1 Acne

  1. 1.

    Acne vulgaris

    • Common inflammatory skin disease, most often in puberty

    • Morphologies include comedonal, papular, pustular, nodulocystic

    • Pathophysiology related to:

      1. 1.

        Increased sebum production

      2. 2.

        Abnormal follicular epidermal turnover/keratinization

      3. 3.

        Overgrowth of bacteria (gram positive diptheroid anaerobe Propionobacterium acnes)

      4. 4.

        Inflammatory response (to foreign body)

    • Typical therapeutic ladder:

      1. 1.

        Benzoyl peroxide in conjunction with topical antibiotic (clindamycin or erythromycin) and topical retinoid (for comedones)

      2. 2.

        Systemic antibiotic (tetracyclines)

      3. 3.

        Systemic retinoid (isotretinoin)

    • Androgenic hormones have significant influence on acne; with suspected strong hormonal component (e.g. acne flares monthly localizing more on jawline, chin), consider oral contraceptives and spironolactone

    • The role of diet in acne is controversial, but no strong evidence for diet connection

  2. 2.

    Follicular occlusion tetrad

    • These four diseases are thought to be closely related and may co-exist; the primary pathophysiology involves occlusion and rupture of hair follicles with associated inflammation

    • This spectrum may be associated with inflammatory bowel disease, pyoderma gangrenosum, acne syndromes

    1. (a)

      Hidradenitis suppurativa

      • Aka “acne inversa”

      • Clinically may see sinus tracts and nodules, “double comedones”

      • Localizes typically to intertriginous areas (axillae, inguinal folds)

      • Previously, thought to be a primarily apocrine disease given the typically apocrine gland bearing affected areas, but now thought that apocrine glands are only secondarily inflamed and fibrosed

      • Associated with smoking, obesity

      • Treatments include intralesional steroids, topical and systemic antibiotics, isotretinoin (often not effective), anti-TNF biologics, surgery

    2. (b)

      Acne conglobata

      • Unusually severe nodulocystic acne with sinuses and scarring

    3. (c)

      Dissecting cellulitis

      • Aka perifolliculitis capitis abscedens et suffodiens

      • Clinically presents as cystic nodules on the scalp

      • May have overlap with folliculitis decalvans, which is more typically a flat and boggy scalp plaque

      • See also Alopecia:Scarring alopecia

    4. (d)

      Pilonidal sinus

      • Involves gluteal cleft

  3. 3.

    Acne syndromes

    1. (a)

      Acne fulminans

      • Severe nodulocystic acne with variable systemic manifestations (fevers, arthralgias, hepatosplenomegaly), may have osteoclastic lesions, especially of the clavicle

    2. (b)

      SAPHO syndrome

      • Syndrome of synovitis, acne conglobata, pustulosis (often palmoplantar), hyperostosis, osteitis

      • Can be associated with Sweet’s

    3. (c)

      PAPA syndrome

      • Sterile pyogenic arthritis, pyoderma gangrenosum, and acne

      • Has been associated with pyrin/nod defects

    4. (d)

      PASH and PAPASH syndromes

      • Pyoderma gangrenosum, acne, and suppurative hidradenitis (PASH) and pyogenic arthritis, pyoderma gangrenosum, acne, and suppurative hidradenitis (PAPASH)

  4. 4.

    Other types of acne

    1. (a)

      Neonatal acne/neonatal cephalic pustulosis

      • No open or closed comedones seen

      • Onset usually first 2–3 weeks of life, resolves on own with no scarring within weeks, therapy not necessary

      • Associated with Malassezia sympodialis

    2. (b)

      Infantile acne

      • Usually begins at 3–6 months, may be associated with precocious secretion of gonadal androgens

      • Can persist; treated with topical retinoid/benzoyl peroxide

    3. (c)

      Drug-induced acne

      • Usually from corticosteroids (“steroid acne”), but also lithium, androgens, phenytoin, ACTH, INH, EGFR inhibitors

      • Can see abrupt eruption of monomorphic papules/pustules without comedones

      • Would also include halogenoderma (includes iododerma) as a potential drug-induced acneiform eruption

      • See also Vascular:Toxic Erythema:Drug Eruptions

    4. (d)

      Chloracne

      • Occupational acne caused by exposure to chlorinated aromatic hydrocarbons (dioxins), such as Agent Orange (herbicide/defoliant used in Vietnam War). Famous case: Ukranian president Viktor Yuschenko poisoned.

      • Particularly seen behind ears and over the malar crescent

    5. (e)

      Acne excoriée (de jeunes filles)

      • Picking at one’s face with history of mild acne

    6. (f)

      Acne aestivalis (Mallorca acne)

      • Monomophous eruption of red papules on the face from UVA light (similar to PMLE), no comedones

    7. (g)

      Trichostasis spinulosa

      • Small dark follicular papules on the nose; from clusters of vellus hairs embedded within hair follicles; may be variant of comedones

    8. (h)

      Favre–Racouchot syndrome

      • Nodular elastosis with cysts and comedones

      • Associated with UV and smoking

    9. (i)

      Solid facial edema

      • Aka Morbihan disease

      • Soft tissue edema associated with acne leading to midline facial distortion

      • Has also been associated with rosacea and Melkersson-Rosenthal syndrome

    10. (j)

      Tropical acne

      • Acneiform eruption from extreme heat or occupational exposure

    11. (k)

      Acne mechanica

      • Caused by repeated rubbing under occlusion

        1. I.

          Fiddler’s neck

2 Rosacea

  • Aka acne rosacea; rosacea is considered a distinct entity from acne with different pathophysiology, though may respond to similar therapeutics

  • Rosacea is classically recognized by central erythema of the face with stinging/burning sensations; however, different types may have different clinical morphologies

  • Classic triggers include sunlight, alcohol, caffeine, spicy foods, emotions, hot drinks

  • Pathophysiology of rosacea is unclear, but it is thought to reflect a vascular dysregulation

  • Has been associated with increased levels of toll-like receptor 2, and increased expression of cathelicidin, LL-37, and kallikrein 5

  • Demodex folliculorum has been implicated in etiology (but circumstantial evidence)

  • Treated topically with metronidazole, azelaic acid, sodium sulfacetamide, even retinoids, permethrin, ivermectin; systemically with oral antibiotics (since etiology unclear, why these work is also unclear), ivermectin; also pulsed dye laser

    1. 1.

