Samter’s Triad: State of the Art

Abstract

Samter’s triad (ST) is a well-known disease characterized by the triad of bronchial asthma, nasal polyps, and aspirin intolerance. Over the past few years, a rapid development in the knowledge of the pathogenesis and clinical characteristics of ST has happened. The aim of this paper is to review the recent investigations on the pathophysiological mechanisms and genetic background, diagnosis, and different therapeutic options of ST to advance our understanding of the mechanism and the therapeutic control of ST. As concern for ST increase, more application of aspirin desensitization will be required to manage this disease successfully. There is also a need for continued research efforts in pathophysiology, treatment, and possible prevention.

Aspirin Exacerbated Respiratory Disease: Epidemiology, Pathophysiology, and Management

“…Aspirin exacerbated respiratory disease is characterized by a non-immunoglobulin E hypersensitivity reaction to ASA/COX-1 inhibitors that is commonly comorbid with but not due to underlying allergic disease [15]. Aspirin exacerbated respiratory disease is thought to be due to abnormalities in arachidonic acid biosynthesis [3,4]. Arachidonic acid can be metabolized through two different pathways: the 5-lipoxygenase (5-LO) pathway and the COX-1 pathway (Figure 1).…”

“…The 5-LO pathway produces cysteinyl-leukotrienes (Cys-LTs) from arachidonic acid, specifically leukotriene C4, D4, and E4 (LTC4, LTD4, and LTE4) while the COX-1 pathway produces prostacyclins, prostaglandins, and thromboxanes. The underlying defect in AERD is thought to relate to constitutive overproduction of Cys-LTs with a concomitant decrease in downstream products of the COX-1 pathway, the latter of which have an inherent inhibitory effect on Cys-LTs [4,16,17]. The release of this physiologic brake, coupled with Cys-LT overproduction, creates a proinflammatory milieu.…”

“…The ingestion of ASA or COX-1 inhibiting NSAIDs by AERD patients further skews Cys-LT production through the inhibition of the COX-1 pathway leading to further shunting of products down the 5-LO pathway [4] (Figure 1). This is evidenced by detection of 5-LO pathway enzyme upregulation in the lungs, sinuses, and nasal polyps in AERD patients, thought to be mostly due to the infiltrating eosinophils and resident mast cells [17].…”

“…Subsequently, in 1968, Samter and Beer described the full clinical characteristics of aspirin sensitivity and elucidated the classic triad of symptoms, eponymously named Samter’s Triad [1,2]. Samter’s Triad is defined as chronic rhinosinusitis with nasal polyposis (CRSwNP), bronchial asthma, and reactions to aspirin or cyclooxygenase-1 (COX-1) inhibitors [3,4,5,6]. Since its first description by Widal, there has been considerable literature published on the epidemiology, pathophysiology, and treatment of what is now termed aspirin exacerbated respiratory disease (AERD).…”

Evaluation of the benefits of functional endoscopic sinus surgery on bronchial asthma in patients with concomitant nasal polyposis

“…Samter's triad is a well-known disease characterized by the triad of bronchial asthma, nasal polyps, and intolerance to aspirin and other non-steroidal anti-inflammatory drugs. 6 On the basis of available evidence, medical therapy for NP should begin with daily application of a topical intra nasal corticosteroid (INCS) in conjunction with high volume saline irrigation, and subsequent therapies are based on the patient polyp status, severity of symptoms, and/or quality of life (impairment). 7 In some mild cases presenting for the first time with large polyps, polypectomy can have a long lasting effect.…”