ALLERGY/IMMUNOLOGY—DANIEL TODD, MD, FACS
Definitions:
Allergy–a genetic defect in the immune system whereby exposure to something in the environment, that is not hamful in and of itself, causes symptoms (the immunologic mechanism is usually limited to type 1/IgE)
The term and concept of “allergy” was coined by a Viennese pediatrician named Clemens von Pirquet in 1906 [1]. He observed that the symptoms of some of his patients might have been a response to outside allergens such as dust, pollen, or certain foods. For a long time all hypersensitivities were thought to stem from the improper action of inflammatory immunoglobulin class IgE, however it soon became clear that several different mechanisms utilizing different effector molecules were responsible for the myriad of disorders previously classified as “allergies”. A new four-class (now five) classification scheme was designed by P. G. H. Gell and R. R. A. Coombs. Allergy has since been kept as the name for Type I Hypersensitivity, characterised by classical IgE mediation of effects.
IT REALLY COMES DOWN TO THE FACT THAT THE IMMUNE SYSTEM IS WORKING TOO WELL–REALLY ALLERGY = HYPERSENSITIVITY. Allergic or hypersensitivity disorders may be manifested by generalized systemic reactions as well as by localized reactions in any organ system of the body. The reactions may be ac ute, subacute, or chronic, immediate or delayed, and may be caused by numerous offending agents. CATARRH=HAY FEVER (HISTAMINIC TYPE SYMPTOMS)
ALLERGY IS THE MOST COMMON CHRONIC DISEASE
ALTHOUGH IS IS OFTEN SAID THAT EVERYONE IS ALLERGIC TO SOMETHING, IN TRUTH ONLY 30% OF THE POPULATION IS IGE ALLERGIC TO ANYTHING
5-20% OF THE POP SUFFERS CLINICALLY
PROBABLY GREATER THAN 50% OF ENT PATIENTS HAVE ALLERGIES AS PART OF THEIR UNDERLYING PROBLEM
THE SKIN, GI TRACT AND RESP TRACT ARE THE TARGET ORGANS FOR ALLERGIC INFLAMMATION
SKIN—DERMATITIS(LATIN)=EXZEMA(GREEK), ENATHEM = A MUCOSAL EXANTHEM(RASH), HIVES = URTICARIA, ANGIOEDEMA = DEEP DERMAL OR DEEP MUCOSAL URTICARIA. PAPULAR=PALPABLE. MACULAR
Anaphylaxis—Erronously named “without protection” a type 1 reaction which is immediate, causes a multisystem reaction. Is fixed, testable by rast, repeatable, beta serum tryptase is markedly elevated. Typically get tachy, hypotension, urticaria, pruritis, angioedema, bronchospasm, angor animi(the feeling of impending doom or death) and circulatory collapse (vs anaphylactoidwhich are not IgE mediated, require a large quantity of the offending agent, directly degranulate mast cells in the tissue and and circulating basophils and eosinophil—contrast media is the most common cause) or vs vasovagal where they are hypotensive and bradycardic with no broncho or laryngospasm or histaminic symptoms.
When it is treated, draw a serum beta tryptase within 8 hours.
Antibody—(Immunoglobulin)a protein substance produced by B-lymphocytes and plasma cells in response to and interacting specifically with an antigen. Made up of heavy and light chains. The variation of heavy chains determines the subtype.
IgG (73%), T1/2=23 days, important in secondary immune response
IgA (19%), T1/2=6days, important in secretory response (tears, nasal secretions, saliva, and other secretions.
IgM (7%), t1/2= 5 days, important in primary immune response
IgD (1%), T1/2 2 days, surface receptor in B lymphocytes
IgE (<1%), T1/2 2 days, “Reaginic Antibody”, discovered in 1967. Binds to receptors on Mast cells and Basophils. When antigen cross binds them they cause the cell to degranulate—-allergic symptoms.
Praus·nitz-Küst·ner reaction (prousnts-küstnr)=A reaction based on passive transfer of allergic sensitivity in which serum from an allergic individual is injected into cutaneous sites on a normal individual and the injected sites are then exposed to antigens to which the donor is allergic; the cutaneous sites show a characteristic wheal-and-flare reaction.
The Jarisch-Herxheimer reaction describes the release of endotoxin when large numbers of organisms are killed by antibiotics.
The model for immune complex diseases is the Arthus reaction, named after its discoverer in 1903. When antigen is injected intradermally into a hypersensitized animal, a localized cutaneous inflammatory reaction occurs that progresses to a hemorrhagic necrotic lesion.
Atopy—the inherited predisposition to IgE allergy– refers to an individual being prone to develop allergies because of a genetic state of hyperresponsiveness to allergens associated with the diseases of atopic diathesis. ATOPY (ATOPIC PATIENT) IS REALLY DEFINED AS THE PROPENSITY TO DEVELOP ALLERGY. USUALLY A GENETIC PREDISPOSITION.
Allergens are often common, usually harmless, substances such as pollens, mold spores, animal danders, dust, foods, insect venoms, cockroaches, latex, and drugs. Allergens can induce IgE antibody responses.
ALLERGEN (ANTIGEN/IMMUNOGEN)= ANY SUBSTANCE CAPABLE OF STIMULATING THE IMMUNE SYSTEM BY ITSELF.
EPITOPE = THAT PORTION OF AN ANTIGEN THAT DETERMINES THE SPECIFICITY OF THE REACTION (THE BINDING SITE).
HAPTEN = ANY SUBSTANCE WHICH CAN BIND A PROTIEN OR MUCOPOLYSACCARIDE COMPLEX TO FORM AN ALLERGEN (CHEMICAL SENSITIVITIES)—the major mechanism for drug allergies.
Anergy—The absence of normal sensitivity to antigenic/immunogenic substances. Typical anergy panel uses mumps, candida, trichophyton
Basophil—1% of circulating leukocytes (of the myeloid cell line), full of basophilic granules that when released participate in allergic reaction (similar the the tissue bound mast cell), but no tryptase.
Concentrate—Antigen as it comes from the supplier.
Phenol—an antibacterial diluent, also known under an older name of carbolic acid, is a colorless crystalline solid with a typical sweet tarry odor. Its chemical formula is C6H5OH and its structure is that of a hydroxyl group (-OH) bonded to a phenyl ring; it is thus an aromatic compound.
Phenol has antiseptic properties, and was used by Sir Joseph Lister in his pioneering technique of antiseptic surgery, though the skin irritation caused by continual exposure to phenol eventually led to the substitution of aseptic (germ-free) techniques in surgery. It is one of the main components of the commercial antiseptic TCP.
Phenol has anesthetic properties, and is the active ingredient in some oral anesthetics such as Chloraseptic spray.
It is also used in the production of drugs (it is the starting material in the industrial production of aspirin), weedkillers, and synthetic resins (Bakelite, one of the first synthetic resins to be manufactured, is a polymer of phenol with formaldehyde). Exposure of the skin to concentrated phenol solutions causes chemical burns which may be severe; in laboratories where it is used, it is usually recommended that polyethylene glycol solution is kept available for washing off splashes. Washing with large amounts of plain water (most labs have a safety shower or eye-wash) and removal of contaminated clothing are required, and immediate ER treatment for large splashes; particularly if the phenol is mixed with chloroform (a commonly used mixture in molecular biology for DNA purification). Notwithstanding the effects of concentrated solutions, it is also used in cosmetic surgery as an exfoliant, to remove layers of dead skin.
Glycerin—(a charbohydrate preservative diluent) is a neutral, sweet-tasting, colorless, thick liquid which freezes to a gummy paste and which has a high boiling point. Glycerin can be dissolved into water or alcohol, but not oils. On the other hand, many things will dissolve into glycerin easier than they do into water or alcohol. So it is a good solvent.
Confiming wheal—wheal that has grown 2mm larger than the first positive wheal (usually 9mm).
CLIA—Clinical Lab Improvement Act
Corticosteroids (adrenocorical steroids)—Produced by the adrenal cortex, divided into minerocorticoids (sodium retention effects) and glucocorticoids (liver glycogen deposition)—these also suppress the inflammatory response by inhibiting phospholipase A2 and stop prostaglandin and leukotriene synthesis. Hydrocortisone (short acting) and less potent, Prednisone (intermediate acting and moderate potency), and Dexamethasone (Decadron) (long acting and high potency)
AVG PERSON MAKES EQUIVELENT OF 5-7MG PREDNISONE Q DAY(PEAKS AROUND 7 AM)
MAX WE CAN MAKE IS 60 MG PRED EQUIVELENT PER DAY (FAR OVERSHOOT THIS IN THERAPY OF OPTIC NEUROPATHY ECT….)
MUST ALWAYS BEWARE OF HPA SUPPRESSION
DECADRON(DEXAMETHASONE)—-POTENT —-LONGER ACTING—NO MINEROCORTICOID EFFECTS—BEST FOR PREGANCY OR HYDROPS
PREDNISONE–LESS POTENT—+MINEROCORTICOID EFFECTS-
SEE PROBLEMS WITH WOUND HEALING, IMMUNOSUPPRESION, ECCYMOSIS, OSTEOPOROSIS, CATARACTS, HYPERTENSION, GLAUCOMA—-POTENTIATES DIABETES AND PEPTIC ULCER Dz—–BENIGN INTRACRANIAL HTN IF ACUTE WITHDRAWL
MEDROL 16 MG PO QOD IS POOR MAN’S MEDROL DOSE PACK
Generally do not affect type 1 reactions
Chromolyn—mast cell stabilizer. Nasochrom, alkeseltzer gold.
Cross Reactivity—The ability of more than one antigen to react with a specific antibody, due to similar or identical epitopes. Proven by competitive rast. Seen in the Oral Allergy Syndrome.
Decongestant— Usually a alpha-adrenergic agonist
Delayed whealing response—a type 4 DHS reaction, often seen to complex mold and food antigens (If neg with normally antigenic proteins pt considered anergic)
Diluent—an antigenically inert substance used for volumetric adjustment in the preparation of various concentrations of antigens. Phenol is primarily an antibacterial diluent and glycerin is primarily a preservative.
End Point—the antigenic concentration at which progressive positive whealing first occurs(usually 7 mm). Is then followed by the confirming wheal(usually 9 mm).
Eosinophils—A leukocyte in the myeloid cell line which granules stain eosinophilic, involved in the late phase allergic reaction and is found in high counts in allergic patients nasal secretions (also in eosinophic fungal rhinosinusitis)
EPITOPE = THAT PORTION OF AN ANTIGEN THAT DETERMINES THE SPECIFICITY OF THE REACTION (THE BINDING SITE).
Flash response—when a series of negative responses is suddenly followed by a large positive wheal (5-5-5-5-13).
Fungi—divided into yeast or molds (mycology is the study of fungi)
Glycerine control (2% glycerine or equivalent of #2 dilution)—application of a 4mm wheal of 2% glycerine.
Gell and Coombs Reactions—A classification of Hypersensitivity reactions that although designed for protection actually cause tissue damage.
HAPTEN = ANY SUBSTANCE WHICH CAN BIND A PROTIEN OR MUCOPOLYSACCARIDE COMPLEX TO FORM AN ALLERGEN (CHEMICAL SENSITIVITIES)—the major mechanism for drug allergies.
Histamine—an acute mediator of inflammation (released by mast cells and basophils).
Histamine control—application of a 4mm wheal of histamine which gives a classic wheal and flare response
Hourglass resoponse–wheals of decreasing size are followed by a clear zone, after which the usual progression appears (9-7-5-5-7-9)
Immunoglobulin=antibody
Intracutaneous=Intradermal test—injection of the antigen just under the outermost layer of the epidermis to form a wheal
IMMUNITY = “FREEDOM FROM”
Immunotherapy is a form of medical treatment based upon the concept of modulating the immune system to achieve a therapeutic goal.
A vaccine is an antigenic preparation used to produce active immunity to a disease, in order to prevent or ameliorate the effects of infection by any natural or “wild” strain of the organism. The term derives from Edward Jenner‘s use of cowpox (“vacca” means cow in Latin), which, when administered to humans, provided them protection against smallpox, which Pasteur and others perpetuated. The process of distributing and administrating vaccines is referred to as vaccination.
Immunotherapy
Hyposensitization is a form of immunotherapy where the patient is gradually vaccinated against progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity altogether. It relies on the progressive skewing of IgG (“the blocking antibody”) production, as opposed to the excessive IgE production seen in hypersensitivity type I cases.
Usually get a drop in allergen specific IgE and a rise in IgG (blocking antibody). Builds tolerance.
In the 1960s, Dr. Len McEwen in the United Kingdom developed a treatment for allergies known as enzyme potentiated desensitization, or EPD. EPD uses much lower doses of antigens than conventional treatment, with the addition of an enzyme. EPD is available in the United Kingdom and Canada, and was available in the United States until 2001, when the Food and Drug Administration revoked its approval for an investigative study being performed. Since that time an American counterpart to EPD, known as Low Dose Antigens, or LDA, has been formulated from components approved by the FDA, and is available for treatment from a small number of doctors in the United States. EPD (and LDA) is still considered experimental by many mainstream doctors and medical insurance companies, and many doubt that it is more effective than a placebo.
