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i

MAYO CLINIC
INTERNAL MEDICINE
BOARD REVIEW
ELEVENTH EDITION
ii

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iii

MAYO CLINIC
INTERNAL MEDICINE
BOARD REVIEW
ELEVENTH EDITION

EDITOR-​I N-​C HIEF

Christopher M. Wittich, MD, PharmD

Consultant, Division of General Internal Medicine
Mayo Clinic, Rochester, Minnesota
Associate Professor of Medicine
Mayo Clinic College of Medicine

SENIOR ASSOCIATE EDITOR

Thomas J. Beckman, MD
Consultant, Division of General Internal Medicine
Mayo Clinic, Rochester, Minnesota
Professor of Medicine and of Medical Education
Mayo Clinic College of Medicine

ASSOCIATE EDITORS

Nerissa M. Collins, MD Nina M. Schwenk, MD

Jason H. Szostek, MD Amy T. Wang, MD

MAYO CLINIC SCIENTIFIC PRESS OXFORD UNIVERSITY PRESS

iv

The triple-shield Mayo logo and the words MAYO, MAYO CLINIC, and MAYO CLINIC SCIENTIFIC PRESS
are marks of Mayo Foundation for Medical Education and Research.

1
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Press in the UK and certain other countries.

Published in the United States of America by Oxford University Press

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© 2016 by Mayo Foundation for Medical Education and Research.

All rights reserved. No part of this publication 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
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Scientific Publications, Plummer 10, Mayo Clinic, 200 First St SW, Rochester, MN 55905.

You must not circulate this work in any other form

and you must impose this same condition on any acquirer.

Library of Congress Cataloging-​in-​Publication Data

Names: Wittich, Christopher M., editor | Mayo Clinic. | Mayo Foundation for
Medical Education and Research.
Title: Mayo Clinic internal medicine board review / editor-in-chief,
Christopher M. Wittich ; senior associate editor, Thomas J. Beckman;
associate editors, Nerissa M. Collins, Nina M. Schwenk, Jason H. Szostek,
Amy T. Wang.
Other titles: Internal medicine board review | Mayo Clinic scientific press
(Series)
Description: Eleventh edition. | Oxford ; New York, NY : Oxford University
Press, [2016] | Series: Mayo Clinic scientific press | Includes
bibliographical references and index.
Identifiers: LCCN 2016006611 | ISBN 9780190464868 (alk. paper)
Subjects: | MESH: Internal Medicine | Examination Questions | Outlines
Classification: LCC RC58 | NLM WB 18.2 | DDC 616.0076—dc23
LC record available at http://lccn.loc.gov/2016006611

Mayo Foundation does not endorse any particular products or services, and the reference to any products or services in this book is
for informational purposes only and should not be taken as an endorsement by the authors or Mayo Foundation. Care has been taken
to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and
publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and
make no warranty, express or implied, with respect to the contents of the publication. This book should not be relied on apart from
the advice of a qualified health care provider.

The authors, editors, and publisher have exerted efforts to ensure that drug selection and dosage set forth in this text are in accordance
with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government
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insert for each drug for any change in indications and dosage and for added wordings and precautions. This is particularly important
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Cover images, clockwise from the upper left: Figure 47.2. chaining of β-​hemolytic Streptococcus in a blood culture (Gram stain);
Figure 26.9. pemphigus vulgaris; Figure 11.5. aortogram of contained rupture of proximal descending thoracic aorta; Figure 37.11. spur
cells (acanthocytes).
v

To my colleagues in the Division of General Internal

Medicine for their collaborative spirit.
To Mayo Clinic internal medicine residents for their inspiration.
To Michelle and Claire for their constant laughter.
Christopher M. Wittich, MD, PharmD
vi
vii
Foreword
The Department of Medicine at Mayo Clinic has a long
and rich history of educating physicians in training and
practice. The Mayo Clinic School of Graduate Medical
Education, which began in 1915, has celebrated its cen-
tennial of training resident physicians. Additionally, the
Department of Medicine’s continuing medical education
courses are nearing their 90th consecutive year of edu-
cating physicians in practice. An ongoing key mission
of the Department of Medicine is to provide lifelong
learning programs to educate learners across the medi-
cal education continuum. The Mayo Clinic Internal
Medicine Board Review, Eleventh Edition, is one such
learning program resource designed to teach internists
and update them on the ever-​changing field of internal
medicine.
For the Eleventh Edition, the chapters have been com-
pletely revised and reorganized to cover the breadth of
internal medicine. In addition, the new edition has an up-
dated design to simplify study and improve readability. All
chapters were written by Mayo Clinic physicians whose
primary mission is to care for patients. The editors added
their depth of experience in general internal medicine and
medical education to develop a text that is relevant to prac-
tice. This textbook will be of value to those preparing for
the American Board of Internal Medicine Certification and
Maintenance of Certification examinations and as a general
reference for those striving to provide outstanding clinical
care for patients.
Morie A. Gertz, MD, MACP
Chair, Department of Internal Medicine, Mayo Clinic,
Rochester, Minnesota
Roland Seidler Jr Professor of the Art of Medicine
Mayo Clinic College of Medicine
viii
ix
Preface
The Mayo Clinic Internal Medicine Board Review,
Eleventh Edition, is the result of the dedicated efforts of
Mayo Clinic physicians in multiple specialties whose pri-
mary mission is to put the needs of the patient first. The
field of internal medicine is constantly changing as sci-
ence is advanced. The goal of this textbook is to provide
the reader with the essential elements for the practice of
internal medicine. Readers preparing for the American
Board of Internal Medicine (ABIM) Certification and
Maintenance of Certification examinations will find the
textbook comprehensive and easy to study. Additionally,
readers who want a reference or a general knowledge
review in internal medicine will find this textbook an
­important addition to their medical library.
The Eleventh Edition uses a new design to improve read-
ability with color-​coded chapter tabs and key facts and key
definitions highlighted separately from the main text. The
oncology and neurology chapters have been completely re-
organized according to disease site. New chapters have been
added on complementary and integrative medicine and qual-
ity improvement. Several major topics have been divided
into shorter chapters for ease of study, and all chapters have
been completely revised with a focus on covering content in
the ABIM Certification Examination Blueprint. The editors
have worked diligently to remove extraneous material that
would not be useful for the practice of general internal medi-
cine, yet the book is comprehensive and easy to study.
I wish to thank all the authors for their careful attention
to detail and hard work. The associate editors, all members
of the Division of General Internal Medicine at Mayo Clinic,
provided incredible insights into what information is truly
needed to practice general internal medicine. I would like
to especially thank Thomas J. Beckman, MD, senior associ-
ate editor, for his years of mentorship, during which he
taught me to be a scholar and medical writer. I would like
to thank Morie A. Gertz, MD, Chair of the Department of
Internal Medicine at Mayo Clinic in Rochester, Minnesota,
and Paul S. Mueller, MD, Chair of the Division of General
Internal Medicine, who provided the encouragement and
resources to make this textbook possible. I also thank
Michael O’Brien for his administrative support. This
book would not exist without the dedication of the Mayo
Clinic Section of Scientific Publications staff, including
Joseph G. Murphy, MD, Chair; Randall J. Fritz, DVM, and
LeAnn M. Stee, with assistance from Patricia M. Flynn and
Colleen M. Sauber, editors; Kenna L. Atherton, manager;
Jane M. Craig, editorial assistant; and John P. Hedlund
and Ann M. Ihrke, proofreaders. I gratefully acknowledge
the support of Mayo Clinic Scientific Press and Oxford
University Press. Finally, I thank Laura M. Sadosty, in the
Department of Medicine, who organized over 70 physician
authors—​a remarkable feat indeed!
In the spirit of the previous editions, I trust that Mayo
Clinic Internal Medicine Board Review, Eleventh Edition,
will serve those in the pursuit of mastering the art and sci-
ence of internal medicine.
Christopher M. Wittich, MD, PharmD
x
╇ xi

Contents

Contributorsâ•…xv 7 • Hypertensionâ•… 75
C. Scott Collins, MD and Christopher M.
Wittich, MD, PharmD
Section I: Allergy
Section editor, Christopher M. 8 • Ischemic Heart Diseaseâ•… 83
Wittich, MD, PharmD Nandan S. Anavekar, MB, BCh

1 • Allergic Diseasesâ•… 3 9 • Pericardial Disease and Cardiac Tumorsâ•… 103

Gerald W. Volcheck, MD Kyle W. Klarich, MD

2 • Asthmaâ•… 15 10 • Valvular and Congenital Heart Diseasesâ•… 107

Gerald W. Volcheck, MD Kyle W. Klarich, MD; Lori A. Blauwet, MD;
and Sabrina D. Phillips, MD
Questions and Answersâ•… 25
11 • Vascular Diseaseâ•… 129
Robert D. McBane, MD

Section II: Cardiology Questions and Answersâ•… 143

Section editor, Nina M. Schwenk, MDa

3 • Arrhythmias and Syncopeâ•… 29 Section III: Endocrinology

Peter A. Noseworthy, MD Section editor, Nina M. Schwenk, MDa

4 • Cardiac Manifestations of Systemic Diseases 12 • Calcium and Bone Metabolism Disordersâ•… 149
and Pregnancyâ•… 45 Marius N. Stan, MD
Lori A. Blauwet, MD; Rekha Mankad, MD;
Sabrina D. Phillips, MD; and Kyle W. Klarich, MD 13 • Diabetes Mellitusâ•… 157
Ekta Kapoor, MBBS
5 • Cardiovascular Physical Examinationâ•… 53
Kyle W. Klarich, MD; Lori A. Blauwet, MD; 14 • Gonadal and Adrenal Disordersâ•… 165
and Sabrina D. Phillips, MD Pankaj Shah, MD

6 • Heart Failure and Cardiomyopathiesâ•… 59 15 • Lipid Disordersâ•… 179

Farris K. Timimi, MD Ekta Kapoor, MBBS

a
Other Section editors reviewed a single chapter in this section.
xii

xii Contents

16 • Obesity and Nutritional Disorders 185 27 • Genetics 315

Ryan T. Hurt, MD, PhD
17 • Pituitary Disorders 191
Pankaj Shah, MD
18 • Thyroid Disorders 203
Marius N. Stan, MD
Questions and Answers
C. Scott Collins, MD and Christopher M.
Wittich, MD, PharmD
28 • Geriatrics 319
Ericka E. Tung, MD, MPH
29 • Medical Ethics 331
Keith M. Swetz, MD, MA and C. Christopher Hook, MD
211
30 • Men’s Health 337
Thomas J. Beckman, MD

