Acne Vulgaris - Pharmacotherapy

1. Skin Diseases
Acne Vulgaris
Allergic Dermatitis
Areej Abu Hanieh

2. Definition
• Acne vulgaris is a common chronic skin
disease involving blockage and/or
inflammation of pilosebaceous units (hair
follicles and their accompanying sebaceous
gland).
• Acne can present as noninflammatory lesions,
inflammatory lesions, or a mixture of both,
affecting mostly the face but also the back and
chest.

3. Causes
Acne develops from the following four factors:
1. follicular epidermal hyperproliferation with subsequent
plugging of the follicle.
2. excess sebum production.
3. the presence and activity of the commensal
bacteria Cutibacterium acnes (formerly Propionibacterium
acnes).
4. inflammation.
5. In addition, genetics is also a key factor in the
pathophysiology of acne.

6. Pathophysiology
• C acnes (formerly P acnes) is an anaerobic organism present in acne
lesions.
• The presence of C acnes (formerly P acnes) promotes inflammation
through a variety of mechanisms.
• C acnes (formerly P acnes) stimulates inflammation by producing
proinflammatory mediators that diffuse through the follicle wall.
• Studies have shown that C acnes (formerly P acnes) activates the
toll-like receptor 2 on monocytes and neutrophils.
• Activation of the toll-like receptor 2 then leads to the production of
multiple proinflammatory cytokines, including interleukins 12 and 8
and tumor necrosis factor.
• Hypersensitivity to C acnes (formerly P acnes) may also explain why
some individuals develop inflammatory acne vulgaris while others
do not

7. • Excess sebum is another key factor in the
development of acne vulgaris.
• Numerous other mediators and receptors,
including growth hormone and insulin like
growth factor, as well as peroxisome
proliferator-activated receptors also regulate
the sebaceous gland and may contribute to
the development of acne.

8. Signs and Symptomes
Acne vulgaris is characterized by:
1. noninflammatory open or closed comedones.
2. inflammatory papules, pustules, and nodules.
3. Acne vulgaris typically affects the areas of skin
with the densest population of sebaceous
follicles (eg, face, upper chest, back).
4. Local symptoms of acne vulgaris may include
pain, tenderness, or erythema.
5. Systemic symptoms are most often absent in
acne vulgaris.

9. Diagnosis
• Examination in patients with acne vulgaris includes the
following features:
1. Comedonal acne: Presence of open and closed
comedones but usually no inflammatory papules or
nodules
2. Mild acne: Presence of comedones and a few
papulopustules
3. Moderate acne: Presence of comedones, inflammatory
papules, and pustules; a greater number of lesions are
present than in milder inflammatory acne
4. Nodulocystic acne: Presence of comedones, inflammatory
lesions, and large nodules greater than 5 mm in diameter;
scarring is often evident

10. Non pharmacological treatments
• Cleansing
• Contributory lipids are deep in the follicle and
are not removed through washing. Antiseptic
cleansers, remove only surface dirt, oil, and
aerobic bacteria. They do not affect P. acnes.
Patients should wash no more than twice daily
with a mild, nonfragranced opaque.

11. • Comedone extractor :
• it is painless and results in immediate cosmetic
improvement. Pretreatment with a peeler for 4 to 6
weeks often facilitates the procedure. Following
cleansing with hot water, a comedone extractor is
placed over the lesion and gentle pressure applied until
the contents are expressed. This removes unsightly
lesions, preventing progression to inflammation.
• It treat the symptomes and the appearance not the
disease.

12. Pharmacological Treatments

13. Exfoliants (Peeling Agents)
• Resorcinol is less keratolytic than salicylic acid and is
classified as category II.
• Salicylic acid is keratolytic, has mild antibacterial activity
against P. acnes, and slightly anti-inflammatory at
concentrations up to 5%.
• Sulfur is keratolytic and has antibacterial activity.

14. Topical Retinoids:
• Adapalene ( the first line), Tretinoin, Tazarotene.
• They inhibit microcomedone formation, decreasing the
number of mature comedones and inflammatory lesions.
• Used alone or in combination with antibiotics and benzoyl
peroxide.
• Side effects include erythema, xerosis, burning, and peeling.

15. • For comedonal, noninflammatory acne:
They inhibit microcomedone formation,
decreasing the number of mature comedones
and inflammatory lesions.
Topical retinoids, adapalene.
Benzoyl peroxide or azelaic acid can be
considered, as alternatives (lower strength
recommendation).

16. • For mild-to-moderate papulopustular inflammatory acne,
it is important to reduce the population of P. acnes in the
follicle.
• fixed-dose combination adapalene and benzoyl peroxide
• or the fixed-dose combination of clindamycin and benzoyl
peroxide are strongly recommended as first choice therapy
(high strength recommendation).
• As alternatives, a different topical retinoid used with a
different topical antimicrobial agent with or without
benzoyl peroxide Azelaic acid .
• fixed-dose combination of isotretinoin and erythromycin.

17. • For severe papulopustular or moderate nodular
acne & For nodular or conglobate acne.
• oral isotretinoin monotherapy (high strength
recommendation).
• As alternatives, medium strength systemic
antibiotics in combination with adapalene,
• fixed-dose combination of adapalene and benzoyl
peroxide or in combination with azelaic acid.

