Higher than normal plasma IL-6 concentrations were associated with a diagnosis of major depression in cancer patients. IL-6 may contribute to sickness behavior that has overlapping symptoms with major depression.
No consensus has yet been reached as to whether or not postpartum depression (PPD) represents a distinct clinical entity. Despite the increasing evidence that gender differences may exist in antidepressant treatment response, there is an absence of studies in women with postpartum onset of major depression. The aim of this study was to assess the clinical efficacy of the selective serotonin reuptake inhibitor (SSRI), sertraline, in the treatment of women with a major depressive episode (MDE) that occurred within 6 months of childbirth using an 8 week, prospective, open‐labelled design. Further, we sought to determine if the Edinburgh Postnatal Depression Scale (EPDS) was a useful instrument to monitor the clinical response to drug treatment. Twenty‐six postpartum women who fulfilled DSM‐IIIR criteria for major depressive episode, non‐psychotic, with symptom onset within 6 months postpartum were enrolled in the study. Biweekly assessments included physician and self‐rated depression measures. Twenty‐one of the women (81%) completed the 8 week study; 20 women exhibited a salutary response as defined by > 50% reduction from baseline in SIGH‐D scores (mean reduction = 15.7 points). Fourteen women demonstrated complete symptom remission with recovery of function (SIGH‐D < 7, CGI = 1, GAP > 80) upon completion of the 8 week study. Three women experienced significant side effects; these included gastrointestinal disturbance (n =1) and anorgasmia (n = 2). Our results indicate that: (1) sertraline is a highly efficacious and well‐tolerated treatment for women with postpartum depression; (2) the EPDS is comparable to the BDI and SIGH‐D for monitoring treatment response in women with postpartum onset MDE; (3) PPD (MDE onset within 4 weeks postpartum, as defined by DSM IV) required significantly less medication and tended to respond faster than MDE onset after 4 weeks postpartum; and (4) the rapid response rate underscores the need to conduct placebo‐controlled studies in this population. Depression 3:49–55 (1995). © 1995 Wiley‐Liss, Inc.
Objective: The purpose of this study was to determine the concentrations of sertraline and desmethylsertraline in both human breast milk and infant serum. Method: Breast milk samples from 12 women were collected at specific time intervals after oral doses of sertraline P regnancy and childbirth represent a period of unique neuroendocrine and psychosocial adjustment during which up to 10% of women meet criteria for major depression. Comprehensive reviews of the management of major depression during pregnancy and lactation focus predominantly on pregnancy (1-5). However, the increasing number of nursing mothers (6) and the numerous professional groups that support breast milk as the ideal form of infant nutrition underscore the need to conduct definitive studies of the transmission of antidepressants to infants during lactation. In a review of the available breast-feeding data, Wisner and colleagues (7) demonstrated the limited quantity of meaningful data.Medications enter breast milk primarily by passive diffusion of the free fraction (8), while specific physiochemical properties of a drug appear to be the best predictor of drug concentrations present in breast milk (9). These properties include: 1) degree of ionization, which is a function of the pKa, 2) molecular weight, 3) blood protein binding, and 4) lipid solubility. The pH gradient between maternal serum and breast milk is a major determinant of the quantity of drug excreted into the milk.Neonatal physiology exhibits unique characteristics that may result in increased circulating drug concentrations after oral dosing relative to that in older individuals. Hepatic maturation in the infant appears to occur at a highly variable rate (10) and is even more delayed in premature infants. Both glucuronidation and oxidative systems are immature at birth (as low as 20% of adult levels); the latter system typically matures by 3
Considerable evidence obtained from neuroanatomical and neurochemical studies suggests an interaction between the endogenous tridecapeptide neurotensin (NT) and central nervous system dopamine (DA) neurons. Centrally administered NT blocks many of the actions of synaptic DA in limbic brain areas; the specific mechanism and receptors involved remain under investigation. The electrophysiological effects of NT were studied using extracellular recording techniques and iontophoretic application in 243 spontaneously active neurons in the nucleus accumbens (NAc), with a positive/negative waveform. NT was directly applied to 208 neurons in a pulsatile fashion by iontophoresis (21+/-1 nA). NT had no effect on the firing rate of 120 neurons ((0.31+/-0.72)%), decreased the firing rate in 51 neurons ((-27.87+/-1.52)%), and increased the firing rates of 37 neurons ((33.38+/-2.6)%). One hundred ninety nine (81.9%) of the neurons studied were sensitive to iontophoretically applied DA (>15% decrease in firing rate). The effects of continuous NT application on DA-induced inhibitions were studied in 169 neurons. NT attenuated neuronal responses to directly applied DA by (49.95+/-4.52)%, with antagonism in the "core" subregion (n=96) of (33.41+/-7.75)% when compared with antagonism in the "shell" subregion (n=71) of (61.39+/-5.2)%. The effects of NT on DA were consistent and independent of the effects of NT alone. These data provide further evidence that NT functions as a true neuromodulator in the NAc, exerting minimal direct effects, but blocking the actions of DA.
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