DOCSLIB.ORG

Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections J Neuroimmune Pharmacol (2011) 6:442–465 DOI 10.1007/s11481-011-9292-5 INVITED REVIEW Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections Sabita Roy & Jana Ninkovic & Santanu Banerjee & Richard Gene Charboneau & Subhas Das & Raini Dutta & Varvara A. Kirchner & Lisa Koodie & Jing Ma & Jingjing Meng & Roderick A. Barke Received: 26 May 2011 /Accepted: 27 June 2011 /Published online: 26 July 2011 # Springer Science+Business Media, LLC 2011 Abstract Infection rate among intravenous drug users opioid withdrawal. Data on bacterial virulence in the (IDU) is higher than the general public, and is the major context of opioid withdrawal suggest that mice undergoing cause of morbidity and hospitalization in the IDU popula- withdrawal had shortened survival and increased bacterial tion. Epidemiologic studies provide data on increased load in response to Salmonella infection. As the body of prevalence of opportunistic bacterial infections such as TB evidence in support of opioid dependency and its immuno- and pneumonia, and viral infections such as HIV-1 and suppressive effects is growing, it is imperative to under- hepatitis in the IDU population. An important component in stand the mechanisms by which opioids exert these effects the intravenous drug abuse population and in patients and identify the populations at risk that would benefit the receiving medically indicated chronic opioid treatment is most from the interventions to counteract opioid immuno- suppressive effects. Thus, it is important to refine the : : : : : existing animal model to closely match human conditions S. Roy J. Ninkovic S. Banerjee S. Das R. Dutta and to cross-validate these findings through carefully V. A. Kirchner : J. Ma : R. A. Barke Department of Surgery, University of Minnesota, controlled human studies. Better understanding of the Minneapolis, MN 55455, USA mechanisms will facilitate the search for new therapeutic : modalities to counteract adverse effects including increased S. Roy J. Meng infection rates. This review will summarize the effects of Department of Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA morphine on innate and adaptive immunity, identify the role : of the mu opioid receptor in these functions and the signal R. G. Charboneau R. A. Barke transduction activated in the process. The role of opioid Department of Surgery, Veterans Affairs Medical Center, withdrawal in immunosuppression and the clinical rele- Minneapolis, MN 55417, USA vance of these findings will also be discussed. L. Koodie School of Dentistry, University of Minnesota, Keywords Opioid drug abuse . Morphine . Immune Minneapolis, MN 55455, USA function . Opportunistic infections S. Roy (*) Division of Infection, Inflammation and Vascular Biology, University of Minnesota, Introduction MMC 195, 420 Delaware Street SE, Minneapolis, MN 55455, USA e-mail: [email protected] The status of the immune system generally dictates the outcome following microbial infection in an organism. S. Roy Invasion of a host by pathogenic infectious agents initiates Department of Surgery and Pharmacology, a sequence of immune responses through interactions University of Minnesota, 11-204 Moos Tower, MMC 195, 420 Delaware Street SE, between a diverse array of pathogen-borne virulence factors Minneapolis, MN 55455, USA and the immune surveillance mechanisms of the host. In J Neuroimmune Pharmacol (2011) 6:442–465 443 human infections, the integrity of the host immune system and only partially dependent on sympathetic activation and an appropriate host response is crucial for pathogen (Peterson et al. 1987;Bryantetal.1991; Casellas et al. clearance. Primary immune deficiencies predispose to 1991; Perez-Castrillon et al. 1992). With the discovery of different infections, depending on the nature of the opioid receptors on leukocytes, research focus has shifted underlying immune defect. An inappropriate immune to direct effects of opioids on immune cells and will response may not only result in lack of protection, but therefore be the topic of discussion of this review. even contribute to disease severity. Chronic opioid use and In this section, we summarize seminal studies and abuse has been documented to severely compromise the current literature investigating how morphine directly immune system and thereby, increase the risk of opportu- inhibits the innate immune system by modulating macro- nistic infection (Roy and Loh 