Table 2.

Current findings about sexual hormones in HS.

References	Type of Source	Aim	Results	Conclusion
Harrison et al., 1985 [20]	case-control study (n = 13; all female)	Investigation of endocrine abnormality in HS	−by adding thyrotropin-releasing hormone and gonadotropin-releasing hormone, the HS prolactin and TSH responses were significantly higher than in controls −there was no difference in the levels of estrogen, progesterone, testosterone, DHEA-S, T3, and T4.	In HS, there could rather be a disturbance of the feedback signals of peripheral hormones.
Mortimer et al., 1986 [17]	case-control study (n = 42; all female)	role of sexual hormones in HS	−13 patients (31%) had irregular menstruation, 22 out of 36 (61.1%) had exacerbation of HS premenstrual −patients had higher testosterone (p < 0.01) and free androgen index (testosterone to sex-hormone-binding globulin concentrations) than healthy controls (p < 0.01) −88.1% of the patients had comedones in typical HS area.	In female patients with follicular type of HS, androgens seem to play a role in the pathogenesis.
Buimer et al., 2015 [15]	experimental im-munohisto-chemical study (n = 22; 16 female and 6 male)	AR and ER immunoreactivity in apocrine glands of HS	−expression of ER in the apocrine glands was weak or absent −AR expression in the apocrine glands was strong, but there was no difference between HS and healthy controls	Expression of AR and ER in apocrine glands has no decisive role in the pathogenesis of HS.
Gauntner 2019 [14]	experimental study (n = 17; gender unknown)	gene expression microarray analysis from skin biopsies in HS	−genes (VDR, NFE2L2, IRF8, RELA, NANOG, AR, TP63, STAT3) were significantly more enriched in lesional skin of HS compared to non-lesional skin.	HS lesions show increased androgen receptor (AR) transcriptional activity, activation of stem-cell-associated transcriptional pathways, and upregulation of Notch-associated genetic loci.
Zouboulis et al., 2020 [16]	experimental study (n = 16; 8 female and 8 male)	Transcriptome analysis to investigate the role of the apocrine glands in HS	−in female patients, the genes MRO, DYRK3, SDK2, GLB1L, CATSPERB, and PRPS2 are upregulated. All the genes mentioned are regulated by androgens. −In male patients, the genes (AGPAT3, GAL, ELOVL3, THRSP, DGAT2L3, OLAH, THRSP, FADS1, NR2F2, FADS2, PTGDS, and HAO2) that play a role in fat metabolism are downregulated −the gene SULF1 showed significant upregulation between lesional skin (LS) and non-lesional skin (NLS)	Androgen-controlled genes are up-regulated in women, and genes that influence fat metabolism are down-regulated in men. The apocrine glands are of secondary importance in HS pathogenesis.
Yu et al., 2021 [13]	experimental immunohistochemical study (n = 10; 6 female and 4 male)	AR immunoreactivity in HS skin tunnels, epidermis, and infundibulum	−AR expression in the epidermis and infundibulum was on average higher in HS than in healthy skin (54% vs. 26%) −AR expression was significantly higher in HS skin tunnels (lining epithelium) in both males and females −Males showed higher AR expression than females (average: 226% and 78%) −Males had an extensive, continuous AR expression pattern, while females had a segmental, patchy pattern −estrogen receptors were predominantly immunohistochemically negative in the epidermis and skin tunnels	Androgens are involved in HS. The segmental AR expression pattern of the skin tunnels in women may be related to a response to antiandrogenic therapy.