Post-Splenectomy Sepsis: a Review of the Literature
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(ACIP) General Best Guidance for Immunization
8. Altered Immunocompetence Updates This section incorporates general content from the Infectious Diseases Society of America policy statement, 2013 IDSA Clinical Practice Guideline for Vaccination of the Immunocompromised Host (1), to which CDC provided input in November 2011. The evidence supporting this guidance is based on expert opinion and arrived at by consensus. General Principles Altered immunocompetence, a term often used synonymously with immunosuppression, immunodeficiency, and immunocompromise, can be classified as primary or secondary. Primary immunodeficiencies generally are inherited and include conditions defined by an inherent absence or quantitative deficiency of cellular, humoral, or both components that provide immunity. Examples include congenital immunodeficiency diseases such as X- linked agammaglobulinemia, SCID, and chronic granulomatous disease. Secondary immunodeficiency is acquired and is defined by loss or qualitative deficiency in cellular or humoral immune components that occurs as a result of a disease process or its therapy. Examples of secondary immunodeficiency include HIV infection, hematopoietic malignancies, treatment with radiation, and treatment with immunosuppressive drugs. The degree to which immunosuppressive drugs cause clinically significant immunodeficiency generally is dose related and varies by drug. Primary and secondary immunodeficiencies might include a combination of deficits in both cellular and humoral immunity. Certain conditions like asplenia and chronic renal disease also can cause altered immunocompetence. Determination of altered immunocompetence is important to the vaccine provider because incidence or severity of some vaccine-preventable diseases is higher in persons with altered immunocompetence; therefore, certain vaccines (e.g., inactivated influenza vaccine, pneumococcal vaccines) are recommended specifically for persons with these diseases (2,3). Administration of live vaccines might need to be deferred until immune function has improved. -
Endogenous Dendritic Cells from the Tumor Microenvironment Support T
Endogenous dendritic cells from the tumor PNAS PLUS microenvironment support T-ALL growth via IGF1R activation Todd A. Tripletta, Kim T. Cardenasa,1, Jessica N. Lancastera, Zicheng Hua, Hilary J. Seldena, Guadalupe J. Jassoa, Sadhana Balasubramanyama, Kathy Chana, LiQi Lib, Xi Chenc,d, Andrea N. Marcogliesee, Utpal P. Davéf, Paul E. Loveb, and Lauren I. R. Ehrlicha,2 aDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712; bSection on Hematopoiesis and Lymphocyte Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892; cDivision of Biostatistics, Department of Health Sciences, University of Miami Miller School of Medicine, Miami, FL 33136; dSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136; eDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030; and fDivision of Hematology/Oncology, Tennessee Valley Healthcare System and Vanderbilt University Medical Center, Nashville, TN 37232 Edited by Zena Werb, University of California, San Francisco, CA, and approved January 14, 2016 (received for review October 15, 2015) Primary T-cell acute lymphoblastic leukemia (T-ALL) cells require tumor growth and metastasis (3). Tumor-associated macrophages stromal-derived signals to survive. Although many studies have (TAMs), which resemble alternatively activated (M2) macro- identified cell-intrinsic alterations in signaling pathways that promote phages (4), also support tumor growth. TAMs suppress antitumor T-ALL growth, the identity of endogenous stromal cells and their immune responses, promote tumor invasion and angiogenesis, and associated signals in the tumor microenvironment that support T-ALL are negatively associated with clinical outcomes (5). -
Complications of Splenectomy 2020; 4(2): 218-222 Received: 08-02-2020 Dr
