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During a khat-chewing session, but no effect was noted with amoxicillin [21]. Licorice Glycyrrhiza glabra ; contains glycyrrhizin, which inhibits 11b-dehydrogenase, 5a-reductase, and 5b-reductase. Glycyrrhizin is metabolized largely to glycyrrhetinic acid an even more potent inhibitor of 5a-, 5b-reductase and 11b-dehydrogenase ; . Liquorice has been shown to increase plasma concentrations of prednisolone [22, 23]. It also potentiated the cutaneous vasoconstrictor response of hydrocortisone [24]. Licorice is a common herb in Chinese and Japanese herbal mixtures. The effect of several such mixtures on prednisolone concentrations has been tested. Both Shosaiko-To and Xiao Chai Hu Tang decreased the plasma AUC of prednisolone [25] whereas Saiboku-To increased it. Sairei-To did not affect it [26]. Both Sho-saiko-To and Rikkunshi-to were found not to affect the pharmacokinetics of a single oral dose of ooxacin [26]. St John's wort affects the clearance of many drugs, including cyclosporin, antidepressants predominantly SSRIs ; , digoxin, indinavir, and phenprocoumon. The underlying mechanism appears to be multifactorial. There is evidence of a strong interaction with P-glycoprotein PgP ; , an ATP-dependent drug efux transporter known to pump drugs out of the cell membrane, thus decreasing intracellular concentrations [27]. St John's wort increases expression of duodenal PgP MDR1 [28]. The herb also induces the activity of an important form of cytochrome P450, CYP3A4. However, results of studies of the effect of St John's wort on CYP3A4 are conicting. While three enzyme marker studies indicated a potent inducing effect of St John's wort 300 mg three times dailyr14 days ; on CYP3A4 activity [29, 30], two others found no effect both 300 mg three times daily, one for 3 days [31], the other for 8 days [32] ; on CYP2D6 or 3A4 activities. It is possible that the negative trials were simply too short in duration. Alternatively, differences in quality of the HMPs used might explain the discrepancy. One study examining the effect of St John's wort on CYP1A2 activity using a caffeine dextromethorphan probe ; found that it 300 mg three times daily for 8 days ; had no effect on 17 DMX caffeine ratios [33], indicating that this HMP has a low potential for drug interactions involving CYP 1A2. Cases of serotonin syndrome could arise if St John's wort increased serotonin levels. However, it cannot be considered an SSRI, because in vitro, St John's wort inhibits the uptake of serotonin, noradrenaline and dopamine only at high concentrations with IC50s of 2.4, 4.5, and 0.9 mg mlx1, respectively [34] which are unlikely to be achieved with oral dosing. However, enough cases of interactions with SSRIs have been reported that a serotonergic or serotonin-amplifying ; effect of St John's wort could occur.
Survival Rates with Surgial versus NonSurgical Tbapy o Squatnous CeIl Carcinoma o the Lung with Nodal f f Metastases Detected a Medfostinoscopy. R D. Bryn; R M. t Yeager; I. G. Butford; M. S. Briggs; R. B. George, FCCP, LSU School of Medicine, Shreveport.
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Author: Robert Harsieber, PhD, is a philosopher, author, and freelance business journalist in Vienna, Austria, covering topics ranging from nuclear physics to spirituality. He is the editor-in-chief of rzte EXKLUSIV and publisher of different conference transcripts and diamox.
FIGURE 38.13. Example of an in vitro study of inhibition of CYP2D6 by two antipsychotic agents, perphenazine and clozapine. A fixed concentration of the substrate dextromethorphan was incubated with liver microsomes, appropriate cofactors, and varying concentrations of perphenazine or clozapine. Rates of formation of dextrorphan mediated by CYP2D6 ; with inhibitor present were expressed as a ratio versus the control velocity with no inhibitor. The relation of the velocity ratio to inhibitor concentration can be used to calculate a 50% inhibitory concentration IC50 ; . The results indicate that perphenazine IC50 0.9 M ; is likely to be a clinically important inhibitor of CYP2D6, whereas clozapine IC50 119 M ; is a weak inhibitor.