A third form of immunotherapy involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free and B-cell IgE signalling such sources for destruction. They do not bind to IgE already bound to the Fc receptor on basophils and mast cells as this would stimulate the allergic inflammatory response.
Inhalant—Allergen entering the body via the resp tract.
Intracutaneous testing—Another term for intradermal testing.
Intradermal testing—injecting the antigen under the outermost layser of the epidermis to form a wheal.
Invitro—“in glass”—blood laboratory testing.
In vivo—testing the patient directly (skin testing).
Late phase Rxn—-part of a type 1 response that is from newly synthesized mediators of inflammation—happens in about 2-4-6 hours. A result of chemotactic factors (leukotrienes, prostaglandins, and other cytokines that call other inflammatory cells in (known as the recruitment phase). The late phase response actuall primes or upregulates the next early phase.
Mast cells—Tissue bound granulocytes, although similar to circulating basophils are of different CD34+ progenitor cell lineage. Have unilobed nucleus and tryptase whereas Basophils are circulating, and have multilobed nucleus and no tryptase.
Molds—A type of fungi, also called fungi imperfecta, having septae mycelia
Multidose vial—a treatment vial containing sufficient quantity for the withdrawal and administration of several immunotherapy injections.
Multitest—A puncture test using a multipronged device for introducing multiple antigens with a single application.
Negative Control—a skin test using only diluent
OSHA—Occupational Safety and Health Administration
Perennial—year round
Plateau reaction—A skin whealing response where 2 or more of the positive wheals are the same size. That is the end point (the first increased wheal (usually 7mm) is followed by another 7mm response instead of the usual increased confirmation wheal (9mm).
Pollen—the fertilizing elements of a flowering plant
Prick test—an epicutaneous skin test wher the skin is punctured at a 45 degree angle through a drop of antigen.
Prick-puncture test—a variant of the pricktest in which the puncture throught antigen droplet is vertical and not 45 degrees.
S.E.T.—Skin Endpoint Titration or serial diltion endpoint tritration, now called IDT (intradermal dilution testing) uses 5 fold dilution concentrations to obtain progressive whealing.
Single dose vial—A treatment vial containing the exact amoung for one immunotherapy injection.
Standardized extract—an allergenic extract in which the biological potency has been expressed in a form, which compares it to known standards developed by an overseeing agency.
Stock vial—Same as concentrate.
Titrate the Vial—Diluting the treatment vial with 5 fold dilutions, then doing a vial test, to determine the safe starting point.
TOE—a term for three fungi: Trichophyton, Oidomycetes, and Epidermophyton.
Vial test—an intradermal test preceding treatment with any new vial. May go ahead if the whealing response is not over 11mm.
Treatment board—a collection of relevant antigens in varying concentrations, often mixed using 10% glycerine for stability, used to prepare treatment vials.
Vertical testing—A screening maneuver in which skin testing for several antigens is done simultaneously.
W/V concentration—Antigen strength expressed as grams of antigen per milliliter of extracting fluid.
PATHOLOGY—INFLAMMATORY, NEOPLASTIC, CONGENITAL, TRAUMATIC,IDIOPATHIC
INFLAMMATION=AND IMMUNE RESPONSE TO PATHOLOGY (ABOVE)—RUBOR, DOLOR, PALLOR, ET TUMOR. “ITIS”
THERE ARE NOW 6 IMMUNE MECHANISMS OF INFLAMMATION.
INFLAMMATION CAN BE INFECTIOUS OR NON INFECTIOUS IN ETIOLOGY.
INFECTION IS COLONIZATION GONE BAD (DETRIMENTAL COLONIZATION), GREATER THAN 10 TO THE FIFTH MICRO-ORGANISMS PER MM3 WITH SOME TYPE OF INVASION (MICRO INVASION)
CULPRITS ARE VIRUSES, BACTERIA, FUNGI—ATYPICALS SUCH AS MYCOPLASMA CHLAMYDIA CAN BE CHRONIC
THE MIDDLE RESP TRACT IS COLONIZED
THE DISTAL REST TRACT IS USUALLY STERILE (PARANASAL SINUSES, MIDDLE EAR, TRACHEA, BRONCHI, AND LUNGS)
ALLERGY IS USUALLY DEFINED AS ONLY TYPE 1 (IgE MEDIATED) HYPERSENSITIVITY. (SOME INCLUDE OTHER IMMUNE MECHANISMS IN THE DEFINITION OF ALLERGY)
ATOPY AND ALLERGY BLURRS WITH OTHER IMMUNE MECHANISMS WHEN YOU GET INTO THE PERENIAL ALLERGENS
SEASONAL INHALANTS ARE VERY IGE MEDIATED (ALL HISTAMINIC SYMPTOMS)—SHOW UP ON A PRICK TEST–RESPOND WELL TO SQIT AS WELL AS MEDS (EASY TO TREAT)
PERENIAL INHALANTS ARE MORE COMPLEX, INVOLVE OTHER MECHANISMS—RESPOND MORE POORLY TO SQIT (PROBABLY BECAUSE WE OVERDOSE THEM—DUE TO THE MYRIAD OF IMMUNE RESPONSES), OFTEN HAVE A DELAYED RXN (TYPE 4), SHOW UP BETTER WITH ID TESTING AND HAVE POSITIVE DHT, RESPOND BETTER TO SLIT OR LOWER DOSE SQIT.
NON INFECTIOUS, NON ALLERGIC INFLAMMATION IS REALLY VERY POORLY UNDERSTOOD—THIS INCLUDES ALL THE AUTOIMMUNITIES AND OTHER CHRONIC INFLAMMATORY CONDITIONS WE STRUGGLE WITH (IBS, FIBROMYALGIA, EOSINOPHILIC FUNGAL RHINOSINUSITIS)
60-90% OF SINUS PATIENTS HAVE ALLERGIES
3% DOCTOR VISITS—-MORE THAN A BILLION $ / YEAR
PROBABLY ACCOUNTS FOR HALF OF OUR PATIENTS COMPLAINTS
20-30% OF THE US POPULATION = 40 MILLION AMERICANS
HUGE DIVERSITY OF SYMPTOMS—HA, HALITOSIS, ITCHY EARS, ITCHY FEET, FATIGUE, MYALGIAS, MIGRAINES, CHRONIC FATIGUE
THE BODY DOESN’T RECOGNIZE HOW THE ALLERGEN GOT IN (NOSE, GUT)—IT RESPONDS THE SAME—THUS CROSS REACTIVITY
80% OF KIDS WHO HAVE RECURRENT AOM AT LESS THAT 1 YEAR HAVE ALLERGY
THE IMMUNE SYSTEM CAN BE MANIPULATED TO ACHIEVE LONG LASTING BENEFITS
BREAST FEEDING AND HAVING A DOG (ENDOTOXIN) HAVE PROVEN HELPFUL IN AVOIDING THE DEVELOPEMENT OF ALLERGIES AND ASTHMA—THE “HYGEINE HYPOTHESIS”
ALLERGIC LOAD PHENOM—THERE ARE THRESHOLDS, THESE ARE LOWERED FOR ALL ALLERGENS AND EVEN IRRITANTS AS THE ALLERGIC LOAD IS INCREASED
BIPOLARITY—KIDS GET HYPER, ADULTS FATIGUED—PEDIATRIC PARODOXICAL REACTION
INDIVIDUALITY—EVERYONE REACTS DIFFERENT AND ALLERGIES ARE LIKE A FINGERPRINT
ADAPTATION—-SOME CAN ADAPT AND SOME CANT—-GENETICS
SPREADING PHENOMENON—TIES INTO THE ALLERGIC LOAD PHENOM
SWITCH PHENOM—-RHINITIS—-TO ULCERATIVE COLITIS (COULD THE COLECTOMY HAVE BEEN PREVENTED IF THE ALLERGIES HAD BEEN AGGRESSIVELY TREATED IN CHILDHOOD? WE KNOW THAT TREATING ASTHMA AGGRESSIVELY IS BENEFICIAL IN PREVENTING AIRWAY REMODELING
HISTORY
1921 FRENCH HANSEL(ENT) PIONEERED SET–HE DID NOT ESCALATE DOSES TO MAX TOLERATED AND THUS THE IMPRESSION THAT ENT ALLERGY IS HOMEOPATHIC
HERBERT RINKEL (INTERNAL MED) REALLY PIONEERED TODAYS USE OF SET
SET ALLOWS STARTING POINT TO BE CLOSER TO MAINTENENCE POINT. ESCALATED DOSE UNTIL SYMPTOMS RELIEVED
ALSO DESCRIBES CYCLIC FOOD ALLERGY THROUGH OBSERVATION
DOR BROWN DESCRIBES PROVOCATION (HIGH DOSES)/ NEUTRALIZATION (LOW DOSES) AS A TEST FOR FOOD ALLERGIES
RAST TESTING PROVED THAT SET ALLOWED A STARTING POINT THAT WAS CLOSER TO THE MAINTANENCE DOSE
SET WAS THE ORIGINAL SKIN TEST, STILL THE GOLD STANDARD, ALL AGREE THAT SKIN TESTING IS THE MOST SENSITIVE (SPECIFICITY IS NOT AN ISSUE) AND QUANTITATIVE TESTING OFFERS MANY ADVANTAGES (ONLY DISADVANTAGE IS THAT IT TAKES A LITTLE LONGER
IMMUNITY = “FREEDOM FROM”–ABILITY TO RECOGNIZE SELF FROM NON-SELF
MAJOR HISTOCOMPATIBILITY ANTIGENS ARE ENCODED ON CHROMOSOME 6p
CONSIDER AN IMMUNE DEFEICENCY OF SOME TYPE WHEN YOU GET—1)TOO MANY INFXNS FOR THEIR AGE GROUP. 2) UNUSUAL INFECTING AGENTS. 3) IMPROPER RESPONSE TO THERAPY
N ONSPECIFIC/INNATE/NATURAL/NON-ADAPTIVE
PHYSICAL BARRIERS–ANATOMIC(SKIN, MUCOUS MEMBRANES, CILIA)
EXAMPLES OF DEFECTS: BURNS, TRAUMA, KARTAGENER’S,IMMOBILE CILIA SYNDROME,CF, EPIDERMAL BULLOSA DYSTROPHICA
CELLS & BIOCHEMICAL BARRIERS(ACID, LYSOZYMES)-–PHAGOCYTES, OTHER CELLS
EXAMPLES OF DEFECTS: NEUTROPENIA (<500)—- CHRONIC GRANULOMATOUS DISEASE (CGDz)–X-LINKED RECESSIVE—NO SUPEROXIDE DISMUTASE OR OXYGEN FREE RADICALS—HIGH STAPH AUREUS INFXNS—+NITROBLUE TETRAZOLIUM DYE REDUCTION TEST—— CHEDIAK HAGASHI (AUTO R)—ABNL MEMBRANE FLUIDITY—CELLS CANNOT BIND LYSOSOMES/DEGRANULATE—GIANT CYTOPLASMIC GRANULES IN THE PTS LEUKOCYTES–LEUKOCYTE ADHESION DEFIECEINCY—DELAYED SEPARATION OF THE UMBILICAL CORD——HIGH INCIDENCE OF URTI’S AND SKIN INFXNS WITH S a. AND ENTERICS