Section IV: Gastroenterology 31 • Otolaryngology and Ophthalmology 345

and Hepatology
Section editor, Nina M. Schwenk, MDa
19 • Colonic Disorders 217
Conor G. Loftus, MD
20 • Diarrhea, Malabsorption, and Small-​Bowel
Disorders 229
Seth R. Sweetser, MD
21 • Esophageal and Gastric Disorders
Amy S. Oxentenko, MD
22 • Hepatic Disorders 251
William Sanchez, MD
and John J. Poterucha, MD
23 • Pancreatic Disorders 271
Conor G. Loftus, MD
Questions and Answers
Nerissa M. Collins, MD
32 • Palliative Care 349
Jacob J. Strand, MD and Keith M. Swetz, MD, MA
33 • Preoperative Evaluation 355
Karna K. Sundsted, MD and Karen F. Mauck, MD, MSc
34 • Preventive Medicine 365
Amy T. Wang, MD and Karen F. Mauck, MD, MSc
241
35 • Quality Improvement and Patient Safety 375
Jordan M. Kautz, MD and Christopher M. Wittich, MD,
PharmD
36 • Women’s Health 379
Nicole P. Sandhu, MD, PhD; Lynne T. Shuster, MD;
and Amy T. Wang, MD
Questions and Answers 391
277

Section VI: Hematology

Section editor, Amy T. Wang, MD
Section V: General Internal Medicine
Section editors, Thomas J. Beckman, MD; 37 • Benign Hematologic Disorders 399
Jason H. Szostek, MD; Amy T. Wang, MD; Naseema Gangat, MBBS
and Christopher M. Wittich, MD, PharmD
38 • Hemostatic Disorders 415
24 • Clinical Epidemiology 285 Rajiv K. Pruthi, MBBS
Scott C. Litin, MD and John B. Bundrick, MD
39 • Malignant Hematologic Disorders 427
25 • Complementary and Alternative Medicine 291 Carrie A. Thompson, MD
Tony Y. Chon, MD and Brent A. Bauer, MD
40 • Thrombotic Disorders 439
26 • Dermatology 297 Rajiv K. Pruthi, MBBS
Carilyn N. Wieland, MD
Questions and Answers 447

a
Other Section editors reviewed a single chapter in this section.
xiii

Contents xiii

Section VII: Infectious Diseases Section IX: Neurology

Section editor, Nerissa M. Collins, MD a
Section editor, Nerissa M. Collins, MD

41 • Central Nervous System Infections 453 53 • Cerebrovascular Diseases 599

Pritish K. Tosh, MD and M. Rizwan Sohail, MD James P. Klaas, MD and Robert D. Brown Jr, MD

42 • HIV Infection 461 54 • Headache, Facial Pain, and “Dizziness” 605

Mary J. Kasten, MD and Zelalem Temesgen, MD Bert B. Vargas, MD

43 • Immunocompromised Hosts 55 • Inflammatory and Autoimmune Central Nervous

and Microorganism-​Specific Syndromes 475 System Diseases and the Neurology of Sepsis 615
Pritish K. Tosh, MD and M. Rizwan Sohail, MD Andrew McKeon, MB, BCh, MD

44 • Infective Endocarditis and Health Care–​Associated 56 • Movement Disorders 619

Infections 491 Anhar Hassan, MB BCh and Eduardo E. Benarroch, MD
M. Rizwan Sohail, MD and Pritish K. Tosh, MD
57 • Neoplastic Diseases 625
45 • Pulmonary and Mycobacterial Infections 505 Alyx B. Porter, MD
Pritish K. Tosh, MD and Elie F. Berbari, MD
58 • Seizure Disorders 633
46 • Sexually Transmitted, Urinary Tract, Lily C. Wong-​Kisiel, MD
and Gastrointestinal Tract Infections 521
M. Rizwan Sohail, MD 59 • Spinal, Peripheral, and Muscular Disorders 639
Lyell K. Jones Jr, MD and Brian A. Crum, MD
47 • Skin, Soft Tissue, Bone, and Joint Infections 539
Elie F. Berbari, MD Questions and Answers 649

Questions and Answers 545

Section X: Oncology
Section editor, Jason H. Szostek, MD
Section VIII: Nephrology
Section editors, Thomas J. Beckman, MD; 60 • Breast Cancer 655
Nerissa M. Collins, MD; and Tufia C. Haddad, MD and Timothy J. Moynihan, MD
Amy T. Wang, MD
61 • Cancer of Unknown Primary Origin
48 • Acid-​Base Disorders 551 and Paraneoplastic Syndromes 661
Qi Qian, MD Michelle A. Neben Wittich, MD

49 • Acute Kidney Injury 557 62 • Gynecologic Cancers: Cervical, Uterine,

Suzanne M. Norby, MD and Kianoush B. Kashani, MD
50 • Chronic Kidney Disease 565
Carrie A. Schinstock, MD
51 • Electrolyte Disorders 571
Qi Qian, MD
52 • Renal Parenchymal Diseases
Suzanne M. Norby, MD
and Fernando C. Fervenza, MD, PhD
Questions and Answers 591
and Ovarian Cancers 667
Andrea E. Wahner Hendrickson, MD
63 • Colorectal Cancer 673
Joleen M. Hubbard, MD
64 • Genitourinary Cancer 677
Brian A. Costello, MD, MS
579
65 • Lung Cancer and Head and Neck Cancer 683
Michelle A. Neben Wittich, MD
and Katharine A. Price, MD

a
Other Section editors reviewed a single chapter in this section.
xiv
xiv Contents
66 • Oncologic Emergencies and Chemotherapy
Complications 689
Timothy J. Moynihan, MD
Questions and Answers
Section XI: Psychiatry
Section editor, Christopher M.
Wittich, MD, PharmD
67 • Mood and Anxiety Disorders
Brian A. Palmer, MD
68 • Psychotic and Somatic Symptom
and Related Disorders 707
Brian A. Palmer, MD
69 • Substance Use Disorders, Personality Disorders,
and Eating Disorders 711
Brian A. Palmer, MD
Questions and Answers
Section XII: Pulmonology
Section editor, Amy T. Wang, MDa
70 • Critical Care Medicine
Cassie C. Kennedy, MD
71 • Cystic Fibrosis, Bronchiectasis,
and Pleural Effusion 729
Vivek N. Iyer, MD
72 • Interstitial Lung Diseases
Fabien Maldonado, MD
and Timothy R. Aksamit, MD
a
Other Section editors reviewed a single chapter in this section.
73 • Obstructive Lung Diseases 741
Vivek N. Iyer, MD
74 • Pulmonary Evaluation 747
695 Vivek N. Iyer, MD
75 • Pulmonary Vascular Disease 767
Rodrigo Cartin-​Ceba, MD, MSc
76 • Sleep-​Related Breathing Disorders 773
Mithri R. Junna, MD
701
Questions and Answers 775
Section XIII: Rheumatology
Section editor, Jason H. Szostek, MDa
77 • Connective Tissue Diseases 781
Floranne C. Ernste, MD
78 • Musculoskeletal Disorders 795
715 Arya B. Mohabbat, MD and Christopher M.
Wittich, MD, PharmD
79 • Osteoarthritis, Gout, and Infectious Arthritis 813
Clement J. Michet, MD and Floranne C. Ernste, MD
80 • Rheumatoid Arthritis and
719 Spondyloarthropathies 829
Clement J. Michet, MD
81 • Vasculitis 839
Matthew J. Koster, MD and Kenneth J. Warrington, MD
Questions and Answers 849
733
Index 853
xv

Contributorsa

Timothy R. Aksamit, MD Rodrigo Cartin-​Ceba, MD, MSc

Consultant, Division of Pulmonary and Critical Care
Medicine, Mayo Clinic; Associate Professor of Medicine
Nandan S. Anavekar, MB, BCh
Consultant, Division of Cardiovascular Diseases,
Mayo Clinic; Associate Professor of Medicine
Brent A. Bauer, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Professor of Medicine
Thomas J. Beckman, MD
Consultant, Division of General Internal Medicine, Mayo
Clinic; Professor of Medical Education and of Medicine
Eduardo E. Benarroch, MD
Consultant, Department of Neurology, Mayo Clinic;
Professor of Neurology
Elie F. Berbari, MD
Consultant, Division of Infectious Diseases, Mayo Clinic;
Professor of Medicine
Lori A. Blauwet, MD
Consultant, Division of Cardiovascular Diseases, Mayo
Clinic; Associate Professor of Medicine
Robert D. Brown Jr, MD
Consultant, Department of Neurology, Mayo Clinic;
Professor of Neurology
John B. Bundrick, MD
Consultant, Division of General Internal Medicine, Mayo
Clinic; Assistant Professor of Medicine
Consultant, Division of Pulmonary and Critical
Care Medicine, Mayo Clinic, Scottsdale, Arizona;
Assistant Professor of Medicine
Tony Y. Chon, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
C. Scott Collins, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Nerissa M. Collins, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Instructor in Medicine
Brian A. Costello, MD, MS
Consultant, Department of Oncology, Mayo Clinic;
Associate Professor of Urology and of Oncology
Brian A. Crum, MD
Consultant, Department of Neurology, Mayo Clinic;
Assistant Professor of Neurology
Floranne C. Ernste, MD
Consultant, Division of Rheumatology, Mayo Clinic;
Assistant Professor of Medicine
Fernando C. Fervenza, MD, PhD
Consultant, Division of Nephrology and Hypertension,
Mayo Clinic; Professor of Medicine

