2018
DOI: 10.1111/jdv.15160
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Anti‐TNF‐α therapy modulates mTORC1 signalling in hidradenitis suppurativa

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Cited by 27 publications
(21 citation statements)
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“…1 HS has a complex pathophysiology that has been linked to several genetic loci; upregulated proinflammatory cytokines; activation of T cells, neutrophils, macrophages and mast cells; bacterial invasion and biofilm formation. [2][3][4] Patients with HS have multiple potential risk factors for serious and antibiotic-resistant infections, including epidermal disruption from suppurating lesions and erosions; treatment with immunosuppressants, topical agents and/or oral antibiotics; and comorbidities such as diabetes that are independently associated with infections. 5,6 Several studies have demonstrated high rates of colonization of lesions with bacteria that can cause soft-tissue and skin infections, such as Staphylococcus aureus, coagulase-negative Staphylococci and mixed anaerobic bacteria.…”
Section: Discussionmentioning
confidence: 99%
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“…1 HS has a complex pathophysiology that has been linked to several genetic loci; upregulated proinflammatory cytokines; activation of T cells, neutrophils, macrophages and mast cells; bacterial invasion and biofilm formation. [2][3][4] Patients with HS have multiple potential risk factors for serious and antibiotic-resistant infections, including epidermal disruption from suppurating lesions and erosions; treatment with immunosuppressants, topical agents and/or oral antibiotics; and comorbidities such as diabetes that are independently associated with infections. 5,6 Several studies have demonstrated high rates of colonization of lesions with bacteria that can cause soft-tissue and skin infections, such as Staphylococcus aureus, coagulase-negative Staphylococci and mixed anaerobic bacteria.…”
Section: Discussionmentioning
confidence: 99%
“…Hidradenitis suppurativa (HS), or acne inversa, is a chronic inflammatory skin disease capable of causing significant pain, pruritus and scarring, and disfiguring nodules, abscesses and suppurating lesions . HS has a complex pathophysiology that has been linked to several genetic loci; upregulated proinflammatory cytokines; activation of T cells, neutrophils, macrophages and mast cells; bacterial invasion and biofilm formation . Patients with HS have multiple potential risk factors for serious and antibiotic‐resistant infections, including epidermal disruption from suppurating lesions and erosions; treatment with immunosuppressants, topical agents and/or oral antibiotics; and comorbidities such as diabetes that are independently associated with infections …”
mentioning
confidence: 99%
“…TNF-α could particularly play a central role in the pathogenesis of the skin manifestations. 4 Indeed, different cases reported the efficacy of TNF inhibitors in these auto-inflammatory conditions. [2][3][4][5][6][7] Treatment of PG remains largely anecdotal, with only two randomised controlled trials; therefore, its management is based largely on case series and poorly evidenced publications.…”
mentioning
confidence: 99%
“…Chest x-ray and abdominal ultrasound ruled out the concomitant presence of other major diseases. Oral antibiotic treatment with rifampicin and clindamycin was administered for 8 weeks (instead of starting the treatment by combining the two antibiotics, the patient started the therapy taking only 300 mg rifampicin twice a day for 7 days and, after the first week, added clindamycin at a dose of 300 mg twice a day), 4 associated with adalimumab. Adalimumab therapy was started with a loading dose of 160 mg, subcutaneously injected at week 0, 80 mg at week 2, and 40 mg every week from week 4 onwards.…”
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confidence: 99%
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