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ABIM Allergy Immunology Review 2014 . Richard D. deShazo, MD with thanks to the many colleagues from whom I have borrowed material. Questions:. What are the major diagnostic criteria for asthma?. How can you separate asthma from COPD?.

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abim allergy immunology review 2014

ABIM Allergy Immunology Review2014

Richard D. deShazo, MD with thanks to the many colleagues from whom I have borrowed material


What are the major diagnostic criteria for asthma?

  • How can you separate asthma from COPD?
  • What does a positive methacholine inhalation test mean?
spirometry before and after an inhaled bronchodilator showing reversible airway obstruction
Spirometry before and after an inhaled bronchodilator showing reversible airway obstruction
asthma diagnosis
Asthma Diagnosis
  • FEV1 improvement of 12% and 200mL after beta-agonist is evidence for asthma according to ATS
  • Decreased FEV1/FVC ratio
    • 20-39yr 85%
    • 40-59yr 80%
    • 60-80yr 70%
  • Methacholine challenge – not diagnostic of asthma
    • + with 20% decrease FEV1 with <8-16mg/mL
    • True benefit is in negative predictive value

What test should be considered in a young asthmatic female with recurrent episodes of wheezing poorly responsive to bronchodilators?


Vocal Cord Dysfunction Is Not Asthma, But May Occur In Asthmatics

Flow volume loops showing maximum inspiratory and expiratory flow-volume relationships in a patient with vocal cord dysfunction during asymptomatic (left) and symptomatic (right) periods. Note also the marked adduction of the vocal cords with severe reduction of the glottic aperture during a symptomatic period (right) of airway obstruction.

vocal cord dysfunction
Vocal Cord Dysfunction
  • Female 2:1
  • Athletes
  • Bronchodilator non responsive
  • Many (up to 1/3) can have coexist asthma
  • Difficulty getting breath in
2 questions
2 Questions:

What is the likely diagnosis in a man with persistent cough, shortness of breath, dyspnea, and episodic wheeze that developed after working as a police officer in the 9/11 exposure area in NYC?

A 22 year old with recent onset cough and wheeze works in a custom sailboat shop in Biloxi sealing the inside of boats with epoxy resins. What is the most likely low molecular weight chemical causing his symptoms?

