Derm- Hidradenitis suppurativa

Question 1

Hidradenitis suppurativa AKA acne inversa (HS/AI) is

Answer 1

a chronic follicular occlusive disease that affects the folliculopilosebaceous unit (FPSU), mainly but not exclusively in intertriginous axillary, groin, perianal, perineal, genital, and inframammary skin.

Question 2

Epidemiology of HS/AI

Answer 2

prevalence 1-4%, onset of symptoms usually occurs between puberty and age 40, with usual onset in the second or third decade of life. Women are more likely to develop HS/AI than men, worse in obese pts

Question 3

pathogenesis of HS/AI

Answer 3

not fully understood; follicular occlusion, follicular rupture, and an associated immune response appear to be important events in the development of the clinical manifestations of HS/AI. progressive and relentless. often has bad odor.

Question 4

actors that may be associated with the development or exacerbation of HS/AI

Answer 4

genetic susceptibility, mechanical stresses on the skin, obesity, smoking, diet, hormonal factors, and drugs such as lithium or oral contraceptives

Question 5

most common site of HS/AI

Answer 5

axilla

Question 6

Sex influences the distribution of HS/AI. Primary sites of involvement in women/ men?

Answer 6

women: groin or upper inner thigh, axilla, chest (including breast and inframammary regions), and the buttocks or gluteal clefts
men: groin or thigh, axilla, perineal or perianal regions, and buttocks or gluteal cleft

Question 7

clinical manifestations

Answer 7

inflammatory nodules, sinus tracts, comedones, scarring

Question 8

physical findings

Answer 8

double or triple comedone is hallmark of disease; may be the first sign of dx. Boil- like lesions smolder and communicate to form sinus tracts that disrupt the dermis and heal with haphazard cord- like bands of scar tissue

Question 9

inflammatory nodules

Answer 9

Most frequently, the first lesion is a solitary, painful, deep-seated inflamed nodule (0.5 to 2 cm in diameter). Dx frequently missed at this stage- misdiagnosed as “boils” aka furunculosis. Painful. Often progresses to form an abscess that may open spontaneously- which relieves pain

Question 10

sinus tracts

Answer 10

typical findings in HS/AI that persist for months or years and contribute to symptomatology. Patients with sinus tracts often experience intermittent release of seropurulent, and at times infected and malodorous, bloody discharge. Not always palpable. Ulceration may accompany sinus tract formation.

Question 11

Open comedones

Answer 11

often appear in long-standing HS/AI, commonly as double-headed or multi-headed open comedones. often described as “tombstone comedones” because they reflect end stage damage to the folliculopilosebaceous unit with associated loss of the sebaceous gland and hair

Question 12

Closed comedones

Answer 12

in HS/AI- essentially tiny cysts that result from continued keratin production by the follicular epithelium lining the residual stub of the follicle above the destroyed sebofollicular junction. Closed comedones are not primary lesions and therefore, are not present in early cases of HS/AI.

Question 13

scarring

Answer 13

The appearance of healed areas ranges from individual pitted acneform scars after resolution of small nodules to dense fibrotic bands or indurated, thick, scarred plaques affecting the whole axillary or groin area. Scars may also be atrophic (particularly on the trunk) or keloidal, and scarring on the buttocks sometimes manifests as multiple pitted scars. In patients with active disease, scarring is accompanied by inflammatory nodules and draining sinuses.