a
Unless otherwise noted, clinical appointments refer to Rochester, Minnesota, and academic appointments refer to Mayo Clinic College
of Medicine.
xvi
xvi Contributors
Naseema Gangat, MBBS
Consultant, Division of Hematology, Mayo Clinic;
Instructor in Oncology and Assistant Professor
of Medicine
Tufia C. Haddad, MD
Consultant, Department of Oncology, Mayo Clinic;
Assistant Professor of Oncology
Anhar Hassan, MB, BCh
Consultant, Department of Neurology, Mayo Clinic;
Assistant Professor of Neurology
C. Christopher Hook, MD
Consultant, Division of Hematology, Mayo Clinic;
Associate Professor of Medicine
Joleen M. Hubbard, MD
Consultant, Department of Oncology, Mayo Clinic;
Instructor in Medicine and Assistant Professor of
Oncology
Ryan T. Hurt, MD, PhD
Consultant, Division of General Internal Medicine, Mayo
Clinic; Associate Professor of Medicine
Vivek N. Iyer, MD
Consultant, Division of Pulmonary and Critical Care
Medicine, Mayo Clinic; Assistant Professor of
Medicine
Lyell K. Jones Jr, MD
Consultant, Department of Neurology, Mayo Clinic;
Associate Professor of Neurology
Mithri R. Junna, MD
Senior Associate Consultant, Department of Neurology
and Division of Pulmonary and Critical Care Medicine,
Mayo Clinic; Assistant Professor of Neurology
Ekta Kapoor, MBBS
Consultant, Divisions of General Internal Medicine and
Endocrinology, Diabetes, Metabolism, & Nutrition,
Mayo Clinic; Assistant Professor of Medicine
Kianoush B. Kashani, MD
Consultant, Divisions of Nephrology and Hypertension
and Pulmonary and Critical Care Medicine, Mayo
Clinic; Assistant Professor of Medicine
Mary J. Kasten, MD
Consultant, Divisions of General Internal Medicine and
Infectious Diseases, Mayo Clinic; Assistant Professor of
Medicine
Jordan M. Kautz, MD
Senior Associate Consultant, Division of General Internal
Medicine, Mayo Clinic; Instructor in Medicine
Cassie C. Kennedy, MD
Consultant, Division of Pulmonary and Critical Care
Medicine, Mayo Clinic; Assistant Professor of Medicine
James P. Klaas, MD
Senior Associate Consultant, Department of Neurology,
Mayo Clinic; Assistant Professor of Neurology
Kyle W. Klarich, MD
Consultant, Division of Cardiovascular Diseases,
Mayo Clinic; Professor of Medicine
Matthew J. Koster, MD
Fellow in Rheumatology, Mayo School of Graduate
Medical Education; Instructor in Medicine
Scott C. Litin, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Professor of Medicine
Conor G. Loftus, MD
Consultant, Division of Gastroenterology and Hepatology,
Mayo Clinic; Assistant Professor of Medicine
Fabien Maldonado, MD
Consultant, Division of Pulmonary and Critical Care
Medicine, Mayo Clinic; Assistant Professor of Medicine
Present address: Vanderbilt University School of
Medicine
Rekha Mankad, MD
Consultant, Division of Cardiovascular Diseases,
Mayo Clinic; Assistant Professor of Medicine
Karen F. Mauck, MD, MSc
Consultant, Division of General Internal Medicine,
Mayo Clinic; Associate Professor of Medicine
Robert D. McBane, MD
Consultant, Division of Cardiovascular Diseases,
Mayo Clinic; Professor of Medicine
Andrew McKeon, MB, BCh, MD
Consultant, Department of Neurology and Division of
Clinical Biochemistry, Mayo Clinic; Associate Professor
of Laboratory Medicine and Pathology and of Neurology
Clement J. Michet, MD
Consultant, Division of Rheumatology, Mayo Clinic;
Associate Professor of Medicine
xvii
Arya B. Mohabbat, MD
Senior Associate Consultant, Division of General Internal
Medicine, Mayo Clinic; Assistant Professor of Medicine
Timothy J. Moynihan, MD
Consultant, Department of Oncology, Mayo Clinic;
Associate Professor of Oncology
Michelle A. Neben Wittich, MD
Consultant, Divisions of Radiation Oncology and General
Internal Medicine, Mayo Clinic; Assistant Professor of
Radiation Oncology
Suzanne M. Norby, MD
Consultant, Division of Nephrology and Hypertension,
Mayo Clinic; Associate Professor of Medicine
Peter A. Noseworthy, MD
Senior Associate Consultant, Division of Cardiovascular
Diseases, Mayo Clinic; Assistant Professor of Medicine
Amy S. Oxentenko, MD
Consultant, Division of Gastroenterology and Hepatology,
Mayo Clinic; Associate Professor of Medicine
Brian A. Palmer, MD
Consultant, Department of Psychiatry & Psychology,
Mayo Clinic; Assistant Professor of Psychiatry
Sabrina D. Phillips, MD
Consultant, Division of Cardiovascular Diseases, Mayo
Clinic; Assistant Professor of Medicine
Present address: Oklahoma University Cardiovascular
Institute
Alyx B. Porter, MD
Consultant, Department of Neurology, Mayo Clinic
Hospital, Phoenix, Arizona; Assistant Professor of
Neurology
John J. Poterucha, MD
Consultant, Division of Gastroenterology and Hepatology,
Mayo Clinic; Professor of Medicine
Katharine A. Price, MD
Consultant, Division of Medical Oncology, Mayo Clinic;
Assistant Professor of Oncology
Rajiv K. Pruthi, MBBS
Consultant, Division of Hematology, Mayo Clinic;
Associate Professor of Medicine
Qi Qian, MD
Consultant, Division of Nephrology and Hypertension,
Mayo Clinic; Professor of Medicine and of Physiology
Contributors xvii
William Sanchez, MD
Consultant, Division of Gastroenterology and Hepatology,
Mayo Clinic; Assistant Professor of Medicine
Nicole P. Sandhu, MD, PhD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Carrie A. Schinstock, MD
Consultant, Division of Nephrology and Hypertension,
Mayo Clinic; Assistant Professor of Medicine
Nina M. Schwenk, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Pankaj Shah, MD
Consultant, Division of Endocrinology, Diabetes,
Metabolism, & Nutrition, Mayo Clinic; Assistant
Professor of Medicine
Lynne T. Shuster, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Associate Professor of Medicine
M. Rizwan Sohail, MD
Consultant, Divisions of Infectious Diseases and
Cardiovascular Diseases, Mayo Clinic; Associate
Professor of Medicine
Marius N. Stan, MD
Consultant, Division of Endocrinology, Diabetes,
Metabolism, & Nutrition, Mayo Clinic;
Assistant Professor of Medicine
Jacob J. Strand, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Karna K. Sundsted, MD
Senior Associate Consultant, Division of General
Internal Medicine, Mayo Clinic; Assistant Professor
of Medicine
Seth R. Sweetser, MD
Consultant, Division of Gastroenterology and Hepatology,
Mayo Clinic; Associate Professor of Medicine
Keith M. Swetz, MD, MA
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Present address: Birmingham Veterans Affairs Medical
Center, Birmingham, Alabama
xviii
xviii Contributors
Jason H. Szostek, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Zelalem Temesgen, MD
Consultant, Division of Infectious Diseases, Mayo Clinic;
Professor of Medicine
Carrie A. Thompson, MD
Consultant, Division of Hematology, Mayo Clinic;
Assistant Professor of Medicine
Farris K. Timimi, MD
Consultant, Division of Cardiovascular Diseases,
Mayo Clinic; Assistant Professor of Medicine
Pritish K. Tosh, MD
Consultant, Division of Infectious Diseases, Mayo Clinic;
Associate Professor of Medicine
Ericka E. Tung, MD, MPH
Consultant, Division of Primary Care Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Bert B. Vargas, MD
Consultant, Department of Neurology, Mayo Clinic
Hospital, Phoenix, Arizona; Assistant Professor of
Neurology
Present address: University of Texas Southwestern
Medical Center
Gerald W. Volcheck, MD
Chair, Division of Allergic Diseases, Mayo Clinic;
Associate Professor of Medicine
Andrea E. Wahner Hendrickson, MD
Consultant, Department of Oncology, Mayo Clinic;
Assistant Professor of Oncology and of Pharmacology
Amy T. Wang, MD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Assistant Professor of Medicine
Present address: Harbor-​UCLA Medical Center
Kenneth J. Warrington, MD
Chair, Division of Rheumatology, Mayo Clinic;
Professor of Medicine
Carilyn N. Wieland, MD
Consultant, Department of Dermatology, Mayo Clinic;
Assistant Professor of Dermatology
Christopher M. Wittich, MD, PharmD
Consultant, Division of General Internal Medicine,
Mayo Clinic; Associate Professor of Medicine
Lily C. Wong-​Kisiel, MD
Consultant, Department of Neurology, Mayo Clinic;
Assistant Professor of Neurology
1

