Effect of Mycophenolate on the White Blood Cell Count and the Frequency

Total Page:16

File Type:pdf, Size:1020Kb

Effect of Mycophenolate on the White Blood Cell Count and the Frequency 10/26/2013 Effect of Mycophenolate on the White Disclosures for Michelle Petri, MD MPH Blood Cell Count and the Frequency of • Clinical Trials Infection in Systemic Lupus – HGS/GSK – Medimmune Erythematosus – Pfizer – TEVA – Anthera – UCB Ananta Subedi M.D. • Consultant Hong Fang M.D. M.S. – Genentech – Lilly Michelle Petri M.D. M.P.H. – Merck Serono Johns Hopkins University School of Medicine Leukopenia, Lymphopenia and Neutropenia Leukopenia Occurs in 4 to 36% of Transplant Are All Frequent in SLE Patients on Mycophenolate Mofetil # of Study Leukopenia (%) Lymphopenia (%) Neutropenia (%) Patients No of Patients with Study Patients Transplant Rivero et al, 1978 158 18 75 ND leukopenia (%) on MMF Isenberg et al, 1982 30 37 57 6 Nossent et al, 1991 126 ND 19.8 47 Fischer et al, 2000 31 Liver 6.5 Ng et al, 2005 91 27 62 ND Hao et al, 2008 63 Liver 36 Vila et al, 2006 591 ND 64.6 ND Becker et al, 2008 297 Liver 10.4 Dias et al, 2009 124 36.3 67 40.3 El-Agroudy et al , 2009 25 Kidney 4 (At least 1 visit) Herlenius et al, 2010 13 Liver 11 Dias et al, 2009 124 12.9 41 4.8 (Persistent) Boudjema et al, 2011 95 Liver 29 Castillo-Martinez et al, 85 ND ND 8 2011 Leukopenia in SLE Patients on Mycophenolate Infection is One of the Most Frequent Adverse Events in May be Less Than Transplant Patients SLE Patients on MMF SLE patients Infection Study with leukopenia (%) Study # of PTS Frequency (%) Chan et al, 2000 0 Chan et al, 2000 21 19 Ginzler et al, 2005 1.2 Weixin et al, 2002 23 17.3 Ong et al, 2005 37 Ong et al, 2005 26 23.1 Houssiau et al, 2010 3.7 Ginzler et al, 2005 83 45.8 Wang et al, 2007 9 11.1 Weng et al, 2010 2.9 Appel et al, 2009 184 68.5 El-Shafey et al, 2010 17 El-Shafey et al, 2010 24 50 Radhakrishnan et al, 2010 0 Dooley et al, 2011 115 79.1 Dooley et al, 2011 0 Li et al, 2012 20 40 1 10/26/2013 MMF is Associated with More Infections than Other Infection Risk of Mycophenolate Mofetil Immunosuppressive Drugs in SLE in Lupus Nephritis Placebo Ocrelizumab 52-week double-blind Long-term continuation period (years 1–4), all placebo-controlled period Belimumab-treated patients * 400 mg 1,000 mg (year 1) (n=125) (n=126) (n=127) Placebo Belimumab Year 1 Year 2 Year 3 Year 4 (n= 113) (n=336) (n= 424) (n= 339) (n= 274) (n= 248) Patients with infections (%) 56.0 68.3 59.1 Patients receiving background ELNT Non MMF immunosuppressant 44.4 61.7 39.6 regimen* (%) Overall infection , % 68.9 71.8 75.6 82.6 73.0 79.7 Serious and severe Patients receiving background MMF (%) 62.5 72.2 70.9 2.7 4.2 11 6.4 2.1 8.1 infection , % MMF Patients with serious infections (%) 14.4 21.4 15.0 Overall infection, % 99.1 83.0 93.7 77.5 74.2 90.0 ELNT regimen (%) 11.1 10.6 10.4 Serious and severe 12.4 14.9 13.1 7 13.2 2.8 MMF (%) 16.3 27.8 19.0 infection, % * Expressed as AEs/100 patient-years * ELNT: Euro-Lupus Nephritis Trial regimen (CYC/AZA) Merrill, J T et al. Arth Rheum 64:3364-73, 2012 Mysler et al. Arth Rheum 65: 2368-79, 2013 Objectives Methods We analyzed the effect of • Patients: Patients on mycophenolate mofetil mycophenolate mofetil on: within the Hopkins Lupus Cohort were included in the study 1. White blood cell count 2. Rate of infection since starting • Definition of infection: mycophenolate – Bacterial or viral – Diagnosed on the basis of the clinical judgment of the treating physician – Recorded at every visit Methods Methods • SLE patients served as their own control • Statistical analysis was performed using (before and after mycophenolate the paired t-test. mofetil). • The P-value was adjusted (for ethnicity • The white blood cell count and rate of and prednisone dose) by using the infection on the day mycophenolate was generalized estimating equation. started were compared with the white blood cell count and rate of infection at the next visit. 