1996; Roy et al. 2006; phage, neutrophil, dendritic, mast and natural killer cell Friedman and Eisenstein 2004; Dinda et al. 2005). This is function. supported by epidemiological studies showing increased prevalence of opportunistic infections such as tuberculosis, Macrophage HIV infection and pneumonia in opioid addicts (Georges et al. 1999;Nathetal.2002; Quaglio et al. 2002). Macrophages are one of the first lines of innate immune Confounding variables such as sharing of unsterilized, defense against invading pathogens. They play an essen- contaminated needles, nutritional status, environment tial role in pathogen clearance through their phagocytic, influences, history of drug use and genetic variability can chemotactic and bactericidal actions. Therefore, any contribute to the frequency of infections in these patients, defects in macrophage function can be detrimental for however, epidemiological studies suggest that the immune the host. Macrophages have been at the center of many modulating effects of morphine abuse to be a major factor studies examining morphine mediated immune suppres- in disease prevalence (Georges et al. 1999;Nathetal. sion and the significant role they play as the key factors in 2002; Quaglio et al. 2002). Furthermore, in animal studies the innate immune system. Opioid inhibition of the innate where these variables can be controlled, morphine treat- immune system has been observed at several levels. ment (used as a surrogate for heroin which is rapidly Morphine treatment has been implicated in the inhibition converted to morphine following first pass metabolism) of cytokine secretion, leukocyte recruitment and bacterial results in significant immune detriment with increased clearance. By decreasing the proliferative capacity of susceptibility to opportunistic infections (Roy and Loh 1996; macrophage progenitor cells and lymphocytes, morphine Roy et al. 2006). Defense against microbes is mediated by treatment reduces the number of macrophages that are the early reactions of innate immunity and the later response available to respond to infection (Roy et al. 2006) thereby of adaptive immunity. Chronic morphine abuse has been compromising the host’s ability to fight off invading shown to affect both arms of immune defense (Vallejo et al. pathogens. Furthermore, morphine treatment has been also 2004). This review will summarize the effects of chronic and shown to directly inhibit macrophages’ ability to ingest acute morphine on innate and adaptive immunity, identify the opsonized pathogens (Casellas et al. 1991; Szabo et al. role of the mu opioid receptor and the signal transduction 1993; Tomei and Renaud 1997). activated in the process. The role of opioid withdrawal in Initial opioid induced immunosuppression studies inves- immunosupression and the clinical relevance of these tigated the role of endogenous opioids such as leucine (leu) findings will also be discussed. or methionine (met) enkephalin. It was observed that in vitro administration of endogenous opioid peptides such as leu- and met-enkephalin resulted in inhibition of phagocy- Morphine modulation of innate immune function tosis by murine macrophages of opsonized sheep red blood cells (Casellas et al. 1991). When the field expanded to Studies supporting a direct role for opioids on immune examine the role of exogenous opioids in this process, system modulation emerged with the discovery of opioid findings showed that morphine treatment also led to receptors on immune cells. The concept of direct and indirect inhibition of macrophage function. Murine peritoneal morphine action was first introduced through work with macrophages undergoing morphine treatment exhibited morphine dependent rodents. Extensive body of literature suppression of phagocytosis, respiratory burst activity now supports that morphine-induced immunosuppression is (Menzebach et al. 2004) while in human monocytes mediated primarily by the mu opioid receptor (MOR), morphine has been implicated to inhibit and chemotaxis although some functions are amplified following sympathetic (Perez-Castrillon et al. 1992). By preventing bacterial activation or in the presence of corticosterone (CORT). The internalization morphine leads to inadequate bacterial inhibition of IFN-gamma synthesis and activation of clearance. Furthermore, through inhibition of respiratory macrophage-cytokine synthesis is CORT-independent burst activity, morphine attenuates bacterial killing which 444 J Neuroimmune Pharmacol (2011) 6:442–465 together with diminished phagocytosis leads to increased et al., which examined respiratory burst activity in response to bacteremia and bacterial escape from latency in mice phorbol myristate acetate (PMA) (Peterson et al. 1987; (Bhaskaran et al. 2001; Wang et al. 2005; Lugo-Chinchilla Peterson et al. 1989). et al. 2006). Human studies and rodent models of drug Along with inhibition of bacterial clearance (Grimm et abuse indicate that morphine impairs the host’s ability to al. 1998a), morphine treatment leads to inhibition of eradicate infection by inhibiting