SOLUBLE FACTORS—-COMPLEMENT—ACTIVATED BY IGM
EXAMPLES OF DEFECTS: C1,2 AND 4 (EARLY COMPONENTS)—RESEMBLES SLE—AUTOIMMUNE DZ IS HIGHTER—SLE, GN, RA, DERMATOSITIS
C3 DEFEICEINCY—-HIGH INCIDENCE OF PYOGENIC INFXNS—SEE ALSO IN LIPODYSTROPHY
C4 AND C1 ESTERASE INHIBITOR—-ANGIOEDEMA
C5,6,7 AND 8 (TERMINAL COMPONENTS/MAC ATTACK)—-HIGH INCIDENCE OF NISSERIA INFXNS (MENINGITIS AND GONNORHEA)
ABNL ALTERNATE PATHWAY (H,I, PROPERDIN)—RECURRENT INFXNS
OTHER FACTORS RELEASED FROM CELLS
SPECIFIC/ADAPTIVE/AQUIRED–-REQUIRES PRIOR EXPOSURE, MAY BE PASSIVELY TRANSFERRED, MEMORY, DIFFERENTIATES SELF FROM NON-SELF
HUMORAL IMMUNITY–TYPICALLY B-CELLS–PLASMA CELLS—HIGH INCIDENCE OF RECURRENT PYOGENIC ENCAPSULATED SINOPULMONARY BACTERIAL(STAPH AND STREP AND H. INF) INFXNS & GIARDIASIS (GENERALIZED & CERVICAL LAD) WITH A NL CLINICAL RESPONSE TO VIRUSES BUT FAILURE TO RESPOND TO IMMUNIZATIONS—-NL LIFE SPAN
LACK SUFFICIENT ANTIBODIES TO FIGHT INFXN
IGM — TO IGG (IGG=73%, IGA–A DIMER WITH A SECRETORY J-CHAIN=17%) IGG4 = A BLOCKING AB
BEST WAY TO TEST FOR THIS IS A QUANTITATIVE SERUM IMMUNOGLOBULIN ASSAY——IF THIS IS LOW CAN GET A B-CELL COUNT AND ANTIBODY RESPONSE TESTS
EXAMPLES OF DEFECTS:
PEDS PATIENTS WITH TOO MANY INFXNS—ORDER QUANTITATIVE IMMUNOGLOBULINS—LATE SPECIFIC RESPONSE TO SAY PNEUMOCOCCAL VACCINE—CAN MEASURE THIS
SELECTIVE IgA DEFEICENCY—#1 IN US (AUTO R) 1/700—-OFTEN ASX, INCREASED INFXNS, ALLERGY AND SUSCEPTIBILITY TO AUTOIMMUNE DZ—-ALSO GUT Dz (CELIAC SPRUE)—ALSO SUSCEPTIBLE TO TRANSFUSION FEACTIONS (MAY HAVE AB TO IGA)
PHYSIOLOGIC—TRANSIENT HYPOGAMMAGLOBULINEMIA OF INFANCY—–TRANSITION TIME WHEN MATERNAL IgG IS WANING (T1/2=25 DAYS) AND NEONATAL IG IS NOT YET TO PROTECTIVE LEVELS (USUALLY ABOUT 4-6 MONTHS)
SEE THIS AS A LARGER PROBLEM IN PREMIES!!—-THEY DELIVERED PRIOR TO GETTING FULL COMPLEMENT OF MATERNAL AB
BRUTON’S CONGENITAL X-LINKED RECESSIVE HYPO-AGGAMMAGLOBULINEMIA—YOUNG MALES RECURRENT PYOGENIC INFECTIONS—LACK CIRCULATING B-CELLS—DEFECT IS IN TYROSINE KINASE—B-CELLS UNABLE TO MATURE—-ABSENT TONSILS AND GERMINAL CENTERS (PEYERS PATCHES)
COMMON VARIABLE HYPOGAMMAGLOBULINEMIA—-AGE 15-35 HAVE INCREASED SINOPULM INFXNS—ALSO MAY HAVE LAD
CMI(CELL MEDIATED IMMUNITY)–PROBABLY MOST IMPORTANT IN COMBATING INTRACELLULAR INFXNS—-VIRAL AND FUNGAL AND PROTOZOAL INFXNS—-PRESENT WITH FTT THE DIARRHEA
LACK LYPHOID TISSUE AND CAN OFTEN GET TRANSFUSION AND TRANSPLANT (GRAFT VS HOST) RXNS
SCREEN FOR THIS WITH A TOTAL LYPHOCYTE COUNT OR AND ANERGY PANEL
ALSO GET MUCOBACTERIAL INFXNS AND DIE EARLY
EXAMPLES OF DEFECTS:
SCID (SEVERE COMBINED IMMUNODEFICIENCY)—X-LINKED (AUTO – R —SWISS TYPE)
PURINE SALVAGE DEFECTS–MHC—-AUTO R
WISKOTT ALDRICH—-X-LINKED—-EXZEMA, THROMBOCYTOPENIA, AND INCREASED INFXNS
DI GEORGE THYMIC HYPO/APLASIA-—SPORATIC (NON HEREDITARY) –EMBRYOLOGIC DEFECT IN THE 5-6TH WEEK GESTATION——FISH MOUTH, HYPOPARATHYROID, LOW SET EARS, NOTCHED PINNA, HYPERTELORISM—ALSO CARDIAC ABNL—-EMPBYOLOGIC ABNL—-ABSENCE OF THYMUS AND PARATHYROIDS—–(3RD POUCH DEFECT)—–HYPCALCEMIA (LOW PTH) NO T-CELLS—-VACCINATION WITH LIVE VACCINES CAN BE FATAL
CHRONIC MUCOCUTANEOUS CANDIDIASIS
JOB’S -(BUCKY) SYNDROME—-HYPER IgE SYNDROME—-EXZEMA (HYPER IgE), ASTHMA, RECURRENT S. a SKIN INFXNS “COLD ABSCESSES”, DEFECT IN PMN MIGRATION
NEZELOF SYNDROME
CARTILAGE HAIR HYPOPLASIA
HOST RESPONSE:
ANAPHYLAXIS = TYPE I RXN–”WITHOUT PROTECTION”—GET TACHY, HYPOTN URTICARIA, PRURITIS, ANGIOEDEMA, BRONCHOSPASM—HIGH TRYPTASE LEVELS
ANAPHYLACTOID = ANAPHYLAXIS LIKE
VASOVAGAL-—-BRADY/DIAPHORESIS, HYPOTN, LACK URTICARIA, PRURITIS, ANGIOEDEMA, BRONCHOSPASM—LOW TRYPTASE LEVELS—–OFTEN A BRIEF SYNCOPAL EVENT WITH NO RESP OR CARDIAC ARREST
TYPE I (ANAPHYLACTIC)–IGE MEDIATED— FIXED ATOPY OR IMMEDIATE HYPERSENSITIVITY REACTIONS—–FIXED, IGE MEDIATED, IMMEDIATE, SEVERE, DETECTABLE BY RAST–(VS ANAPHYLACTOID RXNS WHICH ARE NOT IGE MEDIATED AND USIALLY REQUIRE A LARGE QUANTITY OF THE OFFENDING AGENT)—-DIRECTLY DEGRANULATE MAST CELLS—IN THE TISSUE (CONNECTIVE TISSUES AND MUCOSA) AND BASOPHIL (CIRCULATING) AND EOSINOPHILS (WORMS WHEEZES AND WEIRD DISEASES—-MBP (CONTRAST DYES)
CLASSIC IgE RXN—IMMEDIATE—-PREFOMED AND NEWLY FORMED MEDIATORS LEAD TO A CASCADE OF INFLAMMATION—–ACUTE AND SUBSEQUENTLY LATE PHASE (DELAYED) ALLERGIC REACTION FROM CHEMOTACTIC FACTORS—STILL ALL PART OF THE TYPE I RXN!!!—-THIS IS WHY YOU KEEP YOUR SHOT PTS FOR 20 MINUTES
PERMANENT—STAYS WITH YOU FOR LIFE—–HAVE TO INITIALLY BE SENSITIZED TO IT AT SOME POINT
THE PRIMARY MECHANISM FOR ALLERGIC RHINITIS–—-ALL INHALANT ALLERGIES ARE FIXED ALLERGIES
THE MECHANISM BEHIND URTICARIA, ATOPIC DERMATITIS, ASTHMA, GI SENSITIVITY
GENERALIZED RXN—-ANAPHYLACTIC “SHOCK”—CIRCULATORY COLLAPSE— ANGOR ANIMI—THE FEELING OF IMPENDING DOOM OR DEATH
PROBABLY GOOD TO DRAW A beta TRYPTASE SERUM ENZYME LEVEL TO DOCUMENT THIS PHENOM WITHIN THE FIRST FEW HOURS, POSITIVE IN ANAPHACTIC AND ANAPHYLACTOID RXNS AND IS INDICITIVE OF MASSIVE MAST CELL DEGRANULATION. ELEVATED LEVELS CONFIRM REACTIONS, BUT A NEGATIVE TEST DOES NOT EXCLUDE ANAPHYLAXIS.
LOCALIZED RXN—-ALLERGIC RHINITIS, ASTHMA—AFS(ALLERGIC FUNGAL SINUSITIS)
INSECT BITE
DRUG ALLERGY (PCN)
FOOD—FIXED FOOD ALLERGY, CAN BE VARYING DEGREE —SMALL PERCENTAGE OF FOOD RXNS
LATEX ALLERGY(URTICARIA TO ANAPHYLAXIS)–CONTACT URTICARIA (IgE)
TAKE A HISTORY AND BELIEVE IT—CAN CONFIRM IT WITH RAST—–EOSINOPHILS ARE RELATED TO THIS BUT ARE NOW KNOWN TO ACTUALLY BE TRYING TO SHUT DOWN THE REACTION
TYPE II (CYTOTOXIC)—IgG OR IgM
DELAYED
ANTIBODY, HAPTEN, OR AG FIX TO CELL MEMBRANE—-COMPLEMENT FIXATION—CELL LYSIS
HEMOLYTIC TRANSFUSION RXN, HEMOLYTIC ANEMIA, TRANSFUSION RXNS, HYPERACUTE GRAFT REJECTION, GOODPASTEURES SYNDROME, MG, RHEUMATIC HEART DISEASE, PERHAPS A COMPONENT OF FOOD ALLERGY
TYPE III (AG-ANTIBODY COMPLEX RXN)
DELAYED—OFTEN FOR DAYS
FORMS AG-ANTIBODY AND COMPLEMENT PRECIPITANS (USUALLY INITIALLY AN AG EXCESS—THUS COMPLEXES STAY IN SOLUTION AND FOODS GIVE RELEIF FROM SYMPTOMS)
DELAYED FOOD RXNS, COUGH WHEEZING—ASTHMA, ANGIOEDEMA, ARTHRITIS, CRAMPS AND DIARRHEA—-ALLERGIC ALVEOLITIS, GLOMERULONEPHRITIS, SERUM SICKNESS (ARTHUS RXN), POST STREP G.N.(DIFFERENT THAN RHEMATIC HEART DZ)
TYPE IV (CMI, DHS RXNS)–T-CELL—-DELAYED HYPERSENSITIITY REACTION!—24-48 HOURS
IS THE RXN BETWEEN SENSITIZED T LYMPHOCYTES AND SPECIFIC AG’S—THE PRESENCE OF COMPLEMENT IS NOT REQUIRED
POISION IVY, TB SKIN TEST, COSMETICS—–ACUTE AND CHRONIC DERMATITIS/EXZEMA, URTICARIA, GRANULOMATOUS Dz (TB, SARCOID, ECT.)THYROIDITIS
CONTACT DERMITITIS (LATEX)
TYPE V—STIMULATION AB REACTION (GRAVES DZ)
TYPE VI—-ANTIBODY DEP CELL CYTOTOXICITY—-TRANSPLANT REJECTION (NULL CELLS)
ANAPHYLAXIS = TYPE I RXN—ERRONOUSLY NAMED ”WITHOUT PROTECTION”—GET TACHY, HYPOTN—ALTHOUGH PATIENTS EXPERIENCING ANAPHYLAXIS ARE NOT ALWAYS TACHYCARDIC—USUALLY HAVE SKIN SYMPTOMS
HOWEVER CAN HAVE FATAL RXN WITHOUT SKIN SX
INGESTANTS CAN HAVE BIPHASIC ANAPHYLACTIC RXNS—ADMIT TO HOSPITAL AND OBS FOR AT LEAST 4 HOURS
LOOK AT HX OF EXPOSURE AND SYMPTOMS AND CALL IT AND TREAT IT EARLY!
ANAPHYLACTOID = ANAPHYLAXIS LIKE
VASOVAGAL—– BRADY/DIAPHORESIS/HYPOTENSION
DELAYED—TYPE III (TETANY)
Rx:
CALL 911
EPI 0.1 MG/KG (1:1000) IM OR SQ—-25-30% REQUIRE 2ND INJECTION (EPI-PEN)
BETA BLOCKERS AND ACE INHIBITORS MAKE THE SITUATION MUCH WORSE—EVEN OPTH DROPS—– GIVE GLUCAGON
ACE INHIBITORS CAN ALSO EXACERBATE THE SITUATION—GIVE GLUCAGON
GIVE EPIPEN EARLY AND IM
AIRWAY—-O2
TRENDELENBURG FOR HYPOTN
?TOURNIQUET?
DA 5CC OF 80MCG/CC IN 500 CC IV SOL
DECADRON 10MG IVPUSH — REPEAT Q 6 HOURS
BENEDRYL 50-100 MG OV OR IM
ZANTAC 50 MG IM OR IV
THEOPHYLLINE 6 MG/KG IV OVER 30 MIN—–0.5MG/KG/HR IV DRIP
HEPARIN 10,000 U IM OR IV
ALBUTEROL OR RACEMIC EPI & ATROVENT MDI/HFN
GLUCAGON—ESPECIALLY FOR THOSE ON BETA BLOCKERS—DIRECTLY RELEASES CATACHOLAMINES
VIT C IV/SQ
MGSO (CA++ = ANTIDOTE)
FIND OUT WHO IS ON MAOI’S OR BETABLOCKERS—– GLUCOGON–HAVE NIPRIDE & PHENTOLAMINE AVAILABLE
DOCUMENT WITH SERUM TRYPTASE LEVELS—DOCUMENT CLEARLY IN CHART AND EDUCATE PT—WRITE SCRIPT FOR EPI-PEN X 2—-PLACE ON TYPE I AND 2 ANTIHISTAMINES FOR ABOUT 3-6 MONTHS—HAVE PTS GET AN ARMBAND
ADMIT AND OBS—OFTEN WILL HAVE BIPHASIC OR PROLONGED REACTION (ESPECIALLY WITH INGESTANTS), NO MATTER WHAT ALWAYS OBS >4 HOURS.