2 10/26/2013 Demographics The WBC is Not Reduced by MMF Ethnicity African-American 47% Before During Patient Group Mycophenoalate Mycophenolate P-value Caucasian 43% mofetil mofetil Other ethnicities 10% All patients (n=300) 6.65±3.34 7.02±3.28 0.075 African-American (n=140) 6.30±2.94 6.53±3.23 0.40 Gender Caucasian (n=130) 7.15±3.84 7.36±3.15 0.44 Baseline WBC 2.49±0.46 4.83±2.66 0.0007 Female 87% <3,000/mm3 (n=26) Male 13% African-American Ethnicity Reduced the WBC Mycophenolate Increased and Prednisone Increased It Only Bacterial Infections Effect on white Before After Variable P-value Adjusted blood cell count Variable mycophenolate mycophenolate p-value* Ethnicity mofetil (%) mofetil (%) Infection (Viral African-American vs. 14 18 0.087 -0.91±0.33 0.0049 or bacterial) Caucasian Viral infection 10 10 0.17 Other ethnicity vs. Bacterial -0.52±0.51 0.31 5 9 0.032 Caucasians infection Prednisone (per mg/dl) 0.07±0.01 <0.0001 *p-value adjusted for prednisone dose. Mycophenonate mofetil 0.20±0.18 0.28 (before vs. after) Conclusion Conclusion • We found overall a slight increase in • There was a statistically significant the white blood cell count with increase in the frequency of bacterial mycophenolate mofetil use. infection in SLE patients on • In SLE patients with baseline mycophenolate mofetil. leukopenia (white blood cell count less • There was no difference in the 3 than 3,000/mm ), there was a frequency of viral infection. statistically significant increase in the white blood cell count. 3 10/26/2013 Conclusions Limitations of the study • Improvement in the white • The Hopkins Lupus Cohort visits blood count on MMF was still were outpatient visits, but associated with an increase in ascertainment of infection included any during a hospitalization. bacterial infection. • Lymphocyte or neutrophil counts were not recorded in the database. Supported by a Grant from The Institute for Clinical and Translational Research Clinical Research Units 4 .
Recommended publications
  • Agammaglobulinemia Hypogammaglobulinemia Hereditary Disease Immunoglobulins
    Pediat. Res. 2: 72-84 (1968) Agammaglobulinemia hypogammaglobulinemia hereditary disease immunoglobulins Hereditary Alterations in the Immune Response: Coexistence of 'Agammaglobulinemia', Acquired Hypogammaglobulinemia and Selective Immunoglobulin Deficiency in a Sibship REBECCA H. BUCKLEY[75] and J. B. SIDBURY, Jr. Departments of Pediatrics, Microbiology and Immunology, Division of Immunology, Duke University School of Medicine, Durham, North Carolina, USA Extract A longitudinal immunologic study was conducted in a family in which an entire sibship of three males was unduly susceptible to infection. The oldest boy's history of repeated severe infections be- ginning in infancy and his marked deficiencies of all three major immunoglobulins were compatible with a clinical diagnosis of congenital 'agammaglobulinemia' (table I, fig. 1). Recurrent severe in- fections in the second boy did not begin until late childhood, and his serum abnormality involved deficiencies of only two of the major immunoglobulin fractions, IgG and IgM (table I, fig. 1). This phenotype of selective immunoglobulin deficiency is previously unreported. Serum concentrations of the three immunoglobulins in the youngest boy (who also had a late onset of repeated infection) were normal or elevated when he was first studied, but a marked decline in levels of each of these fractions was observed over a four-year period (table I, fig. 1). We could find no previous reports describing apparent congenital and acquired immunologic deficiencies in a sibship. Repeated infections and demonstrated specific immunologic unresponsiveness preceded gross ab- normalities in the total and fractional gamma globulin levels in both of the younger boys (tables II-IV). When the total immunoglobulin level in the second boy was 735 mg/100 ml, he failed to respond with a normal rise in titer after immunization with 'A' and 'B' blood group substances, diphtheria, tetanus, or Types I and II poliovaccines.
