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Acne Vulgaris

Chronic skin disease involving blockage or inflammation of the hair follicle and sebaceous glands ( pilosebaceous units ) Androgen dependent disorder of pilosebaceous follicles or pilosebaceous unit Four primary pathogenic factors which interact to produce lesions Increased sebum production by the sebaceous glands Alteration in follicular keratinization process Propionibacterium
(Gr +ve anaerobic rod) 
 follicular hypercolonization Release of inflammatory mediators
mild-Typically limited to face with non inflammatory closed and open comedones with few inflammatory lesions moderate-Increased number of inflammatory papules and pustules on face and often mild truncal disease severe-Nodules and cysts are present and often widespread truncal disease Face neck and 
chest have greatest 
density of pilosebeceous 
Nodulocystic-Comedones , inflammatory lesions and large nodules greater than 5 mm in diametre acne conglobata-Severe acne inflammatory lesions predominate and run together , may exudate or bleed- high risk sacrring Acne fulminans-Sudden severe inflammatory reaction that precipitates deep ulcerations and erosions -sometimes with systemic effects others-Acne excorciee Acne mechanica Acne cosmetica Chloracne
Assessment-Assessment of morphology and severity is an important first step Lesion morphology will dictate optimal treatment approach Ascertain severity- Mild , moderate or severe 
( look for scarring , pigmentation ) Consider any aggravating factors ( eg medications ) Address common myths ( Patient education is vital )
○ eg central discoloration is not dirt but oxidized melanin
○ not caused by poor hygiene
○ diet has little or no effect ( eg chocolate consumption )
○ pickering may cause scarring
○ not infectious and cannot be passed
○ sunlight has little benefit on acne
Differential diagnosis-Rosacea Folliculitis and boils Milia Perioral dermatitis Demodex folliculitis ( caused by mites usually in elderly- affects mostly face ) Pityrosporum folliculitis – yeast , predominates on trunk Sebaceeous hyperplasis Dermatological manifestations of Tuberous sclerosis
Rarely misdiagnosed and investigations usually not required Endocrine investigations primarily indicated for patients with clinical features or a history of hypergonadism acne early onset body odour axillary or pubic hair accelerated growth advanced bone age genital maturation irregular menses androgenic alopecia excessive facial or body hair
( hirsuitism ) infertility polycystic ovaries clitromegaly truncal obesity Total and free testosterone LH , FSH ( ratio LH/ FSH altered in PCOS with ↑ LH ) Serum dehydroperiandrosterone ( DHEA )
○ ↑ levels may suggest adrenal tumour or CAH 17-hydroxyprogesterone ( ↑ levels may suggest CAH ) Prolactin ( ↑ levels may suggest hyperprolactinaemia ) 24 hr urinary free cortisol
 Hormonal testing
 and interpretation is complex  ) Consider hormone profile for patients suspected to have Polycystic Ovary Syndrome Consider late onset ( non-classical ) congenital adrenal hyperplasia which is a
○ common autosomal recessive disorder
○ clinical features reflect androgen excess for e.g premature pubarche , hirsuitism , acne , alopecia , anovulation and menstrual dysfunction Consider endocrine referral is above suspected
Topical retinoids-Comedolytic and some times anti-inflammatory effect Vitamin A derivatives that normalizes keratinocyte desquamation 
and adhesion -> comedolysis and preventing formation of new 
microcomedones Increased use recently- consider First line Recommended for all cases except when oral retinoids are used Improvement within weeks with maximal benefit within 3-4 months Combine with antibiotics or benzoyl peroxide if inflammatory lesions present Comes as cream , gel ,liquid and microsphere formulations Evidence that adapalene is the best tolerated retinoid Skin irritation with peeling and redness –> typically resolves within 1st few weeks of use ( try alternate days if irritation persists ) Thin stratum corneum- associated with sun sensitivity

Benzoyl peroxide- Benzoyl peroxide ( BPO ) – if papules pustules present Potent bectericide and significantly reduces P Acni conc in sebaceous follicle Good evidence that reduces both inflammatory and non inflammatory lesions Helps prevent antibacterial resistance Available in conc from 2.5 % to 10 % Irritation increases with higher concentration ( gets better with use) May bleach clothing , bedding and hair Resistance to BPO not reported
Oral antibiotics-Tetracycline , Oxytetracycline , Doxycline , Lymecycline- first line Combine with a topical retinoid or BPO to minimize bacterial resistance and improve treatment efficacy Moderate to severe inflammatory acne If acne on back or shoulders that is extensive or difficult to reach Continue maintenance with BPO/ Retinoid after stopping oral treatment Review treatment at 6-8 weeks