18. • Topical azelaic acid, topical retinoids, adapalene regimens.
• tazarotene or tretinoin.
• maintenance therapy is begun after a 12-week induction
and continues for 3 to 4 months.
• High dose as induction therapy , then maintainance
therapy.
• Patients have signs of hyperandrogenism (eg, hirsutism,
irregular menses, menstrual dysfunction). Serum androgen
levels may or may not be elevated.
• Available options include combination estrogen-progestin
oral contraceptive pills.

19. Allergic Contact Dermatitis

20. Allergic Contact Dermatitis
• the cause of allergic contact dermatitis can be
attributed to:
• chemicals or other elements of outside sources. Some
of the most popular irritating elements include nickel,
fragrances, hair dyes, preservatives, rubber, and latex
products. These elements inflict irritation to the
surface of the skin, causing the rashes you’ll see with
this condition.
• It appears as red, itchy, scaly rashes with visible
borders.

21. Signs & Symptomes
• pruritic papules and vesicles on an erythematous base.
Lichenified pruritic plaques may indicate a chronic form
of the condition.
• Individuals with allergic contact dermatitis typically
develop the condition within a few days of exposure, in
areas that were exposed directly to the allergen.
• Certain allergens (eg, neomycin), however, penetrate
intact skin poorly; in such cases, the onset of dermatitis
may be delayed for up to a week following exposure.

22. Diagnosis
• Potassium hydroxide preparation and/or fungal culture: To
exclude tinea; these tests are often indicated for dermatitis
of the hands and feet.
• Patch testing: To identify external chemicals to which the
person is allergic.
• Repeat open application test (ROAT): To determine whether
a reaction is significant in individuals who develop weak or
1+ positive reactions to a chemical.
• Dimethylgloxime test: To determine whether a metallic
object contains enough nickel to provoke allergic
dermatitis.
• Skin biopsy: May help to exclude other disorders,
particularly tinea, psoriasis, and cutaneous lymphoma.

23. Itiology
• Fragrances
• Preservatives (eg, quaternium-15, parabens, MI
(methylisothiazolinone) or MCI/MI [the combination of
methylchloroisothiazolinone and
methylisothiazolinone, which is marketed as Kathon CG
or Kathon WT], thimerosal).
• Excipients (eg, propylene glycol, lanolin, or colorants)
• Glues (eg, acrylates in nail products)
• Sunscreens
• Hair dyes (para-phenylenediamine and derivatives)
• Surfactants (cocamidopropyl betaine, decyl glucosides)

24. Treatment
• Managements :
• The optimal management of ACD requires a
multipronged approach :
• Identification and avoidance of the offending
allergen
• Alternatives to offending products
• Treatment of skin inflammation
• Restoration of the skin barrier
• Skin protection

25. • Skin protection — Irritant contact dermatitis
is often associated with or precedes the
development of ACD.
• Prework (barrier) creams and after-work
(emollients) creams appear to confer some
degree of protection against irritant contact
dermatitis.

26. • Topical corticosteroids – Topical corticosteroids are the
first line treatment for localized ACD .
• Topical calcineurin inhibitors –
Topical tacrolimus or pimecrolimus may be an
alternative to topical corticosteroids in the
management of chronic, localized ACD.
• localized ACD resistant to topical corticosteroids.
• ACD involving the face or intertriginous areas.
• and ACD induced by topical corticosteroids.
• tacrolimus 0.1% ointment applied twice daily until
resolution .
• or pimecrolimus 1% cream twice daily until resolution.

27. • Other topical treatments – Soothing and drying agents
may be useful for reduction of discomfort and pruritus
in acute ACD.
• These include aluminum acetate compresses, calamine
lotion, and colloidal oatmeal compresses or baths.
• Systemic corticosteroids – Oral corticosteroids are the
first line treatment for ACD involving >20 percent of
the body surface area or for acute ACD involving the
face, hands, feet or genitalia if quick relief is desired
(eg, involvement of the eyelids).
• Mainly for the treatment of poison ivy dermatitis.
• Ivy caused by urushiol , from Toxicodendron
vernicifluum .

28. • Phototherapy – Phototherapy is a therapeutic option
in patients with chronic ACD that is unresponsive to
topical or oral corticosteroids.
• Narrowband UVB is more convenient for the patient
and associated with fewer side effects than PUVA.
• Systemic immunosuppressive agents – Rarely, in cases
of chronic ACD, azathioprine, mycophenolate mofetil,
and cyclosporine have been used.
• Situations such as airborne compositae dermatitis or
photodermatitis, where allergen avoidance is
impossible.

29. Treatment depending on affected
organs
ACD involving the face or flexural areas:
• Topical corticosteroids are applied once or twice daily
for one to two weeks.
• If topical not effective , Treatment is started
with prednisone systemically at a dose of 0.5 to
1 mg/kg per day (maximum 60 mg/day) for seven days.
• The dose may be reduced by 50 percent in the next
five to seven days and then tapered and discontinued
over the following two weeks.
• Tacrolimus 0.1% ointment or pimecrolimus 1% cream is
applied twice daily until resolution.

30. ACD involving the hands, feet, or
nonflexural areas
• Topical corticosteroids are applied once or twice
daily for two to four weeks, or until resolution of
symptoms.
• If the dermatitis is acute and weeping, topical
corticosteroids may be used in combination with
drying agents (eg, aluminum acetate soaks).
• If ACD cover more than 20% of the body use
systemic corticosteroids and calcineurin
inhibitors as before .

31. Chronic ACD
• chronic hand eczema initially treated
with mometasone furoate 0.1% fatty cream
for up to nine weeks or until the dermatitis
cleared.

32. • References:
• Dipiro – Pharmcotherapy
• Up to date
• Medscape