Disease relevance of antipyrine

• Effect of age on antipyrine metabolism in patients with gastric cancer [1].
• Concurrent drug ingestion enhanced antipyrine metabolism in most patients with liver disease as well as in control patients [2].
• Using the plasma disappearance rate of antipyrine (15 mg per kg of body weight) as an index of liver microsomal metabolism, a significant decrease in the half-life of antipyrine has been observed: 11.7 +/- (1 sd) 4.7 hr before treatment as compared to 6.9 +/- 2.3 hr on the 7th day [3].
• The disposition of antipyrine was therefore studied in 15 patients with cirrhosis before and after 13 days of spironolactone treatment (200 mg/day) and in 15 comparable patients not treated by spironolactone [4].
• Prophylaxis of neonatal jaundice with maternal antipyrine treatment [5].

Psychiatry related information on antipyrine

• Influence of short-term water deprivation on antipyrine disposition [6].
• Stepwise multiple regression analysis, incorporating the independent variables of age, height, weight, sex, BSA, LBM, alcohol consumption, smoking status and liver volume and the dependent variable antipyrine clearance, indicated that LBM was the only independent correlate of antipyrine clearance [7].
• These results put forward the importance of the degree of physical activity (1) for the evaluation of antipyrine-loading-test results as expression of liver function and (2) whenever drugs with a low therapeutic index are used in athletes [8].

High impact information on antipyrine

• Prior to the initiation of topotecan treatment, patients were given intravenous injections of ICG, lorazepam, and antipyrine to determine the plasma pharmacokinetics of these compounds [9].
• The verapamil-induced improvement in microcirculatory characteristics was associated with a significant improvement in oxygen consumption (+21%) and antipyrine clearance (+20%) [10].
• While these results are compatible with a common regulatory element in the AP and theophylline polymorphisms, other evidence suggests more than a single genetic polymorphism [11].
• Similar results were obtained for antipyrine clearance per hepatocyte (7.35 +/- 2.27 x 10(-11) mL/min for cirrhotics vs. 6.16 +/- 1.07 x 10(-11) mL/min for noncirrhotics; P greater than 0.10) [12].
• Sixteen patients receiving enteral supplementation had antipyrine half-life (50% vs. 3% reduction), serum bilirubin (25% vs. 0% reduction), and median encephalopathy scores that improved more rapidly than those of controls [13].

Chemical compound and disease context of antipyrine

• The aim of this study was to look for correlations between the metabolic clearance rate of antipyrine and (a) the concentration of cytochrome P-450, and (b) the NADPH cytochrome c reductase, aminopyrine demethylase, and aniline hydroxylase activities in the liver microsomes of 20 patients without liver diseases [14].
• In patients with liver disease, the unbound clearance of oxazepam correlated significantly with antipyrine clearance (r = 0.88; p less than 0.05) [15].
• Proceedings: Antipyrine, lingocaine and paracetamol metabolism in chronic liver disease [16].
• Blood clearance of antipyrine, indocyanine green, and galactose were measured to evaluate the alterations of effective hepatic blood flow and hepatic intrinsic clearances in chronic liver diseases [17].
• The role of hepatic drug-metabolizing enzyme activity for plasma propranolol and sotalol levels was investigated in 68 patients with hypertension or angina pectoris by comparing elimination rate with antipyrine kinetics and cytochrome P-450 content in the liver [18].

Biological context of antipyrine

• Prothrombin time, serum bilirubin, albumin, the antipyrin breath test, and plasma disappearance of indocyanine green were normal initially and did not change [19].
• Alprazolam kinetics in the elderly. Relation to antipyrine disposition [20].
• Thus propranolol prolongs the half-life and reduces the clearance or biotransformation rate of antipyrine, a drug whose clearance is independent of hepatic blood flow [21].
• The putative selective COX-3 inhibitors antipyrine and aminopyrine also reduced basal body temperature and brain PGE(2) levels in normal mice [22].
• Genetic variation in rates of antipyrine metabolite formation: a study in uninduced twins [23].