ALLERGENS/ANTIGENS:
ALLERGENS ARE PROTEINS, THE ANTIBODY RESPONSE IS TO AN EPITOPE ON THE ANTIGEN. COMPETITIVE RAST HAS PROVEN THE CONCEPT OF CROSS REACTIVITY
INHALANTS/AEROALLERGENS —-ALL INHALANT ALLERGIES ARE FIXED ALLERGIES- POLLENS(MALE GAMETE CARRIER)—MUST FUFILL THOMEN’S POSTULATES,
INCLUDES TREES(GYMNO AND ANGIOSPERMAE), GRASSES, WEEDS
POLLENS—-SPRING—TREES, SUMMER—-GRASSES,FALL—–WEEDS
PRIMARILY EARLY MORNING, DECREASE WITH RAIN, INCREASE WITH WIND
MOLDS(IMPERFECT FUNGI), THE ANTIGEN IS THE SPORE. TEND TO BE SEASONAL, REQUIRE MOISTURE, PEAK IN THE SPRING AND FALL WITH WET WEATHER. TEND TO GROW IN DAMP AREA (BASEMENTS AND BATHROOMS) CAN CROSS REACT WITH FOODS (BREADS=RHIZOPUS) TEND TO CLEAR WITH THE FIRST SNOW
MOLDS IMPERFECT SAPROPHYTIC FUNGI — NO CHLOROPHYLL—- AG = SPORE
FLARE AT DUSK, CLEAR WITH SNOW STORM, HIGH COMORBIDITY WITH THOSE WHO HAVE DELAYED LOCAL TYPE III GEL & COOMBS RXN TO IMMUNOTHERAPY
ANIMAL PRODUCTS, (70% OF HOMES CONTAIN CAT DANDER) TAKES OVER 6 MONTHS TO GET IT OUT OF THE HOUSE) SOME CROSS REACTIVITY WITH DOGS
MUST ASK ABOUT ANY ANIMAL EXPOSURE (FARM, LABORATORY, WORK)
ANIMAL DANDER AND SALIVA (NOT HAIR) CATS > DOGS—LICK SELF–SHED SALIVA–6 MONTHS PERSISTENT ALLERGEN AFTER REMOVAL
IF YOU CAN’T GET RID OF ANIMAL—CLEAN IT FREQUENTLY
DUST/MITE/COCKROACH––FECAL PARTICLES AND BODY PARTS
PEAK IN THE INDOOR SEASON(WINTER)
DUST MITE–FECES AND BODY PARTS—-THEY THRIVE IN HUMID ENVIRONMENT—GET A DEHUMIDIFIER, FURNACE FILTER, AND A HEPA AIR FILTER
COCKROACH—-BODY PARTS (CHITIN) A VERY UBIQUITOUS AND POTENT ALLERGEN-PROBABLY CROSS REACTS WITH DUST MITE
SNEEZE IN YOUR SLEEP = DUST MITE ALLERGY
BACTERIA?
THE NOSE IS THE PRINCIPLE TARGET ORGAN—ALLERGIC RHINITIS IS DIVIDED INTO SEASONAL AND PERENIAL
USUALLY A GEL AND COOMBS TYPE I HYPERSENSITIVITY RXN (IGE MEDIATED)
ALLERGIC MUCIN—HIGH EOSINOPHIL COUNT AND CHARCO-LAYDEN CRYSTALS
ALLERGIC RHINITIS—OFTEN YOUNG MALES >FEMALES (AGE 20 OR SO)
SAR–”HAY FEVER”/CATARRH–TENDS TO BE EARLY PHASE TYPE I RXN
POLLENS, MOLD SPORES
# 1 = RAGWEED
PAR—SEEMS TO BE MORE OF A LATE PHASE TYPE I RXN
AGE 2-5—–THINK PERENNIALS (DUST, ANIMAL DANDER, MOLDS)
>5—FIRST APPEARANCE OF OUTDOOR POLLEN AND INHALANT ALLERGIES
SYMPTOMS ON AWAKENING—DUST
MORNING—POLLENS
EVENING–OUTDOOR MOLDS (KILLED BY THE FROST)
WIND–POLLENS, RAIN—-MOLDS, MOWING OR RAKING GRASS—MOLD, FURNACE—DUST, HOTELS—DUST AND MOLDS, AIRPLANES—DUST, FIREPLACE—MOLDS AND VOLATILE CHEMICAL SUBSTANCES IN THE WOOD
THE ORAL (ESOPHAGEAL) ALLERGY SYNDROME IS REALLY CROSS REACTIVITY–LIKE CROSS RXN BETWEEN THE GABHS EPITOPES AND THE HEART VALVE EPITOPES (PROVEN BY COMPETITIVE RAST)
RAGWEED—MELONS (WATERMELON, CANTALOUPE), BANANAS, CUCUMBER, LETTUCE , ZUCCHINI
BIRCH TREE—APPLE, PEAR, HAZEL NUT, CARROT, POTATO, CELERY, KIWI, PEACH
GRASS—-PEACHES, CELERY, KIWI, MELON, TOMATO, WHEAT, GRAINS, ONIONS, GARLIC
TIMOTHY GRASS–APPLE, CARROT, CELERY
MUGWORT—CELERY, CARROT, CHAMOMILE TEA, CORIANDER
DUST MITE-—SHRIMP, SNAIL
LATEX—AVACADO, BANNANA, CHESTNUT, KIWI, ROSE FAMILY FRUITS(CHERRY, PEACH)
INGESTANTS—FOOD
DEFINITIONS:
AAAI—THE ONLY FOOD ALLERGY IS IGE MEDIATED (FIXED, ANAPHALACTIC, ANGIOEDEMA, ORAL ALLERGY SYNDROME)
LIKELY CULPRITS ARE (ADULTS: PEANUTS, SEAFOODS-SHRIMP, LOBSTER, CRAB, CRAYFISH, TREE NUTS-ALMONDSM BRAZIL NUTS, CASHEWS, FILBERTS, WALNUTS, AND PECANS, FISH, SEEDS) (CHILDREN: COW’S MILK, EGGS, PEANUTS, WHEAT, SOY)
EVERYTHING ELSE IS UNDER THE UMBRELLA OF INTORERANCE-CONSIDERED NON IMMUNOLOGIC (ALTHOUGH THEY ACKNOWLEDGE HEINER’S SYNDROME (IGG TYPE 3 TO COWS MILK) AND CELIAC SPRUE (IGG TYPE 4 TO GLUTEN)
INTOLERANCE INCLUDES: ANAPHYLACTOID REACTIONS, FOOD POISONING (PREFORMED TOXINS) IDIOSYNCRATIC RXNS,(LACTOSE INTOLERANCE/ALACTASIA (ENZYME DEFICIENCIES AND UNDIGESTIBLE SUGARS) MSG, FOOD COLORING/DYES, MIGRAINES), PHARMACOLOGIC RXNS
AAOA–THERE IS FIXED IMMEDIATE IGE ALLERGY AND CYCLIC DELAYED IGG FOOD ALLERGY—-BOTH ACTING THROUGH IMMUNOLOGIC MECHANISMS. AGREE WITH ALL THE INTOLERANCES DEFINED ABOVE
BREAD = RHIZOPUS
AN ILL DEFINED ENTITY, CAN INVOLVE ANY OR ALL OF THE 4 TYPES OF GEL & COOMBS RXNS
DESCRIBED BEST BY RINKEL IN THE 1930’S
MOST OFTEN ASSOC WITH INHALANT ALLERGY AND CAN MANIFEST IDENTICALLY
THE YOUNGER THE CHILD–THE MORE LIKELY FOOD IS THE ALLERGEN—6-8% UNDER 3—DROPS TO 3% LATER IN CHILDHOOD
MILK/DAIRY PRODUCTS ARE THE BIGGEST CULPRIT—NOT A BAD MOVE TO EMPIRICALLY ELIMINATE EVEN WITHOUT ANY TESTING
THE GUT WILL ALLOW ALLERGENS TO CROSS—ESPECIALLY THE NEONATAL GUT (MILK PRICIPITANS)
OLDER PTS ARE OFTEN THIN–WITH ILL DESCRIBED Sx—THEY MAY NOT BE CRAZY—SEE BIZZAR SIGNS—UNILAT EYELID EDEMA ECT…MIGRAINE
SULFITES IN WHITE WINE OR YEAST IN RICH GERMAN BEERS CAN EFFECT ADULTS IN THIS MANNER
IF THEY ARE OLD ENOUGH TO HAVE Sx—THEY ARE OLD ENOUGH TO HAVE Rx
USUALLY EITHER TYPE I–(25%)—IMMEDIATE (FIXED) MAY BE VARYING DEGREES OF THIS—
OR TYPE III—(75%)– (IgG) DELAYED (CYCLIC)
FIXED FOOD SENSITIZATION—-CONSTANT SENSITIZATION EVERY TIME THE PATIENT INGESTS THE FOOD—RXN IS USUALLY IMMEDIATE–ALWAYS WITHIN THE HOUR —-SENSITIVITY REMAINS UNCHANGED—-EVEN AFTER 2 YEARS OF AVOIDANCE (TOLERANCE IS NOT POSSIBLE)—-ONLY TREATMENT IS AVOIDANCE AND IT IS BEST NOT TO CHALLENGE THE PATIENT TO PROVE THEM WRONG
IF YOU ARE GOING TO TEST FOR IT USE BLOOD
CYCLIC FOOD SENSITIZATION—-INTERMITTENT SENSITIZATION–DEGREE OF SENSITIZATION DETERMINED BY THE FREQUENCY OF INGESTION (QUANTITY NOT AS IMPORTANT AS FREQUENCY)
PRINCIPLE OFFENDERS—CORN, WHEAT, YEAST, MILK, EGGS, SOYBEANS, WHITE POTATOES, AND BEEF
IF YOU ARE GOING OFF MILK —-GO TO RICE MILK (NOT SOY!!!)
A DIFFICULT DIAGNOSTIC DILEMMA AS THE MOST OFTEN PRESENT IN THE MASKED PHASE (PHASE I)
MASKED PHASE (STAGE I)—-EXCESS AG KEEPS IMMUNE COMPLEXES IN SOLUTION—-BEGIN TO PRECIPITATE OUT AT SOME ARBITRARY POINT—-USUALLY SOME HOURS–DURING THIS PHASE PT HAS BASICALLY CONTINUOUS CHRONIC SYMPTOMS RELEIVED FOR SHORT PERIODS BY INGESTION OF THE OFFENDING FOOD AND PUTTING THE PT INTO AG OVERLOAD—-THUS—-PTS CRAVE WHAT THEY ARE ALLERGIC TO—–OFTEN AWAKEN IN THE NIGHT TO EAT IT!