Load more

Recommended publications
  • ASAM National Practice Guideline for the Treatment of Opioid Use Disorder: 2020 Focused Update
    The ASAM NATIONAL The ASAM National Practice Guideline 2020 Focused Update Guideline 2020 Focused National Practice The ASAM PRACTICE GUIDELINE For the Treatment of Opioid Use Disorder 2020 Focused Update Adopted by the ASAM Board of Directors December 18, 2019. © Copyright 2020. American Society of Addiction Medicine, Inc. All rights reserved. Permission to make digital or hard copies of this work for personal or classroom use is granted without fee provided that copies are not made or distributed for commercial, advertising or promotional purposes, and that copies bear this notice and the full citation on the fi rst page. Republication, systematic reproduction, posting in electronic form on servers, redistribution to lists, or other uses of this material, require prior specifi c written permission or license from the Society. American Society of Addiction Medicine 11400 Rockville Pike, Suite 200 Rockville, MD 20852 Phone: (301) 656-3920 Fax (301) 656-3815 E-mail: [email protected] www.asam.org CLINICAL PRACTICE GUIDELINE The ASAM National Practice Guideline for the Treatment of Opioid Use Disorder: 2020 Focused Update 2020 Focused Update Guideline Committee members Kyle Kampman, MD, Chair (alpha order): Daniel Langleben, MD Chinazo Cunningham, MD, MS, FASAM Ben Nordstrom, MD, PhD Mark J. Edlund, MD, PhD David Oslin, MD Marc Fishman, MD, DFASAM George Woody, MD Adam J. Gordon, MD, MPH, FACP, DFASAM Tricia Wright, MD, MS Hendre´e E. Jones, PhD Stephen Wyatt, DO Kyle M. Kampman, MD, FASAM, Chair 2015 ASAM Quality Improvement Council (alpha order): Daniel Langleben, MD John Femino, MD, FASAM Marjorie Meyer, MD Margaret Jarvis, MD, FASAM, Chair Sandra Springer, MD, FASAM Margaret Kotz, DO, FASAM George Woody, MD Sandrine Pirard, MD, MPH, PhD Tricia E.
    [Show full text]
  • Opioids and Nicotine Dependence in Planarians
    Pharmacology, Biochemistry and Behavior 112 (2013) 9–14 Contents lists available at ScienceDirect Pharmacology, Biochemistry and Behavior journal homepage: www.elsevier.com/locate/pharmbiochembeh Opioid receptor types involved in the development of nicotine physical dependence in an invertebrate (Planaria)model Robert B. Raffa a,⁎, Steve Baron a,b, Jaspreet S. Bhandal a,b, Tevin Brown a,b,KevinSongb, Christopher S. Tallarida a,b, Scott M. Rawls b a Department of Pharmaceutical Sciences, Temple University School of Pharmacy, Philadelphia, PA, USA b Department of Pharmacology & Center for Substance Abuse Research, Temple University School of Medicine, Philadelphia, PA, USA article info abstract Article history: Recent data suggest that opioid receptors are involved in the development of nicotine physical dependence Received 18 May 2013 in mammals. Evidence in support of a similar involvement in an invertebrate (Planaria) is presented using Received in revised form 18 September 2013 the selective opioid receptor antagonist naloxone, and the more receptor subtype-selective antagonists CTAP Accepted 21 September 2013 (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH )(μ, MOR), naltrindole (δ, DOR), and nor-BNI (norbinaltorphimine) Available online 29 September 2013 2 (κ, KOR). Induction of physical dependence was achieved by 60-min pre-exposure of planarians to nicotine and was quantified by abstinence-induced withdrawal (reduction in spontaneous locomotor activity). Known MOR Keywords: Nicotine and DOR subtype-selective opioid receptor antagonists attenuated the withdrawal, as did the non-selective Abstinence antagonist naloxone, but a KOR subtype-selective antagonist did not. An involvement of MOR and DOR, but Withdrawal not KOR, in the development of nicotine physical dependence or in abstinence-induced withdrawal was thus Physical dependence demonstrated in a sensitive and facile invertebrate model.
