Key factors are follicular keratinization, androgens, and Propionibacterium acnes

Follicular plugging (comedone) prevents drainage of sebum; androgens (quantitatively and qualitatively normal in serum) stimulate sebaceous glands to produce more sebum. Bacterial (p. acnes) lipase converts lipids to fatty acids and produce proinflammatory mediators (IL-I, TNF-α) that lead to an inflammatory response. Distended follicle walls break, sebum, lipids, fatty acids, keratin, bacteria enter the dermis, provoking an inflammatory and foreign-body response. Intense inflammation leads to scars.


Acnegenic mineral oils, rarely dioxin, and others.

Drugs. Lithium, hydantoin, isoniazid, glucocorticoids, oral contraceptives, iodides, bromides and androgens (e.g., testosterone), danazol.

Others. Emotional stress can cause exacerbations. Occlusion andpressure on the skin, such as by leaning face on hands is a very important and often unrecognized exacerbating factor (acne mechanica). Acne is not caused by any kind of food.

Clinical Manifestation


Weeks to months.


Often worse in fall and winter.


Pain in lesions (especially nodulocystic type).


Comedones—open (blackheads) or closed (whiteheads); comedonal acne (Fig. 1-1). Papules and papulopustules—i.e., a papule topped by a pustule; papulopustular acne (Fig. 1-2). Nodules or cysts—1–4 cm in diameter (Fig. 1-4); nodulocystic acne. Soft nodules result from repeated follicular ruptures and reencapsulations with inflammation, abscess formation (cysts), and foreign-body reaction (Fig. 1-3). Round isolated single nodules and cysts coalesce to linear mounds and sinus tracts (Fig. 1-4). Sinuses: draining epithelial-lined tracts, usually with nodular acne. Scars: atrophic depressed (often pitted) or hypertrophic (at times, keloidal). Seborrhea of the face and scalp often present and sometimes severe.



There is a multifactorial genetic background and familial predisposition. Most individuals with cystic acne have parent(s) with a history of severe acne. Severe acne may be associated with XYY syndrome (rare).


  • An inflammation of pilosebaceous units,

  • Appears in certain body areas (face, trunk, rarely buttocks).

Acne most commonly develops on the:

  • face – this affects almost everyone with acne
  • back – this affects more than half of people with acne
  • chest – this affects about 15% of people with acne

    • Manifests as comedones, papulopustules, nodules, and cysts.

    • Results in pitted, depressed, or hypertrophic scars.


There are 6 main types of spot caused by acne:

  • blackheads – small black or yellowish bumps that develop on the skin; they're not filled with dirt, but are black because the inner lining of the hair follicle produces pigmentation (colouring)
  • whiteheads – have a similar appearance to blackheads, but may be firmer and won't empty when squeezed
  • papules – small red bumps that may feel tender or sore
  • pustules – similar to papules, but have a white tip in the centre, caused by a build-up of pus
  • nodules – large hard lumps that build up beneath the surface of the skin and can be painful
  • cysts – the most severe type of spot caused by acne; they're large pus-filled lumps that look similar to boils and carry the greatest risk of causing permanent scarring

Image not available.

Papulopustular acne, some inflammatory papules become nodular and thus represent early stages of nodulocystic acne.



Image not available.

“Blackheads” (open comedones) are black because of the oxidation of the keratinaceous debris within the dilated follicles.



What is the life cycle of an inflammatory acne papule?

B. Keratinocytes fail to slough from the follicles as they should. As a result, the follicle becomes plugged (a comedo). The buildup of sebum behind the plug expands the follicle. Propionibacterium acnes overgrowth in the follicle breaks down sebum. Bacterial factors and sebum breakdown products attract neutrophils to the follicle, thus forming a pustule. Follicular rupture induces an intense inflammatory response in the dermis seen clinically as an inflammatory papule or pustule. Scarring may be the end result.



Follicular plugging


Follicular plugging may be corrected with retinoids (vitamin A analogues) either topically or, if the condition is severe enough, orally. Retinoids promote the proper desquamation of keratinocytes. Bacteria are controlled with topical or oral antibiotics. Some common topical antibiotic agents include benzoyl peroxide and clindamycin. Oral antibiotics such as erythromycin or tetracyclineare frequently used in addition to topical antibiotics. These agents are not merely antibacterial but are known to have anti-inflammatory properties independent of their antibacterial action. Last, sebum production may be decreased through the use of retinoids, again topically or orally, although oral therapy is much more effective for this purpose, or with antiandrogen medications such as spironolactone and oral contraceptives.

