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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2008) |
| Samter's triad |
| Classification and external resources |
Aspirin in tablets
|
| ICD-10 |
J45.1, J45.8 |
| ICD-9 |
493.1 |
| OMIM |
208550 |
| MeSH |
D055963 |
Samter's triad is a medical condition consisting of asthma, aspirin and NSAID sensitivity, and nasal/ethmoidal polyposis.[1] It usually begins in young adulthood[2] (twenties and thirties are the most common onset times)[3] and may not include any other allergies.
Contents
- 1 Signs and symptoms
- 2 Cause
- 3 Treatment
- 3.1 Medication
- 3.2 Surgery
- 3.3 Diet
- 4 Alternate and related names
- 5 History
- 6 See also
- 7 References
Signs and symptoms[edit]
Most commonly the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest as sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. The reactions to aspirin vary in severity, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, anaphylaxis, and urticaria in some cases. In addition to aspirin, patients usually also react to other NSAIDs such as ibuprofen, and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses[4] is generally considered safe.
Anosmia (lack of smell) is also common, as inflammation within the nose and sinuses likely reaches the olfactory receptors.
In addition to aspirin and NSAIDs, consumption of even small amounts of alcohol also produces uncomfortable respiratory reactions in many patients.[5]
Cause[edit]
The disorder is caused by an anomaly in the arachidonic acid cascade which leads to increased production of cysteinylleukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of leukotrienes and produces the severe asthma and allergy-like effects.[6] The underlying cause of the disorder is not fully understood, but there have been several important findings:
- Abnormally low levels of prostaglandin E2 (PGE2), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.[7]
- Overexpression of both the cysteinyl leukotriene receptor 1[8] and the leukotriene C4 synthase[9] enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.
- The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.[10]
- There may be a relationship between aspirin-induced asthma and TBX21, PTGER2, and LTC4S.[11]
Treatment[edit]
Medication[edit]
The preferred treatment for many patients is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA,[12] the Massachusetts General Hospital in Boston, MA,[13] the Brigham and Women's Hospital in Boston, MA,[14] National Jewish Hospital in Denver [15] and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. Patients who are desensitized then take a maintenance dose of aspirin daily and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.
Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are often helpful in treating the symptoms of aspirin-induced asthma. Some patients require oral steroids to alleviate asthma and congestion, and most patients will have recurring or chronic sinusitis due to the nasal inflammation.
Surgery[edit]
Often surgery is required to remove nasal polyps,[16] although they typically recur, particularly if aspirin desensitization is not undertaken.
Diet[edit]
A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help.[citation needed]
Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. However, there is little evidence that a low-salicylate diet is beneficial for patients with AERD,[17] and current clinical trials are underway to determine whether or not the difficult dietary changes truly provide worthwhile therapeutic improvement for these patients.[18]
Alternate and related names[edit]
Samter's triad goes by several other names:
- Acetylsalicylic acid triad [19]
- Widal's triad
- Francis' triad
- Aspirin triad
- Aspirin-exacerbated respiratory disease (AERD).[20]
- Aspirin-induced asthma and rhinitis (AIAR)[21]
A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:
- Non-allergic rhinitis
- Non-allergic rhinitis with eosinophilia syndrome (NARES)
History[edit]
It is named for Max Samter.[22]
Initial reports on the link between asthma, aspirin and nasal polyposis were made by Widal in 1922.[23] Further studies were done by Samter & Beers in reports published in 1968.[24]
See also[edit]
- Salicylate sensitivity
- Drug intolerance
References[edit]
- ^ Kim JE, Kountakis SE (July 2007). "The prevalence of Samter's triad in patients undergoing functional endoscopic sinus surgery". Ear, nose, & throat journal 86 (7): 396–9. PMID 17702319.
- ^ "Current Management of Nasal Polyposis". Retrieved 2008-11-02. [dead link]
- ^ Kevin C. Welch, M.D. "Aspirin Desensitization". American Rhinologic Society.
- ^ Settipane RA, Schrank PJ, Simon RA, Mathison DA, Christiansen SC, Stevenson DD. Prevalence of cross-sensitivity with acetaminophen in aspirin-sensitive asthmatic subjects. Journal of Allergy and Clinical Immunology. 1995 Oct;96(4):480-5.