Section

Allergy
I
2
3
Allergic Diseasesa
1 GERALD W. VOLCHECK, MD
Allergy Testing
S
tandard allergy testing relies on identifying the
immunoglobulin (Ig) E antibody specific for the al-
lergen in question. Two classic methods of doing
this are the immediate wheal-​and-​flare skin prick tests
(in which a small amount of antigen is introduced into
the skin and the site is evaluated after 15 minutes for the
presence of an immediate wheal-​and-​flare reaction) and
in vitro (blood) testing.
Methods of allergy testing that do not have a clear scienti­
fic basis include cytotoxic testing, provocation-​neutralization
testing or treatment, and “yeast allergy” testing.
Patch Tests and Prick (Cutaneous) Tests
Patch testing of skin is not the same as immediate wheal-​
and-​flare skin prick testing. Patch testing is used to inves-
tigate only contact dermatitis, a type IV hypersensitivity
skin reaction. Patch tests require 72 to 96 hours for com-
plete evaluation. Many substances cause contact dermati-
tis. Common contact sensitivities include those to nickel,
formaldehyde, fragrances, and latex.
Skin prick testing, in comparison, identifies inhalant
allergens that cause respiratory symptoms, such as allergic
rhinitis and asthma. These allergens include dust mites,
cats, dogs, cockroaches, molds, and tree, grass, and weed
pollens. Food allergy is also assessed by skin prick testing.
Skin prick testing and intradermal testing involve intro-
ducing allergen into the skin layers below the external kera-
tin layer. Intradermal testing, the deeper technique, is used
to evaluate allergy to stinging insect venoms, penicillin, and
a
Portions previously published in Volcheck GW. Clinical allergy: diagnosis and management. Totowa (NJ): Humana; c2009. Used with
permission of Mayo Foundation for Medical Education and Research.
other medications. Intradermal tests are preceded by skin
prick tests.
Drugs with antihistamine properties, such as histamine1
(H1) receptor antagonists, and many anticholinergic and
tricyclic antidepressant drugs can suppress the immediate
response to allergy skin tests. Use of nonsedating antihis-
tamines should be discontinued 5 days before skin testing.
The histamine2 (H2) receptor antagonists have a small sup-
pressive effect. High-​dose corticosteroids can suppress the
delayed-​type hypersensitivity and the immediate response.
In Vitro Allergy Testing
In vitro (blood) allergy testing initially involves chemi-
cally coupling allergen protein molecules to a solid-​phase
substance and ultimately measuring the patient’s specific
IgE to the allergen via radiolabeling, colorimetry, or other
markers.
This test identifies the presence of allergen-​specific IgE
antibody in the same way that the allergen skin test does.
Generally, in vitro allergy testing is not as sensitive as
skin testing and has some limitations because of the po-
tential for chemical modification of the allergen protein
while it is being coupled to the solid phase. Generally, it
is more expensive than allergen skin tests and has no ad-
vantage in routine clinical practice. In vitro allergy test-
ing may be useful clinically for patients who have been
taking antihistamines and are unable to discontinue their
use or for patients who have primary cutaneous diseases
that make allergen skin testing impractical or inaccurate
(eg, severe atopic eczema with most of the skin involved
in a flare).
3
4
4 Section I. Allergy
Chronic Rhinitis
Medical History
The differential diagnosis of chronic rhinitis is given in
Box 1.1. Nonallergic rhinitis is defined as nasal symptoms
occurring in response to nonspecific, nonallergic irritants.
Vasomotor rhinitis is the most common form. Common
triggers of vasomotor rhinitis are strong odors, respiratory
irritants such as dust or smoke, changes in temperature,
changes in body position, and ingestants such as spicy
food or alcohol.
Key Definition
Nonallergic rhinitis: nasal symptoms occurring in
response to nonspecific, nonallergic irritants.
Historical factors favoring a diagnosis of allergic rhini-
tis include a history of nasal symptoms that have a recur-
rent seasonal pattern (eg, every August and September) or
symptoms provoked by being near specific sources of aller-
gens, such as animals. Factors favoring vasomotor rhinitis
include symptoms provoked by strong odors and changes
in humidity and temperature.
Factors common to allergic rhinitis and nonallergic rhi-
nitis (thus, without differential diagnostic value) include
perennial symptoms, intolerance of cigarette smoke, and
history of “dust” sensitivity. Factors that suggest fixed nasal
obstruction (which should prompt physicians to consider
other diagnoses) include unilateral nasal obstruction, uni-
lateral facial pain, unilateral nasal purulence, nasal voice
but no nasal symptoms, disturbances of olfaction without
any nasal symptoms, and unilateral nasal bleeding. Nasal
polyps, septal deviation, and tumor may present with uni-
lateral symptoms. Further evaluation with computed tomo-
graphic (CT) scan of the sinuses or rhinolaryngoscopy is
indicated.
Box 1.1 • Differential Diagnosis of Chronic Rhinitis
Bilateral presentation
Allergic rhinitis
Vasomotor rhinitis
Rhinitis medicamentosa
Sinusitis
Unilateral presentation
Nasal polyposis
Nasal septal deviation
Foreign body
Tumor
Allergy Skin Tests in Allergic Rhinitis
Interpretation of allergy skin test results must be tai-
lored to the unique features of each patient: For pa-
tients with perennial symptoms and negative results on
allergy skin tests, the diagnosis is nonallergic rhinitis.
For patients with seasonal symptoms and appropriately
positive results on allergy skin tests, the diagnosis is
seasonal allergic rhinitis. For patients with perennial
symptoms, positive results on allergy skin tests for
house dust mite suggest house dust mite allergic rhini-
tis. In this case, dust mite allergen avoidance should be
recommended.
Corticosteroid Therapy for Rhinitis
The need for systemic corticosteroid treatment of rhinitis
is limited. Occasionally, patients with severe symptoms
of allergic rhinitis may benefit greatly from a short course
of prednisone (10 mg 4 times daily by mouth for 5 days).
Improvement may be sufficient to allow topical corticoste-
roids to penetrate the nose and satisfactory levels of anti-
histamine to be established in the blood. Severe nasal pol-
yposis, a separate condition, may warrant a longer course
of oral corticosteroid therapy. Sometimes the recurrence
of nasal polyps can be prevented by continued use of topi-
cal corticosteroids. Polypectomy may be required if nasal
polyps do not respond to treatment with systemic and in-
tranasal corticosteroids, but nasal polyps often recur after
surgical intervention.
In contrast to systemic corticosteroids, topical cortico-
steroid agents for the nose are easy to use and have few ad-
verse systemic effects.
KEY FACTS
✓ Patch testing—​used to investigate only contact
dermatitis
✓ Skin prick testing—​identifies inhalant allergens that
cause respiratory symptoms
✓ Nasal symptoms with a recurrent seasonal pattern
favor a diagnosis of allergic rhinitis
✓ Intranasal corticosteroids—​easy to use; few adverse
systemic effects
Long-​term treatment with decongestant nasal sprays
may have “addictive” potential (a vicious cycle of rebound
congestion called rhinitis medicamentosa caused by topi-
cal vasoconstrictors). In contrast, intranasal corticosteroid
therapy does not induce this type of dependence.
A substantial number of patients with nonallergic rhini-
tis also have a good response to intranasal (topical aerosol)
corticosteroid therapy, especially if they have the nasal eo-
sinophilia form of nonallergic rhinitis.
5
A patient who has allergic rhinitis and does not receive
adequate relief with topical corticosteroid plus antihista-
mine therapy may need systemic corticosteroid treatment
and immunotherapy.
An unusual adverse effect of intranasal corticosteroids is
nasal septal perforation. Spray canisters deliver a powerful
jet of particulates, and a few patients have misdirected the
jet to the nasal septum. Instruction on correct nasal inhaler
technique can help in prevention.
Antihistamines and Other Treatments
Antihistamines antagonize the interaction of histamine with
its receptors. Histamine may be more causative of nasal itch
and sneezing than other mast cell mediators. These are the
symptoms most often responsive to antihistamine therapy.
Pseudoephedrine is the most common decongestant
agent in nonprescription drugs for treating cold symptoms
and rhinitis and usually is the active decongestant agent in
widely used prescription agents. Phenylpropanolamine has
been removed from the market because of its association
with hemorrhagic stroke in women. Several prescription
and nonprescription combination agents combine an anti-
histamine and a decongestant. Saline nasal rinses may pro-
vide symptomatic improvement in patients with chronic
rhinitis by helping to remove mucus from the nares.
In men who are middle-​aged or older, urinary retention
may be caused by antihistamines (principally the older
drugs that have anticholinergic effects) and deconges-
tants. Although there has been concern for years that de-
congestants may exacerbate hypertension because they are
α-​adrenergic agonists, a clinically significant hypertensive
response is rare in patients with hypertension that is con-
trolled medically.
Immunotherapy for Allergic Rhinitis
Until topical nasal glucocorticoid sprays were introduced,
allergen immunotherapy was considered first-​line therapy
for allergic rhinitis when the relevant allergen was sea-
sonal pollen of grass, trees, or weeds. Immunotherapy
became second-​line therapy after topical corticosteroids
were introduced, because immunotherapy requires a larger
time commitment during the buildup phase and carries a
small risk of anaphylaxis due to the immunotherapy injec-
tion itself. However, immunotherapy for allergic rhinitis
can be appropriate first-​line therapy for selected patients
and is highly effective.
Immunotherapy is often reserved for patients who do not
receive satisfactory relief from intranasal corticosteroids or
who cannot tolerate antihistamines. Controlled trials have
shown a benefit for pollen, dust mite, and cat allergies and
a variable benefit for mold allergy. Immunotherapy is not
used for food allergy or nonallergic rhinitis. Immunotherapy
has also been shown to decrease the incidence of the de-
velopment of asthma in children with allergic rhinitis and
Chapter 1. Allergic Diseases 5
to decrease the onset of new allergen sensitivities in those
treated for a single allergen.
Environmental Modification
House Dust Mites
The home harbors the most substantial dust mite popu-
lations in bedding, fabric-​upholstered furniture (heavily
used), and carpeting over concrete (when concrete is in
contact with the ground). To decrease mite exposure, bed-
ding (and sometimes, when practical, furniture cushions)
should be encased in mite-​impermeable encasements. To
some degree, encasements also prevent infusion of water
vapor into the bedding matrix. These 2 factors, a mite bar-
rier and decreased humidity, combine to markedly de-
crease the amount of airborne mite allergen. In contrast,
recently marketed acaricides that kill mites or denature
their protein allergens have not proved useful in the home.
Measures for controlling dust mites are listed in Box 1.2.
Pollen
Air-​
conditioning, which enables the home to remain
tightly closed, is the principal defense against pollinosis.
Most masks purchased at local pharmacies cannot exclude
pollen particles and are not worth the expense. Some masks
can protect the wearer from allergen exposure. These are
industrial-​quality respirators designed specifically to pass
rigorous testing by the Occupational Safety and Health
Administration and the National Institute for Occupational
Safety and Health and meet certification requirements for
excluding a wide spectrum of particulates, including pollen
and mold. These masks allow wearers to mow the lawn
and do yard work, which would be intolerable otherwise
because of sensitivity to pollen allergen. It is important to
shower and change clothes when entering the home after
spending significant time outdoors during allergy season.
Animal Dander
No measure for controlling animal dander can compare
with complete removal of the animal from the home. If
complete removal is not tenable, some partial measures
must be considered. Recommendations include keeping
the animal out of the bedroom entirely and attempting to
keep the animal in 1 area of the home. A high-​efficiency
Box 1.2 • Dust Mite Control
Encase bedding and pillows in mite-​impermeable
encasements
Wash sheets and pillowcases in hot water weekly
Remove carpeting from bedroom
Remove upholstered furniture from bedroom
Run dehumidifier
6