Anatomical context of antipyrine

• When this substance, termed anodynin, is microinjected into rat periaqueductal gray matter, it causes a profound, long-lasting analgesia which is prevented by prior injection of the opiate antagonist naloxone [24].
• High-pressure liquid chromatographic analysis of benzo(a)pyrene metabolism by human lymphocytes from donors of different aryl hydrocarbon hydroxylase inducibility and antipyrine half-lives [25].
• Assessment in the cirrhotics included measurement of hepatic vein pressure gradient, indocyanine green extraction ratio, indocyanine green clearance, and antipyrine clearance as indices of portal pressure, intrahepatic shunting, hepatic blood flow and functional hepatocellular mass, respectively [26].
• However, transfer of the highly diffusible marker substance antipyrine was significantly reduced in IDDM placentas (1.79 vs. 2.49 ml/min in IDDM and nondiabetic, respectively; P less than 0.01) [27].
• Widely used to study hepatic drug metabolism, antipyrine rapidly distributes in total body water [28].

Associations of antipyrine with other chemical compounds

• An attempt was made to compare various morphometric parameters, including total hepatocyte number, with the in vivo clearances of aminopyrine and antipyrine in 26 cirrhotic and 14 noncirrhotic patients to evaluate the intact hepatocyte theory [12].
• Comparison of canine COX-3 activity with murine COX-1 and -2 demonstrates that this enzyme is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently inhibited by some nonsteroidal antiinflammatory drugs [29].
• The glucagon-induced change in functional hepatic nitrogen clearance significantly correlated with galactose elimination capacity and antipyrine clearance (r = 0.905 and 0.964, respectively) [30].
• Further, the area under the concentration-time curve (AUC) for epirubicin correlated with prothrombin index (P < .01), antipyrine clearance (P < .01), and serum bile salt concentration (P = .03), and there were similar correlations for epirubicin steady-state concentration (CpSS) [31].
• At 24 h after administration in ovo, AIA simultaneously decreased the Vmax of the isozymes active in 7-ethoxycoumarin deethylation and in biphenyl and antipyrine hydroxylations in control liver and caused new isozymes with higher Km and Vmax values to appear [32].

Gene context of antipyrine

• METHODS: We used the following methods for this study: (1) determination of enzyme kinetics for antipyrine metabolite formation in human liver microsomes, (2) inhibition studies with antibodies and inhibitors, and (3) formation of metabolites by stable expressed human P450 enzymes [33].
• In the first group no significant alterations of antipyrine kinetics or plasma IFN levels were observed after treatment with ZDV [34].
• Evaluation of the influence of diabetes mellitus on antipyrine metabolism and CYP1A2 and CYP2D6 activity [35].
• OBJECTIVE: Antipyrine metabolism is a "gold standard" measure of mixed cytochrome P450 (CYP) mediated drug metabolism in humans [36].
• 5. Antipyrine metabolism, urinary 6-beta-hydroxycortisol excretion, SHBG levels and circulating androgens were unaltered by treatment with OXC [37].

Analytical, diagnostic and therapeutic context of antipyrine

• In spironolactone-treated patients, a 40% increase in elimination rate constant of antipyrine (P less than 0.01) was due both to a decrease in apparent volume of distribution by 11% (P less than 0.01) and to a 20% rise in metabolic clearance rate (P less than 0.01) [4].
• The mean plasma clearance of antipyrine was 0.0475 +/- 0.009 liter/kg/hr in the tumor group and 0.0557 +/- 0.007 liter/kg/hr in the control group (p greater than 0.05) [38].
• The disposition of antipyrine following oral administration of 1200 mg has been investigated in 10 patients with histologically confirmed hepatosplenic schistosomiasis and 11 normal subjects living in Sudan. Drug metabolising activity as assessed by antipyrine clearance was similar in patients when compared with normal controls [39].
• Liver function tests, antipyrine, half-life, plasma clearance, and the apparent volume of distribution were determined in the acute and recovery period [40].
• Blood samples were obtained over 48 hours for HPLC determination of antipyrine plasma concentrations [41].

References