STAGE II—–PT AVOIDS OFFENDING FOOD FOR > 4 DAYS AND PROBLEM AG IS ELIMINATED FROM SERUM—IMMUNE COMPLEXES BEGIN TO DISSAPATE
STAGE III-—5-12 DAYS—PT BECOMES HYPERSENSITIVE AND AN ORAL CHALLENGE FEEDING CAN BE PERFORMED—-DURING THIS STAGE SYMPTOM ONSET IS ALMOST IMMEDIATE AND AN ACURATE Dx CAN BE MADE (AFTER 4 DAYS ELIMINATION GIVE A LOT OF THE OFFENDING FOOD—-WATCH FOR SYMPTOMS—WILL AID GREATLY IN THE FAMILIES UNDERSTANDING AND COMPLIANCE
STAGE IV—-ACTIVE SENSITIZATION—-PT WILL STILL REACT TO THE FOOD QUICKLY AFTER THE CHALLENGE BUT THE SEVERITY LESSENS
STAGE V—-LATENT SENSITIZATION—-PT REACTS ONLY TO A SECOND CHALLENGE OF THE FOOD
STAGE IV——TOLERANCE—AT THIS POINT CAN ALTERNATE THE FOOD INTO THE DIET
<2 YEARS OLD—THINK FOODS—USUALLY IgE MEDIATED—THINK COWS MILK/DAIRY
>2–POSSIBLE INHALANTS—USUALLY NON-IgE
80% OF KIDS WHO HAVE RECURRENT AOM AT LESS THAT 1 YEAR HAVE ALLERGY
BIMODAL INCIDENCE (NEONATES AND OLDER ADULTS)
FOOD ALLERGY MANIFESTS PRIMARILY AS SKIN ( FLEXOR EXZEMA) , ADULT ACNE—THEN GI, AIRWAY, AND SYSTEMIC ILLNESS—ALSO HEIGHTENED ALTERNATING NASAL CYCLE (ALTERNATING OBSTRUCTION)
SERUM IGE NOT ALWAYS RELIABLE FOR FOODS, DIET DIARY, ORAL CHALLENGE, PROVAKATIVE TESTS
NEUTRALIZATION THERAPY (SL OR SQ)
ORAL CHROMALYN SODIUM 20 MIN AC AND HS
AGE 2-5—–THINK PERENNIALS (DUST, ANIMAL DANDER, MOLDS)
>5—FIRST APPEARANCE OF OUTDOOR POLLENS
DIAGNOSIS:
FIXED FOOD ALLERGIES ARE A NO BRAINER (HISTORY, INVITRO, POSSIBLE EPICUTANEOUS TESTING (PRICK, SCRATCH, PUNCTURE, PATCH)
CYCLIC (DELAYED) FOOD ALLERGIES OR INTOLERANCE
HISTORY, ELIMINATION/CHALLENGE, IPDFT(INTRADERMAL PROGRESSIVE DILUTION FOOD TEST)—NEVER USE THIS FOR ANY OF THE HIGH RISK FOODS(PEANUTS, COTTONSEED) OR IN BRITTLE ASTHMATICS, MUST HAVE EATEN IT WITHIN THE PAST 24 HOURS, MUST BE A REGULAR FOOD (AT LEAST EATEN TWICE A WEEK)–IF THESE CRITERIA ARE MET THE TESTING IS SAFE WITH HIGHER VOLUMES AND CONCENTRATIONS OF ANTIGEN THAN WITH TRADITIONAL SET
TREATMENT:
AAAI: REALLY ONLY ELIMINATION AND AN EPIPEN (FORMULA AND FOOD SUBSTITUTION) DO NOT RECOMMEND ANY TYPE OF IMMUNOTHERAPY
AAOA: REC BOTH ELIMINATION–EVENTUAL ROTATION AS WELL AS IMMUNOTHERAPY FOR UBIQUITOUS FOODS IMPRACTICE TO AVOID. THE IMMUNOTHERAPY REALLY IS NOT DESENSITIZATION BUT NEUTRALIZATION
NEUTRALIZATION CAN BE EITHER INJECTION OR SUBLIGUAL, THE DOSES ARE NOT ESCALATED TO THE MAXIMAL TOLERATED DOSE AS IN INHALANT ALLERGIES. ESSENTIALLY THE ONLY IMMUNOTHERAPY UTILIZED BY THE AAAI
NEUTRALIZATION AND EPD DO NOT ELICIT BLOCKING ANTIBODIES BUT ELICIT T-CELL REGULATORY MECHANISMS AND PROSTAGLANDIN LEVELS. THEY ARE NOT UTILIZED BY THE AAAI
FOODS ARE TREATED WITH NEUTALIZATION RATHER THAN ESCALATION IMMUNOTHERAPY BUT THE SAME RULES APPLY–ALTHOUGH NEUTRALIZATION DOSES OF IMMUNOTHERAPY ARE LOWER AND ARE NOT ESCALATED TO THE MAX TOLERATED DOSE
CUTANEUS/CONTACTS (USUALLY TYPE IV DHS)
EXTENSOR EXCZEMA
LATEX ALLERGY
POISON IVY/OAK–RHUS DERMATITIS/RHUS TOXICODENDRON—-WASH OFF THE AG AND IT WILL NOT SPREAD—NEED 2 WEEKS 0F STEROIDS TO AVOID REBOUND—ATARAX FOR PRURITIS
PARENTERAL/INJECTANTS—MEDS, INSECT OR SNAKE BITES (BEE STINGS)
CLINICAL MANIFESTATIONS:
HISTORY (THE MOST IMPORTANT) NEED TO LOOK FOR ALLERGY JUST LIKE REFLUX BUT NOT EVERYTHING CAN BE BLAMED ON ALLERGY
REALLY AFFECTS 3 MAJOR ORGAN SYSTEMS: RESPIRATORY (NOSE> LOWER AIRWAY), GI SYSTEM, AND SKIN
50% ASTHMA, 25% SINUS, 33% OME (ETD), 33% NASAL POLYPS
80% OF KIDS WHO HAVE RECURRENT AOM AT LESS THAT 1 YEAR HAVE ALLERGY
RARELY AFFECTS THE MUSKULOSKELETAL SYSTEM (JOINTS) , CNS, ECT¼.
FHx IS VERY IMPORTANT—-ACTUAL FH RISK SCORE / 40%-1, 80%-2
PRENATAL EVAL—(FETUS FORMS IGE AT 11 WEEKS GESTATION)—= HICCUPING IN UTERO, INCREASED ACTIVITY
REC. MATERNAL AVOIDANCE, IMMUNOTHERAPY DURING PREGNANCY, ROTATION DIET, NURSE CHILDFOR AT LEAST 6 MONTHS, NO COWS MILK, PLAN BIRTH FOR NON ALLERGIC SEASON, NO SOLIDS FOR AT LEAST 6 MONTHS—THEN ROTATE—AVOID CIGARETTES
MAY GET CORD BLOOD IGE—> 0.2 KU/CC—HIGH RISK (CONTROVERSIAL)
IMMATURE GUT THOUGHT TO ALLOW MACROMOLECULES PASS—ANTIGENIC—SENSITIZE THE CHILD
POLLENS WORSE OUTDOORS IN AM HOURS WITH WIND, IMPROVES INDOORS WITH AIRCONDITIONING
DUST INDOORS AND WORSE AT NIGHT
MOLD WORSE IN THE SUMMER, FRESHLY CUT GRASS, LOW-LYING DAMP AREAS IN THE EVENING, WORSE WITH A CHRISTMAS TREE IN THE HOUSE
WORSE WITH A WOOD BURNING FIREPLACE
DIFFUSE RANGE OF Sx
FATIGUE= THE MOST COMMON Sx
COLIC
FUSSY/IRRITABLE
FREQUENT FORMULA CHANGES
FREQUENT URTI’S—OME–CHL
OTOPRURITIS, PALATAL PRURITIS, NASAL CONGESTION, CLEAR RHINORRHEA, CHRONIC PND, HOARSENESS, TEARING, COUGHING, WHEEZING, SNEEZING, PRURITIS (IF IT ITCHES IT IS ALLERGY—- IF IT DON’T ITCH, IT AINT ALLERGY),, GRIMACE, ASTHMA
PYROSIS, ANAL ITCHING
(AUTOPHONIA) PATULOUS ETD—ALLERGIC EDEMA OF THE TVP
MIGRAINS AND ENDOLYMPHATIC HYDROPS—-FATIGUE-HEADACHE, HALITOSIS, ITCHY EARS AND FEET
SIGNS:
GENERAL
ITCHY WATERY EYES, SNEEZING, RHINORRHEA
JECKYLL AND HYDE PERSONALITY
WHEEZING / COUGHING—1/2 OF ASTHMA PTS WHEEZE
WHEEZING IN THE FIRST YEAR OF LIFE —- THINK CF!
SNEEZING—-# OF SNEEZES CORRELATES WELL WITH AG EXPOSURE
SNEEZE IN YOUR SLEEP (DUST MITE)
COUGH, MOUTH BREATHING
COUGH VARIANT ASTHMA
MIDFACE ELONGATION “ADENOID FACIES”, OPEN MOUTH BREATHING, FLATTENED MALAR EMINENCES, APERTOGNATHIA
DERMATOLOGIC
HIVES=URTICARIA
DIAPER RASH–BURNED BUTT SYNDROME
FLEXOR EXZEMA & ADULT ACNE = FOOD ALLERGY UNTIL PROVEN OTHERWISE
EXTENSOR EXZEMA = CONTACT ALLERGENS (DETERGENTS ECT…) TYPE IV—CONTACT URTICARIA
SAD EYES
CHEMOSIS, CONJUNCTIVITIS (BEWARE OF CONTACT DERMATITIS FROM MAKEUP)
ALLERGIC NASAL CREASE (FROM ALLERGIC SALUTE)= LINEA NASALIS
DENNY’S LINES–HORIZONTAL LINES IN THE PALPEBRAL CREASES OF THE LOWER LIDS, LONG PLUSH UNEVEN SILKY EYE LASHES
ALLERGIC SHINERS (HEMOSIDERIN DEPOSITS FROM CHRONIC VENOUS CONGESTION)
TRANTA’S DOTS (EOSINOPHIS AT SCERAL CORNEAL JUNCTION)
EXCZEMA(DERMATITIS)
ALLERGIC KERATOCONJUNCTIVITIS
PACHYDERMA (ELEPHANT SKIN)–PHILTRUM
BURNED BUTT SYNDROME(DIAPER RASH)—ALLERGIC STOOL IS ACIDIC AND CAUSES A TYPE IV RXN TO PERIANAL SKIN “ON FIRE”
DERMATOPHYTID OR ID RXN SECONDARY TO TOE (TRICOPHYTON, OIDIOMYCETES (CANDIDA), EPIDERMOPHYTON)
BRIGHT RED EARS FROM INTENSE VASODILATION FROM FOOD ALLERGIES
EXT OTITIS
MUCOUS MEMBRANES
PALE NASAL MUCOSA, BOGGY, POST INF MULBERRY TURBS ON MIRROR EXAM, PURPLISH POLYPS, COBBLESTONING OF INFERIOR TURBINATES
GOTHIC (HIGH-ARCHED/NARROW) PALATE
NOCTURNAL BRUXISM
MOUTH BREATHER–DESSICATION ANGULAR CHELITIS/CHELOSIS
HALITOSIS, GINGIVAL HYPERPLASIA
T&A HYPERPLASIA—-APERTOGNATHIA, UVULAR EDEMA
ENLARGE/PROMINENT INJECTED PHARYNGEAL BANDS—- GEOGRAPHIC TONGUE
COBBLESTONING/LYMPHOID HYPERPLASIA
IRRITABLE BOWEL SYNDROME——FOOD ALLERGY UNTIL PROVEN OTHERWISE
TYPE I (ANAPHYLACTIC)–IGE MEDIATED— FIXED ATOPY OR IMMEDIATE HYPERSENSITIVITY REACTIONS—–FIXED, IGE MEDIATED, IMMEDIATE, SEVERE, DETECTABLE BY RAST–(VS ANAPHYLACTOID RXNS WHICH ARE NOT IGE MEDIATED AND USIALLY REQUIRE A LARGE QUANTITY OF THE OFFENDING AGENT)—-DIRECTLY DEGRANULATE MAST CELLS—IN THE TISSUE (CONNECTIVE TISSUES AND MUCOSA) AND BASOPHIL (CIRCULATING) AND EOSINOPHILE (WORMS WHEEZES AND WEIRD DISEASES—-MBP (CONTRAST DYES)
CLASSIC IgE RXN—IMMEDIATE—-PREFOMED AND NEWLY FORMED MEDIATORS LEAD TO A CASCADE OF INFLAMMATION—–ACUTE AND SUBSEQUENTLY LATE PHASE (DELAYED) ALLERGIC REACTION FROM CHEMOTACTIC FACTORS—STILL ALL PART OF THE TYPE I RXN!!!—-THIS IS WHY YOU KEEP YOUR SHOT PTS FOR 20 MINUTES
PERMANENT—STAYS WITH YOU FOR LIFE—–HAVE TO INITIALLY BE SENSITIZED TO IT AT SOME POINT
THE PRIMARY MECHANISM FOR ALLERGIC RHINITIS–—-ALL INHALANT ALLERGIES ARE FIXED ALLERGIES
THE MECHANISM BEHIND URTICARIA, ATOPIC DERMATITIS, ASTHMA, GI SENSITIVITY
GENERALIZED RXN—-ANAPHYLACTIC “SHOCK”—CIRCULATORY COLLAPSE— ANGOR ANIMI—THE FEELING OF IMPENDING DOOM OR DEATH
PROBABLY GOOD TO DRAW A TRYPTASE SERUM ENZYME LEVEL TO DOCUMENT THIS PHENOM WITHIN THE FIRST FEW HOURS
LOCALIZED RXN—-ALLERGIC RHINITIS, ASTHMA—AFS(ALLERGIC FUNGAL SINUSITIS)
INSECT BITE
DRUG ALLERGY (PCN)
FOOD—FIXED FOOD ALLERGY, CAN BE VARYING DEGREE —SMALL PERCENTAGE OF FOOD RXNS
LATEX ALLERGY(URTICARIA TO ANAPHYLAXIS)–CONTACT URTICARIA (IgE)
TAKE A HISTORY AND BELIEVE IT—CAN CONFIRM IT WITH RAST—–EOSINOPHILS ARE RELATED TO THIS BUT ARE NOW KNOWN TO ACTUALLY BE TRYING TO SHUT DOWN THE REACTION
ANAPHYLAXIS = TYPE I RXN–”WITHOUT PROTECTION”—GET TACHY, HYPOTN,NO DIAPHORESIS, PRURITIS,RED WARM SKIN, ANGOR ANIMI
ANAPHYLACTOID = ANAPHYLAXIS LIKE
VASOVAGAL—– BRADY/DIAPHORESIS/HYPOTENSION
DELAYED—TYPE III (TETANY)
Rx:
CALL 911
EPI 0.1 MG/KG (1:1000) IM OR SQ—-25-30% REQUIRE 2ND INJECTION (EPI-PEN)
BETA BLOCKERS AND ACE INHIBITORS MAKE THE SITUATION MUCH WORSE
AIRWAY—-O2
TRENDELENBURG FOR HYPOTN
?TOURNIQUET?