International Journal of Surgery Science 2020; 4(2): 218-222 E-ISSN: 2616-3470 P-ISSN: 2616-3462 © Surgery Science Complications of splenectomy www.surgeryscience.com 2020; 4(2): 218-222 Received: 08-02-2020 Dr. Ketan Vagholkar Accepted: 10-03-2020 Dr. Ketan Vagholkar DOI: https://doi.org/10.33545/surgery.2020.v4.i2d.420 Professor, Department of Surgery. DY Patil University School of Abstract Medicine Navi Mumbai, Spleen is an important organ of the reticuloendothelial system. It plays a crucial role in the immunological Maharashtra, India system of the body. Understanding the consequences and diagnosis of hyposlenic and asplenic states is essential. Splenectomy is performed for a variety of indications ranging from haematological conditions to trauma. Complications of splenectomy include surgical as well as immunological. Overwhelming post splenectomy infection is one of the most dreaded complication with high mortality. The physiological basis of immunological function of the spleen, hyposplenism and complications of splenectomy are presented in this paper. Keywords: Post splenectomy, complications, hyposplenia, OPSI Introduction Spleen is a very important constituent organ of the reticuloendothelial system. The organ is crucial in regulating immune homeostasis through its ability to link innate and adoptive immunity in the process of protecting against infection. Hyposplenism is impairment of splenic function. It is usually acquired and caused by severe haematological and immunological disorders. Asplenia refers to the absence of the spleen which is rarely congenital but predominantly post-surgical (splenectomy). The most important complication of asplenic state is infectious complications [1]. These infections have high mortality. In addition to infectious complications, splenectomy can lead to a series of other complications. -
WSC 20-21 Conf 6 Illustrated Results
Joint Pathology CenterJoint Pathology Center Veterinary PathologyVeterinary Services Pathology Services WEDNESDAY SLIDE CONFERENCE 2020-2021 WEDNESDAY SLIDE CONFERENCE 2019-2020 Conference 6 C o n f e r e n c e 16 29 January 2020 30 September 2020 Dr. Ingeborg Langohr, DVM, PhD, DACVP Professor Department of Pathobiological Sciences Louisiana State University School of Veterinary Medicine Joint Pathology Center Baton Rouge, LA Silver Spring, Maryland CASE I: CASE S1809996 1: N16 (JPC-032 4135077(4084301).-00 ) Microscopic2.2x1.5x2 Description: cm firm mass The originatinginterstitium from the dura within themater section (meningioma). is diffusely infiltrated by Signalment:Signalment: A 3-month 13- old,yrs male,of age, mixed spayed- female,moderate to large numbers of predominantly breed pigGolden (Sus scrofa Retriever,) Canis lupus familiaris, caninemononuclear. Laboratory cells along results: with edema. There is abundantCytology: type II pneumocyteIt was reported hyperplasia that ante -mortem History: This pig had no previous signs of History: lining alveolarcytology septae of blood and manysmears of from the this animal were illness, andIt waswas reportedfound dead. that the patient had decreased consistent with lymphoid leukemia. appetite and lethargy for the past 1-2 weeks andalveolar spacesSpecial have staining: central Under areas polarized of light, Congo Gross Pathologyhad diarrhea: Approximately for ~1 day. She70% had of a history ofnecrotic macrophagesRed special admixedstain withrevealed other apple-green the lungs,seizures primarily for thein the past cranial ~3 years; regions her last of seizure wasmononuclear birefringence cells and of fewer material neutrophils. effacing glomeruli and the lobes,1 were month patchy ago. darkThe red,patient and hadfirm a generalizedOccasionally cardiac there vessel is free. -
Well-Differentiated Angiosarcoma of Spleen: a Teaching Case Mimicking