    [Show full text]
  • Medications for Opioid Use Disorder for Healthcare and Addiction Professionals, Policymakers, Patients, and Families
    Medications for Opioid Use Disorder For Healthcare and Addiction Professionals, Policymakers, Patients, and Families UPDATED 2020 TREATMENT IMPROVEMENT PROTOCOL TIP 63 Please share your thoughts about this publication by completing a brief online survey at: https://www.surveymonkey.com/r/KAPPFS The survey takes about 7 minutes to complete and is anonymous. Your feedback will help SAMHSA develop future products. TIP 63 MEDICATIONS FOR OPIOID USE DISORDER Treatment Improvement Protocol 63 For Healthcare and Addiction Professionals, Policymakers, Patients, and Families This TIP reviews three Food and Drug Administration-approved medications for opioid use disorder treatment—methadone, naltrexone, and buprenorphine—and the other strategies and services needed to support people in recovery. TIP Navigation Executive Summary For healthcare and addiction professionals, policymakers, patients, and families Part 1: Introduction to Medications for Opioid Use Disorder Treatment For healthcare and addiction professionals, policymakers, patients, and families Part 2: Addressing Opioid Use Disorder in General Medical Settings For healthcare professionals Part 3: Pharmacotherapy for Opioid Use Disorder For healthcare professionals Part 4: Partnering Addiction Treatment Counselors With Clients and Healthcare Professionals For healthcare and addiction professionals Part 5: Resources Related to Medications for Opioid Use Disorder For healthcare and addiction professionals, policymakers, patients, and families MEDICATIONS FOR OPIOID USE DISORDER TIP 63 Contents
    [Show full text]
  • Opioid and Nicotine Use, Dependence, and Recovery: Influences of Sex and Gender
    Opioid and Nicotine: Influences of Sex and Gender Conference Report: Opioid and Nicotine Use, Dependence, and Recovery: Influences of Sex and Gender Authors: Bridget M. Nugent, PhD. Staff Fellow, FDA OWH Emily Ayuso, MS. ORISE Fellow, FDA OWH Rebekah Zinn, PhD. Health Program Coordinator, FDA OWH Erin South, PharmD. Pharmacist, FDA OWH Cora Lee Wetherington, PhD. Women & Sex/Gender Differences Research Coordinator, NIH NIDA Sherry McKee, PhD. Professor, Psychiatry; Director, Yale Behavioral Pharmacology Laboratory Jill Becker, PhD. Biopsychology Area Chair, Patricia Y. Gurin Collegiate Professor of Psychology and Research Professor, Molecular and Behavioral Neuroscience Institute, University of Michigan Hendrée E. Jones, Professor, Department of Obstetrics and Gynecology; Executive Director, Horizons, University of North Carolina at Chapel Hill Marjorie Jenkins, MD, MEdHP, FACP. Director, Medical Initiatives and Scientific Engagement, FDA OWH Acknowledgements: We would like to acknowledge and extend our gratitude to the meeting’s speakers and panel moderators: Mitra Ahadpour, Kelly Barth, Jill Becker, Kathleen Brady, Tony Campbell, Marilyn Carroll, Janine Clayton, Wilson Compton, Terri Cornelison, Teresa Franklin, Maciej Goniewcz, Shelly Greenfield, Gioia Guerrieri, Scott Gottlieb, Marsha Henderson, RADM Denise Hinton, Marjorie Jenkins, Hendrée Jones, Brian King, George Koob, Christine Lee, Sherry McKee, Tamra Meyer, Jeffery Mogil, Ann Murphy, Christine Nguyen, Cheryl Oncken, Kenneth Perkins, Yvonne Prutzman, Mehmet Sofuoglu, Jack Stein, Michelle Tarver, Martin Teicher, Mishka Terplan, RADM Sylvia Trent-Adams, Rita Valentino, Brenna VanFrank, Nora Volkow, Cora Lee Wetherington, Scott Winiecki, Mitch Zeller. We would also like to thank those who helped us plan this program. Our Executive Steering Committee included Ami Bahde, Carolyn Dresler, Celia Winchell, Cora Lee Wetherington, Jessica Tytel, Marjorie Jenkins, Pamela Scott, Rita Valentino, Tamra Meyer, and Terri Cornelison.