- ^ Juan Carlos Cardet, Andrew A. White, Nora A. Barrett, Anna M. Feldweg, Paige G. Wickner, Jessica Savage, Neil Bhattacharyya, Tanya M. Laidlaw. Alcohol-Induced Respiratory Symptoms Are Common in Patients with Aspirin Exacerbated Respiratory Disease (AERD). The Journal of Allergy and Clinical Immunology: 131(2), Supplement, AB329, February 2013
- ^ Narayanankutty A, Resendiz-Hernandez JM, Falfan-Valencia R, Teran LM. Biochemical pathogenesis of aspirin exacerbated respiratory disease (AERD). Clin Biochem. 2013 May;46(7-8):566-78. doi: 10.1016/j.clinbiochem.2012.12.005. Epub 2012 Dec 13. Review. PubMed PMID 23246457
- ^ Picado C. Aspirin-intolerant asthma: role of cyclo-oxygenase enzymes. Allergy 2002:57(Suppl.72):58–60
- ^ Ana R. Sousa, Ph.D., Abhi Parikh, M.S., Glenis Scadding, M.D., Christopher J. Corrigan, M.D., Ph.D., and Tak H. Lee, M.D., Sc.D. Leukotriene-Receptor Expression on Nasal Mucosal Inflammatory Cells in Aspirin-Sensitive Rhinosinusitis. N Engl J Med 2002; 347:1493-1499
- ^ Cowburn, A. S., K. Sladek, et al. (1998). Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma. JClinInvest 101(4): 834-46
- ^ Laidlaw TM, Kidder MS, Bhattacharyya N, Xing W, Shen S, Milne GL, Castells MC, Chhay H, Boyce JA. Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes. Blood. 2012 Jan 18.
- ^ Online 'Mendelian Inheritance in Man' (OMIM) 208550
- ^ http://www.scripps.org/locations/scripps-clinic/services/immunology__immunology/services__specialized-services__aspirin-desensitization__frequently-asked-questions
- ^ http://www.massgeneral.org/allergy/
- ^ http://aerd.partners.org/
- ^ "Aspirin Desensitization". 2013. National Jewish Health. Accessed 2013-10-15.
- ^ McMains KC, Kountakis SE (2006). "Medical and surgical considerations in patients with Samter's triad". American journal of rhinology 20 (6): 573–6. doi:10.2500/ajr.2006.20.2913. PMID 17181095.
- ^ http://www.aaaai.org/ask-the-expert/salicylate-free-diet-aspirin-exacerbated-respir.aspx
- ^ http://clinicaltrials.gov/ct2/show/NCT01540032?term=aerd&rank=4
- ^ Amar YG, Frenkiel S, Sobol SE (February 2000). "Outcome analysis of endoscopic sinus surgery for chronic sinusitis in patients having Samter's triad". The Journal of otolaryngology 29 (1): 7–12. PMID 10709165.
- ^ Williams AN, Woessner KM (May 2008). "The clinical effectiveness of aspirin desensitization in chronic rhinosinusitis". Current allergy and asthma reports 8 (3): 245–52. doi:10.1007/s11882-008-0041-7. PMID 18589844.
- ^ Bochenek G, Bánska K, Szabó Z, Nizankowska E, Szczeklik A (March 2002). "Diagnosis, prevention and treatment of aspirin-induced asthma and rhinitis". Current drug targets. Inflammation and allergy 1 (1): 1–11. doi:10.2174/1568010023345011. PMID 14561202.
- ^ synd/2240 at Who Named It?
- ^ Widal MF (1922). "Anaphylaxie et idiosyncraise". Press Med (in French) 119: 48–51.
