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Year : 2009  |  Volume : 75  |  Issue : 7  |  Page : 13-25

Clinical features

members Indian Acne Alliance, India

Correspondence Address:
Raj Kubba
Consultant Dermatologist, Kubba Clinic,10, Aradhana Enclave, Ring Road, New Delhi - 110066
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Source of Support: Production and publication of this supplement is made possible by an educational grant from Galderma India Pvt. Ltd., Conflict of Interest: Indian Acne Alliance (IAA) meetings logistics to formulate IAA consensus document DQAcne in India: Guidelines for managementDQ were supported by Galderma India Pvt. Ltd.

PMID: 19282584

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How to cite this article:
Kubba R, Bajaj A K, Thappa D M, Sharma R, Vedamurthy M, Dhar S, Criton S, Fernandez R, Kanwar A J, Khopkar U, Kohli M, Kuriyipe V P, Lahiri K, Madnani N, Parikh D, Pujara S, Rajababu K K, Sacchidanand S, Sharma V K, Thomas J. Clinical features. Indian J Dermatol Venereol Leprol 2009;75, Suppl S1:13-25

How to cite this URL:
Kubba R, Bajaj A K, Thappa D M, Sharma R, Vedamurthy M, Dhar S, Criton S, Fernandez R, Kanwar A J, Khopkar U, Kohli M, Kuriyipe V P, Lahiri K, Madnani N, Parikh D, Pujara S, Rajababu K K, Sacchidanand S, Sharma V K, Thomas J. Clinical features. Indian J Dermatol Venereol Leprol [serial online] 2009 [cited 2021 Jan 22];75, Suppl S1:13-25. Available from:

Acne is the easiest skin condition to diagnose because of its distinctive anatomic distribution, age of occurrence, and polymorphic appearance in which the comedones (blackheads especially) are the most unique and pathognomonic feature [Figure 9],[Figure 10],[Figure 11]. Typically it starts at puberty, in girls between age 12-14 years, and in boys between 14-16 years. Occasionally, it may start at age 7 or 8 years (adrenarche) and when it does, it portends severe acne. Acne waxes and wanes through adolescent years and early adult life, it peaks between 17-21 years. In about 90% of sufferers, acne will spontaneously remit before 30 years of age. In the rest, its course is unpredictable, and it may persist well into the fifth and the sixth decade (persistent acne). Less commonly, acne may make its first appearance in mature adults - after 30 years (adult acne). Adult acne is more common in women and is often a part of cutaneous hyperandrogenism [Figure 12],[Figure 13],[Figure 14]. [1],[2]

Face is the theater of action. It is involved in 99% of acne sufferers. [2] Back is involved in 60% and chest in 15%. [2] Preadolescent acne and early adolescent acne is largely confined to the forehead [Figure 9]. With time there is cephalocaudal migration. Typical adolescent acne involves the entire face but shows predilection for cheeks [Figure 10],[Figure 11],[Figure 15],[Figure 16],[Figure 17]. In men who have grown beard, it relatively spares the lower face and neck. In severe cases, even external ears are involved. Adult acne is largely confined to the jaw area [Figure 18]. Acne vulgaris (common acne) shows variable involvement of seborrheic areas of upper torso, namely, upper back, sternal area, shoulders, and upper arms [Figure 19] and [Figure 20] [Table 2]. In some cases, acne is largely confined to the torso with little or no involvement of the face (acne corporis) [Figure 21] and [Figure 22]. Acne corporis denotes severe acne and often involves the entire back and in some cases even buttocks and thighs. Acne does not occur on the scalp although folliculitis occasionally co-occurs and is misdiagnosed as acne. Concomitant folliculitis , especially pityrosporum folliculitis, is more common than is recognized [Figure 23]. [3]

Acne shows a variable and fluctuating mix of comedones, folliculocentric inflammatory lesions, scars, and pigmentary disturbances. The full spectrum includes many types of comedones [Table 3] - blackheads (open comedones), whiteheads (closed comedones), missed comedones, macrocomedones, sandpaper comedones, submarine comedones [Figure 24],[Figure 25],[Figure 26]; [4] inflammatory lesions - papules, pustules, nodules, cysts, macules [Figure 27],[Figure 28],[Figure 29],[Figure 30],[Figure 31]; atrophic scars - rolling, boxcar, ice-pick; hypertrophic scars and keloids; and acne hyperpigmented macules (AHM) [Figure 32],[Figure 33],[Figure 34],[Figure 35],[Figure 36],[Figure 37],[Figure 38]. [5] The precursor lesion is a microcomedo which evolves into open or closed comedone and further into papule or nodule. Microcomedo may also directly evolve into papule or nodule [Figure 2]. The diagnosis of acne is untenable in the absence of comedones. Yet 7% of acne patients do not show comedones at first evaluation. [4] On the other hand, the presence of a single comedone is enough to diagnose acne! The preadolescent acne and the beginning of adolescent acne is largely comedonal.[6] Acne papules, pustules, and nodules appear later. Acne severity is gauged by the number and types of inflammatory lesions [Table 4] [Figure 39].