    [Show full text]
  • Ataxia Telangiectasia: a Diagnostic Challenge. Case Report
    case reports 2020; 6(2) https://doi.org/10.15446/cr.v6n2.83219 ATAXIA TELANGIECTASIA: A DIAGNOSTIC CHALLENGE. CASE REPORT Keywords: Ataxia Telangiectasia; Neurodegenerative Diseases; Cerebellar Ataxia; Spinocerebellar Degenerations; Telangiectasia. Palabras clave: Ataxia telangiectasia; Enfermedades neurodegenerativas; Ataxia cerebelosa; Degeneraciones espinocerebelosa; Telangiectasia. Natalia Martínez-Córdoba Universidad Militar Nueva Granada - Faculty of Medicine - Pediatric Neurology Research Group - Bogotá D.C. - Colombia. Hospital Militar Central - Pediatric Neurology Service - Bogotá D.C. - Colombia. Eugenia Espinosa-García Universidad Militar Nueva Granada - Faculty of Medicine - Pediatric Neurology Research Group - Bogotá D.C. - Colombia. Hospital Militar Central - Pediatric Neurology Service - Bogotá D.C. - Colombia. Universidad del Rosario - Medical School - Bogotá D.C. - Colombia. Corresponding author Natalia Martínez-Córdoba. Faculty of Medicine, Universidad Militar Nueva Granada. Bogotá D.C. Colombia. Email: [email protected]. Received: 28/10/2019 Accepted: 08/01/2020 case reports Vol. 6 No. 2: 109-17 110 RESUMEN ABSTRACT Introducción. La ataxia-telangiectasia (AT) es Introduction: Ataxia-telangiectasia (AT) is a un síndrome neurodegenerativo con baja inciden- neurodegenerative syndrome with low incidence cia y prevalencia mundial que es causado por una and prevalence worldwide, which is caused by a mutación del gen ATM, es de herencia autosó- mutation of the ATM gene. It is an autosomal re- mica recesiva y se asocia a mecanismos defec- cessive disorder that is associated with defective tuosos en la regeneración y reparación del ADN. cell regeneration and DNA repair mechanisms. It Este síndrome se caracteriza por la presencia de is characterized by progressive cerebellar atax- ataxia cerebelosa progresiva, movimientos ocula- ia, abnormal eye movements, oculocutaneous res anormales, telangiectasias oculocutáneas e telangiectasias and immunodeficiency.
    [Show full text]
  • 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.
