a Coombs'-positive hemolytic anemia after a year of treatment with tolbutamide. An IgG antibody was identified in the patient's serum that caused the agglutination of both the patient's red blood cells and tolbutamide-coated erythrocytes in the absence of complement. Such a reaction did not occur with the patient's erythrocytes when not exposed to tolbutamide. Agglutination of the patient's serum also occurred with erythrocytes treated with other sulfonylureas (chlorpropamide, glibenclamide, carbutamide) but not with phenacetin.

Aged↗

PubMed2002

History of diabetes mellitus.

Clinical features similar to diabetes mellitus were described 3000 years ago by the ancient Egyptians. The term "diabetes" was first coined by Araetus of Cappodocia (81-133AD). Later, the word mellitus (honey sweet) was added by Thomas Willis (Britain) in 1675 after rediscovering the sweetness of urine and blood of patients (first noticed by the ancient Indians). It was only in 1776 that Dobson (Britain) firstly confirmed the presence of excess sugar in urine and blood as a cause of their sweetness. In modern time, the history of diabetes coincided with the emergence of experimental medicine. An important milestone in the history of diabetes is the establishment of the role of the liver in glycogenesis, and the concept that diabetes is due to excess glucose production Claude Bernard (France) in 1857. The role of the pancreas in pathogenesis of diabetes was discovered by Mering and Minkowski (Austria) 1889. Later, this discovery constituted the basis of insulin isolation and clinical use by Banting and Best (Canada) in 1921. Trials to prepare an orally administrated hypoglycemic agent ended successfully by first marketing of tolbutamide and carbutamide in 1955. This report will also discuss the history of dietary management and acute and chronic complications of diabetes.

Diabetes Mellitus↗

PubMedDate not supplied

[Hypersensitivity to hypoglycemic sulfonylurea compounds. Are there cross-reactions?].

We describe 5 observations of cutaneous reactions or immediate hypersensitivity with different hypoglycemic sulfonylurea: Quincke's oedema with glibornuride, three urticaria (one was followed by bronchospasm and collapsus) with glibenclamide, one bullous dermatitis with carbutamide. With special regard to cross reactions between sulfonylurea: we observe the tolerance of glipizide after glibenclamide induced urticaria, tolerance of glicalazide after glibornuride induced Quincke's oedema and eruption, tolerance of glibornuride after chlorporpamide induced urticaria and Quincke's oedema. In the literature, cross reactions between 1st generation sulfonylurea are noted, but not cross reactions between 1st and 2nd generation.

Adult↗

PubMed1986

[The relatively frequent incidence of severe sulfonylurea-induced hypoglycemia in the last 25 years in Switzerland. Results of 2 surveys in Switzerland in 1969 and 1984].

In 1969 and 1984 all emergency wards in Switzerland were asked to report on the incidence of severe episodes of hypoglycemia (HE) during treatment with sulfonylureas. Each of the two surveys referred to a ten-year period (period A 1960-1969, period B 1975-1984). The number of HE reported was 78 for period A and 116 for period B. The number of diabetics treated with sulfonylurea preparations was established on the basis of tablet consumption, which amounted to 35,000 in period A and 47,500 in period B. The incidence of hypoglycemia in each period was comparable (period A 0.22, and period B 0.24 per 1000 patient years), but differed with regard to the sulfonylurea preparations used. In period A hypoglycemic episodes occurred more frequently under chlorpropamide than under tolbutamide and carbutamide. In period B the incidence of episodes under chlorpropamide and glibenclamide was comparable, but was significantly higher than under tolbutamide and glibornuride. The risk of hypoglycemia occurring is thus significantly higher under glibenclamide and chlorpropamide than under glibornuride and tolbutamide. 6.5% of HE were fatal in period A, compared with 4.3% in period B. Advanced age proved to be a risk factor in HE: 77% of patients with HE were over 69 years of age, whereas only 50% of all diabetics treated with sulfonylurea preparations were in this age group. Further risk factors were impaired renal function (21%) and possible drug interactions (27%). There was less likelihood of recurrence of a hypoglycemic episode in period B than in period A.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

[Clinical trial with glypentide. Comparison with the hypoglycemic activity of other sulfonylurea compounds].

In 53 sulphonylurea-treated diabetic patients, the activity of glypentide and the patients' general tolerance of the drug were studied. The results show that the new oral hypoglycemic drug has a similar, and superior in many instances, activity to other similar drugs such as glybenclamide and glypizide, and to the activity of the classical sulphonylureas (chlorpropamide and carbutamide). The patients' tolerance of the drug was excellent. No digestive disorders, undesirable side effects or hypoglycemias were seen in the patients. Analysis of lipid levels showed that glypentide induces a significant decrease in total lipid and cholesterol values, being this action more marked in patients with normal body weight non-treated with a hypocaloric diet.

Administration, Oral↗

PubMed1976

[Non-saturable cooperative binding of tolbutamide to rat endocrine pancreas. Criteria of specificity].

The binding of 3H-tolbutamide to isolated islets, which shows a cooperative non-saturable pattern up to about 5 X 10(-5) M, was confirmed. Binding to exocrine pancreatic tissue shows much less cooperativity. Among congeners of tolbutamide, unlabelled carbutamide and chlorpropamide in isodynamic concentrations, as well as diazoxide in an exactly antagonistic amount, behave like tolbutamide 5 X 10(-5) M itselt by cancelling cooperativity when added to the labelled drug. Glipizide and glibenclamide do not.

Animals↗

PubMed1997

Evaluation of phototoxic properties of oral antidiabetics and diuretics. Photohemolysis model as a screening method for recognizing potential photosensitizing drugs.

The oral hypoglycemic drugs carbutamide, chlorpropamide, glibenclamide, glubornuride, gliclazide, glipizide, gliquidone, glisoxepide, glymidine, tolazamide and tolbutamide, and the diuretics acetazolamide, bemetizide, bendroflumethiazide, benzthiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlorazanile, chlorothiazide, chlortalidone, clopamide, cyclopenthiazide, cyclothiazide, diazoxide, etozoline, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, mefruside, metolazone, piretanide, polythiazide, trichlormethiazide, and xipamide were investigated for photohemolytic properties in vitro. Irradiation with a SOL 3 apparatus (solar simulating irradiation) revealed hemolysis in the presence of five oral hypoglycemic agents and in the presence of 19 out of the 25 tested diuretics. Photohemolysis was induced in the presence of three substances, respectively, after exposure to UVA or visible light. UVB alone did not induce phototoxic hemolysis in the presence of the tested drugs. Compared to clinical reports on photosensitivity reactions, the photohemolysis model seems a good predictive model in recognizing potential photosensitizing sulfonamides.

Dermatitis, Phototoxic↗

PubMed1965