Xu et al. World Journal of Surgical Oncology (2015) 13:300 DOI 10.1186/s12957-015-0716-1 WORLD JOURNAL OF SURGICAL ONCOLOGY CASE REPORT Open Access Well-differentiated angiosarcoma of spleen: a teaching case mimicking hemagioma and cytogenetic analysis with array comparative genomic hybridization Lichen Xu1†, Yimin Zhang1†, Hong Zhao1, Qingxiao Chen2, Weihang Ma1,3* and Lanjuan Li1 Abstract Primary splenic angiosarcoma is extremely rare but aggressive malignant vascular neoplasm. Here, we report a case of vascular tumor in spleen that was initially misinterpreted as hemangioma. Two years after splenectomy, the patient admitted again with aggravated abdomen pain and severe anemia. The magnetic resonance imaging (MRI) scan showed widely metastases. The ensuing biopsy for lesion both in liver and in bone marrow showed the similar pathological findings as that in spleen, which supported the final diagnosis of well-differentiated splenic angiosarcoma with extensive metastases. The patient was dead in 3 months after discharge without chemotherapy. The copy number changes for spleen lesion detected by array comparative genome hybridization showed copy number gain at 11q23.2, 11q24.3, 12q24.33, 13q34, copy number loss at 1q24.2-q31.3, 1q41-q42.2, 1 q42.3-q43, 2q36.3-q37.3, 2q37.7, 3q13.33-q26.2, 3q28 - q29, 9p11.2, 13q11, 15q11, homozygous copy loss at 8p11.22, 22q11.23. Less than 200 cases of splenic angiosarcoma have been published in literature of English. To the best of our knowledge, this is the first time analyzed cytogenetic alteration in a well-differentiated primary splenic angiosarcoma. Keywords: Angiosarcoma, Well-differentiation, Splenectomy, Array comparative genomic hybridization, Copy number change Background cytogenetic changes to this subgroup of angiosarcoma Primary splenic angiosarcoma (PSA) is a rare malignant has been published. -
Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck. -
Asplenia Vaccination Guide
Stanford Health Care Vaccination Subcommitee Revision date 11/308/2018 Functional or Anatomical Asplenia Vaccine Guide I. PURPOSE To outline appropriate vaccines targeting encapsulated bacteria for functionally or anatomically asplenic patients. Routine vaccines that may also be indicated but not addressed here include influenza, Tdap, herpes zoster, HPV, MMR, and varicella.1,2,3 II. Background Functionally or anatomically asplenic patients should be vaccinated to decrease the risk of sepsis due to organisms such as Streptococcus pneumoniae, Haemophilus influenzae type B, and Neisseria meningitidis. Guidelines are based on CDC recommendations. For additional information, see https://www.cdc.gov/vaccines/schedules/hcp/imz/adult-conditions.html. III. Procedures/Guidelines1,2,3,6,7,8 The regimen consists of 4 vaccines initially, followed by repeat doses as specified: 1. Haemophilus b conjugate (Hib) vaccine (ACTHIB®) IM once if they have not previously received Hib vaccine 2. Pneumococcal conjugate 13-valent (PCV13) vaccine (PREVNAR 13®) IM once • 2nd dose: Pneumococcal polysaccharide 23-valent (PPSV23) vaccine (PNEUMOVAX 23®) SQ/IM once given ≥ 8 weeks later, then 3rd dose as PPSV23 > 5 years later.4 Note: The above is valid for those who have not received any pneumococcal vaccines previously, or those with unknown vaccination history. If already received prior doses of PPSV23: give PCV13 at least 1 year after last PPSV23 dose. 3. Meningococcal conjugate vaccine (MenACWY-CRM, MENVEO®) IM (repeat in ≥ 8 weeks, then every 5 years thereafter) 4. Meningococcal serogroup B vaccine (MenB, BEXSERO®) IM (repeat in ≥ 4 weeks) Timing of vaccination relative to splenectomy: 1. Should be given at least 14 days before splenectomy, if possible. -
Standards of Medical Fitness