    [Show full text]
  • Neonatal Leukopenia and Thrombocytopenia
    Neonatal Leukopenia and Thrombocytopenia Vandy Black, M.D., M.Sc., FAAP March 3, 2016 April 14, 2011 Objecves • Summarize the differenHal diagnosis of leukopenia and/or thrombocytopenia in a neonate • Describe the iniHal steps in the evaluaon of a neonate with leukopenia and/or thrombocytopenia • Review treatment opHons for leukopenia and/ or thrombocytopenia in the NICU Clinical Case 1 • One day old male infant admiUed to the NICU for hypoglycemia and a sepsis rule out • Born at 38 weeks EGA by SVD • Birth weight 4 lbs 13 oz • Exam shows a small cephalohematoma; no dysmorphic features • PLT count 42K with an otherwise normal CBC Definions • Normal WBC count 9-30K at birth – Mean 18K • What is the ANC and ALC – <1000/mm3 is abnormal – 6-8% of infants in the NICU • Normal platelet count: 150-450,000/mm3 – Not age dependent – 22-35% of infants in the NICU have plts<150K Neutropenia Absolute neutrophil count <1500/mm3 Category ANC* InfecHon risk • Mild 1000-1500 None • Moderate 500-1000 Minimal • Severe <500 Moderate to Severe (Highest if <200) • Recurrent bacterial or fungal infecHons are the hallmark of symptomac neutropenia! • *ANC = WBC X % (PMNs + Bands) / 100 DefiniHon of Neutropenia Black and Maheshwari, Neoreviews 2009 How to Approach Cytopenias • Normal vs. abnormal (consider severity) • Malignant vs. non-malignant • Congenital vs. acquired • Is the paent symptomac • Transient, recurrent, cyclic, or persistent How to Approach Cytopenias • Adequate vs. decreased marrow reserve • Decreased producHon vs. increased destrucHon/sequestraon Decreased neutrophil/platelet producon • Primary – Malignancy/leukemia/marrow infiltraon – AplasHc anemia – Genec disorders • Secondary – InfecHous – Drug-induced – NutriHonal • B12, folate, copper Increased destrucHon/sequestraon • Immune-mediated • Drug-induced • Consumpon à Hypersplenism vs.
    [Show full text]
  • On Lupus, Vitamin D and Leukopenia
    r e v b r a s r e u m a t o l . 2 0 1 6;5 6(3):206–211 REVISTA BRASILEIRA DE REUMATOLOGIA w ww.reumatologia.com.br Original article On lupus, vitamin D and leukopenia ∗ Juliana A. Simioni, Flavia Heimovski, Thelma L. Skare Rheumatology Unit, Hospital Universitário Evangélico de Curitiba, Curitiba, PR, Brazil a r t i c l e i n f o a b s t r a c t Article history: Background: Immune regulation is among the noncalcemic effects of vitamin D. So, this Received 7 October 2014 vitamin may play a role in autoimmune diseases such as systemic lupus erythematosus Accepted 24 June 2015 (SLE). Available online 4 September 2015 Objectives: To study the prevalence of vitamin D deficiency in SLE and its association with clinical, serological and treatment profile as well as with disease activity. Keywords: Methods: Serum OH vitamin D3 levels were measured in 153 SLE patients and 85 controls. Data on clinical, serological and treatment profile of lupus patients were obtained through Systemic lupus erythematosus Vitamin D chart review. Blood cell count and SLEDAI (SLE disease activity index) were measured simul- Leukopenia taneously with vitamin D determination. Granulocytopenia Results: SLE patients have lower levels of vitamin D than controls (p = 0.03). In univariate analysis serum vitamin D was associated with leukopenia (p = 0.02), use of cyclophos- phamide (p = 0.007) and methotrexate (p = 0.03). A negative correlation was verified with prednisone dose (p = 0.003). No association was found with disease activity measured by SLEDAI (p = 0.88).
    [Show full text]
  • Interactions of the Classical and Alternate Complement Pathway with Endotoxin Lipopolysaccharide EFFECT on PLATELETS and BLOOD COAGULATION
    Interactions of the Classical and Alternate Complement Pathway with Endotoxin Lipopolysaccharide EFFECT ON PLATELETS AND BLOOD COAGULATION Michael A. Kane, … , Joseph E. May, Michael M. Frank J Clin Invest. 1973;52(2):370-376. https://doi.org/10.1172/JCI107193. Research Article The contributions of the classical and alternate pathways of complement activation to the biological effects of endotoxin have been examined in the guinea pig, with particular reference to thrombocytopenia, leukopenia, and the development of the hypercoagulable state. Injection of endotoxin into normal guinea pigs led to a 95% fall in the level of circulating platelets within 15 min as well as a fall in circulating granulocytes. C4-deficient guinea pigs, known to have a complete block in the activity of the classical complement pathway, but with the alternate pathway intact, sustained no fall in platelets. The development of granulocytopenia proceeded normally. Endotoxin did activate the alternate complement pathway in C4D guinea pigs, as evidenced by the fall in C3-9 titers. With restoration of serum C4 levels, endotoxin- induced thrombocytopenia was observed in C4D animals. Thus, function of the classical complement pathway was an absolute requirement for the development of thrombocytopenia. Experiments performed in cobra venom factor (CVF)- treated normal guinea pigs, with normal levels of C1, C4, and C2, but with less than 1% of serum C3-9 demonstrated the importance of the late components in the development of thrombocytopenia but not leukopenia. C4-deficient guinea pigs had normal clotting times demonstrating that C4 was not required for normal clotting. In addition, development of the hypercoagulable state, evidenced by a marked shortening of the clotting […] Find the latest version: https://jci.me/107193/pdf Interactions of the Classical and Alternate Complement Pathway with Endotoxin Lipopolysaccharide EFFECT ON PLATELETS AND BLOOD COAGULATION MICHAEL A.
