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Association analysis between variants of the interleukin-1β and the interleukin-1 receptor antagonist gene and antidepressant treatment response in major depression
André Tadic,Dan Rujescu,Matthias J Müller,Ralf Kohnen
Neuropsychiatric Disease and Treatment , 2008,
Abstract: André Tadic1, Dan Rujescu2, Matthias J Müller3, Ralf Kohnen4, Hans H. Stassen5, Armin Szegedi6, Norbert Dahmen11Department of Psychiatry, University of Mainz, Germany; 2Department of Psychiatry, University of Munich, Germany; 3Clinic for Psychiatry and Psychotherapy, Marburg-Sued, Germany, and Clinic for Psychiatry and Psychotherapy, Giessen, Germany; 4IMEREM, Nuernberg, Germany; 5Department of Psychiatry, University of Zurich, Switzerland; 6Organon, Roseland, NJ, USAAbstract: This study investigated the possible association of the interleukin-1 beta (IL-1β) C-511T promoter polymorphism and the interleukin-1 receptor antagonist (IL-1Ra) (86bp)n variable number of tandem repeats (VNTR) polymorphism with antidepressant response to paroxetine and mirtazapine treatment. The study group consisted of 101 patients suffering from DSM-IV major depression participating in a randomized double-blind controlled clinical trial. Patients homozygous for the IL-1β-511T allele had a significantly faster and more pronounced response to paroxetine treatment than IL-1β-511C allele carriers. No association was found for the IL-1β C-511T polymorphism with mirtazapine treatment response. The IL-1Ra VNTR showed neither an association with paroxetine nor with mirtazapine treatment response. Our results provide further suggestive evidence that time course of response and antidepressant efficacy of paroxetine, but not of mirtazapine, is influenced in a clinically relevant manner by the IL-1β C-511T gene variant. Our data do not support the hypothesis that the IL-1Ra (86bp)n VNTR affects antidepressant treatment response to paroxetine or mirtazapine. An independent replication of our finding is needed. If replicated, the IL-1β C-511T promoter polymorphism could be considered useful for prospective confirmatory pharmacogenetic trials in patients with major depression.Keywords: major depression, antidepressive agents, treatment outcome, interleukin-1 beta, interleukin-1 receptor antagonist, genetic polymorphisms
Interleukin-1B and Interleukin-1 Receptor Antagonist in Patients with Helicobacter pylori Associated Diseases  [PDF]
Olga V. Shtygasheva, PhD, ScD,Elizaveta S. Ageeva, PhD
International Journal of BioMedicine , 2012,
Abstract: The ethnic people of the Republic of Khakassia (the Khakas) with ulcer disease show a significant T-cell activation and humoral immune response when compared with the Europoids. The reasons for such differences could be due to certain ethno-specific allelic variants of the interleukins, which considerably change the degree of cytokine expression. The aim was to study the peculiarities of the association of the interleukin-1 (IL-1) gene polymorphisms and interleukin-1 receptor antagonist (IL-1Ra). Patients with chronic gastritis and ulcer disease were examined using the restriction analysis method. The most wide-spread allelic variants among the Khakas were discovered to be СС IL-1β and R4R4 IL-1Ra. In this study, we suggest the necessity to define the population’s risk and the protective genotypes that promote Helicobacter pylori-associated ulcer disease among the Khakas people.
Mice Lacking NMDA Receptors in Parvalbumin Neurons Display Normal Depression-Related Behavior and Response to Antidepressant Action of NMDAR Antagonists  [PDF]
Laura Pozzi, Iskra Pollak Dorocic, Xinming Wang, Marie Carlén, Konstantinos Meletis
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0083879
Abstract: The underlying circuit imbalance in major depression remains unknown and current therapies remain inadequate for a large group of patients. Discovery of the rapid antidepressant effects of ketamine - an NMDA receptor (NMDAR) antagonist – has linked the glutamatergic system to depression. Interestingly, dysfunction in the inhibitory GABAergic system has also been proposed to underlie depression and deficits linked to GABAergic neurons have been found with human imaging and in post-mortem material from depressed patients. Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit function through perisomatic inhibition and their activity is NMDAR-dependent, providing a possible link between NMDAR and the inhibitory system in the antidepressant effect of ketamine. We have therefore investigated the role of the NMDAR-dependent activity of PV interneurons for the development of depression-like behavior as well as for the response to rapid antidepressant effects of NMDAR antagonists. We used mutant mice lacking NMDA neurotransmission specifically in PV neurons (PV-Cre+/NR1f/f) and analyzed depression-like behavior and anhedonia. To study the acute and sustained effects of a single NMDAR antagonist administration, we established a behavioral paradigm of repeated exposure to forced swimming test (FST). We did not observe altered behavioral responses in the repeated FST or in a sucrose preference test in mutant mice. In addition, the behavioral response to administration of NMDAR antagonists was not significantly altered in mutant PV-Cre+/NR1f/f mice. Our results show that NMDA-dependent neurotransmission in PV neurons is not necessary to regulate depression-like behaviors, and in addition that NMDARs on PV neurons are not a direct target for the NMDAR-induced antidepressant effects of ketamine and MK801.
