Drugs online research references
Int J Fertil Womens Med. 2001 Jul-Aug;46(4):228-31.
Intermittent versus continuous sertraline therapy in the treatment of premenstrual dysphoric disorders.
Alpay FB, Turhan NO.
Department of Psychiatry, Fatih University, School of Medicine, Ankara, Turkey.
OBJECTIVE: Premenstrual dysphoric disorder (PMDD) is a combination of mood disturbances and physical symptoms that reduce the quality of individual life and the functionality of the individual. Many women do not consider the complaints arising in the luteal phase of the menstrual cycle as a psychiatric disorder and, thus, do not seek treatment. Those who take their complaints to doctors usually apply to gynecology clinics. The aim of the present study is to analyze the psychiatric disorders observed in patients with PMDD and to compare the continuous and intermittent administration of sertraline. MATERIALS AND METHODS: PMDD was investigated in the patients admitted to the Gynecology Clinic of the Medical School of Fatih University. The patients were asked to fill out forms designed in accordance with PMDD diagnosis criteria as defined in DSM IV. RESULTS: Among the 267 patients who filled out the forms, 162 (60.7%) were PMDD positive. Of the PMDD-positive patients, 133 accepted a psychiatric interview; 36 (27%) of them had depression, obsessive-compulsive disorder, anxiety and somatoform disorders as an accompanying disorder. Out of 162 PMDD-positive patients 94 accepted medical treatment; 71 patients were given sertraline on a continuous basis, and 23 patients took sertraline intermittently in the luteal phase of the cycle. Because of side effects, 44 (62%) of the continuous therapy and 22 (96%) of the intermittent therapy group stopped medication. At the end of 6-month follow-up, continuous use of sertraline was found to be significantly more tolerated than intermittent therapy in the treatment of PMDD (chi2 = 7.88, p = 0.005). CONCLUSION: In patients with the symptoms of PMDD, psychiatric evaluation should be encouraged by gynecology clinics, and continuous administration of sertraline should be the choice because of patients' greater acceptance of the therapy.
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Drug Metab Dispos. 1999 Jul;27(7):763-6.
Sertraline N-demethylation is catalyzed by multiple isoforms of human cytochrome P-450 in vitro.
Kobayashi K, Ishizuka T, Shimada N, Yoshimura Y, Kamijima K, Chiba K.
Laboratory of Biochemical Pharmacology and Toxicology Faculty of Pharmaceutical Sciences Chiba University, Chiba, Japan.
Sertraline, a new antidepressant of the selective serotonin reuptake inhibitor class, is extensively metabolized to desmethylsertraline in humans. We identified the cytochrome P-450 (CYP) isoforms involved in sertraline N-demethylation using pooled human liver microsomes and cDNA-expressed CYP isoforms. Eadie-Hofstee plots for the sertraline N-demethylation in human liver microsomes were monophasic. The estimated Michaelis-Menten kinetic parameters were: KM = 18.1 +/- 2.0 microM, Vmax = 0.45 +/- 0.03 nmol/min/mg of protein, and Vmax/KM = 25.2 +/- 4.3 microl/min/mg of protein. At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal. The anti-CYP2B6 antibody inhibited the sertraline N-demethylation activities by 35%. Sertraline N-demethylation activities were detected in all cDNA-expressed CYP isoforms studied. In particular, CYP2C19, CYP2B6, CYP2C9-Arg, CYP2D6-Val, and CYP3A4 all showed relatively high activity. When the contributions of CYP2D6, CYP2C9, CYP2B6, CYP2C19, and CYP3A4 were estimated from the Vmax/KM of cDNA-expressed CYP isoforms and from their contents in pooled human liver microsomes, the values were found to be 35, 29, 14, 13, and 9%, respectively. The results suggest that at least five isoforms of CYP (CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP3A4) are involved in the sertraline N-demethylation in human liver microsomes and that the contribution of any individual isoform does not exceed 40% of overall metabolism. Therefore, concurrent administration of a drug that inhibits a specific CYP isoform is unlikely to cause a marked increase in the plasma concentration of sertraline.
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yale.edu
OBJECTIVE: Pharmacological treatment of postpartum depression is frequently complicated by the mother's desire to breast-feed. Although breast milk levels of several selective serotonin reuptake inhibitors (SSRIs) have been reported to be relatively low, a critical question is whether SSRI exposure during nursing results in clinically significant blockade of serotonin (5-HT) reuptake in infants. This study determined the degree of transporter blockade in infants exposed to sertraline through maternal breast milk. METHOD: The extent of maternal and infant transporter blockade was assessed by measurement of platelet levels of 5-HT in 14 breast-feeding mother-infant pairs before and after 6-16 weeks of maternal treatment with sertraline for major depression with postpartum onset. Plasma sertraline and desmethylsertraline levels were obtained in 13 of these mothers and 11 of their infants. RESULTS: Marked declines in platelet 5-HT levels of 70%-96% were observed in mothers after sertraline treatment, 25-200 mg/day. In contrast, infants showed little or no change in platelet 5-HT levels after exposure through breast-feeding. Mean levels of maternal plasma sertraline and its major metabolite, desmethylsertraline, were 30.7 ng/ml and 45.3 ng/ml, respectively. Drug and drug metabolite concentrations in the infants were at or below the lower limit of quantitation. CONCLUSIONS: The data indicate that while mothers receiving clinical doses of sertraline experience substantial blockade of the platelet 5-HT transporter, platelet 5-HT uptake in nursing infants of treated mothers is unaltered. The observations suggest that mothers taking sertraline can breast-feed without appreciably affecting peripheral or central 5-HT transport in their infants.
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