    [Show full text]
  • Blood and Immunity
    Chapter Ten BLOOD AND IMMUNITY Chapter Contents 10 Pretest Clinical Aspects of Immunity Blood Chapter Review Immunity Case Studies Word Parts Pertaining to Blood and Immunity Crossword Puzzle Clinical Aspects of Blood Objectives After study of this chapter you should be able to: 1. Describe the composition of the blood plasma. 7. Identify and use roots pertaining to blood 2. Describe and give the functions of the three types of chemistry. blood cells. 8. List and describe the major disorders of the blood. 3. Label pictures of the blood cells. 9. List and describe the major disorders of the 4. Explain the basis of blood types. immune system. 5. Define immunity and list the possible sources of 10. Describe the major tests used to study blood. immunity. 11. Interpret abbreviations used in blood studies. 6. Identify and use roots and suffixes pertaining to the 12. Analyse several case studies involving the blood. blood and immunity. Pretest 1. The scientific name for red blood cells 5. Substances produced by immune cells that is . counteract microorganisms and other foreign 2. The scientific name for white blood cells materials are called . is . 6. A deficiency of hemoglobin results in the disorder 3. Platelets, or thrombocytes, are involved in called . 7. A neoplasm involving overgrowth of white blood 4. The white blood cells active in adaptive immunity cells is called . are the . 225 226 ♦ PART THREE / Body Systems Other 1% Proteins 8% Plasma 55% Water 91% Whole blood Leukocytes and platelets Formed 0.9% elements 45% Erythrocytes 10 99.1% Figure 10-1 Composition of whole blood.
    [Show full text]
  • Immunodeficiency Disorders Ivan K
    Immunodeficiency Disorders Ivan K. Chinn, MD,*† Jordan S. Orange, MD, PhD‡x *Department of Pediatrics, Section of Immunology, Allergy, and Rheumatology, Baylor College of Medicine, Houston, TX †Center for Human Immunobiology, Texas Children’s Hospital, Houston, TX ‡Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York, NY xNew York Presbyterian Morgan Stanley Children’s Hospital, New York, NY Education Gaps Immunodeficiencies are no longer considered rare conditions. Although susceptibility to infections has become well-recognized as a sign of most primary immunodeficiencies, some children will present with noninfectious manifestations that remain underappreciated and warrant evaluation by an immunologic specialist. Providers must also consider common secondary causes of immunodeficiency in children. Objectives After completing this article, readers should be able to: 1. Recognize infectious signs and symptoms of primary immunodeficiency that warrant screening and referral to a specialist. 2. Understand noninfectious signs and symptoms that should raise concern for primary immunodeficiency. 3. Determine appropriate testing for patients for whom immunodeficiency is suspected. AUTHOR DISCLOSURE Dr Chinn has disclosed that he is the recipient of a 4. Discuss the management of patients with primary immunodeficiency. Translational Research Program grant from the Jeffrey Modell Foundation. Dr Orange has 5. Appreciate secondary causes of immunodeficiency. disclosed that he is a consultant on the topic of therapeutic immunoglobulin for Shire, CSL Behring, and Grifols and that he serves on the scientific advisory board for ADMA Biologics. This commentary does contain a discussion of INTRODUCTION an unapproved/investigative use of a commercial product/device. Immunodeficiency disorders represent defects in the immune system that result in weakened or dysregulated immune defense.