Question 14

In areas of lax flexural skin, such as the axilla, scarring can result in

Answer 14

thick, linear, rope-bands. Severe scarring in the axilla may result in reduced mobility of the arm or lymphatic obstruction leading to lymphedema. Groin involvement may lead to lymphedema of the pubis or the entire vulvar area in women or penile and/or scrotal lymphedema in men

Question 15

Clinical staging with

Answer 15

the Hurley clinical staging system

Question 16

stage I

Answer 16

Abscess formation (single or multiple) without sinus tracts and cicatrization/scarring

Question 17

stage II

Answer 17

Recurrent abscesses with sinus tracts and scarring, single or multiple widely separated lesions

Question 18

stage III

Answer 18

Diffuse or almost diffuse involvement, or multiple interconnected sinus tracts and abscesses across the entire area

Question 19

diagnose through

Answer 19

the patient history and recognition of the characteristic clinical manifestations

Question 20

The three main clinical features that support a diagnosis of HS/AI include

Answer 20

1. Typical lesions (eg, multiple deep-seated inflamed nodules, tombstone comedones, sinus tracts, abscesses and/or fibrotic scars)
2. Typical locations (eg, axillae, groin, inframammary areas; often bilateral distribution)
3. Relapses and chronicity

Question 21

HS/AI primarily occurs

Answer 21

on intertriginous skin. (axilla most common site)

Question 22

skin biopsy for HS/AI?

Answer 22

usually not necessary. bacterial cultures also not necessary. dx based on examination/ recognition of clinical manifestations

Question 23

Acne vulgaris

Answer 23

the less serious clinical variant of HS/AI, has been strongly associated with the “Western diet” [5], a dairy-
laden and calorie-dense food style that is also the basis of the metabolic syndrome.

Question 24

treatment goals for HS/AI

Answer 24

1. To prevent the formation of new lesions and thus reduce
   the extent and progression of the disease
2. To treat new lesions quickly and effectively to prevent development of chronic sinuses
3. To eliminate existing nodules and sinus tracts to limit or prevent scar formation

Question 25

non- pharmacologic and nonsurgical measures in the

management of patients with HS/AI to attempt to reduce the severity and emotional impact of the disease include

Answer 25

education/support, avoidance of skin trauma (wear loose clothing, avoid excessive heat/friction), daily hygiene (gentle cleanser), a-traumatic dressings, smoking cessation, weight management, diet (avoid “western diet” of too much dairy and high glycemic foods)

Question 26

treatment for Hurley Stage I

Answer 26

non pharm measures; Local therapy is the preferred approach- topical clindamycin (1st line therapy). For acute, individual nodules tx is punch debridement (mini- unroofing) which is a minor surgical procedure that leads to resolution of these lesions

Question 27

Topical resorcinol

Answer 27

Resorcinol is a topical chemical peeling agent with keratolytic and antiinflammatory properties that we occasionally find useful for our patients with HS/AI. Topical 15% resorcinol in a proprietary cream base is applied directly to inflammatory nodules (not entire area just inflamed nodule). reduces pain and promotes healing

Question 28

other tx options for stage I

Answer 28

Intralesional corticosteroid therapy is often useful as an adjunctive therapy for reducing symptoms of HS/AI. Also a short course of systemic abx (7-10 days) can quiet intermittent, acute flares in patients with mild disease. (doxy or minocycline or alt therapy- clindamycin.

Question 29

2 major treatment options for Hurley Stage II

Answer 29

systemic antibiotics (usually given for several weeks or longer) and long- term hormonal therapy. procedural 
interventions are usually beneficial. Also intralesional corticosteroid injections may be used to calm acute, painful inflammatory lesions. (just like tx for stage I)

Question 30

abx therapy

Answer 30

tetracyclines usually first line (tetracycline, doxycycline, and minocycline). Combination therapy with clindamycin and rifampin is an option for patients who fail to respond to conventional antibiotic therapy- diarrhea common s/e of this regimen, alternative therapy- usually not first line. dapsone (sulfone drug) another alternative

Question 31

treatment for stage III

Answer 31

similar to stage II both medical and surgical therapies to prevent the development of new lesions and to treat existing lesions

Question 32

medical therapy for stage III/ severe or refractory HS/AI

Answer 32

TNF- alpha inhibitors— Biologic TNF- alpha inhibitors: infliximab (IV), adalimumab (SQ), and etanercept (SQ)