Army Regulation 40–501 Medical Services Standards of Medical Fitness Rapid Action Revision (RAR) Issue Date: 23 August 2010 Headquarters Department of the Army Washington, DC 14 December 2007 UNCLASSIFIED SUMMARY of CHANGE AR 40–501 Standards of Medical Fitness This rapid action revision, dated 23 August 2010-- o Clarifies waiver authorities for officer accessions and commissions for the U.S. Military Academy, Reserve Officers’ Training Corps, and Officer Candidate School (paras 1-6c and 1-6e). o Updates the medical retention standards for psychiatric disorders and hearing (paras 3-10 and 3-31). o Adds a requirement for referral to a Medical Evaluation Board for rhabdomyolysis (para 3-40). o Provides new definitions for heat illness and reasons for a Medical Evaluation Board (para 3-45). o Clarifies who has ultimate responsibility to determine whether to deploy a Soldier (para 5-14d, 5-14e, and 5-14f). o Updates deployment-limiting psychiatric medical conditions (para 5-14f(8)). o Updates functional activities to reflect content changes to DA Form 3349, Physical Profile (chap 7). o Requires review of all permanent 3 and 4 profiles by a Medical Evaluation Board physician or other physician approval authority (para 7-4b). o Establishes and defines the term Medical Retention Determination Point (para 7-4b(2)). o Allows physician assistants, nurse practitioners, and nurse midwives to write permanent profiles as the profiling officer (para 7-6a(4)). o Changes administrative code designations for physical profiles (table 7-2). o Adds psychiatric evaluations for certain administrative separations (paras 8-24a(1) and 8-24a(2)). -
Human Autoimmunity and Associated Diseases
Human Autoimmunity and Associated Diseases Human Autoimmunity and Associated Diseases Edited by Kenan Demir and Selim Görgün Human Autoimmunity and Associated Diseases Edited by Kenan Demir and Selim Görgün This book first published 2021 Cambridge Scholars Publishing Lady Stephenson Library, Newcastle upon Tyne, NE6 2PA, UK British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Copyright © 2021 by Kenan Demir and Selim Görgün and contributors All rights for this book reserved. No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the copyright owner. ISBN (10): 1-5275-6910-1 ISBN (13): 978-1-5275-6910-2 TABLE OF CONTENTS Preface ...................................................................................................... viii Chapter One ................................................................................................. 1 Introduction to the Immune System Kemal Bilgin Chapter Two .............................................................................................. 10 Immune System Embryology Rümeysa Göç Chapter Three ............................................................................................. 18 Immune System Histology Filiz Yılmaz Chapter Four .............................................................................................. 36 Tolerance Mechanisms and Autoimmunity -
Accessory Spleen ORIGINAL RESEARCH ARTICLE
IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN: 2279-0853, p-ISSN: 2279-0861.Volume 14, Issue 10 Ver.III (Oct. 2015), PP 01-03 www.iosrjournals.org Accessory spleen ORIGINAL RESEARCH ARTICLE V. Durgesh*1, CH. Roja Rani2 1Associate Professor Department of Anatomy Faculty of Medicine Maharajah Institute of Medical Sciences Nellimarla Vizianagaram district Andhra Pradesh 2.Assistant Professor Mims, Nellimarla Vizianagaram Distrct Andhrapradesh Abstract: Accessory spleen is a congenital failure of fusion of splenicules usually found close to the splenic hilum or in the greater omentum or tail of the pancreas. Though mostly asymptomatic, these could confuse the diagnosis of certain tumors and also be the cause of relapse post splenectomy. The aim of this article is to present a case of accessory spleen found during the dissection and discuss the various diagnostic procedures, clinical implications and focus on splenosis. Key words: accessory spleen, splenosis, dorsal mesogastrium I. Introduction During the fifth week of intrauterine life, mesenchymal condensations called ‘splenicules” start to appear in the left leaf of dorsal mesogastrium which eventually fuse to form the spleen. Any failure of this fusion results in small splenic tissues developing separately and resulting in accessory spleens. They are relatively common, with an autopsy study involving 3000 patients identifying 364 accessory spleens, of which 61 were found in the pancreatic tail. The pancreatic tail and the splenic hilum are the most common sites though accessory spleens can be found anywhere along the line of dorsal mesogastrium and close to the urogenital ridge such as the stomach, jejunum, mesentery as well as the ovaries, spermatic cord,scrotum1and testis. -
