Drugs online research references
J Toxicol Clin Toxicol. 1996;34(3):267-70.
Five year retrospective evaluation of sulfonylurea ingestion in children.
Quadrani DA, Spiller HA, Widder P.
Western New York Regional Poison Control Center, Children's Hospital of Buffalo 14222, USA.
BACKGROUND: Oral hypoglycemic medications are frequently used for Type II diabetes and accidental ingestions by children may occur. There are no comprehensive pediatric studies documenting poison center experiences. STUDY OBJECTIVE: To evaluate the toxicity of oral sulfonylurea ingestion in children and the efficacy of treatments instituted in these cases. METHOD: Retrospective review of all ingestions of oral sulfonylureas reported to a single regional poison control center 1987-1991. RESULTS: Ninety-three cases were identified, one to 16 years old (mean of 3.5 years). Eighty cases (86%) were less than six years of age. Of the six medications used, three, chlorpropamide, glipizide and glyburide made up 88 (95%) cases. Twenty-five patients (27%) became hypoglycemic (glucose < 60 mg/dL). The mean minimum blood glucose in these patients was 46.5 mg/dL (minimum 20 mg/dL). Time of onset of hypoglycemia ranged from 0.5 to 16 h (mean 4.3 h; median 2 h). Only four patients had the onset of chemical hypoglycemia more than four hours postexposure. Persistent hypoglycemia occurred in nine children (10%) despite intravenous glucose therapy. There were no seizures. Mean time to decontamination of patients with and without hypoglycemia was 1.4 and 1.2 h respectively. Intravenous glucose of the following concentrations was administered: 5% (40), 10% (15), 20% (1), and 50% (3). Accidental ingestion of a single tablet of chlorpropamide (250 mg), glipizide (5 mg). and glyburide (2.5 mg) each produced hypoglycemia in children ages one to four years. Accidental ingestion of 5-10 mg glyburide produced a blood glucose of 57 mg/dL in an 11-year-old child. All patients recovered fully. There were no neurological sequelae noted. CONCLUSION: Children ingesting oral hypoglycemics should be admitted to a health care facility for 24 h observation. In this series a single tablet produced hypoglycemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8667462&dopt=Abstract
J Am Geriatr Soc. 1996 Jul;44(7):751-5.
Individual sulfonylureas and serious hypoglycemia in older people.
Shorr RI, Ray WA, Daugherty JR, Griffin MR.
Department of Preventive Medicine, Vanderbilt University, School of Medicine, Nashville, Tennessee, USA.
OBJECTIVE: To compare the risk of serious hypoglycemia associated with the use of individual sulfonylureas in older people. DESIGN: A retrospective cohort study. SETTING: The Tennessee Medicaid Program. PATIENTS: A total of 13,963 Medicaid enrollees, aged 65 years or older, who were prescribed one of six sulfonylureas from 1985 to 1989. MAIN OUTCOME MEASURE: Hospitalization, emergency room admission, or death associated with neuroglycopenic or autonomic symptoms, myocardial infarction, stroke, or injury, with a concomitant blood glucose determination of less than 2.8 mmol/L (50 mg/dL). RESULTS: We identified 255 persons with a first episode of serious hypoglycemia during 20,715 person-years of sulfonylurea use. The crude rate (per 1000 person-years) of serious hypoglycemia was highest in glyburide users, 16.6 (95% confidence interval [CI], 13.2 to 19.9 and lowest among users of tolbutamide, 3.5 (95% CI, 1.2 to 5.9). Users of tolbutamide, tolazamide, and glipizide had lower risks of serious hypoglycemia than users of chlorpropamide, whereas the risk of serious hypoglycemia among glyburide users did not differ from that of chlorpropamide users. Among second generation sulfonylureas, the adjusted relative risk of severe hypoglycemia among glyburide users, compared with glipizide users, was 1.9 (95% CI, 1.2 to 2.9). An increased risk of serious hypoglycemia associated with use of glyburide compared with glipizide occurred in all strata, including those defined by gender, race, nursing home residence, dose, and duration of use. CONCLUSIONS: Significant differences in risk of serious hypoglycemia were observed among users of individual agents. This may be explained by duration, timing, or potency of hypoglycemic action. These data confirm previous findings that chlorpropamide use is associated with high risk of hypoglycemia and indicate that among second generation sulfonylureas, glipizide is less associated with hypoglycemia than is glyburide. More information comparing the effectiveness of glycemic control among individual sulfonylureas is needed to assist prescribers in selecting a specific agent for use in clinical practice.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8675920&dopt=Abstract
Xenobiotica. 1995 Dec;25(12):1345-54.
Gliclazide hydroxylation by rat liver microsomes.
Rieutord A, Stupans I, Shenfield GM, Gross AS.
Department of Clinical Pharmacology, Royal North Shore Hospital, St Leonards, NSW, Australia.
1. The metabolism of gliclazide to hydroxygliclazide has been investigated in Sprague-Dawley rat liver microsomes. 2. The kinetics of hydroxygliclazide formation are consistent with Michaelis-Menten kinetics (mean (+/- SD, n = 3) apparent K(m) and Vmax = 256 +/- 27 microM and 1.85 +/- 0.10 nmol/ min/mg respectively). 3. Tolbutamide competitively inhibited hydroxygliclazide formation (Ki = 840 microM) and gliclazide competitively inhibited hydroxytolbutamide formation (Ki = 240 microM) with Ki similar to K(m). Therefore gliclazide and tolbutamide may be metabolized by the same enzyme in the rat. In nine livers the formation of hydroxygliclazide correlated with the formation of hydroxytolbutamide (rs = 0.82, p < 0.01). 4. Diclofenac (Ki = 64 microM), phenytoin (Ki = 38 microM), mephenytoin (Ki = 66 microM), glibenclamide (Ki = 14 microM) and glipizide (Ki = 189 microM) were fully competitive inhibitors of gliclazide hydroxylation. The rank order of Ki constants differed for gliclazide and tolbutamide suggesting that gliclazide and tolbutamide hydroxylases are not identical enzymes. 5. Quinine (Ki = 0.3 microM) and quinidine (Ki = 4.3 microM) were partially competitive inhibitors of hydroxygliclazide formation. Hydroxylation of gliclazide was related to the activity of CYP2D1 as assessed by dextrorphan production from dextromethorphan (rs = 0.83, p = 0.01). 6. In the rat gliclazide is metabolized to hydroxygliclazide by at least two cytochrome P450 isoforms, including tolbutamide hydroxylase and 2D1, which have similar affinities for gliclazide.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8719909&dopt=Abstract
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