    [Show full text]
  • A Clinical Correlation Made Between Opioid-Induced Hyperalgesia and Hyperkatifeia with Brain Alterations Induced by Long-Term Prescription Opioid Use
    Research & Reviews: A Journal of Neuroscience Volume 2, Issue 2, August 2012, Pages 1-11 __________________________________________________________________________________________ A Clinical Correlation Made Between Opioid-induced Hyperalgesia and Hyperkatifeia with Brain Alterations Induced by Long-term Prescription Opioid Use John K. Grandy (B.S., M.S., RPA-C )* North Country Urgent Care, Rte. 12f, Outer Coffeen street, Watertown NY 13601 ABSTRACT The goal of this article is to establish a correlation between the clinical manifestations of opioid-induced hyperalgesia and hyperkatifeia with the morphological and functional connectivity changes seen in the human brain that can be caused by long-term prescription opioid use. This will be accomplished by reviewing the imaging results found in a small but unique study that demonstrated morphological and functional connectivity changes in long-term prescription opioid users. The primary regions that were affected were the amygdala and the white matter tracts connected to it. Therefore, by reviewing the known functions of the amygdala and the white matter tracts - uncinate fasciculus, stria terminalis, and ventral amygdalofugal- and then doing a comparative analysis between the signs and symptoms of the clinical syndromes of opioid-induced hyperalgesia and hyperkatifeia a very obvious correlation has been recognized. Keywords: amygdala, POATS, opioid-induced neuron atrophy, intracellular messenger phosphokinase C, and NMDA receptors. *Author for Correspondence: E-mail [email protected] 1. INTRODUCTION physiological and behavioral functions [2], the majority of existing studies have been done on There has been an enormous increase in the heroin and methadone users. long-term use of prescription opioids over the past decade and a half. The use of opioids for The most frequently prescribed opioids are pain management can cause several hydrocodone [3] and oxycodone [4].
    [Show full text]
  • NIH Public Access Author Manuscript Am J Drug Alcohol Abuse
    NIH Public Access Author Manuscript Am J Drug Alcohol Abuse. Author manuscript; available in PMC 2015 February 17. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Am J Drug Alcohol Abuse. 2012 May ; 38(3): 187–199. doi:10.3109/00952990.2011.653426. Opioid Detoxification and Naltrexone Induction Strategies: Recommendations for Clinical Practice Stacey C. Sigmon, Ph.D.1, Adam Bisaga, M.D.2, Edward V. Nunes, M.D.2, Patrick G. O'Connor, M.D., M.P.H.3, Thomas Kosten, M.D.4, and George Woody, M.D.5 1Department of Psychiatry, University of Vermont College of Medicine, Burlington, VT, USA 2Department of Psychiatry, New York State Psychiatric Institute and Columbia University, New York, NY, USA 3Yale University School of Medicine, New Haven, CT, USA 4Baylor College of Medicine, Houston, TX, USA 5Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, USA Abstract Background—Opioid dependence is a significant public health problem associated with high risk for relapse if treatment is not ongoing. While maintenance on opioid agonists (i.e., methadone, buprenorphine) often produces favorable outcomes, detoxification followed by treatment with the μ-opioid receptor antagonist naltrexone may offer a potentially useful alternative to agonist maintenance for some patients. Method—Treatment approaches for making this transition are described here based on a literature review and solicitation of opinions from several expert clinicians and scientists regarding patient selection, level of care, and detoxification strategies. Conclusion—Among the current detoxification regimens, the available clinical and scientific data suggest that the best approach may be using an initial 2–4 mg dose of buprenorphine combined with clonidine, other ancillary medications, and progressively increasing doses of oral naltrexone over 3–5 days up to the target dose of naltrexone.
    [Show full text]
  • HHS Guide for Clinicians on the Appropriate Dosage Reduction Or
    This HHS Guide for Clinicians on the Appropriate Dosage HHS Guide for Clinicians on the Reduction or Discontinuation of Long-Term Opioid Analgesics provides advice to clinicians who are contemplating or initiating a reduction in opioid dosage or discontinuation Appropriate Dosage Reduction of long-term opioid therapy for chronic pain. In each case the clinician should review the risks and benefits of the or Discontinuation of current therapy with the patient, and decide if tapering is appropriate based on individual circumstances. Long-Term Opioid Analgesics After increasing every year for more than a decade, annual needs.2,3,4 Coordination across the health care team is critical. opioid prescriptions in the United States peaked at 255 million in Clinicians have a responsibility to provide or arrange for 2012 and then decreased to 191 million in 2017.i More judicious coordinated management of patients’ pain and opioid-related opioid analgesic prescribing can benefit individual patients as problems, and they should never abandon patients.2 More well as public health when opioid analgesic use is limited to specific guidance follows, compiled from published guidelines situations where benefits of opioids are likely to outweigh risks. (the CDC Guideline for Prescribing Opioids for Chronic Pain2 At the same time opioid analgesic prescribing changes, such and the VA/DoD Clinical Practice Guideline for Opioid Therapy as dose escalation, dose reduction or discontinuation of long- for Chronic Pain3) and from practices endorsed in the peer- term opioid analgesics, have potential to harm or put patients at reviewed literature. risk if not made in a thoughtful, deliberative, collaborative, and measured manner.