Transplantation Antitumor Activity After Bone Marrow Graft-Versus-Host
The Journal of Immunology Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation1 Asha B. Pillai,* Tracy I. George,† Suparna Dutt,* Pearline Teo,* and Samuel Strober2* Allogeneic bone marrow transplantation is a curative treatment for leukemia and lymphoma, but graft-vs-host disease (GVHD) remains a major complication. Using a GVHD protective nonmyeloablative conditioning regimen of total lymphoid irradiation and antithymocyte serum (TLI/ATS) in mice that has been recently adapted to clinical studies, we show that regulatory host NKT cells prevent the expansion and tissue inflammation induced by donor T cells, but allow retention of the killing activity of donor T cells against the BCL1 B cell lymphoma. Whereas wild-type hosts given transplants from wild-type donors were protected against progressive tumor growth and lethal GVHD, NKT cell-deficient CD1d؊/؊ and J␣-18؊/؊ host mice given wild-type transplants cleared the tumor cells but died of GVHD. In contrast, wild-type hosts given transplants from CD8؊/؊ or perforin؊/؊ donors had progressive tumor growth without GVHD. Injection of host-type NKT cells into J␣-18؊/؊ host mice conditioned with TLI/ATS markedly reduced the early expansion and colon injury induced by donor T cells. In conclusion, after TLI/ATS host conditioning and allogeneic bone marrow transplantation, host NKT cells can separate the proinflammatory and tumor cytolytic functions of donor T cells. The Journal of Immunology, 2007, 178: 6242–6251. raft-vs-host disease (GVHD)3 remains a major compli- taining antitumor activity. Preclinical studies of a TLI and anti- cation of human hemopoietic cell transplantation in the thymocyte serum (ATS) regimen in mice showed that the G treatment of leukemia and lymphoma (1). -
Heterotaxy: Associated Conditions and Hospital- Based Prevalence in Newborns Angela E
May/June 2000. Vol. 2 . No. 3 Heterotaxy: Associated conditions and hospital- based prevalence in newborns Angela E. Lin, MD',~,*, Baruch S. Ticho, MD, phD3j4,Kara Houde, MA1,Marie-Noel Westgate, ME^', and Lewis B. Holmes, MD',~,~ Purpose: To provide insight into the possible etiology and prevalence of heterotaxy, we studied conditions associated with heterotaxy in a consecutive hospital population of newborns. Methods: From 1972 to March, 1999 (except February 16, 1972 to December 31, 1978), 58 cases of heterotaxy were ascertained from a cohort of 201,084 births in the ongoing Active Malformation Surveillance Program at the Brigham and Women's Hospital. This registry includes livebirths, stillbirths, and elective abortions. Prevalence among nontransfers (i.e., patients whose mothers had planned delivery at this hospital) was calculated as approximately 1per 10,000 total births (20 of 201,084). Results: We analyzed a total of 58 patients consisting of 20 (34%) nontransfers and 38 (66%) transfers. Patients were categorized by spleen status as having asplenia (7 nontransfers, 25 total), polysplenia (8, 20), right spleen (4, ll),normal left (0, I), and unknown (1, 0). Among the 20 nontransfer and 59 total heterotaxy patients, the following associated medical conditions were present: chromosome abnormality (1nontransfer, 2 total), suspected Mendelian or chromosome microdeletion disorder (1nontransfer, 6 total), and maternal insulin- dependent diabetes mellitus (1 nontransfer, 2 total). There were 6 twins (1 member each from 6 twin pairs including 1dizygous, 4 monozygous, 1conjoined; 2 were nontransfers). An associated condition occurred in 5 (25%) nontransfer and 16 (28%) total patients, or among 10 of 53 singleton births (19%).