reactive airways dysfunction syndrome rads not asthma
Reactive Airways Dysfunction Syndrome (RADS): Not Asthma
  • Treatment – Time + corticosteroids
  • Occurs after a single inhalation of a caustic irritant in a non-asthmatic
  • Obstruction on PFT
  • (+) methalcholine inhalation challenge
  • Limited PFT-response to beta-agonists
  • Not “reactive airways disease”
occupational asthma
Occupational Asthma
  • Basically, asthma occurring because of exposure at work.
  • Testing difficult, so sometimes need to do pulmonary evaluation at the workplace. (Start with peak flows at work versus home).
  • Earlier you diagnose the better, because may lead to permanent asthma even when removed from environment.
risk factors for asthma death
Risk Factors for Asthma Death
  • Previous life-threatening asthma such as respiratory arrest
  • Hospitalization or ED visit for asthma within the last year
  • Use of 2 or more canisters of rescue inhaler/month
  • Poor perception of hypoxia or airway obstruction
  • Psychosocial disturbance
asthma pharmacotherapy
Asthma Pharmacotherapy
  • Rescue medicines
    • Short acting agonists (SABA)
    • Anticholinergic
  • Controller medicines
    • Inhaled corticosteroids (ICS)
    • Long acting agonists (LABA)
    • Leukotriene receptor antagonists (LTRA)
    • Combinations of ICS & LABA
    • Anti-IgE (omalizamab)
    • Others
things to consider in the out of control asthmatic
Things to consider in the out of control asthmatic
  • Vocal cord dysfunction
  • GERD
  • Sinusitis
  • Churg-Strauss syndrome
  • ABPA
  • Compliance/technique
3 eosinophilic lung diseases
3 Eosinophilic Lung Diseases
  • Churg-Strauss Vasculitis
    • Sinusitis, asthma, eosinophilia, vasculitis
    • Transient pulmonary infiltrates
    • Small vessel vasculitis
    • Neuropathies (mononeuritis multiplex)
    • MPO- ab/P-ANCA test (+) in about 50%
    • RX: steroids (cyclophosphamide/azathioprine in severe)
    • ? relationship to LTRA
allergic bronchopulmonary mycosis abpm
Allergic Bronchopulmonary Mycosis (ABPM)
  • Includes allergic bronchopulmonaryaspergillosis (ABPA) and other allergic mycoses
  • Criteria
    • Asthma
    • Fleeting pulmonary infiltrates
    • High total IgE (>1000 ng/mL or 417 kU/L)
    • Positive immediate skin test (IgE) to fungus (A. fumigatus, etc.) or Positive RAST test
    • Elevated serum specific IgE to fungus (A. fumigatus, etc.)
    • CT with central bronchiectasis reflects chronic disease
treatment of abpm
Treatment of ABPM
  • Oral corticosteroids
  • Follow total serum IgE and CXR
  • No long term studies on Itraconazole as steroid sparing agent
hypereosinophilic syndrome
Hypereosinophilic Syndrome
  • No increase asthma but may have allergic – like dermatitis
  • Paramalignant syndrome
  • Peripheral blood eos count >1500 µL for at least 6 months
  • Absence of any other known cause of eosinophilia
  • Presumptive signs/symptoms of organ invasion by eosinophils
  • 9:1 male:female
  • Systemic disease
  • Cardiac disease (thrombosis, fibrosis, necrosis) is the most common cause of death
  • FIP1L1/PDGFA fusion-gene present in some patients
organs involved in hypereosinophlic syndrome
Organs Involved in Hypereosinophlic Syndrome
  • Heart
  • Skin, Lungs, GI tract, Nervous System
  • Vascular thrombosis is a feared complication
  • Treatment
    • Steroids
    • Hydroxyurea
    • Interferon α
    • Gleevac (imatinib) - for FIP1L1-PDGFRα gene rearrangement

A 50 year old woman with asthma and atopic dermatitis has her 3rd episode of food impaction. What findings should be sought from endoscopy to confirm the diagnosis?

eosinophilic gastroenteritis
Eosinophilic Gastroenteritis
  • Atopic individuals
  • Usually in upper tract
  • Food impaction in esophagus
  • Mucous furrowing and white specks on endoscopy
  • More than 12 eosinophils/HPF on biopsy
  • Food allergy in some
  • Treated with non-absorbable steroids

A 50 year old bird breeder has persistent shortness of breath, cough, and dyspnea. What should be done?

hypersensitivity pneumonitis
Hypersensitivity Pneumonitis
  • Fever, chills, malaise, cough, dyspnea
  • Acute, subacute, chronic
  • A systemic illness
  • Also known as “extrinsic allergic alveolitis”
  • Non allergic, not IgE mediated, no eosinophilia, no asthma except pigeon breeder’s (bird fancier’s) lung
  • T-cell mediated
  • CXR/CT scan abnormal: ground glass/diffuse alveolar pattern
  • PFT – restriction not obstruction except for pigeon breeders
  • Chronic  pulmonary fibrosis
approach to allergic rhinitis
Approach to Allergic Rhinitis
  • Characterize chronicity looking for seasonal variation.
  • Ask for family history, indoor triggers and nasal itching.
  • Swollen nasal mucosa usually more blue that red.
  • Treat
  • If there is treatment failure, do allergy skin tests or RASTs to determine specific allergen and consider allergy shots.
  • Allergy shots are very effective for allergic rhinitis and insect anaphylaxis.
allergic rhinitis
Allergic Rhinitis
  • Nasal steroids – first line treatment
  • Antihistamines and leukotriene receptor antagonists – second line (about equal efficacy as second line agents)
  • To prevent symptoms on planned exposures, chromolyn or antihistamines work best
  • Allergen immunotherapy by subcutaneous or sublingual techniques
mimics of allergic rhinitis
Mimics of Allergic Rhinitis
  • Vasomotor rhinitis
  • Rhinitis medicamentosa
  • Nasal manifestations of systemic disease:
    • Diabetes mellitus – mucor mycosis (nasal eschar; black crust)
    • Wegener’s granulomatosis (saddle nose)
    • Midline granuloma (saddle nose)
    • Relapsing polychondritis (saddle nose)
    • Sarcoidosis (bloody crusts)
    • Cystic fibrosis (nasal polyps)
    • CSF leak – check beta 2 transferrin (very specific)
rhinosinusitis syndromes with nasal polyposis
Rhinosinusitis Syndromes withNasal Polyposis
  • Immunodeficiency
  • Cystic fibrosis
  • Aspirin – sensitive respiratory disease
  • Allergic fungal sinusitis
  • Anosmia is a big tip off for polyps