DA 5CC OF 80MCG/CC IN 500 CC IV SOL
DECADRON 10MG IVPUSH — REPEAT Q 6 HOURS
BENEDRYL 50-100 MG OV OR IM
ZANTAC 50 MG IM OR IV
THEOPHYLLINE 6 MG/KG IV OVER 30 MIN—–0.5MG/KG/HR IV DRIP
HEPARIN 10,000 U IM OR IV
ALBUTEROL OR RACEMIC EPI & ATROVENT MDI/HFN
GLUCAGON—ESPECIALLY FOR THOSE ON BETA BLOCKERS—DIRECTLY RELEASES CATACHOLAMINES
VIT C IV/SQ
MGSO (CA++ = ANTIDOTE)
FIND OUT WHO IS ON MAOI’S OR BETABLOCKERS—–HAVE NIPRIDE & PHENTOLAMINE AVAILABLE
DOCUMENT WITH SERUM TRYPTASE LEVELS—DOCUMENT CLEARLY IN CHART AND EDUCATE PT—WRITE SCRIPT FOR EPI-PEN X 2—-PLACE ON ANTIHISTAMINES FOR ABOUT 3-6 MONTHS—HAVE PTS GET AN ARMBAND
DIAGNOSING ALLERGIES
Dx: DIVIDED INTO INVITRO (IN GLASS) OR INVIVO (SKIN TESTING)
INVITRO TESTING (ELISA) (SERUM IgE)—I-CAP (IMMUNOCAP) OR RAST—RADIOSORBENT ALLERGEN SERUM TEST
CAN TREAT BASED ON THESE RESULTS
ADVANTAGES:
NO RISK OF ANAPHYLAXIS
MEDS DO NOT AFFECT RESULTS
NOT DEPENDENT ON SKIN CONDITION
BETTER DOCUMENTATION ON QUALITY CONTROL
MORE CONVENIENT FOR PATIENTS
PERCEIVED AS BEING MORE SCIENTIFIC
CAN PERFORM ON SICK, PREGNANT, OLD, YOUNG
DISADVANTAGES:
LESS SENSITIVE, REALLY ONLY LOOKING AT A SINGLE PATHWAY FOR ALLERGY
MORE EXPENSIVE
RESULTS NOT IMMEDIATELY AVAILABE
PTS CANNOT SEE AND FEEL THE RESULTS, NO TEACHING TIME
MODIFIED RAST OR ELISA
ALWAYS USE TO LOOK FOR ANAPHALATIC RXNS
ALWAYS USE IN PREGNANCY
TOTAL IGE, ONLY USEFULNESS WOULD BE TO CLUE YOU IN THAT YOU ARE MISSING SOMETHING, PUSH YOU TO TEST MORE ANTIGENS
IN INFANTS ANDCHILDREN CAN CLUE YOU INTO THE “ALLERGY MARCH” FOR THE DEVELOPMENT OF ATOPY AND ASTHMA (INGESTANTS TO INHALANTS)
INVIVO TESTING–SKIN TESTING
HISTORY: BLACKLY 1872, NOON 1911, HANSEL 1:10 DILUTIONS, RINKEL 1:5 DILUTIONS
ADVANTAGES:
HIGHEST SENSITIVITY (INVITRO TEST FELT TO BE ABOUT 75% SENSITIVE)
RESULTS IMMEDIATELY AVAILABLE
GREATER SELECTION IS ALLERGENS FOR TESTING
LESS PERSONNEL AND REAGENT EXPENSE PER TEST
MINIMAL EQUIPMENT REQUIRED
PATIENT CAN SEE AND FEEL THE RESULTS OF THE TEST, TEACHING TIME
DISADVANTAGES:
NEED TO BE OFF ANTIHISTAMINES, TCA’S, BETA BLOCKERS
PT NEEDS TO BE WELL
PT NEEDS GOOD SKIN
PT NEEDS TO TOLERATE TESTING
EFFECTORS
AGE—INFANTS AND OVER 50 MAY HAVE LESS SKIN REACTIVITY
RACE—HIGHER FITZPATRICK SCORES MAY HAVE LESS REACTIVITY
TIME OF DAY—HIGHEST REACTIVITY IN EVENING (7-11PM)
DISTANCE BETWEEN SITES—MAY COALESC
BODY SITE—UPPER BACK> LOWER BACK> UPPER ARM> FOREARM
TIME OF YEAR—COSEASONAL TESTING IS MORE REACTIVE
MEDS—ANTIHISTAMINES VS BETA BLOCKERS
EPICUTANEOUS TESTS
SCRATCH TESTS=OBSOLETE
PATCH TESTING FOR CONTACT ALLERGENS
SKIN PRICK TESTING (SPT)—PRIMARILY MULTITEST DEVICES
SAFE, FAST, ANED COST EFFECTIVE
LOWER SENSITIVITY (IDT 2-3)/FALSE -, LOWER SPECIFICITY (DERMATOGRAPHIC RESPONSES)/FALSE +
SPT FOLLOWED BY IDT STILL HAS THE WEAKNESSES OF SPT
INTRADERMAL DILUTION TITRATION (IDT)= THE BEST (MOST SENSITIVE AND SPECIFIC)
RAISE A 4 MM WHEAL 0.01CC AND WAIT 10-15 MIN—READ THE WHEAL ONLY (THE FLARE IS PROBABLY NOT IGE MEDIATED—IT IS THE RESULT OF OTHER LOCALNEUROTRANSMITTERS)—-A 2-3 MM WHEAL IS PROBABLY SIGNIFICANT
END POINT IS THE DILUTION THAT INITIATES PROGRESSIVE POSITIVE WHEALING
IT IS CONFIRMED BY PROGRESSIVE WHEALING
PEDS AND GERIATRICS MAY HAVE WEAK SKIN TEST RESULTS
SKIN TESTS MAY GIVE YOU A DELAYED INDICATION OF FOOD ALLERGY
ALTHOUGH STEROIDS DO NOT INTERFERE WITH THE TYPE I SKIN TEST REACTION THEY SHOULD BE AVOIDED TO ALLOW THE DELAYED REACTION TO APPEAR—-THEY BLUNT YOUR DATA
MUST GET OFF ANTIHISTAMINES (H1 AND H2 BLOCKERS AND KETOFIN (ANTIASTHMATIC) AND TRICYCLIC ANTIDEPRESSANTS BEFORE SKIN TESTING
NEED TO BE OFF ZYRTEC ONLY 5 DAYS FOR SKIN TESTING WHERE AS HISMANAL CAN TAKE 6 WEEKS
PROBABLY SHOULD GET OFF ALL HOMEOPATHIC/HERBAL MEDS 1 WEEK PRIOR TO SURGERY AND ALLERGY TESTING(GINKO, ASA, NSAIDS, ANTIHISTIMINES, BETA BLOCKERS)
R/O MORE SERIOUS PROBLEMS—-CF (SWEAT CHLORIDE), IMMOTILE CILIA, OTHER IMMUNE DEFECTS (IGA AND IGG SUBCLASSES)
TREATMENT
THE EARLIER YOU TREAT—THE BETTER—PREVENTS PERMANENT ORGANIC CHANGES—AVOID THE “ALLERGIC MARCH” FOOD ALLERGIES, INHALANT ALLERGIES, ASTHMA—IF THEY ARE OLD ENOUGH TO HAVE SYMPTOMS THEY ARE OLD ENOUGH TO HAVE TREATMENT
AVOIDANCE
THERE IS SOME THOUGHT TO AVOIDING ANTIGENS AS A CHILD TO HELP AVOID SENSITIZATION
THERE IS ALSO SOME RECENT THOUGHT THAT ANTIGEN EXPOSURE (ENDOTOXIN) IS HELPFUL
1ST MUST ID ANTIGENS—-INVITRO, IN VIVO, NASAL CYTOLOGY, DIETARY MANIPULATION, ECT….
CONCENTRATE ON THE BEDROOM
MITE PROOF BEDDING COVERS, “DUST COVERS”, HOT WATER WASHING OF BEDDING (130 DEGREES WEEKLY)
DUST MITES FEED ON HUMAN SKIN AND LIKE HIGH HUMIDITY, KEEP HUMIDIFICATION <50%
GET RID OF CARPET, BOOKS, SHELVES, HORIZONTAL BLINDS, STUFFED ANIMALS
PET DANDER
REMOVE CAT OR DOG—NEED 6 MONTHS TO GET THE DANDER OUT, HEPA FILTER, KEEP THE HOUSE
CAT DANDER FROM THE PELT AND SALIVA
CLOSED FOR SAR—AC ON—KEEP THE HOUSE OPEN FOR PAR
POLLENS-STAY IN, WEAR A MASK, SHOWER WHEN YOU GET IN
SPRING (TREES) SUMMER (GRASSES) FALL (WEEDS)
MOLDS
INDOOR–ASPERGILLUS, PENICILIUM, RHIZOPUS
DAMP BASEMENTS, CURTAINS, OLD BOOKS, FIREWOOD, PILED NEWSPAPERS, OLD CHRISTMAS TREE
BASEMENT DEHUMIDIFICATION FOR MOLDS
OUTDOOR-ALTERNARIA, CLADOSPORIUM, HELMINTHOSPORIUM
PEAK AT SUNSET WHEN THE TEMP DROPS
RAIN CLEARS THE MOLDS FOR ABOUT 2 HOURS (ANOTHER PEAK)
AVOID RAKING LEAVES, BAILING HAY ETC.
ELIMINATION DIET——ACHIEVE TOLERANCE THEN INSTITUTE APPROPRIATE ROTATION DIET
LATEX FREE GLOVE OR AT LEAST POWDER FREE LATEX GLOVE—LOTION MEKES YOU MORE SENSITIVE TO CONTACT ALLERGENS
PHARMACOTHERAPY
EPI (0.1MG/KG SQ)
GIVE EPIPEN OUT FREQUENTLY IF SUSPICIOUS HISTORY
STEROIDS
AVG PERSON MAKES EQUIVELENT OF 5-7MG PREDNISONE Q DAY(PEAKS AROUND 7 AM)
MAX WE CAN MAKE IS 60 MG PRED EQUIVELENT PER DAY (FAR OVERSHOOT THIS IN THERAPY OF OPTIC NEUROPATHY ECT….)
MUST ALWAYS BEWARE OF HPA SUPPRESSION
DECADRON(DEXAMETHASONE)—-POTENT —-LONGER ACTING—NO MINEROCORTICOID EFFECTS—BEST FOR PREGANCY OR HYDROPS
PREDNISONE–LESS POTENT—+MINEROCORTICOID EFFECTS-
SEE PROBLEMS WITH WOUND HEALING, IMMUNOSUPPRESION, ECCYMOSIS, OSTEOPOROSIS, CATARACTS, HYPERTENSION, GLAUCOMA—-POTENTIATES DIABETES AND PEPTIC ULCER Dz—–BENIGN INTRACRANIAL HTN IF ACUTE WITHDRAWL
MEDROL 16 MG PO QOD IS POOR MAN’S MEDROL DOSE PACK
NASAL STEROIDS—TEACH PTS HOW TO USE THEM—AIM AWAY FROM THE SEPTUM—TO THE IPSI EAR
AVOID IN GLUACOMA PTS—-IF >65 HAVE THEM FOLLOW THEIR PRESSURES—-EVIDENCE THAT PTS USING INHALED ORAL STEROIDS GET MORE CATARACT EXTRACTIONS
DEXACORT—HAS SYSTEMICALLY DETECTABLE BLOOD LEVELS—-EXCELLENT FOR POLYPOSIS
S.A.=CANDIDAL INFXN, EPISTAXIS, BURNING
FLONASE CAN BE USED DOWN TO AGE 4 NOW—ONCE A DAY—VERY EFFECTIVE BUT CAN BE A BIT HARSH
RHINOCORT = ONCE A DAY AND CHEAPER—NO PRESERVATIVE—-VERY GENTLE!
