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Haemorrhoids are extremely common, and approximately 10 million people are affected by haemorrhoidal disease in the USA.1 Many causes have been proposed to explain the pathogenesis of symptomatic haemorrhoids. The pathophysiological theory, made popular by Thomson’s studies, in which the elastic support of the anal cushions is thought to be broken, is currently the best accepted.1
The function and control of anorectal arteriovenous anastomoses remain unclear as does the existence of individual susceptibility to haemorrhoidal disease, which is influenced by socioeconomic, cultural, and psychological factors.1 Previous studies have established that intake of hot pepper and alcohol abuse may influence disease progression and cause acute exacerbation of haemorrhoidal disease.2
We investigated haemorrhoidal disease and transient receptor potential vanilloid 1 (TPVR1), the receptor for capsaicin, the spicy component contained in plants of the genus Capsicum.3 TPVR1 is a non-selective cation channel that is expressed and stimulates primary sensory neurones. Noxious heat and capsaicin directly activate TPVR1. TPVR1 acts as an ion channel with increased permeability to Na+ and Ca2+ ions, which in turn causes neuronal depolarisation with sensation …
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