A 30 year old nurse has a severe chronic dry and cracking dermatitis of both hands. What should you do first?


Irritant vs. Allergic Contact Dermatitis

Patch testing can detect both irritant and allergic contact dermatitis, if the tests are read at appropriate times. Consider a patch test a TB skin test. Positive results are erythema and induration maximum at 24-48 hours.



Most Frequently Positive Patch -Test Results

in Allergic Contact Dermatitis


A 16 year old male with asthma has a chronic pruritic dermatitis in the flexural areas of his elbows and knees. What treatment would be best for this problem?


Atopic Dermatitis (Eczema) (1)

Atopic dermatitis with involvement of a flexural surface. The frequently involved anticubital and popliteal fossae.

atopic dermatitis 2
Atopic Dermatitis (2)
  • Increased susceptibility to
    • Staph aureus, HSV (eczema herpeticum), vaccinia
  • Differential diagnosis
    • Allergic contact dermatitis
    • Irritant contact dermatitis (gloves)
    • Cutaneous T – cell lymphoma

An adult presenting with eczematous dermatitis with an erythrodermatous appearance by skin biopsy with genetic studies

    • Atopic dermatitis is associated with abnormalities in the filaggrin gene which encodes for filaggrin protein important in statiumcorneammoisturization
treatment of atopic dermatitis
Treatment of Atopic Dermatitis
  • Skin hydration/moisturization (Aquaphor)
  • Medium strength topical corticosteroids and combinations (equal parts 0.1% triamcinolone and Aquaphor)
  • Oral antibiotics (Staph)
  • Antihistamines (control itch)
  • Topical calcineurin inhibitors (protopic/ elidel)

MKSAP Clinical Clues to the

Diagnosis of Selected Causes of Erythroderma

  • Classification of Urticaria
  • Acute urticaria (<6 weeks)
  • Chronic urticaria (>6 weeks)
  • Physical urticaria (pressure, cold, vibratory, etc.)
  • Urticarial vasculitis
  • Contact urticaria (touching a cat)
  • Urticaria and angioedema as components of anaphylaxis

Palpable purpura is a clinical sign of a small vessel (leukocytoclastic) vasculitis which may present as chronic urticaria.


A 68 year old female with chronic mylogenous leukemia presents with non itchy swelling of the lips and throat. What diagnostic tests would be most useful to diagnose acquired angioedema?

