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Doses were informed based on a study that examined gastric emptying in mice and humans (Urva et al

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However, it is considered to be a disorder of multifactorial origin, resulting from a complex interaction between genetic, hormonal and environmental factors and immune dysregulation, both in the onset and maintenance of the disease.8,9 There are 3 fundamental pathophysiological events in HS: hyperkeratosis and dilatation of the hair follicle, follicular rupture and subsequent inflammatory response and chronic inflammation, with architectural changes in the tissue.4 Genetic factors It is estimated that 3040% of HS patients have a family member affected by the disease.3,4 In some families, inactivating mutations have been described in genes encoding essential components of the multiprotein complex -secretase (NCSTN, PSEN1, PSENEN and POGLUT1 genes), which could lead to alterations in the Notch1 signalling pathway and affect keratinocyte proliferation and follicular differentiation.4,10 Moreover, a recently published study found an association between the HLA-DQB1*03 group, in particular the DQB1*03:01 allele, and susceptibility to the development of HS in a series of patients from northern Spain.11 Other genetic alterations that have also been linked to HS include variations in the expression of microRNAs and single nucleotide polymorphisms in the promoter region of the tumour necrosis factor-alpha (TNF-) gene.3 Endocrine factors The role of hormones in the aetiopathogenesis of HS is unclear