Antidepressant-Resistant Depression and Antidepressant-Associated Suicidal Behaviour: The Role of Underlying Bipolarity  [PDF]
Zoltan Rihmer,Xenia Gonda
Depression Research and Treatment , 2011, DOI: 10.1155/2011/906462
Abstract: The complex relationship between the use of antidepressants and suicidal behaviour is one of the hottest topics of our contemporary psychiatry. Based on the literature, this paper summarizes the author's view on antidepressant-resistant depression and antidepressant-associated suicidal behaviour. Antidepressant-resistance, antidepressant-induced worsening of depression, antidepressant-associated (hypo)manic switches, mixed depressive episode, and antidepressant-associated suicidality among depressed patients are relatively most frequent in bipolar/bipolar spectrum depression and in children and adolescents. As early age at onset of major depressive episode and mixed depression are powerful clinical markers of bipolarity and the manic component of bipolar disorder (and possible its biological background) shows a declining tendency with age antidepressant-resistance/worsening, antidepressant-induced (hypo)manic switches and “suicide-inducing” potential of antidepressants seem to be related to the underlying bipolarity. 1. Introduction Treatment-resistant and particularly antidepressant-resistant major depression (AD-RD) is a great clinical challenge both in the cases of unipolar and bipolar depression [1, 2]. While it is well documented that the optimal clinical response to antidepressants is much rare in bipolar I and II than in unipolar major depression [3–5] only the most recent clinical studies have focused on the boundaries between treatment-resistant unipolar major depressive disorder and bipolar disorder. These studies seem to be more promising in understanding both antidepressant-resistance and antidepressant-associated suicidal behaviour in patients with major mood disorders. 2. Antidepressant Resistance in Major Depressive Episode: Its Relationship with Bipolar Disorder The generally accepted definition of AD-RD refers that the depressed patient does not show a clinically significant response after at least two adequate trials of different classes of antidepressants. In spite of the fact that there are several causes of AD-RD in general [1, 6], one of the most common sources of it is the unrecognized bipolar nature of the “unipolar” major depressive disorder, when the patients receive antidepressant monotherapy—unprotected by mood stabilizers/atypical antipsychotics [4–11]. Unrecognized bipolar depressives are generally treated as “unipolar” major depressives which means that these patients do not receive mood stabilizers [3, 12]. This can result in a very high rate of treatment resistance, which is about two-times higher than in patients with
Antidepressant Treatment for Acute Bipolar Depression: An Update  [PDF]
Ben H. Amit,Abraham Weizman
Depression Research and Treatment , 2012, DOI: 10.1155/2012/684725
Abstract: While studies in the past have focused more on treatment of the manic phase of bipolar disorder (BD), recent findings demonstrate the depressive phase to be at least as debilitating. However, in contrast to unipolar depression, depression in bipolar patients exhibits a varying response to antidepressants, raising questions regarding their efficacy and tolerability. Methods. We conducted a MEDLINE and Cochrane Collaboration Library search for papers published between 2005 and 2011 on the subject of antidepressant treatment of bipolar depression. Sixty-eight articles were included in the present review. Results. While a few studies did advocate the use of antidepressants, most well-controlled studies failed to show a robust effect of antidepressants in bipolar depression, regardless of antidepressant class or bipolar subtype. There was no significant increase in the rate of manic/hypomanic switch, especially with concurrent use of mood stabilizers. Prescribing guidelines published in recent years rely more on atypical antipsychotics, especially quetiapine, as a first-line therapy. Conclusions. Antidepressants probably have no substantial role in acute bipolar depression. However, in light of conflicting results between studies, more well-designed trials are warranted. 