The pathology, presentation, and management of acne vulgaris.

1. ACNE VULGARIS
Presentor: Daudi Chiranzi, MED/1004/16
Facilitator: Dr. Kiprono

2. CONTENTS
• Introduction
• Epidemiology
• Aetiology
• Pathogenesis and Pathophysiology
• Clinical features
• Complications
• Diagnosis and Investigations
• Differential diagnosis
• Treatment

3. Introduction
• An inflammatory illness which results from enhanced
sebum production, changes in keratin structure, swelling
and accumulation of bacteria around hair follicles mostly on
face, neck, chest and back.

4. Variants of Acne
1. Acne vulgaris
• Classical acne- 9-12 years
• Infantile/juvenile- Seen in infants 3-12 months of age.
• Late onset- Beyond 20 years of age.
• Severe forms of acne- E.g. conglobata and nodulocystic.
• Acne with associated systemic symptoms- Acne fulminans

5. Variants of Acne
2. Secondary acne
• Endocrine associated.
• Medicine associated.
• Mineral oils.
• Chloracne
3. Hidradenitis suppurative

6. Epidemiology
• The prevalence of acne was found to be 11.2%.
• Majority of the affected cases are women.
• Patient age ranges from 9-52 years, with median age of onset-15 years.
• Present in 49.6% of family members with the condition.
• The most common acne is the classical type (60.9%).
• The most affected body part is the face (93.2%).
• Hyperpigmentation is the most reported complication.

7. Aetiology
• Endocrine abnormalities- Such as PCOS and Pregnancy.
• Bacteria- Cutibacterium acnes (Propionic bacterium), Staphylococcus
epidermis, and Malassezia furfur located on the face, neck, chest and
back.
• Oils.
• Dioxin poisoning- Leading to chloracne
• Medication- Lithium, steroids and anticonvulsants
• Genetics.

8. Associated Factors
• Sunlight exposure.
• Skin trauma- Repetitive mechanical trauma.
• Dietary factors- Increase activity of sebaceous glands.
E.g. milk.
• Stress- Psychological stress
• Insulin-resistance- May stimulate increased androgen
production and insulin-like growth factor.
• BMI- Obesity is proportional to risk of acne.

9. Pathogenesis
• Androgens cause increase in sebum secretion as 5-alpha reductase converts
testosterone to more potent DHT.
• Increased sebum secretion leads to hyperkeratosis of follicular epidermis, keratin
becomes denser, hence blocking secretion of sebum.
• Linoleic acid, that regulates the keratinocytes proliferation, is diminished in ance.
• The increased sebum provides substrate material for Cutibacterium acnes growth,
leading to increased production of lipase enzyme.
• Lipase enzyme converts lipid to fatty acids, and produce proinflammatory
mediators (IL-1 and TNF-α).
• Distended follicles eventually rupture and release the pro-inflammatory mediators,
sebum, lipids, fatty acids and bacteria into the dermis, stimulating inflammation.
• Inflammation in the pilosebaceous unit (hair follicle and sebaceous gland)- Innate,
especially cellular immune response.

11. Pathophysiology
• The microcomedo- A hyperkeratotic plug in the lower
portion of the follicular infundibulum- the precursor for the
lesions.
• Closed comedones (whiteheads)- Keratin and sebum
plugging the pilosebaceous orifice below the skin surface.
• Open comedones (blackheads)- Plugging of the
pilosebaceous orifice by sebum on the skin surface.
• Papules, pustules and nodules- Rupture of follicle and
accumulation of Cutibacterium acnes- inflammation after
translocation of bacteria.

13. Secondary Acne
• Endocrine abnormalities. E.g. PCOS associated with hirsutism,
menstrual irregularities and infertility.
• Medicine- E.g. topical steroids are associated with inducing
comedones and occasional papules.
• Oil-induced acne- When mineral oils come into contact with the skin.
• Dioxin poisoning- Comedones appear after exposure to the chlorinated
compound, leading to chloracne.

14. Clinical Features
Acne occurs on face, deltoid and neck,
chest and back.
• Grade 1- Comedones
1. Closed comedones (White heads)-
Easily felt, and most numerous on the
forehead.
2. Open comedones (Black heads)-
Easily seen, and most numerous on
the cheeks and deltoid.

15. Clinical Features
• Grade 2- Papule with erythema
1. Inflammatory lesions present
as a small papule with
erythema.

16. Clinical Features
• Grade 3: Pustules
1. Develop from papules.

17. Clinical Features
• Grade 4- Nodules and cysts
1. Many pustules coalesce to form
nodules and cysts.
2. May develop to acne conglobata
when patient present with large
numbers of coalesces.
3. Characteristic with pain and
permanent cyst formation.

18. Clinical Features
Acne excoriee
• Presents as chronic comedones or papules that are obsessively
excoriated, leading to erosions and scarring.
• Underlying psychiatric disorder usually present.

19. Clinical Features
Acne Fulminans
• When acne vulgaris presents with systemic
symptoms.
• Severe nodules and cysts are accompanied by:
1. Fever
2. Malaise
3. Joint pain
4. Facial oedema.

20. Clinical Features
Hidradenitis suppurative
• Unpleasant, chronic relapsing sepsis in
the apocrine areas of the axillae and
groins.
• Recurrent painful abscesses and sinus
tracks develop.
• Hx of concurrent acne, or previous
diagnosis of acne.

21. Complications of Acne Vulgaris
1. Post-inflammatory hyperpigmentation.
2. Scarring
3. Gram-negative folliculitis
4. Facial oedema
5. Psychological effect.

22. • History- Age of onset, medication history, menstrual history, current
and prior treatment, psychological impact.
• Physical exam- Distribution, grading, signs of hyperandrogenism,
associated sequelae.
• Investigation- Limited to patients who present with signs of associated
disease or severe acne variants.
Diagnosis and Investigations

23. Differential diagnosis
• Rosacea
• Perioral dermatitis
• Pseudofolliculitis barbae
• Facial angiofibromasin tuberous sclerosis
• Sebaceous hyperplasia
• Nevus comedonicus
• Folliculitis
• Keratosis pellaris
• Steatocystoma multiplex

24. Treatment
1. Topical medication
• Topical retinoids
• Azelaic acid
• Clascoterone
• Salicylic acid
• Topical antibiotics- Dapsone or tetracycline
2. Oral medication
• Oral isotretinoin
• Spironolactone
• Oral contraceptives
• Oral antibiotics

25. Treatment
3. Intralesional glucorcotcoids- Triamcinolone
4. Phototherapy
5. Comedo extraction