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Results for “TOLAZAMIDE”

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PubMed1987

Combined therapy of insulin and tolazamide decreases insulin requirement and serum triglycerides in obese patients with noninsulin-dependent diabetes mellitus.

Insulin requirements, C-peptide levels, and serum lipids have been assessed in 12 obese, insulin-requiring (greater than 60 U/day) patients with type II diabetes mellitus, in a randomized crossover fashion with two treatment regimens: NPH alone and combined NPH and tolazamide, over a period of 3 months each, with maintenance of weight and glycemic control (HgA1, 2hpp and mean 24h glucose profile) at comparable levels. Serum cholesterol improved in both groups compared to their respective baseline values (p less than 0.05). In addition, serum triglyceride was lower (p less than 0.05) in the combined therapy as compared with NPH alone therapy. Insulin requirements were decreased by 23% (p less than 0.002) in the combined therapy group, without significant change in weight, glycemic control, or C-peptide levels. However, C-peptide increments in the combined therapy group were significantly higher than the baseline by 70% (p less than 0.02). NPH plus tolazamide therapy as compared with NPH alone lowers insulin requirement in obese, type II diabetic women without significant alteration in glycemic control, possibly by an increased tissue sensitivity to insulin, and decreases serum triglyceride levels.

Adult↗

PubMed1990

An unusual ring contraction in the formation of N-nitrosohexamethyleneimine and N-nitrosopiperidine from tolazamide.

The previously reported reaction of tolazamide with nitrite, under physiological conditions, to form N-nitrosohexamethyleneimine and surprisingly, N-nitrosopiperidine was confirmed. By using the six-membered ring analogue of tolazamide, 1-(piperidyl)-3-(p-tolylsulfonyl)urea, which yields the corresponding N-nitrosopiperidine and N-nitrosopyrrolidine, the present study shows that an unusual ring contraction occurs, excising the carbon alpha to the nitrogen.

Carbon Radioisotopes↗

PubMed1986

Transketolase abnormality in tolazamide-induced Wernicke's encephalopathy.

We studied a thiamine-dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke's encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke-Korsakoff syndrome. In addition to this patient, we also studied this enzyme from three diabetic kindreds without any history of Wernicke's encephalopathy and from four normal controls. We found that the above-mentioned patient and one of the diabetic kindreds with no history of Wernicke's encephalopathy had abnormal transketolase as determined by its Km for TPP. These data suggest a similarity between postalcoholic Wernicke-Korsakoff syndrome and the patient with tolazamide-induced Wernicke's encephalopathy from the standpoint of transketolase abnormality.

Fibroblasts↗

PubMed1967

Clinical experience with the oral antidiabetic compound, tolazamide.

In clinical experience totalling 82 patient-years with the sulfonylurea tolazamide, satisfactory control of glycemia was obtained in 70% of diabetics. The preponderance of elderly and newly diagnosed diabetics in the group probably increased the percentage of successes, because when tolazamide was compared with tolbutamide in the same patients the frequency of clinical effectiveness was similar. The ratio of effectiveness by weight for tolbutamide/tolazamide was 6.6/1.0. No toxic effects were detected, side effects were minimal and there appeared to be little tendency to induce unwarranted hypoglycemia.

Adolescent↗

PubMed1984

Lichenoid drug reactions to chlorpropamide and tolazamide.

Many medications, including gold, antimalarials, quinidine, and thiazide diuretics have been implicated in lichenoid drug reactions. Chlorpropamide and tolazamide are sulfonylurea oral hypoglycemic agents, neither of which has previously been implicated in cutaneous lichenoid reactions. We report a case of lichenoid drug reaction related to both chlorpropamide and tolazamide.

Aged↗

PubMed1978

Tolazamide-induced hepatic dysfunction.

A case of tolazamide-induced hepatic injury is reported. Injury was documented by abnormal liver tests, including an elevated alkaline phosphatase, 5' nucleotidase and serum glutamic oxaloacetic transaminase. Liver biopsy confirmed the degree and type of injury which consisted of severe portal inflammation, bile duct proliferation and early fibrosis. The case is reported to further establish tolazamide as a drug capable of producing hepatic injury and to report a new form of hepatic injury attributable to a sulfonylurea agent.

Adult↗

PubMed1987

Monitoring a potential carcinogen in pharmaceutical formulations at the low part per billion level. High-performance liquid chromatographic determination of N-nitrosohexamethyleneimine in tolazamide.

A method is described for the determination of N-nitrosohexamethyleneimine, a potential carcinogen, in tolazamide bulk drug and pharmaceutical dosage forms. The technique of trace enrichment high-performance liquid chromatography is employed to obtain accurate quantitation of the analyte at levels approaching 1 ppb. Following extraction in diethyl ether and on-line cleanup and enrichment, the nitrosamine is detected by UV at 228 nm.