- ^ Samter M, Beers RF (1968). "Intolerance to aspirin. Clinical studies and consideration of its pathogenesis". Ann. Intern. Med. 68 (5): 975–83. PMID 5646829.
|
Pathology of respiratory system (J, 460–519), respiratory diseases
|
|
Upper RT
(including URTIs,
Common cold) |
|
Head
|
- sinuses
- Sinusitis
- nose
- Rhinitis
- Vasomotor rhinitis
- Atrophic rhinitis
- Hay fever
- Nasal polyp
- Rhinorrhea
- nasal septum
- Nasal septum deviation
- Nasal septum perforation
- Nasal septal hematoma
- tonsil
- Tonsillitis
- Adenoid hypertrophy
- Peritonsillar abscess
|
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Neck
|
- pharynx
- Pharyngitis
- Strep throat
- Laryngopharyngeal reflux (LPR)
- Retropharyngeal abscess
- larynx
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- Laryngopharyngeal reflux (LPR)
- Laryngospasm
- vocal folds
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- Vocal fold nodule
- Vocal cord paresis
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- epiglottis
- Epiglottitis
- trachea
- Tracheitis
- Tracheal stenosis
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Lower RT/lung disease
(including LRTIs) |
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Bronchial/
obstructive
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- acute
- Acute bronchitis
- chronic
- COPD
- Chronic bronchitis
- Acute exacerbations of chronic bronchitis
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- Emphysema)
- Asthma (Status asthmaticus
- Aspirin-induced
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- Bronchiectasis
- unspecified
- Bronchitis
- Bronchiolitis
- Bronchiolitis obliterans
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restrictive
(fibrosis) |
External agents/
occupational
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Other
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- Pulmonary edema
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- Respiratory hypersensitivity
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restrictive
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pneumonitis
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IIP
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Pleural disease
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anat (n, x, l, c)/phys/devp
|
noco (c, p)/cong/tumr, sysi/epon, injr
|
proc, drug (R1/2/3/5/6/7)
|
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Immune disorders: hypersensitivity and autoimmune diseases (279.5–6)
|
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Type I/allergy/atopy
(IgE) |
|
Foreign
|
Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy
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Autoimmune
|
none
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Type II/ADCC
(IgM, IgG) |
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Foreign
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Pernicious anemia · Hemolytic disease of the newborn
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Autoimmune
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Cytotoxic
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Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura · Bullous pemphigoid · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome
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"Type 5"/receptor
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Graves' disease · Myasthenia gravis
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Type III
(Immune complex) |
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Foreign
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Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
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Autoimmune
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Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis
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Type IV/cell-mediated
(T-cells) |
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Foreign
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Allergic contact dermatitis · Mantoux test
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Autoimmune
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Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome · Multiple sclerosis · Coeliac disease · Giant-cell arteritis
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GVHD
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Transfusion-associated graft versus host disease
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multiple |
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Foreign
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Autoimmune
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Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease
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cell/phys/auag/auab/comp, igrc
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Genetic disorder, membrane: cell surface receptor deficiencies
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G protein-coupled receptor
(including hormone) |
| Class A |
- TSHR (Congenital hypothyroidism 1)
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- EDNRB (ABCD syndrome, Waardenburg syndrome 4a, Hirschsprung's disease 2)
- AVPR2 (Nephrogenic diabetes insipidus 1)
- PTGER2 (Aspirin-induced asthma)
|
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| Class B |
- PTH1R (Jansen's metaphyseal chondrodysplasia)
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| Class C |
- CASR (Familial hypocalciuric hypercalcemia)
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| Class F |
- FZD4 (Familial exudative vitreoretinopathy 1)
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Enzyme-linked receptor
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| RTK |
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| STPK |
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|
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| Lipid receptor |
- LRP: LRP2 (Donnai-Barrow syndrome)
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- LRP5 (Worth syndrome, Familial exudative vitreoretinopathy 4, Osteopetrosis 1)
- LDLR (LDLR Familial hypercholesterolemia)
|
|
| Other/ungrouped |
- Immunoglobulin superfamily: AGM3, 6
- Integrin: LAD1
- Glanzmann's thrombasthenia
- Junctional epidermolysis bullosa with pyloric atresia
EDAR (EDAR Hypohidrotic ectodermal dysplasia)
- PTCH1 (Nevoid basal cell carcinoma syndrome)
- BMPR1A (BMPR1A Juvenile polyposis syndrome)
- IL2RG (X-linked severe combined immunodeficiency)
|
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- See also
- cell surface receptors
- B structural
- perx
- skel
- cili
- mito
- nucl
- sclr
- DNA/RNA/protein synthesis
- membrane
- transduction
- trfk
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