6 Section I. Allergy

KEY FACTS Box 1.4 • Causes of Persistent or Recurrent Sinusitis

✓ Used long term, decongestant nasal sprays may cause Nasal polyposis
rebound congestion (rhinitis medicamentosa) Mucormycosis
✓ Immunotherapy became second-​line therapy for Allergic fungal sinusitis
allergic rhinitis after topical corticosteroids were
introduced Ciliary dyskinesia
✓ Highest dust mite populations in bedding, Granulomatosis with polyangiitis (Wegener)
upholstered furniture, and carpeting over concrete Hypogammaglobulinemia
✓ Principal defense against pollinosis—​air-​conditioning Tumor

particulate air (HEPA) room air purifier should be placed Untreated sinusitis may lead to osteomyelitis, orbital
in the bedroom. The person should avoid close contact and periorbital cellulitis, meningitis, and brain abscess.
with the animal and should consider using a mask if han- Cavernous sinus thrombosis, an especially serious compli-
dling the animal or entering the room where the animal is cation, can lead to retrobulbar pain, extraocular muscle pa-
kept. Bathing cats about once every other week may reduce ralysis, and blindness.
the allergen load in the environment. Chronic noninfectious sinusitis is most often due to eo-
sinophilic inflammation of the sinus tissue with or without
Sinusitis polyp formation. Treatment consists primarily of topical
and systemic corticosteroids and saline irrigations. Sinus
Sinusitis is closely associated with edematous obstruction
surgery can be helpful but is not curative, given the recur-
of the sinus ostia (ostiomeatal complex). Poor drainage of
rent inflammatory component of this disease.
the sinus cavities predisposes to infection, particularly by
Persistent, refractory, and complicated sinusitis should
microorganisms that thrive in low-​oxygen environments
be evaluated by a specialist. Sinus CT is the preferred imag-
(eg, anaerobes). In adults, Streptococcus pneumoniae,
ing study for these patients (Figure 1.1).
Haemophilus influenzae, anaerobes, and viruses are
common pathogens. In addition, Moraxella (Branhamella)
catarrhalis is an important pathogen in children.
Important clinical features of acute sinusitis are purulent
nasal discharge, tooth pain, cough, and poor response to de-
congestants. Findings on paranasal sinus transillumination
may be abnormal.
Physicians should be aware of the complications
of sinusitis, which can be life threatening (Box 1.3).
Mucormycosis can cause recurrent or persistent sinusitis
refractory to antibiotics. Allergic fungal sinusitis is char-
acterized by persistent sinusitis, eosinophilia, increased
total IgE level, antifungal (usually Aspergillus) IgE antibod-
ies, and fungal colonization of the sinuses. Granulomatosis
with polyangiitis (Wegener), ciliary dyskinesia, and hypo-
gammaglobulinemia are medical conditions that can cause
refractory sinusitis (Box 1.4).