    [Show full text]
  • Ribotag-Seq Reveals a Compensatory Camp Responsive Gene Network in Striatal Microglia Induced by Morphine Withdrawal Kevin R
    bioRxiv preprint doi: https://doi.org/10.1101/2020.02.10.942953; this version posted February 12, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. RiboTag-Seq Reveals a Compensatory cAMP Responsive Gene Network in Striatal Microglia Induced by Morphine Withdrawal Kevin R. Coffey1, Atom J. Lesiak1, Russell G. Marx1, Emily K. Vo1, Gwenn A. Garden2, and John F. Neumaier1 *Corresponding Author: John F. Neumaier, MD, PhD Phone: 206-897-5803 Email: [email protected] 1. Psychiatry & Behavioral Sciences University of Washington School of Medicine Seattle, WA, 98104, USA 2. Department of Neurology University of North Carolina Chapel Hill, NC, 27514, USA Microglia have recently been implicated in dependence to currently available treatments for opioid withdrawal are not opioids. To investigate this directly, we used RNA sequencing sufficiently effective and developing new strategies for of ribosome associated RNAs from striatal microglia (RiboTag- diminishing withdrawal may offer important health benefits and Seq) after the induction of morphine tolerance and then the increase the chances of those suffering from substance abuse precipitation of withdrawal by naloxone. We detected large, choosing to discontinue opioids. Molecular and behavioral inverse changes in RNA translation following opioid tolerance responses to opioids have been thought to be mediated and withdrawal, and bioinformatics analysis revealed an primarily by neurons, but there is accumulating evidence that intriguing upregulation of cAMP-associated genes that are other cell types play a prominent role in drug addiction 3-5.
    [Show full text]
  • Resilience Recovery
    Recovery Reintegration Substance Use Disorder Reintegration Resilience Recovery Pocket Guide Overview Pocket Guide Overview Tab 1: POCKET GUIDE OVERVIEW Intended Patient Outcomes of Clinical Practice Guideline Use and Substance Use Disorder (SUD) Pocket Guide: Reduction of consumption Improvement in quality of life, including social and occupational functioning Improvement of symptoms Improvement of retention and patient engagement Improvement in co-occurring conditions Reduction of mortality 2 OVERVIEW Background VA/DoD Clinical Practice Guideline for the Management of Substance Use Disorder Developed by the Department of Veterans Affairs (VA) and the Department of Defense (DoD) – From recommendations generated by the substance use disorder (SUD) working group — a group of VA/DoD clinical experts from primary care, psychological health and other disciplines – Methodology included: determining appropriate treatment criteria (e.g., effectiveness, efficacy, population benefit, patient satisfaction) and reviewing literature to grade the level of evidence and formulate recommendations – Last updated in August 2009 Substance Use Disorder Pocket Guide Provides medical and psychological health providers with a useful, quick reference tool for treating patients with SUD Derived directly from the VA/DoD SUD Clinical Practice Guideline (CPG): – Developed by the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury (DCoE) in collaboration with the VA/DoD – Content derived from a January 2011 VA/DoD working group
    [Show full text]
  • Medication Assisted Treatment Guidelines for Opioid Use Disorders
    STATE OF MICHIGAN Medication Assisted Treatment Guidelines for Opioid Use Disorders MAT Work Group R. Corey Waller MD, MS 9/17/2014 This document was developed to be a consolidated, short form set of updated, evidence-based guidelines for the treatment of opioid use disorders. Prior to starting the manuscript, current relevant guidelines were reviewed. These included, but were not limited to, the World Health Organization Guidelines, the Baltimore Buprenorphine guidelines, the Vermont Buprenorphine Guidelines, the Australian Ministry of Health Methadone Guidelines as well as the Canadian Department of Health Guidelines for use of Methadone and Buprenorphine. All National Institutes of Drug Addiction (NIDA) as well as SAMHSA materials were used in the initial review. Once this was done all information was updated to current as of April 2014. R. Corey Waller MD, MS was the primary author with Shelly Virva LMSW having authored most of the General Behavioral Health Section. The material was then reviewed by the Medication Assisted Treatment workgroup as directed by Lisa Miller (Michigan Department of Community Health) and suggested changes were incorporated. This document was not meant to be an exhaustive philosophical or theoretical journey about treatment beliefs, but rather a consolidation of current evidence that can guide the treatment, safety, efficacy and payment models driving the treatment of opioid use disorders moving forward. SECTION PG 01 Introduction ..................................................................................................................................................................................................................................
