The following laboratory tests may be helpful in the evaluation of hidradenitis suppurativa HS:
Medical anti-inflammatory or antiandrogen therapy eg, oral or topical antibiotics, intralesional triamcinolone, spironolactone, finasteride Biological therapy The following medications are used in the management of hidradenitis suppurativa: Antibiotics eg, tetracycline, doxycycline, minocycline, trimethoprim-sulfamethoxazole, clindamycin, erythromycin, dapsone Retinoids eg, isotretinoin Corticosteroids eg, triamcinolone, prednisolone, prednisone Antiandrogens eg, cyproterone acetate, spironolactone Immunosuppressants eg, adalimumab, infliximab, other biologic agents Estrogen derivatives eg, ethinyl estradiol 5-Alpha-reductase inhibitors eg, finasteride Surgery Surgery is most valuable in the chronic and recurrent stages of hidradenitis suppurativa.
YAG laser treatment of lesions Exteriorization Electrocoagulation of the sinus tracts Deroofing and skin-tissue-saving excision with electrosurgical peeling Simple excision of the troublesome areas with direct closure Reconstruction with skin grafting and negative-pressure wound healing therapy Placement of local cutaneous flaps, musculocutaneous flaps, pedicled and free flaps, or skin grafts Secondary-intention healing Radiotherapy Nonablative radiofrequency therapy can be used for patients with Harley stage I and II disease.
Background Hidradenitis suppurativa HS is a disorder of the terminal follicular epithelium in the apocrine gland—bearing skin. Hidradenitis suppurativa is characterized by comedolike follicular occlusion, chronic relapsing inflammation, mucopurulent discharge, and progressive scarring.
Pathophysiology Hidradenitis suppurativa HS has traditionally been considered a disorder of the apocrine glands. Hidradenitis suppurativa was first described as a distinct entity inwhen Velpeau reported a patient with superficial abscess formation in the axillary, mammary, and perianal regions.
For many years, the condition was described as Verneuil disease, but it subsequently became known as hidradenitis suppurativa.
Ustekinumab in adolescent patients age 12 to 17 years with moderate-to-severe plaque psoriasis: Results of the randomized phase 3 CADMUS study. Practice Essentials. Hidradenitis suppurativa is a disorder of the terminal follicular epithelium in the apocrine gland–bearing skin. This condition is a chronic disabling disorder that relentlessly progresses, frequently causing keloids, contractures, and immobility. Atopic dermatitis is a chronic, relapsing inflammatory skin disease that is characterized by the up-regulation of type 2 immune responses (including those involving type 2 helper T cells), 1,2 an.
Not having performed any histopathologic studies himself, Verneuil conceded that his conclusion was based purely on the characteristic distribution of the condition. He observed the primary cellular reaction in the lumen of the apocrine glands and in the neighboring periglandular connective tissue.
Detailing the clinical features of the disease, Brunsting highlighted its frequent association with acne. He noted that hidradenitis suppurativa, dissecting cellulitis of the scalp and the neck, and acne conglobata commonly occur in the same patient.
He thought that the central pathogenetic event in all 3 conditions was a tendency for follicular hyperkeratinization with secondary bacterial infection. InPlewig and Kligman added pilonidal sinus as another component to the ensemble, and they introduced the term acne tetrad. InPlewig and Steger suggested the term acne inversa as an inclusive and accurate name for what was previously called the follicular occlusion triad, or follicular occlusion tetrad.
The term acne inversa links the pathogenesis to acne and reflects the fact that it is an expression of follicular occlusion in localizations inverse to acne vulgaris.
Etiology The exact etiology of hidradenitis suppurativa remains obscure. All proposed etiologic factors, such as occlusion and bacterial infection, genetics, host defense defects, hormones, cigarette smoking, and irritants, are likely to be only secondary factors.