Box 1.3 • Complications of Sinusitis

Meningitis
Subdural abscess
Extradural abscess
Orbital infection Figure 1.1 Sinusitis. Sinus computed tomogram shows
Cellulitis opacification of the osteomeatal complex on the left, sub-
Cavernous sinus thrombosis total opacification of the right maxillary sinus, and an air-​
fluid level in the left maxillary antrum.
7
Amoxicillin (500 mg 3 times daily) or trimethoprim-​
sulfamethoxazole (1 double-​strength capsule twice daily)
for 10 to 14 days is the treatment of choice for uncompli-
cated maxillary sinusitis.
KEY FACTS
✓ Common sinusitis pathogens in adults—​
Streptococcus pneumoniae, Haemophilus influenzae,
anaerobes, and viruses
✓ Clinical features of acute sinusitis—​purulent nasal
discharge, tooth pain, cough, and poor response to
decongestants
✓ Chronic noninfectious sinusitis—​usually due to
eosinophilic inflammation with or without polyps
✓ Amoxicillin or trimethoprim-​sulfamethoxazole—​
choice for uncomplicated maxillary sinusitis
Plain radiography of the sinuses is less sensitive than
CT (using the coronal sectioning technique). CT scans show
greater detail about sinus mucosal surfaces, but CT usually
is not necessary in acute, uncomplicated sinusitis. CT is in-
dicated, though, for patients in whom a sinus operation is
being considered and for those in whom standard treatment
of sinusitis fails. However, patients with extensive dental
restorations that contain metal may generate too much ar-
tifact for CT to be useful. For these patients, magnetic reso-
nance imaging techniques are indicated.
Urticaria and Angioedema
Duration of Urticaria
The distinction between acute urticaria and chronic urti-
caria is based on duration. If urticaria has been present for
6 weeks or longer, it is called chronic urticaria.
Secondary Urticaria
In most patients, urticaria is simply a skin disease (chronic
idiopathic urticaria). Many of these patients have an anti-
body that interacts with their own IgE or IgE receptor and
produces the urticaria. Occasionally urticaria is the pre-
senting sign of more serious internal disease. It can be a
sign of lupus erythematosus and other connective tissue
diseases, particularly the “overlap” syndromes that are
more difficult to categorize. Thyroid disease, malignancy
(mainly of the gastrointestinal tract), lymphoproliferative
diseases, and occult infection (particularly of the intes-
tines, gallbladder, and dentition) may be associated with
urticaria. Immune complex disease has been associated
with urticaria, usually with urticarial vasculitis; hepatitis
B virus has been identified as an antigen in cases of urti-
caria and immune complex disease.
Chapter 1. Allergic Diseases 7
A common cause of acute urticaria and angioedema
(other than the idiopathic variety) is drug or food allergy.
However, drug or food allergy usually does not cause
chronic urticaria.
Relationship Between Urticaria and Angioedema
In common idiopathic urticaria, the hives last 2 to 18
hours, and the lesions itch intensely because histamine is
the primary cause of wheal formation.
The pathophysiologic mechanism is similar for urticaria
and angioedema. The critical factor is the type of tissue
in which the capillary leak and mediator release occur.
Urticaria occurs when the capillary events are in the tissue
wall of the skin—​the epidermis. Angioedema occurs when
the capillary events affect vessels in the loose connective
tissue of the deeper layers—​the dermis. Virtually all pa-
tients with common idiopathic urticaria also have angio-
edema at some point.
Hereditary Angioedema
Hereditary angioedema (HAE), a rare genetic condition
due to C1 esterase inhibitor dysfunction, is characterized
by recurrent episodes of angioedema, typically without
urticaria. The duration, size, and location of individual
swellings vary. Many patients with HAE have also had
symptoms resembling intestinal obstruction. These symp-
toms usually resolve in 3 to 5 days. HAE episodes may be
related to local tissue trauma in a high percentage of cases,
with dental work often regarded as the classic precipitating
factor. The response to epinephrine is a useful differential
point: HAE lesions do not respond well to epinephrine.
If HAE is strongly suspected, the diagnosis can be
proved by appropriate measurement of complement factors
(decreased levels of C1 esterase inhibitor [quantitative and
functional] and C4 [also C2, during an episode of swelling]).
Treatment of C1 esterase inhibitor dysfunction includes
plasma-​derived C1 esterase inhibitor given intravenously
and bradykinin antagonists: ecallantide, a kallikrein inhibi-
tor, and icatibant, a bradykinin receptor antagonist.
Physical Urticaria
Heat, light, cold, vibration, and trauma or pressure can
cause hives in susceptible persons. Obtaining the history
is the only way of suspecting the diagnosis, which can be
confirmed by applying each of the stimuli to the patient’s
skin. Heat can be applied by placing coins soaked in hot
water for a few minutes on the patient’s forearm. Cold can
be applied with coins kept in a freezer or with ice cubes.
For vibration, a laboratory vortex mixer or any common
vibrator can be used. A pair of sandbags connected by a
strap can be draped over the patient to create enough
pressure to cause symptoms in those with delayed pres-
sure urticaria. Unlike most cases of common idiopathic
8
8 Section I. Allergy
urticaria, in which the lesions affect essentially all skin
surfaces, many cases of physical urticaria seem to involve
only certain areas of skin. Thus, results of challenges will
be positive only in the areas usually involved and negative
in other areas.
Food Allergy in Chronic Urticaria
Food allergy almost never causes chronic urticaria.
However, urticaria (or angioedema or anaphylaxis) can be
an acute manifestation of true food allergy.
Histopathologic Features of Chronic Urticaria
Chronic urticaria is characterized by mononuclear cell
perivascular cuffing around dermal capillaries, par-
ticularly involving the capillary loops that interdigitate
with the rete pegs of the epidermis. Urticarial vasculitis
shows the usual histologic features of leukocytoclastic
vasculitis.
Management of Urticaria
The history is of utmost importance for discovering the
2% to 10% of cases of chronic urticaria due to second-
ary causes. A complete physical examination is needed,
with particular attention paid to the skin (including test-
ing for dermatographism) to evaluate for the vasculitic
nature of the lesions and to the liver, lymph nodes, and
mucous membranes. Laboratory testing need not be ex-
haustive but may include the following: chest radiogra-
phy, a complete blood cell count with differential count
(to discover eosinophilia), measurement of liver en-
zymes, tests for thyroid function and antibodies, eryth-
rocyte sedimentation rate, serum protein electrophoresis
(in patients older than 50 years), urinalysis, and stool
examination for parasites. Allergy skin testing is indi-
cated only if the patient has an element in the history
suggesting an allergic cause. However, patients with id-
iopathic urticaria often have fixed ideas about an allergy
causing their problem, and skin testing often helps to
dissuade them of this idea.
Management of urticaria and angioedema consists of
blocking histamine, beginning usually with nonsedating H1
antagonists. The addition of leukotriene antagonists may
be helpful. The role of H2 antagonists is unclear; they may
help a small percentage of patients. Doxepin, a tricyclic an-
tidepressant, has potent antihistamine effects and is useful.
Systemic corticosteroids can be administered for acute urti-
caria and angioedema.
Anaphylaxis
There is no universally accepted clinical definition of
anaphylaxis. The manifestations of anaphylaxis vary,
Box 1.5 • Most Common Causes of Anaphylaxis
Foods (peanuts, tree nuts, fish, and shellfish)
Medications (antibiotics, neuromuscular blockers, and
anticonvulsants)
Insect stings (bee, fire ant, and vespid)
Latex
Aspirin and other nonsteroidal anti-​inflammatory
agents
depending on the severity, and can include any combi-
nation of urticaria, angioedema, flushing, pruritus, upper
airway obstruction, lower airway obstruction, diarrhea,
nausea, vomiting, syncope, hypotension, tachycardia, and
dizziness. Approximately 90% of anaphylactic episodes
include urticaria or angioedema. A cellular and molecular
definition of anaphylaxis is a generalized allergic reaction
characterized by activated basophils and mast cells releas-
ing many mediators (preformed and newly synthesized).
The dominant mediators of acute anaphylaxis are hista-
mine and prostaglandin D2. The serum levels of tryptase
peak at 1 hour after the onset of anaphylaxis and may stay
elevated for 5 hours. Physiologically, the hypotension of
anaphylaxis is caused by peripheral vasodilatation and not
by impaired cardiac contractility. Anaphylaxis is charac-
terized by a hyperdynamic state. For these reasons, ana-
phylaxis can be fatal in patients with preexisting fixed vas-
cular obstructive disease in whom a decrease in perfusion
pressure leads to a critical reduction in flow (stroke) or
in patients in whom laryngeal edema develops and com-
pletely occludes the airway.
The most common causes of anaphylaxis are listed in
Box 1.5. The vast majority of anaphylactic events occur
within 1 hour, often within minutes, after exposure to the
offending agent.
Food Allergy
Clinical History
The clinical syndrome of food allergy may include the fol-
lowing: Very sensitive persons experience tingling, itch-
ing, and a metallic taste in the mouth while the food is still
in the mouth. Within 15 minutes after the food is swal-
lowed, epigastric distress may occur. There may be nausea
and rarely vomiting. Abdominal cramping is felt chiefly
in the periumbilical area (small-​bowel phase), and lower
abdominal cramping and watery diarrhea may occur.
Urticaria or angioedema may occur in any distribution,
or there may be only itching of the palms and soles. With
increasing clinical sensitivity to the offending allergen,
9
Box 1.6 • Common Causes of Food Allergy
Eggs
Milk
Nuts
Peanuts
Shellfish
Soybeans
Wheat
anaphylactic symptoms may emerge, including tachycar-
dia, hypotension, generalized flushing, and alterations of
consciousness.
In extremely sensitive persons, generalized flushing,
hypotension, and tachycardia may occur before the other
symptoms. Most patients with a food allergy can identify
the offending foods. The diagnosis should be confirmed by
skin testing or in vitro measurement of allergen-​specific IgE
antibody. Items considered to be the most common causes
of food allergy are listed in Box 1.6.
Food-​Related Anaphylaxis
Food-​induced anaphylaxis is the same process as acute
urticaria or angioedema induced by food allergens,
except that the reaction is more severe in anaphylaxis.
Relatively few foods are commonly involved in food-​
induced anaphylaxis; the main ones are peanuts, shell-
fish, and nuts, although any food has the potential to
cause anaphylaxis. In patients with latex allergy, food
allergy can develop to banana, avocado, kiwifruit, and
other fruits.
KEY FACTS
✓ Hereditary angioedema—​recurrent angioedema,
typically without urticaria
✓ Heat, light, cold, vibration, and trauma or pressure
can cause physical urticaria
✓ Urticaria and angioedema are managed by blocking
histamine
✓ Food-​induced anaphylaxis—​same process but more
severe reaction than acute food-​induced urticaria or
angioedema
Allergy Skin Testing in Food Allergy
Patients presenting with food-​ related symptoms may
have food allergy, food intolerance, irritable bowel syn-
drome, nonspecific dyspepsia, or a nonallergic condition.
A careful and detailed history on the nature of the “reac-
tion,” the reproducibility of the association of food and
Chapter 1. Allergic Diseases 9
symptoms, and the timing of symptoms in relation to the
ingestion of food can help the clinician form a clinical
impression.
In many cases, allergy skin tests to foods can be help-
ful. If the results are negative (and the clinical suspicion for
food allergy is low), the patient can be reassured that food
allergy is not the cause of the symptoms. If the results are
positive (and the clinical suspicion for food allergy is high),
the patient should be counseled about management of the
food allergy. The patient should strictly avoid the food and
possible cross-​ reactive foods. These patients should also
be given an epinephrine kit for self-​administration in an
emergency. Although some food allergies may be outgrown,
peanut, tree nut, fish, and shellfish allergies are typically
lifelong.
If the diagnosis of food allergy is uncertain or if the
symptoms are mild and nonspecific, oral food challenges
may be helpful. An open challenge is usually performed
first. If the results are negative, the diagnosis of food allergy
is excluded. If the results are positive but there is suspicion
about them, a blinded placebo-​controlled challenge test can
be performed.
Stinging Insect Allergy
In patients clinically sensitive to Hymenoptera, reactions
to a sting can be either large local reactions or systemic,
anaphylactic reactions. With a large local sting reaction,
swelling at the sting site may be dramatic, but there are no
symptoms distant from that site. Stings of the head, neck,
and dorsum of the hands are particularly prone to large
local reactions.
Anaphylaxis caused by allergy to stinging insects is
similar to all other forms of anaphylaxis. Thus, the onset of
anaphylaxis may be very rapid, often within 1 or 2 minutes.
Pruritus of the palms and soles is the most common initial
manifestation. Frequently, 1 or more of the following occur
next: generalized flushing, urticaria, angioedema, or hypo-
tension. The reason for attaching importance to whether a
stinging insect reaction is a large local or a generalized one
is that allergy skin testing and allergen immunotherapy are
recommended only for generalized reactions. Patients who
have a large local reaction are not at significantly increased
risk for future anaphylaxis.
Bee and Vespid Allergy
Yellow jackets, wasps, and hornets are vespids, and their
venoms cross-​react to a substantial degree. The venom of
honeybees (family, Apidae) does not cross-​react with that
of vespids. Thus, it usually is appropriate to conduct skin
testing for allergy to honeybee and to each of the vespids.
In most cases, the patient will not be able to identify the
causative stinging insect.
10
10 Section I. Allergy
Box 1.7 • Indications for Insect Venom
Immunotherapy
History of mild, moderate, or severe anaphylaxis to a sting
Positive results on skin tests to the venom that was
implicated historically in the anaphylactic reaction
Urticaria distant from the site of the sting (adults only)
Allergy Testing
Patients who have had a generalized reaction need allergen
skin testing. Patients who have had a large local reaction to
a Hymenoptera sting do not need allergen skin testing be-
cause they are not at significantly increased risk for future
anaphylaxis.
In many cases, skin testing should be delayed for at least
1 month after a sting-​induced generalized reaction because
tests conducted closer to the time of the sting have a sub-
stantial risk of false-​negative results. Positive results that
correlate with the clinical history are sufficient evidence for
considering Hymenoptera venom immunotherapy.
Venom Immunotherapy
General indications for venom immunotherapy are listed
in Box 1.7. Patients must understand that after immuno-
therapy is begun, the injection schedule must be main-
tained and that immunotherapy itself has a small risk of
allergic reaction. Patients also need to understand that
despite receiving allergy immunotherapy, they must carry
epinephrine when outdoors because of the possibility
(from 2% with vespid stings to 10% with apid stings) that
immunotherapy will not provide suitable protection. Most,
but not all, patients can safely discontinue venom immu-
notherapy after 5 years of treatment.
Avoidance
The warnings that every patient with stinging insect hyper-
sensitivity should receive are listed in Box 1.8. A patient’s
specific circumstances may require additions to this list. Also,
patients need to know how to use self-​injectable epinephrine.
Many patients wear an anaphylaxis identification bracelet.
Drug Allergy
Drug Allergy Not Involving IgE
or Immediate-​Type Reactions
Patients with drug allergy not involving IgE or immediate-​
type reactions have negative results on skin prick and in-
tradermal testing.
Box 1.8 • Do’s and Don’ts for Patients With
Hypersensitivity to Insect Stings
Avoid looking or smelling like a flower
Avoid wearing flowered-​print clothing
Avoid using cosmetics and fragrances, especially ones
derived from flowering plants
Never drink from a soft-​drink can outdoors during the
warm months—​a yellow jacket can land on or in the
can while you are not watching, go inside the can,
and sting the inside of your mouth (a dangerous
place for a sensitive patient to be stung) when you
take a drink
Never reach into a mailbox without first looking
inside it
Never go barefoot
Always look at the underside of picnic table benches
and park benches before sitting down
Stevens-​Johnson Syndrome
Stevens-​ Johnson syndrome is a bullous skin and mu-
cosal reaction; very large blisters appear over much of
the skin surface, in the mouth, and along the gastroin-
testinal tract. Because of the propensity of the blisters
to break down and become infected, the reaction often
is life-​threatening. Treatment consists of stopping use of
the drug that causes the reaction, giving corticosteroids
systemically, and providing supportive care. The pa-
tients are often treated in burn units. Penicillin, sulfon-
amides, barbiturates, diphenylhydantoin, warfarin, and
phenothiazines are well-​known causes. A drug-​induced
Stevens-​Johnson reaction is an absolute contraindication
to administering the causative drug to the patient in the
future.
Toxic Epidermal Necrolysis
Clinically, toxic epidermal necrolysis is almost indistin-
guishable from Stevens-​Johnson syndrome. Histologically,
the cleavage plane for the blisters is deeper than in Stevens-​
Johnson syndrome. The cleavage plane is at the basement
membrane of the epidermis, so even the basal cell layer
is lost. This makes toxic epidermal necrolysis even more
devastating than Stevens-​ Johnson syndrome, because
healing occurs with much scarring. Often, healing cannot
be accomplished without skin grafting, so the mortality
rate is even higher than for Stevens-​Johnson syndrome.
Patients with toxic epidermal necrolysis should always be
cared for in a burn unit because of full-​thickness damage
over 80% to 90% of the skin. The very high mortality rate
is similar to that for burn patients with damage of this
extent.
Another random document with
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The Project Gutenberg eBook of Dante
 This ebook is for the use of anyone anywhere in the United
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Title: Dante

Author: Edmund G. Gardner

Release date: October 31, 2023 [eBook #71990]

Language: English

Original publication: New York: E. P. Dutton and Company, 1923

Credits: Tim Lindell and the Online Distributed Proofreading

Team at https://www.pgdp.net (This file was produced
from images generously made available by The
Internet Archive/American Libraries.)

*** START OF THE PROJECT GUTENBERG EBOOK DANTE ***

 DANTE
BY
EDMUND G. GARDNER, M.A.

