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At least 19 recordsLinked to original sources
PubMed1991

A case of acetohexamide-induced hypoglycemia: the influence of hypothyroidism on the metabolism of acetohexamide.

Prolonged hypoglycemia induced by acetohexamide (AH) in a patient with noninsulin dependent diabetes mellitus accompanied by primary hypothyroidism was presented. A 74-year-old man who had been treated with AH (500mg, daily) for diabetes mellitus since 1973 was admitted to our hospital in Oct. 1988 because of hypoglycemic coma. On admission, the level of blood glucose was 20mg/dl. Continuous intravenous administration of 10 per cent glucose solution led to improvement in the mental state on the second day. However, the level of blood glucose remained between 30 to 45mg/dl for four days after admission. On the fifth day, a fasting blood glucose level finally reached 75mg/dl. In a thyroid function test, the serum levels of thyroid hormone showed the following decreases: T3 68ng/dl, T4 2.8 micrograms/dl, free T4 0.3ng/dl, while basal TSH levels increased to 50.3 microU/ml. Since anti-thyroid microsomal antibody was positive and thyroid 99mTc-pertechnetate uptake was slightly elevated, the hypothyroidism in this patient was considered to be caused by chronic thyroiditis. Urinalysis was positive for protein. In a renal function test, the blood urea nitrogen was 26.7mg/dl and creatinine 1.7mg/dl, and creatinine clearance decreased to 22ml/min. After thyroid function returned to euthyroid, creatinine clearance improved (41 ml/min). To clarify the relationship between hypothyroidism and the metabolism of AH, the serum levels of AH and its metabolite hydroxyhexamide (HH) following oral administration of AH (500mg) were evaluated before and after thyroxine replacement therapy. The blood glucose level before therapy was lower than that after therapy, and hypoglycemic symptoms were observed early in the second and third morning after AH administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetohexamide↗
PubMed1977

Acetohexamide hypoglycemia: treatment by peritoneal dialysis.

Acetohexamide hypoglycemia in a patient with renal failure has been successfully treated by peritoneal dialysis. Peritoneal dialysis was done in such a patient, and specimens of serum were collected to measure levels of acetohexamide and its main active metabolite, hydroxyhexamide. During dialysis, hypoglycemia was corrected. After 17 1/2 hours of dialysis, serum acetohexamide level was essentially unchanged. Serum hydroxyhexamide level had decreased at a slower rate than the rate of decrease previously measured in a uremic patient not on dialysis. Although peritoneal dialysis may correct the hypoglycemia, the data suggest that acetohexamide and hydroxyhexamide are not dialyzable. Due to these problems this drug should not be used in patients with chronic renal failure. The drug of choice to control hyperglycemia in patients with renal insufficiency is insulin. If for any reason insulin cannot be used, tolbutamide is the oral hypoglycemic agent of choice.

Acetohexamide↗
PubMed1991

Postnatal development of acetohexamide reductase activities in microsomes and cytosol of rat liver.

The postnatal development of acetohexamide reductase activities in liver microsomes and cytosol were examined in male rats. The developmental pattern of acetohexamide reductase activity in liver microsomes was distinguished from that in liver cytosol. Furthermore, acetohexamide reductase activity in liver microsomes was effectively suppressed by castration, but the activity in liver cytosol was not affected by castration. These results clearly indicate that enzymes with physiologically different roles can catalyze the metabolic reduction of acetohexamide in rat liver.

Age Factors↗
PubMed1990

Drug-metal interactions: copper(II) complex of the antidiabetic drug acetohexamide and pyridine.

The preparation, spectral properties, and crystal structure of a copper(II) complex of 4-acetyl-N-[(cyclohexylamino)carbonyl]benzenesulfonamide, which is known as acetohexamide, and pyridine are reported. The complex Cu(AH)2(py)2, where AH = acetohexamide and py = pyridine, was prepared and characterized by X-ray and ESR. The complex is monoclinic, space group P2(1)/a, with a = 17.412(6), b = 9.039(2), c = 26.531(10) A, beta = 102.24(2) degrees, and Z = 4. The final refinement used 3892 unique reflections and gave an R value of 0.0646. The copper atom is surrounded by four nitrogen atoms in a square-planar arrangement, two from the acetohexamide ligands (Cu-N = 2.009 A) and two from the pyridine molecules (Cu-N = 2.016 A) in a trans geometry. The ESR data support a similar coordination behavior of the copper (g parallel greater than g perpendicular greater than ge) with the unpaired electron in the dx2-y2 orbital.