differential diagnosis cutaneous and or laryngeal swelling
Differential Diagnosis: Cutaneous and/or Laryngeal Swelling
  • Allergic reactions and anaphylaxis
  • Idiopathic angioedema
  • Drug induced angioedema
  • Allergic contact dermatitis
  • Autoimmune conditions
  • Thyroid disorders
  • Superior vena cava syndrome and tumors
  • Cheilitisgranulomatosa (Miescher’scheilitis) and Melkersson-Rosenthal syndrome
  • Trichinosis
  • Low C-4 levels
hereditary angioedema
Hereditary Angioedema
    • Autosomal Dominant
  • Hiveless, itchless edema
  • Hereditary angioedema form more likely to have symptoms precipitated by trauma - dental visit, surgery, auto accident, menses, puberty
    • Visceral attacks may present as an acute abdomen with normal findings at surgery
symptoms painless itchless angioedma with without family history
Symptoms: Painless, itchlessangioedma with/without family history
  • Diagnosis of HAE5
    • HAE 1 - low C41, 2 low C1 INH, low C1INH-F
    • HAE2 - low C41, 2normal C1 INH, low C1INH-F
    • Acquired – low C41, 3low C1 INH, low C1INH-F, low Clq
    • HAE3 – normal C4 4 normal C1 INH, normal C1INH-F, normal C1f level
    • Always low during attacks
    • SERPING1 gene abnormalities
    • Antibodies to C1INH
    • Abnormalities in Factor XII genes
    • Family members should be screened in all types
acquired angioedema
Acquired Angioedema
  • Associated with lymphoproliferative disorders
  • Have low C1q levels
  • Mechanism unclear
  • Low C1 of levels appear to reflect autoactivation
  • Anti – C1 esterase inhibitor antibodies have been described as well
tests for hereditary acquired angioedema
Tests for Hereditary/Acquired Angioedema
  • C4 – is a great screening test, but is normal in HAE Type 3
  • Test for C1 esterase inhibitor level and function to discriminate between two hereditary types
  • Test C1q level for the acquired form
  • Genetic testing for HAE Type 3
therapy of hae
Therapy of HAE
  • On-demand treatment
    • Treatment of attacks with upper airways symptoms is mandatory
    • Acute attacks should be treated with
      • C1INH (plasma derived) Berinert
      • Escallantide (inhibits HMW Kininogen to bradykinen) Kalbitor
      • Icatibant (bradykinenrecepptor antagonist) Firazyr
    • Intubation or trachestomy should be early in progressive airway obstruction
    • Antifibronolytics are not to be used
    • Procedural prophylaxis with procedures involving the upper airway is recommended without evidence
    • Pregnancy – C1INH advised
    • Long-term Prophylaxis
      • C1INH - immunizations, screens
      • Androgens – frequent screens for liver toxicity
      • Antifibrolyticsnot recommended
first line therapies for acute attacks of hae include
First-line therapies for acute attacks of HAE include
  • Purified (C1INHRP) or recombinant (rhC1INH) human C1 inhibitor (various products available worldwide)
  • Ecallantide, a kallikrein inhibitor (available only in the United States)
  • Icatibant, a bradykinin B2 receptor antagonist (available in the United States and the European Union)
question 23
Question 23:

What should be prescribed for a patient after treatment for acute anaphylaxis and how should it be used?

  • Usually starts with urticaria and itching but can present with syncope, hypotension, or erythoderma.
  • Most common causes are foods (peanut/ tree nut ingestion, etc.), insect stings, drug allergy (beta lactam)
  • Don’t forget latex, especially in medical spaces
  • No obvious trigger- think mastocytosis (check serum mast cell tryptase) or idiopathic anaphylaxis
  • All who have insect anaphylaxis patients require evaluation for venom immunotherapy
anaphylaxis early management
AnaphylaxisEarly Management
  • Hypotension - supine, IV (NS)
  • Respiratory distress - oxygen and albuterol, intubation
  • Epinephrine
    • 1:1000 .3-.5cc IM for adults (note this is NOT the 1:10,000 dilution - (1mg/10ml) on crash carts
    • Can repeat in 5 minutes
    • If on beta blocker and not responsive to epi, consider glucagon 1mg IM, IV, SC
    • Can start epi infusion if not responsive to IM epi
      • (1:10,000) 1-3 mg over 3 min, then 3-5mg over 3 minutes, then 4-10ug/min infusion
  • All who recover must leave with an Epipen®.
  • Consider 1 mg of glucagon IV if on beta blocker
cutaneous mastocytosis
  • CutaneousMastocytosis
    • Have urticariapigmentosa – reddish brown or tan macules. Darier’s sign
    • Indolent, benign course
  • Itching, burning skin, flushing, CNS symptoms
criteria for systemic mastocytosis
Criteria for Systemic Mastocytosis
  • Major
    • Multifocal dense infiltrates of mast cells in bone marrow or extracutaneous organ
  • Minor
    • >25% mast cells are spindle-shaped or atypical
    • Presence of c-kit point mutation
    • Mast cells co-express Kit and CD2
    • Persistent serum tryptase >20ng/mL
  • Need one major and one minor, or 3 minor
  • Other:
    • Skin involvement improves prognosis
    • Insect stings may induce anaphylactoid reactions in patients with mastocytosis.
drug reactions
Drug Reactions