The primary events in the hair follicles of the affected areas remain unidentified. The classic view of hidradenitis suppurativa is that it is an occlusive and pyogenic disease of the apocrine glands, a hypothesis that seemed to be confirmed with its experimental reproduction by Shelley and Cahn in No progression to the characteristically chronic condition of hidradenitis suppurativa occurred.
The inflammation of the apocrine glands did not occur in the absence of an adjacent folliculitis; thus, apocrine gland involvement was incidental or secondary. The earliest change is plugging, which occurs in follicular hyperkeratosis with infundibulofolliculitis.
This obstructs the apocrine gland ducts and perifolliculitis around the ducts. Whether this initial inflammatory change is due to a bacterial infection or factors similar to those involved in acne formation is not known.
In the later stages of hidradenitis suppurativa, bacterial infection seems to be a risk factor for the destructive scarring and extension of hidradenitis suppurativa lesions, and, once the sinuses have formed, the risk of secondary infection is obvious.
A similar mechanism may be important in the pathogenesis of hidradenitis suppurativa. The cause of the rupture is not known, although friction in intertriginous locations may be a contributing factor.
The rupture is followed by the spillage of foreign-body material into the dermis, which initiates an inflammatory response, resulting in foreign-body granuloma formation. Epithelial strands form draining sinuses in this inflammatory tissue.
Colonization with bacteria, usually coagulase-negative staphylococci, can aggravate the chronic inflammation. The apocrine glands may play a role in hidradenitis suppurativa since an abnormal secretion either the excess or absence could be influencing an effect on the acroinfundibulum, distal from the gland itself.
The sinus tract formation is an early feature of hidradenitis suppurativa, arising not from hair follicles but rather from invaginations of epidermis as cysts.
Resident bacteria, such as coagulase-negative staphylococci may cause adherence of the epidermis in the closed serrated tissue of intertriginous areas, leading to the formation of cysts and hidradenitis suppurativa lesions.
Although the inciting influences for the follicular occlusion and sinus tract formation have not been fully elucidated, genetic factors may play a role. More than 15 years ago, the existence of a familial form of hidradenitis suppurativa with autosomal dominant inheritance was proposed.
Gamma-secretase appears integral to normal skin function, through effects on notch signaling, such as the biological role in the hair follicle. The pattern of mutations suggests that loss of function of components of the gamma-secretase complex underlies the disease: Although these mutations only appear in a minority of cases of hidradenitis suppurativa, their identification delineated the first genetically defined clinical subgroup of patients with hidradenitis suppurativa and primary involvement of the hair follicle instead apocrine gland, suggesting that the primary event is follicular occlusion.
They are different heterozygous mutations in subunits of gamma-secretase. Genetic factors might influence not only the appearance of hidradenitis suppurativa, but also the phenotype of disease.
The release of oxygen radicals from peripheral neutrophils that are activated in vitro was studied in patients with inactive hidradenitis suppurativa.
The generation of free oxygen radicals after the stimulation of peripheral neutrophils with protein kinase C PKC activator and phorbolmyristate acetate PMA was significantly higher in patients with hidradenitis suppurativa than in healthy control subjects.Atopic dermatitis is a chronic, relapsing inflammatory skin disease that is characterized by the up-regulation of type 2 immune responses (including those involving type 2 helper T cells), 1,2 an.
Practice Essentials. Hidradenitis suppurativa is a disorder of the terminal follicular epithelium in the apocrine gland–bearing skin. This condition is a chronic disabling disorder that relentlessly progresses, frequently causing keloids, contractures, and immobility.
Oct 19, · Hidradenitis suppurativa is a disorder of the terminal follicular epithelium in the apocrine gland–bearing skin. This condition is a chronic disabling disorder that relentlessly progresses, frequently causing keloids, contractures, and immobility.
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A3: Accurate, Adaptable, and Accessible Error Metrics for Predictive Models: abbyyR: Access to Abbyy Optical Character Recognition (OCR) API: abc: Tools for.