الفهرس 
Microanatomy and physiology of apocrine gland, Definition, Epidemiology and Etiopathogenesise of hidradenitis SuppurativaOnly 14 pages are availabe for public view
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Abstract
H
idradenitis suppurativa is a chronic, recurrent, debilitating disease that presents with painful, inflammed lesions in the apocrine-gland-bearing areas of the body, most commonly the axillary, inguinal, and anogenital areas.
The exact aetiology of hidradenitis suppurativa is obscure but there are many suggested causes such as occlusion of the pilosebaceous apparatus, bacterial infections, obesity, excessive sweating, and cigarette smoking as predisposing factors. Since HS begins after puberty, improves with pregnancy, and improves with cyclic elevations of estrogen during the menstrual cycle, these serve to support the role of hormonal influence in the pathogenesis of HS. Also, the relation between HS and hyperandrogenism is largely based on the finding of an increase free androgen index due to a low sex hormone binding globulin. HS also seems to have a genetic component.
The severity of hidradenitis suppurativa varies from a few suppurating lesions to widespread,disabling disease and it leads to a significant long term adverse effect on the mental and physical health where it is characterized by comedo like follicular occlusion, chronic relapsing inflammation, mucopurulent discharge and progressive scarring, which affect axillae, groins, buttocks, perianal area and submammary regions in females.
The condition has classically been thought to occur when apocrine gland outlets become blocked by perspiration or are unable to drain normally because of incomplete gland development. Secretions trapped in the glands force perspiration and bacteria into surrounding tissue, causing subcutaneous induration, inflammation, and infection. However, recent studies have indicated that hidradenitis suppurativa is caused by follicular occlusion first, which, in turn, occludes the apocrine glands and causes perifolliculitis. Therefore, it is actually a disorder of the terminal follicular epithelium located in the apocrine gland-bearing skin areas.
Tumor necrosis factor alpha (TNF-α) was suggested to be involved in the pathogenesis of hidradenitis suppurativa. TNF-α is a cytokine produced by monocytes and macrophages and it exerts host-damaging effects in different autoimmune and inflammatory diseases. It is a key regulator of other pro-inflammatory cytokines and of leukocyte adhesion molecules and it is a priming activator of immune cells. Also, TNF-α mediates the immune response by increasing the transport of white blood cells to the sites of inflammation, and through additional molecular mechanisms which initiate and amplify the inflammation as it leads to the development of inflammatory responses that are hallmarks of many diseases including autoimmune diseases. Because of the numerous roles of TNF-α, it was thought that inhibition of TNF may aid in the treatment of certain dermatological diseases such as hidradenitis suppurativa, psoriasis, pyoderma gangrenosum, and Behcet’s syndrome.
There are many types of therapeutic modalities of hidradenitis suppurativa such as: antibiotics, hormonal treatment, retinoids, steroids, oral cyclosporines, cimetidine, zinc salts and TNF-α antagonist.
It was found that Infliximab and etanercept, TNF-α antagonist, have a role in curing hidradenitis, which gives further support to the suggested role of TNF-α in the pathogenesis.
In our study, the role of TNF-α was evaluated by estimating the serum levels of TNF-α in patients with hidradenitis suppurativa in correlation to the disease severity, general condition, sex of patients and smoking.
Twenty patients with hidradenitis suppurativa were diagnosed by clinical picture were encountered in this study. Ten apparently healthy subjects matched for age and sex were included as controls. At presentation, all patients were subjected to full history taking; full general and dermatological examination as well as estimation of serum TNF-α using the commercially available ELISA kit.
The serum level of TNF- α was significantly elevated in all patients of hidradenitis compared to healthy controls, also there was a highly significant increase in serum TNF-α in moderate than mild cases, and a significant higher serum level of TNF-α among cases with bad general condition as compared to those with good general condition. TNF-α serum level did not correlate with cigarette smoking or the sex of the patients.