Disease relevance of chlorpropamide

• Chlorpropamide-induced hypoglycemia. A dramatic presentation of celiac disease [1].
• Chlorpropamide-induced granulomas. A probable hypersensitivity reaction in liver and bone marrow [2].
• Chlorpropamide-induced agranulocytosis [3].
• To our knowledge, this is the first report of a patient with liver and bone marrow inflammation characterized by granulomas with eosinophilic infiltration following intake of chlorpropamide [2].
• Anicteric hepatitis, associated with fever and exfoliative dermatitis, developed in a diabetic patient two weeks after intake of a long-acting sulfonylurea, chlorpropamide (Diabinese) [2].

Psychiatry related information on chlorpropamide

• Patients with IF have features that distinguish them from individuals with flushing from other causes, such as CS, postmenopausal state, chlorpropamide-alcohol flush, panic attacks, medullary thyroid carcinoma, and autonomic epilepsy [4].
• RESULTS: Other than a longer duration of diabetes in users of chlorpropamide, no differences were observed among users of different sulfonylurea agents with respect to diabetic complications, adequacy of diabetic control, obesity, smoking, and excessive alcohol consumption [5].

High impact information on chlorpropamide

• Chlorpropamide action on renal concentrating mechanism in rats with hypothalamic diabetes insipidus [6].
• Our patient had been taking chlorpropamide, but she had no evidence of liver disease before administration of tolazamide [7].
• Facial skin temperature and the chlorpropamide/alcohol flush in diabetics [8].
• The blocking effects of aspirin, chlorpheniramine, and cimetidine were tested against the flush provoked by alcohol in twenty-four chlorpropamide-treated patients with non-insulin-dependent diabetes mellitus [9].
• Chlorpropamide alcohol flushing and diabetic retinopathy [10].

Chemical compound and disease context of chlorpropamide

• To determine an optimal glyburide dosage schedule, the effects of glyburide once (every morning) or twice daily and chlorpropamide once daily (every morning) were compared in 18 men with non-insulin-dependent diabetes mellitus in a randomized, double-blind fashion [11].
• Resistance was associated with a high titer of antibodies that disappeared once vasopressin therapy was withdrawn and the diabetes insipidus was controlled with chlorpropamide [12].
• The failure of chlorpropamide to maintain the reduction in serum and VLDL triglyceride could be of importance in the genesis of coronary heart disease in maturity onset diabetics [13].
• Inhibition of prostaglandin synthesis with nonsteroidal anti-inflammatory agents enhances expression of the ADH effect on the kidney, but it does not appear to potentiate chlorpropamide hyponatremia [14].
• Improved control of non-insulin-dependent diabetes mellitus by combined halofenate and chlorpropamide therapy [15].

Biological context of chlorpropamide

• Chlorpropamide raises fructose-2,6-bisphosphate concentration and inhibits gluconeogenesis in isolated rat hepatocytes [16].
• Euglycemia during chlorpropamide therapy appears to allow full expression of the action of chlorpropamide on CH2O; hyperglycemia with attendant osmotic diuresis protects chlorpropamide-treated patients against hyponatremia [14].
• The relationship of the ALDH2 genotype with proliferative retinopathy is interesting, because it resembles that of chlorpropamide alcohol flushing with severe diabetic retinopathy [17].
• Hormonal and metabolic effects of chlorpropamide, glibenclamide and placebo in a cross-over study in diabetics not controlled by diet alone [18].
• Higher rises in facial skin temperature and heart rate, higher flush-score and higher acetaldehyde levels resulted from chlorpropamide therapy than followed placebo [19].

Anatomical context of chlorpropamide

• The addition of chlorpropamide to hepatocytes isolated from fed rats raised the cellular concentration of fructose-2,6-bisphosphate (F-2,6-P2), a regulatory metabolite that plays a relevant role in the control of hepatic glucose metabolism [16].
• We conclude that short-term use of chlorpropamide in addition to insulin in IDDM does not alter insulin binding to circulating monocytes or erythrocytes [20].
• Hepatic effects of chlorpropamide: inhibition of glucagon-stimulated gluconeogenesis in perfused livers of fasted rats [21].
• It is concluded that stimulation of the pancreatic beta cells during chlorpropamide toxicity leads to hyperinsulinemia and hypoglycemia [22].
• The significance of the cerebrospinal fluid examination in the management of chlorpropamide-induced hypoglycemia [23].

Associations of chlorpropamide with other chemical compounds

• Acetaldehyde measurement is an objective method to study the chlorpropamide alcohol flush and it appears superior to the measurement of skin temperature [24].
• Measurements of metabolic intermediates suggest that chlorpropamide may inhibit gluconeogenesis by antagonizing the action of glucagon on the phosphoenolpyruvate cycle [21].
• The binding of insulin to rat hepatocyte monolayers was not altered in cells previously exposed to gliclazide at 0.7, 7.0 or 70 micrograms/ml; and to glibenclamide, chlorpropamide, or glipizide at 0.1, 1.0 and 10 micrograms/ml [25].
• Recording of facial skin temperature, measurement of chlorpropamide, ethanol and acetaldehyde concentrations have been proposed for this purpose [19].
• RESULTS: Indapamide revealed a 40.56% +/- 9.70% (mean +/- SD) (range, 19.6%-55.0%) reduction in 24-hour urinary volume and an increase in urinary osmolality, as well as a decrease in serum osmolality, and was as effective as chlorpropamide (P<.05) in the treatment of CDI [26].

Gene context of chlorpropamide

• In contrast, no differences in chlorpropamide pharmacokinetics were observed for subjects with the CYP2C19 extensive metabolizer vs. poor metabolizer genotypes [27].
• CONCLUSIONS: These results suggest that chlorpropamide disposition is principally determined by CYP2C9 activity in vivo, although both CYP2C9 and CYP2C19 have a catalysing activity of chlorpropamide 2-hydroxylation pathway [27].
• Chlorpropamide did not decrease the phosphaturic response to any dose of PTH [28].
• Effect of chlorpropamide on renal response to parathyroid hormone in normal subjects and in patients with hypoparathyroidism and pseudohypoparathyroidism [28].
• Water retention after oral chlorpropamide is associated with an increase in renal papillary arginine vasopressin receptors [29].

Analytical, diagnostic and therapeutic context of chlorpropamide

• Reversible mild diabetes in children after treatment with chlorpropamide [30].
• Potenitation by chlorpropamide of the hepatic action of insulin does not require administration of the drug prior to perfusion [31].
• To investigate the effect of hyperglycemia on normal islets, rats were made diabetic by a 95% partial pancreatectomy and treated with insulin, saline, or chlorpropamide for 3 mo [32].
• Twelve additional subjects were entered into a 16-wk double-blind study testing chlorpropamide plus either placebo or halofenate [15].
• Seventy-seven adults with hyperglycemia despite diet therapy were randomly assigned to chlorpropamide or insulin [33].

References