Acne papules are conical, measure 3 mm or less, and often show a pore at the summit. Pustules are similar in size and represent more intense inflammation; they are sterile on routine cultures. Nodules measure 4 mm or larger and show tenderness that is proportional to size. Nodules sometimes soften and become fluctuant when they are erroneously described as cysts; at best they are pseudocysts [Figure 40],[Figure 41]. Such lesions may further evolve into hemorrhagic crusts, abscesses, or sinus tracts [Figure 42]. Nodules carry high potential for scarring, especially in the genetically prone. Acne macules represent resolved papules/nodules and often precede atrophic scars [Figure 29]. Acne scars [Table 5] are invariably atrophic on the cheeks, and hypertrophic/ keloidal over the jaw angles [Figure 35], shoulders, upper back, and sternal areas. Papular scars are sometimes encountered on the chin [Figure 37] and nose, perifollicular fibrosis and perifollicular elastolysis on the back, chest, and neck. Macular atrophic scars are large, 5-20 mm, somewhat circular, soft, and erythematous, and occur on the back. Mixed scars and unclassifiable scars are also encountered [Figure 43]. Scarring is seen in 22% of acne sufferers. Rarely, severe acne scars are complicated with osteoma cutis. [8]

Acne variants [Figure 44],[Figure 45],[Figure 46],[Figure 47],[Figure 48],[Figure 49],[Figure 50],[Figure 51],[Figure 52],[Figure 53],[Figure 54],[Figure 55]: Acne offers a wide spectrum of clinical subtypes. Some subtypes are aggressive or severe and are associated with constitutional symptoms and systemic involvement. This group includes acne conglobata [Figure 44], acne fulminans, pyoderma faciale (rosacea fulminans) [Figure 45], and SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis) [Figure 46]. SAHA syndrome (seborrhea, acne, hirsutism, alopecia) [Figure 47],[Figure 48],[Figure 49] denotes acne in the context of endocrine abnormality, particularly polycystic ovarian syndrome. Infantile acne is sometimes severe and prolonged and warrants evaluation for adrenal or gonadal tumor. Acne excoriθe [Figure 29] and [Figure 56] is often a manifestation of dysmorphophobia. Frictional acne, acne mechanica, acne cosmetica, and tropical acne (acne Mallorca) are mild variants or acne look alikes. Drug-induced acne includes drug aggravation of pre-existing acne (androgenic hormones, anabolic steroids, INH, lithium) or a de novo acneiform eruption (oral corticosteroids, halogens) [Table 1].

Clinical differential diagnosis: Many skin conditions mimic acne [Table 6]. Some are more acneiform than others. This is a large group and includes: rosacea, perioral dermatitis, folliculitides - namely, Gram-negative folliculitis, other bacterial folliculitides, pityrosporum folliculitis, candida folliculitis, demodex folliculitis, herpetic folliculitis, and HIV-associated eosinophilic pustular folliculitis, lupus miliaris disseminatus facei, adenoma sebaceum, milia, verruca plana, and molluscum contagiosum. All of the above conditions lack comedones and are thus easily distinguished from acne. However, some of these conditions may co-occur with acne and that may pose diagnostic difficulty[9].

  References Top

1.Cunliffe WJ, Gollnick HP. Acne: Diagnosis and management. London: Martin Dunitz; 2001. p. 49-103.  Back to cited text no. 1    
2.Simpson NB, Cunliffe WJ. Disorders of the sebaceous glands. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's textbook of dermatology. 7 th ed. Oxford: Blackwell Science; 2004. p. 43.28-43.34.  Back to cited text no. 2    
3.Ayers K, Sweeney SM, Wiss K. Pityrosporon folliculitis : Diagnosis and management in 6 adolescent patients with acne vulgaris. Arch Pediatr Adolesc Med 2005;159:64-7.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Cunliffe WJ, Holland DB, Clark SM, Stables GI. Comedogenesis: Some new aetiological, clinical and therapeutic strategies. Br J Dermatol 2000;142:1084-91.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Taylor SC, Cook-Bolden F, Rahman Z, Strachan D. Acne vulgaris in skin of color. J Am Acad Dermatol 2002;46:S98-106.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Lucky AW, Biro FM, Hustar GA, Leach AD, Morrison JA, Ratterman J. Acne vulgaris in premenarcheal girls: An early sign of puberty associated with rising levels of dehydroepiandrosterone Arch Dermatol 1994;130:308-14.   Back to cited text no. 6    
7. Cunliffe WJ, Holland DB, Clark SM, Stables GI. Comedogenesis: Some new aetiological, clinical and therapeutic strategies. Br J Dermatol 2000;142:1084-91.  Back to cited text no. 7    
8.Thielen AM, Stucki L, Braun RP, Masouyι I, Germanier L, Harms M, et al . Multiple cutaneous osteomas of the face associated with chronic inflammatory acne. J Eur Acad Dermatol Venereol 2006;20:321-6.  Back to cited text no. 8    
9.Jacob CI, Dover JS, Kaminer MS. Acne scarring: A classification system and review of treatment options. J Am Acad Dermatol 2001;45:109-17.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]


  [Figure 2], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 27], [Figure 28], [Figure 29], [Figure 30], [Figure 31], [Figure 32], [Figure 33], [Figure 34], [Figure 35], [Figure 36], [Figure 37], [Figure 38], [Figure 39], [Figure 40], [Figure 41], [Figure 42], [Figure 43], [Figure 44], [Figure 45], [Figure 46], [Figure 47], [Figure 48], [Figure 49], [Figure 50], [Figure 51], [Figure 52], [Figure 53], [Figure 54], [Figure 55], [Figure 56]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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