1. Introduction Bipolar disorder (BD) is a devastating illness, carrying an immense burden of both morbidity [1] and all-cause mortality [2], including high rates of completed suicide [3]. With a lifetime prevalence of 1.5–2% in Europe [4] and a similar prevalence in the USA [5], much attention has been drawn to assessing potential treatments for alleviating the symptoms of this condition, manic and depressive alike. However, while clinical focus in the past tended to be more on the manic phase of the disorder, recent findings illustrate the need to focus on effective treatment strategies for the depressive phase, for several reasons. First, observations of the natural course of BD show the considerable amount of time spent in the depressive phase compared to the manic phase (30% on average compared to 10% in bipolar 1 disorder) [6], leading to severe morbidity, including a marked occupational impairment [7]. Second, the depressive phase of BD is more prone to suicide [8]. Incomplete remission, with enduring subsyndromal depressive symptoms, has been demonstrated both to cause functional impairment [9] and increase the risk of relapse [10], emphasizing the importance of optimizing the treatment for the depressive phase of BD. Since their conception, antidepressants have been the mainstay of
Interleukin Expression after Injury and the Effects of Interleukin-1 Receptor Antagonist  [PDF]
Connie S. Chamberlain, Ellen M. Leiferman, Kayt E. Frisch, Stacey L. Brickson, William L. Murphy, Geoffrey S. Baer, Ray Vanderby
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071631
Abstract: Ligament healing follows a series of complex coordinated events involving various cell types, cytokines, as well as other factors, producing a mechanically inferior tissue more scar-like than native tissue. Macrophages provide an ongoing source of cytokines to modulate inflammatory cell adhesion and migration as well as fibroblast proliferation. Studying interleukins inherent to ligament healing during peak macrophage activation and angiogenesis may elucidate inflammatory mediators involved in subsequent scar formation. Herein, we used a rat healing model assayed after surgical transection of their medial collateral ligaments (MCLs). On days 3 and 7 post-injury, ligaments were collected and used for microarray analysis. Of the 12 significantly modified interleukins, components of the interleukin-1 family were significantly up-regulated. We therefore examined the influence of interleukin-1 receptor antagonist (IL-1Ra) on MCL healing. Transected rat MCLs received PBS or IL-1Ra at the time of surgery. Inhibition of IL-1 activation decreased pro-inflammatory cytokines (IL-1α, IL-1β, IL-12, IL-2, and IFN-γ), myofibroblasts, and proliferating cells, as well as increased anti-inflammatory cytokines (IL-10), endothelial cells/blood vessel lumen, M2 macrophages, and granulation tissue size without compromising the mechanical properties. These results support the concept that IL-1Ra modulates MCL-localized granulation tissue components and cytokine production to create a transient environment that is less inflammatory. Overall, IL-1Ra may have therapeutic potential early in the healing cascade by stimulating the M2 macrophages and altering the granulation tissue components. However, the single dose of IL-1Ra used in this study was insufficient to maintain the more regenerative early response. Due to the transient influence on most of the healing components tested, IL-1Ra may have greater therapeutic potential with sustained delivery.
Persistence and compliance to antidepressant treatment in patients with depression: A chart review
Norifusa Sawada, Hiroyuki Uchida, Takefumi Suzuki, Koichiro Watanabe, Toshiaki Kikuchi, Takashi Handa, Haruo Kashima
BMC Psychiatry , 2009, DOI: 10.1186/1471-244x-9-38
Abstract: In this retrospective chart-review, 6-month adherence to antidepressants was examined in 367 outpatients with a major depressive disorder (ICD-10) (170 males; mean ± SD age 37.6 ± 13.9 years), who started antidepressant treatment from April 2006 through March 2007. Additionally, we evaluated Medication Possession Rate (MPR), defined as the total days a medication was dispensed to patients divided by the treatment period.Only 161 patients (44.3%) continued antidepressant treatment for 6 months. Among 252 patients who discontinued their initial antidepressant, 63.1% of these patients did so without consulting their physicians. Sertraline use was associated with a higher persistence rate at month 6 (odds ratio 2.59 in comparison with sulpiride), and the use of anxiolytic benzodiazepines had a positive effect on persistence to antidepressant treatment only at month 1 (odds ratio 2.14). An overall MPR was 0.77; 55.6% of patients were considered compliant (i.e., a MPR of ≥ 0.8).Given a high rate of antidepressant discontinuation without consulting their physicians, closer communication between patients and their physicians should be encouraged. Although the use of anxiolytic benzodiazepines was associated with a higher persistence to antidepressant treatment at month 1, the use of these drugs should be avoided as a rule, given their well-known serious adverse effects.While antidepressants have played an important role in the treatment of depression, good adherence to medications is prerequisite to maintain those therapeutic benefits. Despite this self-evident fact, the available evidence has generally shown low adherence rates to antidepressant treatment in patients with a major depressive disorder [1-3]. For example, the adherence rate was found to be 51% at week 16 and further dropped to 21% at week 33 in a sample of 4,312 privately insured outpatients in the US [1]. Similarly, the Vantaa Depression Study showed a one-year continuation rate as low as 50% in Finland (n =
