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.
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.
The correlation of asthma, nasal polyps (NPs), and aspirin intolerance
Samter’s triad (ST):
There are many other terms to describe this disease: aspirin-induced asthma, aspirin-sensitive asthma, aspirin hypersensitivity, and aspirin-exacerbated respiratory disease (AERD) including chronic rhinosinusitis (CRS) with as a fourth hallmark of this disease .
Although the exact mechanism of ST remains unclear, evidence was found that the pathogenesis of ST is nonallergic hypersensitivity reaction . It is associated with the abnormal metabolism of arachidonic acid, which suggest both the lipoxygenase (LO) pathway and the cyclooxygenase (COX) pathway . This abnormality causes an imbalance in the synthesis of eicosanoid, prostaglandins (PG) and leukotrienes (LTs). Anti-inflammatory PG, especially E2, decrease and the synthesis of cysteinyl LT (Cys-LT C4, D4, E4) is increased . Many patients with ST first visited the otorhinolaryngology department because nasal obstruction and anosmia are the most common symptoms of ST. These patients usually have intractable sinonasal disease that requires multiple endoscopic sinus surgery (ESS).
The provocative challenges test with aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is the only diagnostic methods. Aspirin desensitization is an important therapeutic option in patients with ST, especially in those patients suffering from recurrent NPs, anosmia, and overdependence on systemic corticosteroids .