NASONEX—NO FRAGERANCE
STERIOD EAR DROPS AND CREAMS (EXT EAR CARES)
DECONGESTANTS
S/A OF INSOMNIA, PROSTATISM, BLADDER CONSTRICTION
MUCOLYTICS
ROBITUSSIN (SSKI)—-S/A OF SEDATION AND GI UPSET
GUAIFENESIN 2,400 MG/DAY IN DIVIDED DOSES
5000 U HEPARIN S.Q.—ANTI INFLAMMATORY
HI AND H2 BLOCKERS—ZYRTEC 10 MG PO QHS AND ZANTAC 300 MG PO QHS WORK WELL FOR URTICARIA AND PRURITIS—IV BENEDRYL (ZYRTEC CAN GIVE HA’S—BEST TO GIVE QHS)
1ST GERNERATION ARE GOOD BUT CAUSE SEDATION, CONSTIPATION AND URINARY RETENTION—-DRY UP RHINORHEA FAIRLY WELL—BENEDRYL, DIMETAP, CHLORPHENIRAMINE, DRIXORAL, ATARAX, HYDROXAZINE, TRINOLIN, POLYHISTINE-(D)—ASTELIN (TOPICAL ANTIHISTAMINE—WORKS WELL)
SELDANE(TERFENIDINE), ASTEMIZOLE, MACROLIDES, ANTIFUNGALS, AND GRAPEFRUIT JUICE CAN ALL POTENTIATE TORSAD—-
2ND GENERATION—LESS SEDATING—-NOW NO BLACK BOX WARNING ABOUT DYSRHYMIAS
ANTICHOLINERGICS
ATROVENT(IPRATROPIUM BROMIDE—TOPICAL WITH VERY LOW SYSTEMIC ABSORBTION OR 1ST GENERATION ANTIHISTAMINES ARE GOOD AT COMBATING RHINORHEA—VASOMOTOR RHINITIS—-IF THIS DON’T WORK DO A PARTIAL INF TURB
ATROVENT 0.03 OR 0.06% NASAL SPRAY
BETA-2 AGONISTS—VENTOLIN, PROVENTIL, AND SEREVENT (SALMEDEROL POWDER)—-CAN GET TACHYPHYLAXIS TO THESE SO BEST NOT TO NEED THEM TOO OFTEN
AMINOPHYLLINE—–ALWAYS CHECK LEVELS
CHROMALYN SODIUM—STABALIZES MAST CELLS—-IS AN ELIXER FORM FOR FOOD ALLERGIES—GASTROCHROME 200 MG PO QID FOR ADULTS AND 100 MG PO BID FOR CHILDREN, 100-200MG PO 20 MIN AC
NASOCHROME (OTC) INTAL (MDI) AND GASTROCHROM= ALL THE SAME DRUG IN DIFFERING FORMS
CHROMALYN AND PSEUDOPHED ARE OK IN PREGNANCY
NEDOCHROMIL (SON OF CHROMALYN)—GOOD FOR CHILDREN (TILADE) TILADE—EXCELLENT FOR COUGH VARIANT ASTHMA—CAN SPRAY IT IN YOUR NOSE—HAS A VERY BITTER BAD AFTERTASTE IN SOME PTS AND IS QID
PATANOL—-AN EYE DROP FOR ALLERGIC CONJUNCTIVITIS/OCULAR PRURITIS —HAS BOTH ANTIHISTAMINIC AND MAST CELL STABALIZING EFFECTS (CHROMALYN EFFECTS)—-2 DROPS OU BID
OTC ANTIHISTAMINE EYE DROPS AVAILABLE
* DERMATITIS MEDICAMENTOSA = RXN TO TOPICAL MEDICINE SUCH AS NEOMYCIN OTHPH OR OTO DROPS—SWITCH TO VOSOL HC
LEUKOTRIENE ANTAGONISTS—ACCOLATE ——LEUKOTRIENE SYNTHESIS INHIBITORS (B4)–SAFER AT 20MG BID—-ZYFLO (MUST FOLLOW LFTS)USUALLY QID—MORE EFFECTIVE AND PAINFUL TO USE—–ESPECIALLY USEFUL IN SAMPTER’S TRIAD ASMTHMA—–REPORTS OF CORRELATION WITH OR POSSIBLY UNMASKING CHURG STRAUSS DISEASE
SINGULAIR—-USE IT!!
IMMUNOTHERAPY–DESENSITIZATION
HOLD IMMUNOTHERAPY FOR FEVER, SEVERE OUT OF CONTROL ASTHMA, INFECTIONS WITH FEVER, OUT OF CONTROL DM OR PTS ON BETA BLOCKERS
THE TH2—TO—TH1 SWITCH (SWITCHING TO THE NON-ALLERGIC PROFILE)—-BLOCKING AB, AND BLUNTING THE INCREASE IN AG SPECIFIC IGE
SET (SKIN END POINT TITRATION)
SL OR SQ NEUTRALIZATION OR ORAL CHROMALYN SODIUM 20 MIN AC AND HS FOR FOOD SENSITIVITY—-GET SL THERAPY TO THE MAX ASAP
EPD (ENZYME [B-GLUCURONIDASE] POTENTIATED DESENSITIZATION)
TAKES ADVANTAGE OF CROSS REACTIVITY TO ANTIGENS
FIRST GET INCREASE IN IgG BLOCKING AB—MAY TAKE A FEW MONTHS
THEN GET A DECREASE INALLERGEN SPECIFIC IgE SERUM AB
INCREASE IN SECRETORY IgA AND IgG
USUALLY PTS FEEL BETTER IN 6-12 WEEKS—SEE THEM BACK IN 6 WEEKS
USUALLY TRY FOR 3-5 YEARS (USUALLY 5 YEARS—80-90% SUCCESS AND NEVER NEED IT AGAIN—-“TRAIN THE IMMUNE SYSTEM”
SET POINT VERY SAFE—-CAN DO OFF OF THE INVITRO TESTS—-ALWAYS DO A VIAL TEST (A INTRADERMAL SKIN TEST WITH THE ANTIGEN)—-SHOULD BE OFF THE ANTIHISTAMINE FOR THE VIAL TEST—SHOULD BE ON THE ANTIHISTAMINES FOR ROUTINE SHOTS
VIAL TESTS IN GENERAL
ALWAYS IMPERATIVE AFTER BLOOD TESTING AS THE PATIENT HAS NEVER ACTUALLY BEEN EXPOSED TO THE LABORATORY ANTIGEN (THIS IS TRUE FOR FOODS AND INHALANTS)
ALWAYS VIAL TEST THE FIRST VIAL IN THE OFFICE
VIAL TESTING MAY NOT BE NECESSARY AFTER THE FIRST VIAL PROVIDED THAT NO ANTIGENS HAVE BEEN ADDED–EVEN DURING ESCALATION (I THINK ERRING ON THE SIDE OF VIAL TESTING IS A GOOD IDEA)
BEGIN AT 0.05 – 0.1 CC SQ INJECTIONS—ADVANCE TO 0.5 CC BY EITHER 0.05 OR 0.1 CC INCREMENTS
ADVANCE TO STRONGER VIALS AS TOLERATED
MODIFICATION OF THE LATE PHASE RESPONSE
1 CC = 15 DROPS
GLYCERINE = A PRESERVATIVE, SWEET TASTE (CHARBOHYDRATE), USUALLY A 50% SOLUTION
PHENOL = A BACTERIOSTATIC AGENT, HAS DETRIMENTAL DEGRATIVE EFFECTS ON THE AG
NEW ANTI IgE MAY REVOLUTIONIZE THE TREATMENT OF ALLERGY—–ESPECIALLY WHEN IT BECOMES GENETICALLY ENGINEERED AND MANUFACTURED IN A DEPO FOMULATION WHICH WOULD ONLY REQUIRE Q 6 MONTH INJECTIONS
THE ONLY DOWNSIDE TO BEING IgE DEFIECIENT IS INCREASED SUSCEPTIBITY TO WORMS WHEEZES AND WEIRD DISEASES—PARASITES ECT…..
CAVEATES:
ALWAYS ASK—-FHx, PETS, SMOKE, CARPET, AGE OF HOUSE, BASEMENT(FINISHED), SEASONAL, PILLOW TYPE (COVERS), BEDDING, MATTRESS, INFANT EATING PATTERNS—-BREAST FED, INTRO TO DAIRY, COLIC, FORMULA/FOOD INTOLERANCE, WHAT DO THEY CRAVE(SUGAR—THINK CORN(SYRUP)), SKIN PROBLEMS AS AN INFANT
PEOPLE CRAVE THE FOODS THEY ARE ALLERGIC TO—PROBABLY GIVES TEMP RELEIF BY CREATING AN AG OVERLOAD AND DRIVING IT BACK INTO SOLUTION
ALACTASIA = LACTOSE INTOLERANCE (LAC OPERON) OF ADULTHOOD IS MUCH DIFFERENT THAN ALLERGY TO DAIRY PRODUCTS
IgE—PERILYMPH
IgA—- (A DIMER WITH A SECRETORY PEICE—J-CHAIN)—ENDOLYMPH (ELS–THE INNER EAR SEAT OF THE IMMUNE SYSTEM)
SNEEZE IN YOUR SLEEEP = DUST MITE ALLERGY
FLEXOR EXZEMA = FOOD ALLERGY UNTIL PROVEN OTHERWISE
EXTENSOR EXZEMA = CONTACT ALLERGENS (DETERGENTS ECT…) TYPE IV
POLLENS—-TREES, GRASSES, WEEDS
PRIMARILY EARLY MORNING, DECREASE WITH RAIN, INCREASE WITH WIND
# 1 = RAGWEED
BREAD = RHIZOPUS
MOLDS IMPERFECT SAPROPHYTIC FUNGI — NO CHLOROPHYLL
AG = SPORE
FLARE AT DUSK, CLEAR WITH SNOW STORM, HIGH COMORBIDITY WITH THOSE WHO HAVE DELAYED LOCAL
DEATH WITH BARIUM ENEMA = LATEX ALLERGY
COWS MILK AND BEEF OFTEN SHARE EPITOPES (AG) CROSS REACT
ENTITIES:
ASTHMA-–REALLY A SECOND COUSIN TO ALLERGY—REALLY A CHRONIC INFLAMMATORY DZ OF THE AIRWAY
A FREQUENT COMORBIDITY, GREATER THAN 90% PEDS HAVE ALLERGY (PRIMARILY DUST MITE AND OTHER PERENIALS SUCH AS COCKROACH)
Rx: THE EARLIER YOU TREAT—THE BETTER—PREVENTS PERMANENT ORGANIC CHANGES
THE CORNERSTONE OF THERAPY IS INHALED STEROIDS—DECREASES RELIANCE ON BETA-2 AGONISTS
MONITOR WITH PEAK FLOWS
RASHES
EXANTHEM = A CUTANEOUS ERUPTION(RASH)
ENANTHEM = A MUCOSAL ERUPTION
A EPITHELIAL MANIFESTATION OF AN INFXOUS Dz
USUALLY AN IMMUNOLOGIC PHENOM TO A VIRAL OR BACTERIAL AG
DERMATITIS (LATIN) = EXCZEMA (GREEK)
URTICARIA = SUPERFICIAL DERMIS
HIVES = NETTLE RASH = URTICARIA (70% IDIOPATHIC)
<6 WEEKS = ACUTE (90%)
> 6 WEEKS = CHRONIC URTICARIA (10%)
CAN EFFECT UP TO 15% OF POP, (50% ASSOC WITH ANGIOEDEMA)
A SUPERFICIAL DERMIS PHENOM (VS QUINKES ANGIOEDEMA = DEEP DERMAL)
TYPES: PHYSICAL (DERMATOGRAPHIA, CHOLINERGIC, COLD) VS ALLERGIC
LOOK FOR ACE INHIBITORS AND NSAIDS
BEST Rx = H2 BLOCKER (ZANTAC)—–AND ZYRTEC
INTERMITTENT SHORT COURSE OF STEROIDS, ALTERNATE DAY THERAPY
MORE LIKELY TO BE A ALLERGIC PHENOM (TYPES I OR IV)
>25% HAVE ASSOC THYROID ABNORMALITIES (CHECK LEVELS AND ANTIBODIES)
ANGIONEUROTIC EDEMA (QUINKE’S Dz)
ANGIOEDEMA = DEEP DERMIS AND SQ TISSUE
DEFINITELY AN IMMUNE PHENOM
NON-PITTING – LOCALIZED EDEMA—PALMES SOLES, UPPER AIRWAY
GI TRACT MAY MANIFEST AS COLIC
PEDIATRIC CASES ARE MORE AMENABLE TO ANTI-INFLAMMATORY THERAPY
HEREDITARY (AUTO D)
STAY SWOLLEN > 24 HOURS
TYPE I (85%) COMMON— DEFICIENT CI INH (C1 ESTERASE INHIBITOR)
TYPE II (15%) VARIABLE—-DEFECTIVE CI INH, DECREASED C4
AQUIRED
B-CELL MALIGNANCY
CT Dz/AUTOIMMUNE Dz (SLE)
ALLERGEN? DRUG INDUCED ( ACE INHIBITORS!)—–MECHANISM NOT WORKED OUT–PROBABLY RETARDS THE BREAKDOWN OF BRADYKININ—INCIDENCE IS 0.1-0.7%, 60% IN THE FIRST WEEK BUT –LATE ONSET (UP TO 1 YEAR—EVEN AFTER 7 YEARS HAS BEEN REPORTED) IS COMMON—-CAPTOPRIL (1/1000)—ASSOC. COUGH AND DYSGUESIA
USUALLY SWELLING GOES DOWN FAST
IDIOPATHIC—PROBABLY THE MOST COMMON TYPE
ALSO HAVE LOW TITERS OF C2 AND C4
ATTACKS ARE SELDOM PRIOR TO PUBERTY
DO NOT PRESENT WITH URTICARIA
Dx: Hx, PE C4, C2, CI INH LEVELS– –REVEIW MEDS—-NEVER SEEN THESE LEVELS BE HELPFUL IN AN ADULT
SCREE WITH C4 LEVELS—-IF LOW THEN GET C1 INH LEVELS AND FUNCTION
CHECK SERUM TRYPTASE
Rx: D/C ACE INHIBITORS—BE CAREFUL ABOUT ARB’S AS WELL
EPI S Q AND INHALED RACEMIC
DECADRON 10 MG IV Q 6 HOURS
5000 U HEPARIN S.Q.
HI AND H2 BLOCKERS (DOXEPIN IS AN EXCELLENT TCA WITH ANTIHISTAMINIC ACTIONS)
FOR AIRWAY TRY INHALED RACEMIC EPI, BETA 2 AGONISTS ECT…..