    [Show full text]
  • Hyperimmunoglobulin E Syndrome: Genetics, Immunopathogenesis, Clinical Findings, And
    Hyperimmunoglobulin E syndrome: Genetics, immunopathogenesis, clinical findings, and TICLE R treatment modalities A Hassan Hashemi1,2, Masoumeh Mohebbi1,2, Shiva Mehravaran1,3, Mehdi Mazloumi2, Hamidreza Jahanbani-Ardakani4,5, Seyed-Hossein Abtahi4,5,6 1Noor Ophthalmology Research Center, Noor Eye Hospital, Tehran, 2Department of Ophthalmology, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, 4Isfahan Eye Research Center, Feiz Eye Hospital, Isfahan University of Medical Sciences, Isfahan, 5Isfahan Medical Students Research Center (IMSRC), Isfahan University of Medical Sciences, Isfahan, 6Department of Ophthalmology, Feiz Eye Hospital, 3 EVIEW Isfahan University of Medical Sciences, Isfahan, Iran, Department of Ophthalmology, Stein Eye Institute, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California, USA R The hyperimmunoglobulin E syndromes (HIESs) are very rare immunodeficiency syndromes with multisystem involvement, including immune system, skeleton, connective tissue, and dentition. HIES are characterized by the classic triad of high serum levels of immunoglobulin E (IgE), recurrent staphylococcal cold skin abscess, and recurrent pneumonia with pneumatocele formation. Most cases of HIES are sporadic although can be inherited as autosomal dominant and autosomal recessive traits. A fundamental immunologic defect in HIES is not clearly elucidated but abnormal neutrophil chemotaxis due to decreased production or secretion of interferon γ has main role in the immunopathogenesis of syndrome, also distorted Th1/Th2 cytokine profile toward a Th2 bias contributes to the impaired cellular immunity and a specific pattern of infection susceptibility as well as atopic‑allergic constitution of syndrome. The ophthalmic manifestations of this disorder include conjunctivitis, keratitis, spontaneous corneal perforation, recurrent giant chalazia, extensive xanthelasma, tumors of the eyelid, strabismus, and bilateral keratoconus.
    [Show full text]
  • Practical Guidance for the Evaluation and Management of Drug Hypersensitivity: Specific Drugs
    Specific Drugs Practical Guidance for the Evaluation and Management of Drug Hypersensitivity: Specific Drugs Chief Editors: Ana Dioun Broyles, MD, Aleena Banerji, MD, and Mariana Castells, MD, PhD Ana Dioun Broyles, MDa, Aleena Banerji, MDb, Sara Barmettler, MDc, Catherine M. Biggs, MDd, Kimberly Blumenthal, MDe, Patrick J. Brennan, MD, PhDf, Rebecca G. Breslow, MDg, Knut Brockow, MDh, Kathleen M. Buchheit, MDi, Katherine N. Cahill, MDj, Josefina Cernadas, MD, iPhDk, Anca Mirela Chiriac, MDl, Elena Crestani, MD, MSm, Pascal Demoly, MD, PhDn, Pascale Dewachter, MD, PhDo, Meredith Dilley, MDp, Jocelyn R. Farmer, MD, PhDq, Dinah Foer, MDr, Ari J. Fried, MDs, Sarah L. Garon, MDt, Matthew P. Giannetti, MDu, David L. Hepner, MD, MPHv, David I. Hong, MDw, Joyce T. Hsu, MDx, Parul H. Kothari, MDy, Timothy Kyin, MDz, Timothy Lax, MDaa, Min Jung Lee, MDbb, Kathleen Lee-Sarwar, MD, MScc, Anne Liu, MDdd, Stephanie Logsdon, MDee, Margee Louisias, MD, MPHff, Andrew MacGinnitie, MD, PhDgg, Michelle Maciag, MDhh, Samantha Minnicozzi, MDii, Allison E. Norton, MDjj, Iris M. Otani, MDkk, Miguel Park, MDll, Sarita Patil, MDmm, Elizabeth J. Phillips, MDnn, Matthieu Picard, MDoo, Craig D. Platt, MD, PhDpp, Rima Rachid, MDqq, Tito Rodriguez, MDrr, Antonino Romano, MDss, Cosby A. Stone, Jr., MD, MPHtt, Maria Jose Torres, MD, PhDuu, Miriam Verdú,MDvv, Alberta L. Wang, MDww, Paige Wickner, MDxx, Anna R. Wolfson, MDyy, Johnson T. Wong, MDzz, Christina Yee, MD, PhDaaa, Joseph Zhou, MD, PhDbbb, and Mariana Castells, MD, PhDccc Boston, Mass; Vancouver and Montreal,
    [Show full text]