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1. Kaufman RD, Walts LF. Tourniquet-induced hypertension. Br J Anaesth 1982; 54: 333 Hagenouw RR, Bridenbaugh PO, van Egmond J, Stuebing R. Tourniquet pain: a volunteer study. Anesth Analg 1986; 65: 1175 Valli H, Rosenberg PH, Kytta J, Nurminen M. Arterial hypertension associated with the use of a tourniquet with either general or regional anaesthesia. Acta Anaesthesiol Scand 1987; 31: 279 Kam PC, Kavanaugh R, Yoong FF. The arterial tourniquet: pathophysiological consequences and anaesthetic implications. Anaesthesia 2001; 56: 534 Valli H, Rosenberg PH. Effects of three anaesthesia methods on haemodynamic responses connected with the use of thigh tourniquet in orthopaedic patients. Acta Anaesthesiol Scand 1985; 29: 1427. Chabel C, Russell LC, Lee R. Tourniquet-induced limb ischemia: a neurophysiologic animal model. Anesthesiology 1990; 72: 1038 Maclver MB, Tanelian DL. Activation of C fibers by metabolic perturbations associated with tourniquet ischemia. Anesthesiology 1992; 76: 61723. Tetzlaff JE, O'Hara J, Yoon HJ, Schubert A. Tourniquet-induced hypertension correlates with autonomic nervous system changes detected by power spectral heart rate analysis. J Clin Anesth 1997; 9: 138 Heropoulos M, Schieren H, Seltzer JL, et al. Intraoperative hemodynamic, renin, and catecholamine responses after prophylactic and intraoperative administration of intravenous enalaprilat. Anesth Analg 1995; 80: 58390. Satsumae T, Yamaguchi H, Sakaguchi M, et al. Preoperative small-dose ketamine prevented tourniquet-induced arterial pressure increase in orthopedic patients under general anesthesia. Anesth Analg 2001; 92: 1286 Dickenson AH, Sullivan AF, Stanfa LC, Mcquay HJ. Dextromethorphan and levorphanol on dorsal horn nociceptive neurones in the rat. Neuropharmacology 1991; 30: 1303 Elliott KJ, Brodsky M, Hynansky AD, et al. Dextromethorphan suppresses both formalin-induced nociceptive behavior and the formalin-induced increase in spinal cord c-fos mRNA. Pain 1995; 61: 4019. Weinbroum AA, Rudick V, Paret G, Ben-Abraham R. The role of dextromethorphan in pain control. Can J Anaesth 2000; 47: 58596. Price DD, Mao J, Frenk H, Mayer DJ. The N-methyl-d-aspartate receptor antagonist dextromethorphan selectively reduces temporal summation of second pain in man. Pain 1994; 59: 16574 and dicloxacillin.
RECOMBINANT HUMAN GROWTH HORMONE rhGH ; HAS NO EFFECT ON ACTIVITIES OF HEPATIC CYTOCHROME P4501A2 CYP1A2 ; , N-ACETYLTRANSFERASE 2 NAT2 ; , XANTHINE OXIDASE XO ; OR CYTOCHROME P4502D6 IN CHILDREN WITH IDIOPATHIC GROWTH HORMONE GH ; DEFICIENCY. M. J. Kennedy, PharmD, D. A. Davis, MD, N. B. Smith, PhD, W. M. Pierce, PhD, T. Lin, M.S., R. E. Pearce, PhD, A. Gaedigk, PhD, G. L. Kearns, PharmD, PhD, Kosair Charities Pediatric Clinical Research Unit; Departments of Pediatrics and Pharmacology Toxicology, School of Medicine, University of Louisville, Division of Clinical Pharmacology and Medical Toxicology, Children's Mercy Hospitals and Clinics, Louisville, KY. BACKGROUND: Growth hormone GH ; is a known modulator of hepatic drug metabolizing enzyme activity. However, previous investigations have used polyfunctional enzyme substrates and the effect on GH on individual hepatic enzyme isoforms remains unknown. This investigation assessed the activities of CYP1A2, NAT-2, XO and CYP2D6 in children receiving GH replacement using the specific probe substrates caffeine and dextromethorphan DM ; . METHODS: Pre-pubertal children 4-14y, n 12 ; with idiopathic GH deficiency received DM 0.5mg kg ; and caffeine 11.5mg ; prior to and 3 and 6 months following initiation of rhGH therapy. Urine was collected for 8 hours and analyzed via HPLC. Blood was also obtained for CYP2D6 genotyping. The following molar ratios and 95% CI estimation for the mean were calculated: AFMU 1X 1U 17U CYP1A2 ; , AFMU AFMU 1X 1U NAT2 ; , 1U 1X CYP2D6 ; . Mean baseline ratios were also compared to those obtained at 3 and 6 months using the Student's t-test. RESULTS: Mean 95% CI ; ratio and values in NAT-2 slow acetylators and CYP2D6 EMs were as follows.