Antidepressant and Neurocognitive Effects of Isoflurane Anesthesia versus Electroconvulsive Therapy in Refractory Depression  [PDF]
Howard R. Weeks, Scott C. Tadler, Kelly W. Smith, Eli Iacob, Mikala Saccoman, Andrea T. White, Joshua D. Landvatter, Gordon J. Chelune, Yana Suchy, Elaine Clark, Michael K. Cahalan, Lowry Bushnell, Derek Sakata, Alan R. Light, Kathleen C. Light
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0069809
Abstract: Background Many patients have serious depression that is nonresponsive to medications, but refuse electroconvulsive therapy (ECT). Early research suggested that isoflurane anesthesia may be an effective alternative to ECT. Subsequent studies altered drug, dose or number of treatments, and failed to replicate this success, halting research on isoflurane's antidepressant effects for a decade. Our aim was to re-examine whether isoflurane has antidepressant effects comparable to ECT, with less adverse effects on cognition. Method Patients with medication-refractory depression received an average of 10 treatments of bifrontal ECT (n = 20) or isoflurane (n = 8) over 3 weeks. Depression severity (Hamilton Rating Scale for Depression-24) and neurocognitive responses (anterograde and retrograde memory, processing speed and verbal fluency) were assessed at Pretreatment, Post all treatments and 4-week Follow-up. Results Both treatments produced significant reductions in depression scores at Post-treatment and 4-week Follow-up; however, ECT had modestly better antidepressant effect at follow-up in severity-matched patients. Immediately Post-treatment, ECT (but not isoflurane) patients showed declines in memory, fluency, and processing speed. At Follow-up, only autobiographical memory remained below Pretreatment level for ECT patients, but isoflurane patients had greater test-retest neurocognitive score improvement. Conclusions Our data reconfirm that isoflurane has an antidepressant effect approaching ECT with less adverse neurocognitive effects, and reinforce the need for a larger clinical trial.
The safety of interleukin-1 receptor antagonist (anakinra) in the treatment of rheumatoid arthritis  [cached]
L. Riente
Reumatismo , 2011, DOI: 10.4081/reumatismo.2004.1s.74
Abstract: The safety profile of interleukin-1 receptor antagonist (anakinra) has been studied with randomised, placebo-controlled trials involving 2932 patients affected by rheumatoid arthritis. The most frequently reported adverse events were represented by injection site reactions (71%) and headache (13.6%). No statistically significant difference in the incidence of infections was observed among the patients treated with the interleukin-1 receptor antagonist and the patients receiving placebo. In particular, the incidence of serious infections was 1,8% in rheumatoid arthritis patients on anakinra therapy and 0,7% in patients on placebo. The reported serious infections consisted of pneumonia, cellulitis, bone and joint infections, bursitis. No case of opportunistic infections or tubercolosis was observed. The results of clinical studies suggest that anakinra is a new well-tolerated drug for the treatment of patients affected by rheumatoid arthritis.
Melatoninergic Antidepressant in Post-Stroke Depression Therapy  [PDF]
Victor V. Kuznetsov
Advances in Aging Research (AAR) , 2018, DOI: 10.4236/aar.2018.72003
Abstract: This paper presents the results of the effects of Melitor (25 mg during two months) on the psychic-emotional state, cerebral hemodynamic and bioelectrical activity of the brain in 30 patients (average age 66.2 ± 3.2 years) with ischemic post-stroke depression. It has been found that this drug possesses a multimodal action which is characterized by the decrease of the level of depression, widening of the range of social-environmental activity, improvement of the cerebral blood circulation and harmonization of the brain electrogenesis. In the patients with right versus left hemisphere stroke, the effect of Melitor on the functional state of the brain was more pronounced. Based on the results obtained in our study, we can recommend Melitor to use it in complex scheme of rehabilitation care of patients of the given nosological category.
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