      Classic types of rosacea

      1. (a)

        Erythematotelangiectatic

      2. (b)

        Papulopustular

      3. (c)

        Phymatous (including rhinophyma)

      4. (d)

        Ocular (including blepharoconjunctivitis)

    2. 2.

      Pyoderma faciale/rosacea fulminans

      • A more severe inflammatory form of rosacea

      • Some use former term to mean more localized, latter term for whole face

      • Presents as eruption of inflamed papules and yellow pustules in the centrofacial region

    3. 3.

      Perioral/periorificial dermatitis

      • May be within rosacea spectrum, but also can be caused by topical steroid use; classically spares vermillion border of lips

      • Includes periorificial dermatitis of childhood

    4. 4.

      Granulomatous rosacea

      • Clinically consistent with rosacea, but with lesions with granulomatous clinical morphology (red-brown/orange papules) and pathology

      • See also Dermal:Inflammatory:Granulomatous/histiocytic

    5. 5.

      Lupus miliaris disseminatus faciei

      • Aka acne agminata

      • Granulomatous eruption on face; some consider a form of rosacea

      • Previously thought to be a tuberculid reaction

3 Folliculitis

3.1 Superficial Folliculitis

  1. (a)

    Bacterial

    1. I.

      Impetigo of Bockhart (Staph)

    2. II.

      Gram negative folliculitis

    3. III.

      Hot tub folliculitis (Pseudomonas)

  2. (b)

    Fungal

    1. I.

      Dermatophytes

      1. 1.

        Tinea barbae (T. mentagrophytes and T. verrucosum)

      2. 2.

        Tinea capitis (especially T. tonsurans and M. canis)

    2. II.

      Candida

    3. III.

      Pityrosporum

  3. (c)

    Viral

    1. I.

      Herpes simplex (HSV)

  4. (d)

    Eosinophilic pustular folliculitis (EPF)

    • Three types

      1. I.

        HIV-associated EPF

        • Presents as pruritic papules on chest/back/face; can mimic acne

      2. II.

        Ofuji’s disease

        • Seen primarily in Asians/Japanese

      3. III.

        Eosinophilic pustulosis of infancy

        • Ddx erythema toxicum neonatorum

  5. (e)

    Demodex folliculitis

  6. (f)

    Other non-infectious

    1. I.

      Disseminate and recurrent infundibulofolliculitis (DRIF)

      • Aka Hitch and Lund disease

      • Numerous monomorphic follicular papules on chest

      • Can appear like lichen spinulosus

      • Ddx juxtaclavicular beaded lines, an entity perhaps related to sebaceous hyperplasia

    2. II.

      Irritant/frictional

3.2 Deep Folliculitis

  1. (a)

    Infectious

    1. I.

      Furunculosis

      • Aka boils or follicular abscesses

      • From Staph and Strep primarily

      • Primary treatment is incision and drainage; may also use systemic antibiotics

      • See also Infectious Diseases: Bacterial: Staph and Strep

    2. II.

      Sycosis barbae (Staph/mycotic/herpetic)

      • Homophone with “psychosis”

      • Localizes to the beard area

    3. III.

      Majocchi’s granuloma (deep dermatophyte folliculitis)

      • T. rubrum

      • Often on legs, with topical steroid use

3.3 Pseudofolliculitis

  • From in-grown hairs

    1. (a)

      Pseudofolliculitis barbae (PFB)

      • Often treated with topical antibiotics for presumed associated folliculitis; also treated with decreased shaving frequency

    2. (b)

      Acne keloidalis/Acne keloidalis nuchae (AKN)

      • May represent a scarring reaction to pseudofolliculitis

      • See also Alopecia:Scarring alopecia

4 Follicular Cysts

  • See also Neoplastic:Cysts

    1. 1.

      Milia

      • Benign, keratin-filled cysts (small epidermoid cysts); do not confuse with miliaria (from obstruction of sweat gland ducts)

        1. (a)

          Primary milia

          • From vellus hair follicles

        2. (b)

          Secondary milia

          • From damage to pilosebaceous unit (as in subepidermal blistering diseases)

    2. 2.

      Epidermal inclusion cysts

      • Aka epidermoid cysts or sebaceous cyst (misnomer) or infundibular cyst (from the infundibulum)

      • Associated with Gardner syndome/FAP

      • Has granular layer

    3. 3.

      Pilar cysts

      • Aka trichilemmal cysts, sometimes autosomal dominant

      • Derived from the outer root sheath trichilemma of the hair follicle

      • Lacks granular layer

    4. 4.

      Foreign body granulomatous reaction to ruptured follicular cyst (ruptured cyst/keratin granuloma)

    5. 5.

      Eruptive vellus hair cysts

      • Small bluish papules typically on mid chest/sternum, rarely extremities

      • See also Neoplastic:Cysts

    6. 6.

      Steatocystoma/steatocystoma multiplex

      • Cystic papules with oily, yellow liquid

      • See also Neoplastic:Cysts