Acetohexamide↗
PubMed1977

Peritoneal dialysis in the treatment of acetohexamide-induced hypoglycemia.

Severe hypoglycemia in a 67-year-old black male as a result of the ingestion of acetohexamide is described. Because of both his renal status as well as the severity of the hypoglycemia, the patient received peritoneal dialysis. Sequential specimens of serum, urine and dialysate were collected to measure the levels of acetohexamide and its main active metabolite, hydroxyhexamide. The data indicate that these compounds are not dialyzable. In patients with reduced renal function, peritoneal dialysis may be one way to administer large amounts of glucose with very little administration of fluid in the treatment of acetohexamide-induced hypoglycemia. For those azotemic patients whose hypoglycemia is difficult to manage, intensive dialysis might be a means to correct the abnormality of glucose metabolism imposed by uremia.

Acetohexamide↗
PubMed1977

Inadvertent substitution of acetohexamide for acetozolamide.

In three cases acetohexamide (Dymelor), an oral hypoglycemic agent, was mistakenly given to patients instead of acetazolamide (Diamox), which had been prescribed for their glaucoma. A number of similarities, including the fact that both medications are 250-mg white tablets, with similar generic and brand names which are generically repackaged medications juxtaposed on the pharmacist's shelf, predispose to the inadvertent substitution of one medication for the other. In one instance a systemic hypoglycemic reaction resulting in head trauma and confusion ended in an emegency hospital admission following the substitution of acetohexamide for acetazolamide.

Acetohexamide↗
PubMed1992

Factors affecting acetohexamide reductase activities in microsomes and cytosol from the kidney of male rats: age and castration.

Acetohexamide reductase activity in microsomes from the kidney of male rats increased markedly at puberty to approach the maximum level at 8 weeks of age; it was not detected until 4 weeks of age. Furthermore, castration suppressed effectively the activity in kidney microsomes at 8 weeks of age. These findings clearly indicate that the activity in kidney microsomes can be regulated by androgens. On the other hand, in cytosol from the kidney of male rats, a higher acetohexamide reductase activity was observed at all weeks of age tested. Castration had no significant effect on the activity in kidney cytosol.

Aging↗
PubMed1977

GLC determination of acetohexamide and hydroxyhexamide in biological fluids.

A sensitive and specific GLC assay was developed for acetohexamide and hydroxyhexamide, its major metabolite, in plasma and urine. The assay uses tolbutamide as a mass internal standard. Compounds are extracted from acidified plasma or urine with toluene, converted to methylated derivatives with dimethyl sulfate, and measured by GLC using a flame-ionization detector. With GLC-mass spectrometry, the compounds measured are the N-methylsulfonamides resulting from GLC pyrolysis. Plasma and urine data are presented from a bioavailability study to demonstrate the utility of this method.

Acetohexamide↗
PubMed1990

Mechanism of pharmacodynamic and pharmacokinetic interactions between acetohexamide and phenylbutazone in rabbits.

The interaction of acetohexamide (AH) with phenylbutazone (PBZ) was investigated in rabbits. Orally administered PBZ caused a potentiation of hypoglycaemic action after oral administration of AH. This can be explained by the fact that the co-administration of PBZ significantly increased both the serum concentrations of AH and its pharmacologically active metabolite. (-)-hydroxyhexamide [(-)-HH], after AH administration. The co-administration of PBZ decreased the renal clearance (Clr) and non-renal clearance (Clnr) of AH. PBZ inhibited the in vitro reduction of AH to (-)-HH and decreased the accumulation of (-)-HH by the kidney cortical slices. These results indicate that the mechanism of in vivo interaction of AH with PBZ is complicated.

Acetohexamide↗