NEW YORK
E. P. DUTTON & COMPANY
681 Fifth Avenue
 Copyright, 1923
By E. P. Dutton & Company

All Rights Reserved

PRINTED IN THE UNITED STATES OF AMERICA

 TO
PHILIP H. WICKSTEED
A SMALL TRIBUTE
OF
DEEP AFFECTION AND HIGH ESTEEM
 AUTHOR’S NOTE
I would ask the reader to take the present volume, not as a new
book on Dante, but merely as a revision of the Primer which was first
published in 1900. It has been as far as possible brought up to date,
the chief modifications being naturally in the sections devoted to the
poet’s life and Opere minori, and in the bibliographical appendix; but
the work remains substantially the same. Were I now to write a new
Dante Primer, after the interval of nearly a quarter of a century, I
should be disposed to attach considerably less importance to the
allegorical meaning of the Divina Commedia, and to emphasise,
more than I have here done, the aspect of Dante as the symbol and
national hero of Italy.
E. G. G.
London, July, 1923.
 N.B.—The “Sexcentenary Dante” (the testo critico published under
the auspices of the Società Dantesca Italiana) adopts a slightly
different numbering of the chapters, or paragraphs, of the Vita Nuova
and the second treatise of the Convivio from that presented by the
“Oxford Dante” and the “Temple Classics.” I have kept to the latter
(which is indicated in brackets in the testo critico). Similarly, I have
followed the numbering of the Epistolae in Dr. Toynbee’s edition and
the “Oxford Dante” (also given in brackets in the testo critico). In the
section on the lyrical poetry, Rime refers to the testo critico as edited
by Professor Barbi, O. to the new Oxford edition revised by Dr.
Toynbee. In the closing passage of the Letter to a Florentine friend, I
have followed the reading retained by Dr. Toynbee. I have frequently
availed myself of Dr. Wicksteed’s translation of the Letters and
Monarchia, of Mr. A. G. F. Howell’s version of the De Vulgari
Eloquentia, and occasionally of Carlyle’s rendering of the Inferno.
Every student of Dante must inevitably owe much to others; but, in
this new edition of my Primer, I would express my indebtedness in
particular to the writings of Dr. Paget Toynbee, Dr. Philip H.
Wicksteed, the late Ernesto Giacomo Parodi, and Prof. Michele
Barbi.
⁂ To the Bibliographical Appendix should be added: A.
Fiammazzo, Il commento dantesco di Graziolo de’ Bambaglioli
(Savona, 1915), and P. Revelli, L’Italia nella Divina Commedia
(Milan, 1923).
 CONTENTS
CHAPTER I
Dante in his Times—
i. The End of the Middle Ages.—ii. Dante’s 1
Childhood and Adolescence.—iii. After the
Death of Beatrice.—iv. Dante’s Political Life.
—v. First Period of Exile.—vi. The Invasion of
Henry VII.—vii. Last Period of Exile.—viii.
Dante’s Works and First Interpreters
CHAPTER II
Dante’s Minor Italian Works—
i. The Vita Nuova.—ii. The Rime.—iii. The 67
Convivio
CHAPTER III
Dante’s Latin Works—
i. The De Vulgari Eloquentia.—ii. The 102
Monarchia.—iii. The Epistolae.—iv. The
Eclogae.—v. The Quaestio de Aqua et Terra
CHAPTER IV
The “Divina Commedia”—
i. Introductory.—ii. The Inferno.—iii. The 136
Purgatorio.—iv. The Paradiso
Bibliographical Appendix 223
Diagrams and Tables 233
Index 249
DANTE
 CHAPTER I
DANTE IN HIS TIMES
1. The End of the Middle Ages
From Gregory VII. to Frederick II.—The twelfth and thirteenth
centuries cover the last and more familiar portion of the Middle Ages.
They are the period of chivalry, of the crusades and of romance,
when the Neo-Latin languages bore fruit in the prose and poetry of
France, the lyrics of the Provençal troubadours, and the earliest
vernacular literature of Italy; the period which saw the development
of Gothic architecture, the rise of scholastic philosophy, the
institution of the Franciscan and Dominican orders, the recovery by
western Europe of the works of Aristotle, the elevation of Catholic
theology into a systematic harmony of reason and revelation under
the influence of the christianised Aristotelianism of Albertus Magnus
and Thomas Aquinas. The vernacular literature of Italy developed
comparatively late, and (until the time of Aquinas and Bonaventura)
her part in the scholastic movement was secondary to that of
France, but she had led the way in the revival of the study of Roman
law and jurisprudence, which centred at Bologna, where the great
Irnerius taught at the beginning of the twelfth century. It was thus that
the first European university, studium generale, came into being, and
Bologna boasts the proud title alma mater studiorum.
There are two predominant political factors in Italy which appear at
the end of the twelfth century, and hold the field up to the time of
Dante’s birth. Out of the war of investitures between Pope and
Emperor, the struggle which we associate mainly with the name of
Hildebrand (Gregory VII.), emerged the Italian city-states, the free
communes of northern and central Italy, whose development
culminated in the heroic resistance offered by the first Lombard
League to the mightiest of mediaeval German Caesars, Frederick I.
(Barbarossa), which won the battle of Legnano (1176) and obtained
the peace of Constance (1183). In the south, the Normans—
conquering Apulia and Calabria, delivering Sicily from the Saracens
—consolidated their rule into a feudal monarchy, making their capital
Palermo one of the most splendid cities of the mediaeval world. The
third and last of these Norman kings of Sicily, William II. (Par. xx. 61-
66), died in 1189. The son of Barbarossa, Henry VI., claimed the
kingdom in the right of his wife Constance (Par. iii. 115-120), and
established the Suabian dynasty on the throne. His son, Frederick
II., continued the cultured traditions of the Norman kings; but the
union in his person of the kingdom of Sicily with the Empire led to a
continuous struggle with the Italian communes and the Papacy,
which embittered his closing years until his death in 1250. The reign
of Frederick II. is the period of the Guelf and Ghibelline factions, and
the beginning of the rise of tyrants in the Italian cities, tyrants of
whom the most terrible example was Ezzelino da Romano (Inf. xii.
110).
The Battle of Benevento.—The policy of Frederick II. was
continued by his son Manfred (crowned King of Sicily in 1258),
against whom Pope Clement IV., claiming the right to dispose of the
kingdom as a fief of the Church, summoned Charles of Anjou, the
brother of St. Louis of France. Charles entered Italy (Purg. xx. 67),
encountered and defeated Manfred on the plains of Grandella near
Benevento, in February 1266, and the papal legate refused the rites
of Christian burial to the fallen king (Purg. iii. 124-132). This battle of
Benevento marks an epoch in Italian history. It ended for the time the
struggle between the Roman Pontiffs and the German Caesars; it
initiated the new strife between the Papacy and the royal house of
France. Henceforth the old ideal significance of “Guelf” and
“Ghibelline,” as denoting adherents of Church and Empire
respectively, becomes lost in the local conflicts of each Italian district
and city. The imperial power was at an end in Italy; but the Popes, by
calling in this new foreign aid, had prepared the way for the
humiliation of Pope Boniface at Anagni and the corruption of
Avignon. The fall of the silver eagle from Manfred’s helmet before the
golden lilies on Charles’s standard may be taken as symbolical. The
preponderance in Italian politics had passed back from Germany to
France; the influence of the house of Capet was substituted for the
overthrown authority of the Emperor (Purg. xx. 43, 44). Three weeks
after the battle Charles entered Naples in triumph, King of Apulia and
Sicily; an Angevin dynasty was established upon the throne of the
most potent state of Italy.
Art and Letters.—This political transformation was profoundly
felt in Italian literature. A new courtly poetry, that of the so-called
“Sicilian School,” had come into being in the south, partly based on
Provençal models, in the first quarter of the thirteenth century. Its
poets—mainly Sicilians and Apulians, but with recruits from other
parts of the peninsula—had almost given to Italy a literary language.
“The Sicilian vernacular,” writes Dante in his De Vulgari Eloquentia,
“seems to have gained for itself a renown beyond the others; for
whatever Italians produce in poetry is called Sicilian, and we find that
many native poets have sung weightily.” This he ascribes to the
fostering influence of the imperial rule of the house of Suabia:
“Those illustrious heroes, Frederick Caesar and his well-begotten
son Manfred, showing their nobility and rectitude of soul, as long as
fortune lasted, followed human things, disdaining the bestial;
wherefore the noble in heart and endowed with graces strove to
cleave to the majesty of such great princes; so that, in their time,
whatever the excellent among Italians attempted first appeared at
the court of these great sovereigns. And, because the royal throne
was Sicily, it came about that whatever our predecessors produced
in the vernacular is called Sicilian” (V. E. i. 12). The house of Anjou
made Naples their capital, and treated Sicily as a conquered
province. After Benevento the literary centre of Italy shifted from
Palermo and the royal court of the south to Bologna and the
republican cities of Tuscany. Guittone d’Arezzo (Purg. xxvi. 124-126)
founded a school of Tuscan poets, extending the field of Italian
lyrical poetry to political and ethical themes as well as love (which
had been the sole subject of the Sicilian School). The beginnings of
Italian literary prose had already appeared at Bologna, with the first
vernacular models for composition of the rhetoricians, the masters of
the ars dictandi. Here, within the next eight years, St. Thomas
Aquinas published the first and second parts of the Summa
Theologica; and the poetry of the first great singer of modern Italy,
Guido Guinizelli (Purg. xxvi. 91-114), rose to spiritual heights
undreamed of in the older schools, in his canzone on Love and true
nobility: Al cor gentil ripara sempre Amore; “To the gentle heart doth
Love ever repair.” And, in the sphere of the plastic arts, these were
the years that saw the last triumphs of Niccolò Pisano, “the Father of
Sculpture to Italy,” and the earliest masterpieces of Cimabue, the
teacher of Giotto (Purg. xi. 94-96), the shepherd boy who came from
the fields to free Italian painting from Byzantine fetters, and who
“developed an artistic language which was the true expression of the
Italian national character.”