Common Drug Reaction Patterns

vancomycin reactions
Vancomycin Reactions
  • “Red man syndrome” – pruritis and erythema of face, neck, upper torso, occasionally with hypotension
  • Non-immunologic release of histamine
  • Not IgE mediated
  • Rx: slow the infusion and pre-treat
anticonvulsant hypersensitivity
Anticonvulsant Hypersensitivity
  • Cause the “hypersensitivity syndrome”
  • Deficiency of epoxidehydrolase
  • Fever, maculopapular rash, generalized lymphadenopathy
  • Node bx resembles Hodgkin’s
  • Phenytoin, carbamazepine, phenobarb
  • Can also cause DRESS: Drug reaction with eosinophilia and systemic symptoms. Rash, fever, multi-organ failure
  • ½ actually have eosinophilia
question 24
Question 24:

A 21 year old college student has recurrent sinupulmonary infections. What test in addition to HIV should be performed to exclude immunodeficiency?

  • T- cell (cellular immunity) – virus, fungi, protozoa, mycobacteria and other intracellular organisms
  • Humoral (antibody mediated immunity) – infection with extracellular pyogenic organisms
    • Haemophilus
    • Pneumococcus
    • Streptococcus
    • Increased infections
    • Recurrent respiratory infections
    • Multiple systems involved
    • Unusual organisms
    • Malabsorption
    • Big LNs or absent LNs
common variable immunodeficiency
Common Variable Immunodeficiency
  • Decreased IgG, M, A, normal to increased IgE
  • Recurrent sinopulmonary infections
  • Lymph tissue present or enlarged
  • High incidence of autoimmune disease (22%)
  • Increased risk of adenocarcinoma and lymphomas
  • In addition to encapsulated organisms
    • Giardia, yersinia, H. pylori, and H. jejuni are common
iga deficiency
IgA deficiency
  • Most common form of primary immunodeficiency (1:333)
  • IgA <5mg/dL (VERY LOW)
  • Most patients with IgA def. are NORMAL
  • Have increased risk of infections: collagen vascular , allergic, and GI disease, and malignancy
  • Can make anti-IgA antibodies
    • Leads to anaphylaxis with IgA containing blood products
  • Indicated for common variable immunodeficiency and specific antibody deficiency
  • Not indicated for IgA deficiency
  • Side effects
    • Never transmitted of HIV
    • Fever, chills, HA, muscle pain.
    • Aseptic meningitis
    • Renal failure (was due to osmotic load, not as common now), stroke, MI
complement deficiency
Complement Deficiency
  • C2 deficiency (most common) – sepsis, pneumonia, meningitis, pyogenic arthritis with Strep pneumo
  • C2 deficiency – increased risk of rheumatoid arthritis, SLE
  • Terminal Complement Components – Neisseria sp infections
    • Think about if recurrent meningitis or if unusual strain
live vaccines to avoid in cellular immune deficiency
Live Vaccines to Avoid in Cellular Immune Deficiency
  • Measles
  • Mumps
  • Oral Polio
  • Rubella
  • Varicella
  • MMR
  • Smallpox (vaccinia)
  • Flumist
egg allergy and vaccines
Egg Allergy and Vaccines
  • Influenza and Yellow fever
question 28
Question 28:

What dietary pattern do bedbugs follow?


Bedbug Bites Often

Occur in a Series

“Breakfast, lunch, and dinner”

Lesions are usually painless and appear as pruritic, urticarial-like papules.





Bedbugs are nocturnal, hiding in cracks and crevices within 10 feet of a bed and especially on the cords of the mattress during the day and biting at night.