tetracyclines-Tetracyline class can be considered first line Inhibit protein synthesis and notable antiinflammatory effect Avoid in pregnancy and children ( tooth discoloration ) Women childbearing age- consider contraception Lymecycline -408 mg OD- can be taken with food and compliance is good Doxycline @ 100 mg od -Can cause photosensitivity Minocycline can rarely cause skin hyperpigmentation and drug induced SLE , risk hepatotoxicity ( no longer recommended )
Macrolides-Use if tetracyclines contraindicated
○ eg can be used in pregnant women and children < 12 yrs Bacterial resistance- high levels Erythromycin @ 500 mg bd or claithromycin 250 mg bd
No antibiotic has
 been shown to be more effective than any other
hormonal-COCP ( standard formulation )
○ suppress ovarian androgen production
 Androgen receptor blockers -
○ cyproterone acetate ( ↑ ed risk thromboembolism 1.5 to 2 times )
○ spironolactone
○ flutamide
 Recent Cochrane review confirmed efficacy of COCPs ( in inflammatory and non inflammatory acne ) but showed no difference in efficacy of different types
 It is therefor nor clear if formulations containing cyproterone acetate should be favored
Isotretinoin-Systemic retinoid Efficacious in treatment of severe disease and in treatment of treatment resistance moderate disease Exact mechanism not elucidated in detail Suppression of sebaceous gland activity Normalization of epidermal differentiation Dermal anti-inflammatory effect Teratogenic and embryotoxic ( animal experiments) 16-24 week course- works within 1-2 months Atleast 1/2 the patients achieve permanent remission after 1 course Relapse more likely in younger or female wax Chapped skin , dry eyes , epistaxis , myalgias and altered lipids , transminase
Referral-Suspected endocrine cause of acne ( eg PCOS ) People who are developing scarring or at risk of scarring despite primary care treatment Treatment failure after 6 months Acne fulminans Severe acne eg with painful deep nodules or cysts ( nodulocystic acne ) Severe psychosocial problems including morbid fear of deformity 
( body dysmorphic disorder )


British Skin Foundation on acne
Acne Support Org UK has sections on types , causes , treatment , scarring etc- a comprehensive useful patient resource – this has been setup by BAD and consider informing all patients about this
British Association of Dermatology acne leaflet
Printable concise 3 page leaflet from The Society of Pediatric Dermatology 
Australian College of Dermatologists about acne with an introductory video
American Academy of  Dermatology patient resource centre on Acne –
Acne Management in Primary Care – a downloadable guide from ICGP by Dr Johnny Loughanane
American Dermatology Association’s work on acne -Clinical Guideline
Primary Care Dermatology Society on acne  – a very useful contribution
Dermnet NZ on acne
Cardiff Acne Disability Index
Access required for Acne Quality of Life Questionnaire ( Acne-QoL )
Chinese Guidelines for the Management of Acne Vulgaris

European evidence‐based (S3) guideline for the treatment of acne – update 2016 – short version

A4Medicine on Acne management
Acne Vulgaris – A Review of management by Christine Chim , Pharm D , BCACP 2016

  1. Guidelines of care for the management of acne vulgaris : American Academy of Dermatology February 2016
  2. Clinical Review : Acne vulgaris BMJ 2013 ; 346:f2634
  3. CKS NHS Acne vulgaris September 2014
  4. Acne Vulgaris Medscape Updated May 2016
  5. Acne Vulgaris MSD Professional Version
  6. Acne Best practice management Australian Family Physician Vol 39 , No9 , September 2010
  7. Acne : acne vulgaris Primary Care Dermatological Society accessed via

  8. A systemic review of the evidence for ‘ myths and misconceptions’ in acne management : diet , face -washing and sunlight Parker Magin et al Oxford University Press January 2015
  9. Combined oral contraceptive pills for treatment of acne ; Cochrane Database Syst Rev . 2004; (3) : CD004425 ( abstract)
  10. Antibiotic Resistance in Acne Treatment JAMA Dermatol . 2017
  11. Isotretinoin from Medicine compendium
  12. Non classical Congenital Adrenal Hyperplasia Selma Feldman and Ricardo Azziz Internationa Journal of Paediatrics
  13. Lynn, Darren D et al. “The epidemiology of acne vulgaris in late adolescence.” Adolescent health, medicine and therapeutics vol. 7 13-25. 19 Jan. 2016, doi:10.2147/AHMT.S55832
  14. Sutaria AH, Masood S, Schlessinger J. Acne Vulgaris. [Updated 2019 Dec 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  15. Bhate, K. and Williams, H. (2013), Epidemiology of acne vulgaris. British Journal of Dermatology, 168: 474-485. doi:10.1111/bjd.12149
  16. Heng, A.H.S., Chew, F.T. Systematic review of the epidemiology of acne vulgaris. Sci Rep 10, 5754 (2020).



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