    [Show full text]
  • Hippocampal TNF-Α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss
    Molecular Neurobiology https://doi.org/10.1007/s12035-021-02322-z Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss Shveta V. Parekh1 & Jacqueline E. Paniccia1 & Lydia O. Adams 1 & Donald T. Lysle1 Received: 6 November 2020 /Accepted: 4 February 2021 # The Author(s) 2021 Abstract There is significant comorbidity of opioid use disorder (OUD) and post-traumatic stress disorder (PTSD) in clinical populations. However, the neurobiological mechanisms underlying the relationship between chronic opioid use and withdrawal and devel- opment of PTSD are poorly understood. Our previous work identified that chronic escalating heroin administration and with- drawal can produce enhanced fear learning, an animal model of hyperarousal, and is associated with an increase in dorsal hippocampal (DH) interleukin-1β (IL-1β). However, other cytokines, such as TNF-α, work synergistically with IL-1β and may have a role in the development of enhanced fear learning. Based on both translational rodent and clinical studies, TNF-α has been implicated in hyperarousal states of PTSD, and has an established role in hippocampal-dependent learning and memory. The first set of experiments tested the hypothesis that chronic heroin administration followed by withdrawal is capable of inducing alterations in DH TNF-α expression. The second set of experiments examined whether DH TNF-α expression is functionally relevant to the development of enhanced fear learning. We identified an increase of TNF-α immunoreactivity and positive cells at 0, 24, and 48 h into withdrawal in the dentate gyrus DH subregion. Interestingly, intra-DH infusions of etanercept (TNF-α inhibitor) 0, 24, and 48 h into heroin withdrawal prevented the development of enhanced fear learning and mitigated withdrawal-induced weight loss.
    [Show full text]
  • Management of Drug and Alcohol Withdrawal
    The new england journal of medicine review article current concepts Management of Drug and Alcohol Withdrawal Thomas R. Kosten, M.D., and Patrick G. O’Connor, M.D., M.P.H. From the Departments of Psychiatry (T.R.K.) ach year in the united states, approximately 8.2 million persons and Medicine (P.G.O.), Yale University are dependent on alcohol and 3.5 million are dependent on illicit drugs, includ- School of Medicine, New Haven, Conn.; e 1 and Veterans Affairs Connecticut Health- ing stimulants (1 million) and heroin (750,000). In a sample from primary care care System, West Haven, Conn. (T.R.K.). practice, 15 percent of patients had either an “at-risk” pattern of alcohol use or an alco- Address reprint requests to Dr. Kosten at hol-related health problem, and 5 percent had a history of illicit-drug use.2 With rates of Veterans Affairs Connecticut Healthcare System, Psychiatry 151D, 950 Campbell substance use so high, all patients should be carefully screened with validated instru- Ave., Bldg. 35, West Haven, CT 06516, or ments such as the CAGE questionnaire for alcohol dependence, which consists of the at [email protected]. following questions: Can you cut down on your drinking? Are you annoyed when asked N Engl J Med 2003;348:1786-95. to stop drinking? Do you feel guilty about your drinking? Do you need an eye-opener Copyright © 2003 Massachusetts Medical Society. drink when you get up in the morning? Physicians should be prepared to treat patients who have withdrawal syndromes.3 A carefully taken history should include the time of last use for each substance involved, and toxicologic screening should be performed to identify any additional substances used.
    [Show full text]