AMINOPHYLLINE
STANAZOL 2 MG/KG/DAY—WEAN TO 0.5 MG/KG/DAY (INCREASE THE C1INH LEVELS)
DANAZOL 200 MG/KG/DAY—WEAN TO 200 MG Q D
AMICAR (EPSILON AMINOCAPROIC ACID)—PRIMARILY IN CHILDREN
FFP
CIq ESTERASE INHIBITOR CONCENTRATE IN 5% D5W OVER 10-45 MINUTES—IF UNAVAILABE– GIVE FFP
ALLERGIC FUNGAL SINUSITIS = A TYPE I HYPERSENSITIVITY RXN—-ALSO POSIBLE TYPE III
HIGH ASSOC WITH ATOPY AND ASTHMA—DATA FROM MAYO SUGGESTS YOU CAN GROW FUNGUS OUT OF MOST ALL CHRONIC SUNUSITIS PTS (USED A MUCOLYUTIC TO EXTRACT) FEEL IT IS NOT ALLERGIC BUT JUST A OPPORTUNISTIC PATHOGEN ON DISEASED MUCOSA—LONG TERM STEROIDS MAY BE THE BEST
CONSIDERED THE SINONASAL CORRELATE TO BRONCHOPULMONARY ASPERGILOSIS(BPA)—THUS IMMUNOTHERAPY IS CONTROVERSIAL AS IT IS CONTRAINDICATED HERE–HOWEVER IN SINUSITIS THE ANTIGEN IS SUPPOSEDLY ALL REMOVED PRIOR TO BEGINNING IMMUNOTHERAPY!
CHARACTERIZED BY 1) ALLERGIC MUCIN 2) FUNGAL ELEMENTS 3) POSITIVE FUNGAL CULTURE —-MEASURE OF FUNGAL SPECIFIC IgE, 30-50% SKIN TEST + FOR FUNGAL ANTIGENS
OFTEN HAVE AN EOSINOPHILIA (+MBP)—-MAY PLAY A MAJOR ROLE
CALCIUM PHOSPHATE CALCIUM SULFATE CRYSTALS/FE++/MG++/MN WITH INCREASED HOUNDSFIELD UNITS ON CT—CHARACTERISTIC HETEROGENOUS OPACIFICATIONS–THOUGHT TO REPRESENT CENTRAL NECROTIC REGIONS—–DECREASED SIGNAL INTENSITY ON T2 MRI
OFTEN HAVE CONCOMMITANT NASAL POLYPOSIS
BIOPSY — ONOIN SKIN LESIONS ON H & E
CHARACTERISTIC ALLERGIC MUCIN INSPISSATED MUCOUS(LIKE GREEN PEANUT BUTTER)—SNOTOMA—NOT INVASIVE
CHARCOT-LAYDEN CRYSTALS–EOSINOPHILIC INFILTRATE-“TIDE WATER LIKE ARCHITECTURE”
EOSINOPHIS ARE PROBABLY ATTACKING THE FUNGUS—(A RESPONSE)
GOMORI METHENAMINE SILVER (GMS) STAIN WITH MUCIN + CHONDROID MATERIAL—H & E STARIN
OFTEN ASSOC REMODELING OF BONE AND CAUSES PERIOSTEAL THICKENING(DOES NOT INVADE OR DESTROY BONE)
ALLERGIC FUNGAL SINUSITIS/ALLERGIC SINONASAL ASPERGILLOSIS–OTHERWISE HEALTHY HOST (IMMUNE COMPETENT)
DERMATIACIOUS FAMILY (BIPOLARIS)—-GENERA—FAMILY OF DARKLY PIGMENTED FUNGUS
Rx FOR AFS = DEBRIDEMENT—MANY WOULD USE AN OPENFRONTOETHMOIDECTOMY AND CALDWELL LUC TO EXENT Dz—-INITIAL TREATMENT IS ALWAYS REMOVAL
BEFORE INSTITUTING TREATMENT SECURE THE Dx AND REVIEW THE HISTOPATH WITH SILVER STAIN
HTSI
SYSTEMIC STEROIDS ONLY AFTER THE DIAGNOSIS IS FIRMLY SECURE AND INVASIVE DZ IS RULED OUT/ANTIHISTAMINES/DIFLUCAN/ITRACONAZOLE (SPORANOX)
IMMUNOTHERAPY MAY BE OF BENEFIT (RICHARD MABERY–DALLAS)—MAY BE PAN ALLERGIC COMMON EPITOPE AT 18 KD
BRANCHING(45 DEGREES), SEPTATE HYPHAE “A”—THE PROBLEM IS THE HIGH ANTIGEN LOAD
TOPICAL STEROIDS INDEFINITLY
FUNGAL SINUSITIS IS DIVIDED INTO 1) ACUTE FULMINANT—PRIMARILY IMMUNOCOMPROMISED PTS WITH FACIAL PAIN, INVASIVE AND LIFE THREATENING 2) NON-INVASIVE (MYCETOMA) AND (AFS)
MELKERSON-ROSENTHAL SYNDROME (1931)
RECURRENT OROFACIAL EDEMA
RECURRENT FACIAL PARALYSIS(POSSIBLY PROGRESSIVE)
LINGUAL PLICATA(FISSURED TONGUE)–POSSIBLY PERMANENT ORAL CAVITY/LIP DEFORMITY(CHELITIS)
+/- MIGRAINE HA
TRIAD: CHRONIC RECURRENT UNI OR B FACIAL PARALYSIS, FACIAL SWELLING(LIPS AND TONGUE), FISSURED TONGUE (LINGUAL PLICAE/SCROTAL TONGUE)
COMPLETE TRIAD IN ONLY 25%–USUALLY SEQUENTIAL TRIAD OF SIGNS
USUALLY STARTS IN CHILDHOOD OR 2nd DECADE
FEMALE>MALE
UNILATERAL ON IPSI SIDE OF SWELLING
PROBABLY A LOCALIZED VARIANT OF ANGIONEUROTIC (QUINKE’S) EDEMA VS A VARIANT OF SARCOIDOSIS (HIGH ACE LEVELS/GRANULOMATOUS CHANGES)
Dx: LIP BIOPSY-GRANULOMATOUS CHANGES-NON-CASEATING
Rx: STEROIDS
ACYLOVIR? THALIDOMIDE
PROPHYLACTIC DECOMPRESSION(FACIAL PARALYSIS TENDS TO WORSEN)
CAVEATE:
MAY BE A COUSIN TO (A LOCALIZED VARIANT OF) ANGIOEDEMA
AUTO D
PEAKS AGE 20-30
HIGH [ACE] LEVELS WITH ATTACKS
DIGEORGE SYNDROME AND VELOCARDOIOFACIAL SYNDROME HAVE SOME OVERLAP
POLYPOSIS
THE END POINT OF MULTIPLE CAUSES OF INFLAMMATION
ONLY THE HUMAN AND CHIMPANZEES INVOLVED
MUST R/O OTHER MASSES (ENCEPHALOCELE AND INVERTING PAPILLOMA)
ONLY 50% OF POLYPOSIS IS IN ALLERGY PTS (SKIN TEST +)—PROBABLY NO LINK—-HOWEVER—ATOPIC PTS WILL REQUIRE MORE REVISIONS IF NOT DESENSITIZED
LENGTH OF TIME PTS HAS HAD THEM, AGO OF ONSET, ANOSMIA, HX OF EXZEMA, ASA SENSITIVE, ASTHMA—-AFFECTS PROGNOSIS
THINK OF ASA TRIAD AND CF!
ASA TRIAD AND AFS ARE DIFFERENT IN PATHO PHYS
ASPIRIN/ASTHMA/SAMPTER’S/SAINT’S TRIAD
SYNDROME OF ASA INTOLERANCE, ASTHMA, AND NASAL POLYPOSIS
NOT ALLERGIC!
MALE = FEMALE
NOT HELPED VERY MUCH BY SINUS SURGERY
IF YOU DO OPERATE—USE HUMMER, ABX, AND BRONCHODILATORS LIBERALLY
SEEMS TO RESPOND EXCELLENTLY TO NEW LEUKOTRIENE INHIBITORS
AVOID NSAIDS AS THESE CROSS REACT—-USE TYLENOL
ASA DESENSITIZATION (SCRIPTS) IS MOVING INTO THE OFFICE AS A PER HOUR PROCEDURE WITH SINGULAIR, NASAL TORADOL, AND ALKASELTZER.
RHINITIS
VASOMOTOR–NO ALLERGIC SYMPTOMS AND NO EOSINOPHILS—-ATROVENT 80 MCG Q 6 HOURS, HTSI, HUMIDIFICATION, PSEUDOPHED, REGULAR EXERCISE PROGRAM
ALLERGIC—-ALLERGIC Sx, SKIN TEST +, EOSINOPHILS UNLESS (NARES)
INFLAMMATORY/INFXOUS—PMS ON NASAL SMEAR OR POSSIBLY A MANIFESTATION OF A SYSTEMIC PROBLEM
STRUCTURAL/NEOPLASTIC
MULT CHEMICAL SENSITIVITY
A FELLOW TRAVELER WITH ALLERGY—HARD TO OBJECTIVELY QUANTIFY BUT DEFINITELY A PROBLEM FOR MANY INDIVIDUALS—SEEMS TO BE GETTING MORE PREVELENT IN OUR INDUSTRIAL AGE
LATEX ALLERGY
A COMPLICATED ENTITY CONSISTING OF A TYPE IV HYPERSENSITIVITY (CONTACT) RXN OR A TYPE I IGE MEDIATED ANAPHYLACTIC RXN
AG CONTACT IS EITHER THROUGH THE SKIN OR MUCOUS MEMBRANES (OR OPERATIVE WOUNDS) OR THROUGH INHALED PARTICLES GREATLY FACILITATED BY THE CORNSTARCH POWDER
1ST REPORT IN ‘79—ONLY DEATHS HAVE BEEN WITH BARIUM ENEMAS
ACCOUNTS FOR >80% OF PERIOPERATIVE ALLERGIC RXNS—DIFFICULT TO DIAGNOSE
POTENTIATED BY ETHYLENE OXIDE GAS
AEROALLERGENS FORMED BY CORNSTARCH PARTICLES ADHERING TO THE LATEX AG
THE AG = NATURAL RUBBER LATEX FROM THE RUBBER TREE HAVEA BRAZILIENSIS
HIGHEST IN HEALTHCARE WORKERS AND SPINA BIFIDA PTS
7% OF POP HAS IGE TO THE AG (2% HIGH LEVELS)
12% OF HEALTH CARE WORKERS ARE +—–MOST ARE YOUNG
IT IS A REAL PAIN TO GET A TRULY LATEX FREE ENVIRONMENT
CROSS REACTING FOODS: BANNANAS, AVACODO, CHESNUT, KIWI, PAPAYA, FIG
CROSS REACTING AEROALLERGENS: RAGWEED, BLUEGRASS
GIVE ZYRTEC, ZANTAC, EPIPEN, AND ARMBAND