2. Dante’s Childhood and Adolescence

Birth and Family.—Dante Alighieri, in its Latin form Alagherii, was
born at Florence in 1265, probably in the latter part of May, some
nine months before the battle of Benevento. His father, Alighiero di
Bellincione di Alighiero, came of an ancient and honourable family of
that section of the city named from the Porta San Piero. Although
Guelfs, the Alighieri were probably of the same stock as the Elisei,
decadent nobles of supposed Roman descent, who took the
Ghibelline side in the days of Frederick II., when the city was first
involved in these factions after the murder of young Buondelmonte in
her “last peace” in 1215 (Par. xvi. 136-147). Among the warriors of
the Cross, in the Heaven of Mars, Dante meets his great-great-
grandfather Cacciaguida. Born probably in 1091, Cacciaguida
married a wife from the valley of the Po, a member of one or other of
the families afterwards known as the Aldighieri or Alighieri at Ferrara,
Parma, and Bologna, was knighted by Conrad III., and died in battle
against the infidels in the disastrous second crusade (Par. xv. 137-
148). None of Cacciaguida’s descendants had attained to any
distinction in the Republic. Brunetto di Bellincione, Dante’s uncle,
probably fought for the Guelfs at Montaperti in 1260, where he may
have been one of those in charge of the carroccio, the battle-car
which accompanied the army. Besides Cacciaguida and his son
Alaghiero, or Alighiero, the first to bear the name, who is said by his
father to be still in the purgatorial terrace of the proud (Par. xv. 91-
96), the only other member of the family introduced into the Divina
Commedia is Geri del Bello, a grandson of the elder Alighiero and
cousin of Dante’s father, a sower of discord and a murderer (Inf. xxix.
13-36), whose violent and well-deserved death had not yet been
avenged.
The Florentine Republic.—As far as Florence was concerned,
the real strife of Guelfs and Ghibellines was a struggle for
supremacy, first without and then within the city, of a democracy of
merchants and traders, with a military aristocracy of partly Teutonic
descent, who were gradually being deprived of their territorial and
feudal sway, which they had held nominally from the Emperor in the
contado, the country districts of Tuscany included in the continually
extending Florentine commune. Although the party names were first
introduced into Florence in 1215, the struggle had virtually begun
after the death of the great Countess Matilda in 1115; and had
resulted in a regular and constitutional advance of the power of the
people, interrupted by a few intervals. It was in one of these intervals
that Dante was born. The popular government (Primo Popolo), which
had been established shortly before the death of Frederick II. in
1250, and worked victoriously for ten years, had been overthrown in
1260 at the disastrous battle of Montaperti, “the havoc and the great
slaughter, which dyed the Arbia red” (Inf. x. 85, 86). The patriotism of
Farinata degli Uberti saved Florence from total destruction, but all
the leading Guelf families were driven out, and the government
remained in the power of a despotic Ghibelline aristocracy, under
Manfred’s vicar, Count Guido Novello, supported by German
mercenaries. After the fall of Manfred, an attempt was made to effect
a peace between the Ghibellines and the people; but a revolution on
St. Martin’s Day, November 11th, 1266, led to the expulsion of Guido
Novello and his forces, and the formation of a provisional democratic
government. In January 1267 the banished Guelfs—many of whom
had fought under the papal banner at Benevento—returned; on
Easter Day French troops entered Florence, the Ghibellines fled, the
Guelfs made Charles of Anjou suzerain of the city, and accepted his
vicar as podestà. The government was reorganised, with a new
institution, the Parte Guelfa, to secure the Guelf predominance in the
Republic.
 The defeat of young Conradin, grandson of Frederick II., at
Tagliacozzo in 1268, followed by his judicial murder (Purg. xx. 68),
confirmed the triumph of the Guelfs and the power of Charles in Italy.
In Florence the future conflict lay between the new Guelf aristocracy
and the burghers and people, between the Grandi and the Popolani;
the magnates in their palaces and towers, associated into societies
and groups of families, surrounding themselves with retainers and
swordsmen, but always divided among themselves; and the people,
soon to become “very fierce and hot in lordship,” as Villani says,
artisans and traders ready to rush out from stalls and workshops to
follow the standards of their Arts or Guilds in defence of liberty. In the
year after the House of Suabia ended with Conradin upon the
scaffold, the Florentines took partial vengeance for Montaperti at the
battle of Colle di Valdelsa (Purg. xiii. 115-120), where the Sienese
were routed and Provenzano Salvani (Purg. xi. 109-114) killed. It is
said to have been Provenzano Salvani who, in the great Ghibelline
council at Empoli, had proposed that Florence should be destroyed.
Dante’s Boyhood.—It is not clear how Dante came to be born in
Florence, since he gives us to understand (Inf. x. 46-50) that his
family were fiercely adverse to the Ghibellines and would naturally
have been in exile until the close of 1266. Probably his father, of
whom scarcely anything is known, took no prominent part in politics
and had been allowed to remain in the city. Besides the houses in
the Piazza San Martino, he possessed two farms and some land in
the country. Dante’s mother, Bella (perhaps an abbreviation of
Gabriella), is believed to have been Alighiero’s first wife, and to have
died soon after the poet’s birth. Her family is not known, though it
has been suggested that she may have been the daughter of
Durante di Scolaio degli Abati, a Guelf noble. Alighiero married
again, Lapa di Chiarissimo Cialuffi, the daughter of a prominent
Guelf popolano; by this second marriage he had a son, Francesco,
and a daughter, Tana (Gaetana), who married Lapo Riccomanni.
Another daughter, whose name is not known, married Leone Poggi;
it is not quite certain whether her mother was Bella or Lapa. Dante
never mentions his mother nor his father, whom he also lost in
boyhood, in any of his works (excepting such indirect references as
Inf. viii. 45, and Conv. i. 13); but, in the Vita Nuova, a “young and
gentle lady, who was united to me by very near kindred,” appears
watching by the poet in his illness. In the loveliest of his early lyrics
she is described as

Adorna assai di gentilezze umane,

which Rossetti renders:

Exceeding rich in human sympathies.

This lady was, perhaps, one of these two sisters; and it is tempting to
infer from Dante’s words that a tender affection existed between him
and her. It was from Dante’s nephew, Andrea Poggi, that Boccaccio
obtained some of his information concerning the poet, and it would
be pleasant to think that Andrea’s mother is the heroine of this
canzone (V. N. xxiii.); but there are chronological difficulties in the
identification.
Sources.—Our sources for Dante’s biography, in addition to his
own works, are primarily a short chapter in the Chronicle of his
neighbour Giovanni Villani, the epoch-making work of Boccaccio,
Filippo Villani’s unimportant sketch at the end of the fourteenth and
the brief but reliable life by Leonardo Bruni at the beginning of the
fifteenth century. In addition we have some scanty hints given by the
early commentators on the Divina Commedia, and a few documents,
including the consulte or reports of the deliberations of the various
councils of the Florentine Republic. Boccaccio’s work has come
down to us in two forms: the Vita di Dante (or Trattatello in laude di
Dante) and the so-called Compendio (itself in two redactions, the
Primo and Secondo Compendio); the researches of Michele Barbi
have finally established that both are authentic, the Compendio
being the author’s own later revision. The tendency of recent
scholarship has in a considerable measure rehabilitated the once
discredited authority of Boccaccio, and rejected the excessive
scepticism represented in the nineteenth century by Bartoli and
Scartazzini.
Beatrice.—Although Leonardo Bruni rebukes Boccaccio, “our
Boccaccio that most sweet and pleasant man,” for having lingered so
long over Dante’s love affairs, still the story of the poet’s first love
remains the one salient fact of his youth and early manhood. We
may surmise from the Vita Nuova that at the end of his eighteenth
year, presumably in May 1283, Dante became enamoured of the
glorious lady of his mind, Beatrice, who had first appeared to him as
a child in her ninth year, nine years before. It is not quite certain
whether Beatrice was her real name or one beneath which Dante
conceals her identity; assuredly she was “Beatrice,” the giver of
blessing, to him and through him to all lovers of the noblest and
fairest things in literature. Tradition, following Boccaccio, has
identified her with Bice, the daughter of Folco Portinari, a wealthy
Florentine who founded the hospital of S. Maria Nuova, and died in
1289 (cf. V. N. xxii.). Folco’s daughter is shown by her father’s will to
have been the wife of Simone dei Bardi, a rich and noble banker.
This has been confirmed by the discovery that, while the printed
commentary of Dante’s son Pietro upon the Commedia hardly
suggests that Beatrice was a real woman at all, there exists a fuller
and later recension by Pietro of his own work which contains a
distinct statement that the lady raised to fame in his father’s poem
was in very fact Bice Portinari. Nevertheless, there are still found
critics who see in Beatrice not a real woman, but a mystically exalted
ideal of womanhood or a merely allegorical figure; while Scartazzini
at one time maintained that the woman Dante loved was an
unknown Florentine maiden, who would have been his wife but for
her untimely death. This can hardly be deduced from the Vita Nuova;
in its noblest passages the woman of Dante’s worship is scarcely
regarded as an object that can be possessed; death has not robbed
him of an expected beatitude, but all the world of an earthly miracle.
But, although it was in the fullest correspondence with mediaeval
ideals and fashions that chivalrous love and devotion should be
directed by preference to a married woman, the love of Dante for
Beatrice was something at once more real and more exalted than
the artificial passion of the troubadours; a true romantic love that
linked heaven to earth, and was a revelation for the whole course of
life.
Poetry, Friendship, Study.—Already, at the age of eighteen,
Dante was a poet: “I had already seen for myself the art of saying
words in rhyme” (V. N. iii.). It was on the occasion of what we take as
the real beginning of his love that he wrote the opening sonnet of the
Vita Nuova, in which he demands an explanation of a dream from
“all the faithful of Love.” The new poet was at once recognised.
Among the many answers came a sonnet from the most famous
Italian lyrist then living, Guido Cavalcanti, henceforth to be the first of
Dante’s friends: “And this was, as it were, the beginning of the
friendship between him and me, when he knew that I was he who
had sent that sonnet to him” (cf. Inf. x. 60). In the same year, 1283,
Dante’s name first occurs in a document concerning some business
transactions as his late father’s heir.
There are no external events recorded in Dante’s life between
1283 and 1289. Boccaccio represents him as devoted to study. He
certainly owed much to the paternal advice of the old rhetorician and
statesman, Brunetto Latini, who had been secretary of the commune
and, until his death in 1294, was one of the most influential citizens
in the state: “For in my memory is fixed, and now goes to my heart,
the dear, kind, paternal image of you, when in the world, from time to
time, you taught me how man makes himself eternal” (Inf. xv. 82). Of
his growing maturity in art, the lyrics of the Vita Nuova bear witness;
the prose narrative shows that he had studied the Latin poets as well
as the new singers of Provence and Italy, had already dipped into
scholastic philosophy, and was not unacquainted with Aristotle. At
the same time, Leonardo Bruni was obviously right in describing
Dante as not severing himself from the world, but excelling in every
youthful exercise; and it would seem from the Vita Nuova that, in
spite of his supreme devotion for Beatrice, there were other
Florentine damsels who moved his heart for a time. Dante speaks of
“one who, according to the degrees of friendship, is my friend
immediately after the first,” and than whom there was no one nearer
in kinship to Beatrice (V. N. xxxiii.). Those who identify Dante’s
Beatrice with the daughter of Messer Folco suppose that this second