Buffers↗

PubMed1986

2-Deoxyglucose tissue levels and insulin levels following tolazamide dosing in normal and obese mice.

The effect of tolazamide (TZ), a sulfonylurea, on 14C-2-deoxyglucose (14C-2DG) tissue distribution and insulin levels of normal and obese mice was investigated using an in vivo physiological method. Acute doses of TZ (50 mg/kg ip) increased 14C-2DG levels in gastrocnemius muscle and retroperitoneal fat and produced a transient elevation of insulin which most likely accounts for the increased 14C-2DG levels in muscle and fat. The results demonstrate that the in vivo 14C-2DG method produced results consistent with known actions of sulfonylureas on in vitro hexose assimilation in muscle and fat. Subchronic treatment (7 days) with TZ 50 mg/kg ip twice daily did not result in increased insulin-stimulated 14C-2DG tissue levels in normal mice when compared to saline treated controls. However, insulin levels were lower in mice treated subchronically with TZ compared to saline controls suggesting an enhancement of insulin action. Viable yellow obese mice represent a model of maturity onset obesity presenting with insulin resistance. The insulin resistance of this obese strain appears to reside in the fat tissue as assessed by comparing 14C-2DG tissue levels of obese mice with lean littermate controls. Subchronic TZ treatment had no effect on 14C-2DG uptake in fat or muscle tissue of viable yellow obese mice and did not alter their plasma insulin levels. It appears that genetically obese viable yellow mice may be resistant to subchronic treatment with TZ.

Adipose Tissue↗

PubMed1980

Impaired granulocyte adherence in mildly diabetic patients: effects of tolazamide treatment.

Granulocyte adherence in 10 of 15 untreated asymptomatic hyperglycemic diabetic outpatients (mean fasting glucose +/- SEM, 289 +/- 16 mg/100 ml) was 62 +/- 7% of control values. After treatment (2--4 wk) with tolazamide (500 mg daily), adherence to the nylon fiber columns employed in this study returned to control levels in the seven patients whose fasting glucose levels fell, (mean, 192 +/- 16 mg/100 ml) and deteriorated in the three in whom fasting hyperglycemia worsened. Results of this study indicate that, even in some mildly diabetic patients, a reduction in granulocyte adherence similar to that found in insulin-dependent diabetics may impair the inflammatory response.

Cell Adhesion↗

PubMedDate not supplied

Glyburide and glipizide in treatment of diabetic patients with secondary failures to tolazamide or chlorpropamide.

We evaluated therapeutic usefulness of the second-generation sulfonylurea agents glyburide and glipizide in non-insulin-dependent diabetic patients who were secondary failures on chlorpropamide or tolazamide. Twenty patients were treated with glyburide, and 10 of them were subsequently treated with glipizide. Fasting and postprandial serum glucose, insulin, C-peptide, glycosylated hemoglobin, urinary C-peptide, and glucose levels all failed to show significant improvement. We concluded that both glyburide and glipizide proved ineffective in the treatment of secondary failures to first-generation sulfonylureas.

Blood Glucose↗

PubMed1980

Pseudoinsulinoma syndrome from inadvertent tolazamide ingestion.

A 70-year-old woman with rheumatoid arthritis presented with fasting hypoglycemia, inappropriately elevated insulin and C-peptide levels, and negative insulin antibodies, all compatible with the diagnosis of an insulinoma. However, results of a 72-hour fast were subsequently negative. Medication identification revealed that the patient had been taking tolazamide (Tolinase; The Upjohn Company, Kalamazoo, Michigan) instead of tolmetin (Tolectin; McNeil Laboratories, Inc., Fort Washington, Pennsylvania).

Adenoma, Islet Cell↗

PubMed1967

A comparison of the effects of tolazamide and tolbutamide upon blood glucose and serum insulin and lipid levels in diabetic subjects.

The effects of tolazamide (300 mg. daily), a new oral hypoglycemic sulfonylurea, and tolbutamide on the blood glucose, serum insulin, cholesterol and triglyceride levels were compared in 14 subjects with maturity-onset diabetes of varying severity. The mean effects of the two drugs in the pharmacologically equivalent doses were the same. In particular, the mean reduction of the blood glucose level was 19% and of the serum triglyceride level was 17% with both agents. However, an individual subject might respond to one agent and not to the other; neither the blood glucose nor the serum lipid response could be predicted from the pretreatment blood glucose level or the per cent of ideal body weight.

Adult↗

PubMedDate not supplied