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| Dextromethorphan side effectsCharacterizing the chemical's fate and disposition. Once the major toxicokinetic factors governing chemical fate are known, then the approaches that follow can be evaluated for utility and feasibility. Use of surrogate chemicals typically therapeutic agents ; for which pharmacokinetic data in children exist. Even if the target chemical s ; has not been evaluated in children, a chemical that is similarly processed may have been tested. Information for surrogate chemicals can help delineate the maturation of key pathways and how the target chemical will be handled at certain developmental stages. This section describes the kinds of data sets and resources available for this part of the phase II assessment. Over the past several years children's pharmacokinetic databases have been developed in which therapeutic drugs tested in both children and adults are identified and key pharmacokinetic parameters are compared across ages Ginsberg et al. 2002; Renwick 1998; Renwick et al. 2000 ; . The metabolism and clearance pathways of many of the drugs are known, making them useful indicators for particular pathways. For example, dextromethorphan and debrisoquine are known substrates for a particular cytochrome P450 CYP ; enzyme, CYP2D6; trimethadione, chlorzoxazone, and halothane are markers for CYP2E1 activity; morphine is predominantly processed by glucuronidation; and a host of antibiotics are not extensively metabolized but are mostly excreted unchanged by the kidneys Bertz and Granneman 1997; Dollery 2000; Kurata et al. 1998; Tanaka 1998 ; . A well-known example of childadult differences in metabolic processing is caffeine, a process in which an initial N-demethylation reaction is catalyzed by CYP1A2, and a secondary N-acetylation step is catalyzed by N-acetyltransferase Welfare et al. 2000 ; . The CYP1A2 reaction is the primary factor governing the half-life of this drug. Caffeine's half-life in newborns is 14-fold higher than in adults, which is likely the result of the immaturity of CYP1A2 at this age Dorne et al. 2001; Ginsberg et al. 2002; Parsons et al. 1976; Parsons and Neims 1978 ; . The metabolic clearance of caffeine and another CYP1A2 substrate, theophylline, becomes more like the adult rate by 26 months of age, after which time the half-life becomes significantly shorter than in that in adults Dorne et al. 2001; Ginsberg et al. 2002 ; . This suggests that once CYP1A2 function approaches adult levels, the greater size and blood flow to the liver per body weight ; in young children can lead to greater enzymatic clearance of CYP substrates Gibbs et al. 1997 ; . However, this also means that chemicals activated to toxicants by this pathway [e.g., aromatic amines, polycyclic aromatic hydrocarbons PAHs ; , aflatoxin B1] may produce more active metabolite in this age.
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Cal and retinal neuron responses to dextromethorphan may be related to differences in type and distribution of receptors in the cells within these two areas of the central nervous system. Some neuronal subpopulations have heightened vulnerability to excitatory amino acids.30-31 Sensitivity to excitatory amino acids also changes during development32'33 and may explain why dextromethorphan did not protect our cultured newborn rat neurons, whereas it was effective in the retinas of adult rabbits subjected to hypoxia.28 In conclusion, the results of our study show that MK-801 was very effective in protecting rat retinal neurons from hypoxic damage and from the toxicity of exogenous L-glutamic acid and N-methyl-D-aspartic acid. These data support the hypothesis that synaptically released neurotransmitters, most likely glutamate or aspartate, are responsible for hypoxic retinal neuron damage. Compounds related to MK-801 may prove therapeutically beneficial in protecting the human retina from hypoxic or ischemic insult in conditions such as central retinal artery or vein occlusion and diabetic retinopathy and dihydroergotamine.
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FIGURE 4. The original image, the NNE image, the significance image and the 3 s.d. masked image are shown for a single axial section of the cortex for a subject with Alzheimer's disease.
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The traditional view of migraine as being an episodic pain disorder is being supplanted by a disease model where migraine is considered a chronic disease with episodic manifestations.
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