  • Immunology of the Acquired Immunodeficiency Syndrome
    Henry Ford Hospital Medical Journal Volume 32 Number 2 Article 6 6-1984 Immunology of the Acquired Immunodeficiency Syndrome Patrick W. McLaughlin Carl B. Lauter Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation McLaughlin, Patrick W. and Lauter, Carl B. (1984) "Immunology of the Acquired Immunodeficiency Syndrome," Henry Ford Hospital Medical Journal : Vol. 32 : No. 2 , 107-115. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol32/iss2/6 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hospital Med J Vol. 32, No. 2, 1984 Immunology of the Acquired Immunodeficiency Syndrome Patrick W. McLaughlin, MD* and Carl B. Lauter, MD** The Acquired Immunodeficiency Syndrome (AIDS) first known to cause immunodeficiency. Simian AIDS, an recognized in 1981, has been extensively studied, and animal model of virus-induced immunodeficiency, is the most recent studies have demonstrated that its also discussed. Recommendations are made regarding defects extend well beyond the apparent deficient the interpretation and limitations of immune testing in cell-mediated immunity to include humoral immunity, AIDS, includinga discussion of how apparently healthy autoimmunity, and abnormal immunoregulation. The homosexuals and groups at risk develop an immu­ recent discovery ofa retrovirus, HTLV III, as a possible nologic profile which mimics that of patients with AIDS. etiologic agent is discussed in relation to other viruses J\r\ce late 1981, an unexpected outbreak of oppor­ The immune system has "surveillance" functions to tunistic infections and unusual neoplasms has been protect humans (and other vertebrates) from infections noted, described, and studied (1-4).
    [Show full text]
  • Chronic Lymphocytic Leukemia Early Detection, Diagnosis, and Staging Detection and Diagnosis
    cancer.org | 1.800.227.2345 Chronic Lymphocytic Leukemia Early Detection, Diagnosis, and Staging Detection and Diagnosis Finding cancer early often allows for more treatment options. Some early cancers may have signs and symptoms that can be noticed, but that's not always the case. ● Can Chronic Lymphocytic Leukemia Be Found Early? ● Signs and Symptoms of Chronic Lymphocytic Leukemia ● How Is Chronic Lymphocytic Leukemia Diagnosed? Stages and Outlook (Prognosis) After a cancer diagnosis, staging provides important information about the extent of cancer in the body and anticipated response to treatment. ● How Is Chronic Lymphocytic Leukemia Staged? Questions to Ask About CLL Here are some questions you can ask your cancer care team to help you better understand your CLL diagnosis and treatment options. ● Questions to Ask About Chronic Lymphocytic Leukemia 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Can Chronic Lymphocytic Leukemia Be Found Early? For certain cancers, the American Cancer Society recommends screening tests1 in people without any symptoms, because they are easier to treat if found early. But for chronic lymphocytic leukemia (CLL) , no screening tests are routinely recommended at this time. Many times, CLL is found when routine blood tests are done for other reasons. For instance, a person's white blood cell count may be very high, even though he or she doesn't have any symptoms. If you notice any symptoms that could be caused by CLL, report them to your doctor right away so the cause can be found and treated, if needed. Hyperlinks 1. www.cancer.org/healthy/find-cancer-early/cancer-screening-guidelines/american- cancer-society-guidelines-for-the-early-detection-of-cancer.html Last Revised: May 10, 2018 Signs and Symptoms of Chronic Lymphocytic Leukemia Many people with chronic lymphocytic leukemia (CLL) do not have any symptoms when it is diagnosed.
    [Show full text]