However, some exogenous substances such as oily cosmetics or petrolatum-based hair care products may promote comedone formation and thus exacerbate acne.

Cleansing does not affect any of the four steps essential to the development of acne, because all steps occur within the follicles. Cleansing merely removes surface debris and oil. The patient should be advised to use a gentle soap or nonsoap cleanser designed for the face and to avoid scrubbing the skin with rough cloths, towels, or scrubbing pads, which is not helpful in ameliorating acne and may cause secondary irritation, making topical treatments less tolerable. She should also be advised to use nongreasy cosmetics, usually those labeled as “noncomedogenic,” as well as hair care products without petrolatum.





A.L. Zaenglein


Acne is a primary inflammatory disorder involving the pilosebaceous unit. The pathogenesis is multifactorial, involving four key factors with interrelated mechanisms: increased sebum production, hyperkeratinization of the follicular infundibulum, inflammation, and Cutibacterium acnes (formerly Propionibacterium acnes).

Clinical Pearls
Clinical Pearl  What is the role of retinoids in the treatment of acne?

A topical retinoid should be used as the foundation for most acne treatment regimens. Topical retinoids are comedolytic, normalize desquamation at the follicular infundibulum, and have antiinflammatory properties. In the United States, three topical retinoids are used in patients with acne: tretinoin, adapalene, and tazarotene. All the retinoids are mildly photosensitizing, but this situation can be managed easily with sunscreen use.

Clinical Pearl  What combinations of topical medications are typically used to treat acne?

In addition to topical retinoids, benzoyl peroxide is a key component of acne therapy. Benzoyl peroxide is highly effective at reducing C. acnes through the release of free oxygen radicals, without allowing microbial resistance. The combination of a topical retinoid and benzoyl peroxide has greater efficacy than either product alone. Topical antibiotics, primarily clindamycin and erythromycin, also reduce C. acnes. The combination of benzoyl peroxide with a topical antibiotic has been shown to decrease the concentration of antibiotic-resistant strains of C. acnes and has greater efficacy than either product alone. However, owing to the excellent bactericidal properties of benzoyl peroxide alone, the complementary comedolytic and antiinflammatory effects of topical retinoids, and efforts to reduce antibiotic use overall, the use of topical antibiotics in patients with acne is declining.

Table 1. Algorithm for the Management of Acne Vulgaris.

Morning Report Questions
Q. If oral antibiotics are used to treat acne, what duration of treatment is recommended?

A. Oral antibiotics are widely used in patients with acne to gain control of the inflammation in moderate-to-severe acne. Given concerns regarding increasing antibiotic resistance, current acne treatment guidelines recommend limiting the use of oral antibiotics to 3 to 4 months whenever possible. Clinical improvement should be maintained with the continued use of a topical retinoid, with or without benzoyl peroxide, depending on lesion types. Typically, tetracyclines are prescribed for acne treatment because they decrease the concentration of C. acnes, but they also have anti-inflammatory effects. They decrease retinoic acid and enzyme degradation, are antiapoptotic and antioxidant, and regulate cell proliferation. In the United States, minocycline is the most commonly used antibiotic for acne, followed closely by doxycycline. Tetracycline is less often used, owing to inconsistent bioavailability and the need for it to be taken on an empty stomach.

Q. What side effects or potential complications are associated with use of isotretinoin for acne?

A. Isotretinoin is a systemic retinoid that is highly effective for treating recalcitrant nodulocystic acne. It is also used in patients with moderate-to-severe acne who do not have a response to other therapy, including oral antibiotics. It is a potent teratogen, and various pregnancy-prevention programs are in place worldwide. Common cutaneous side effects of isotretinoin include dryness of skin and mucosa. Elevations in serum triglyceride, low-density lipoprotein cholesterol, and aminotransferase levels may occur, although they are usually mild. One serious concern is a possible link between isotretinoin use and depression and suicide. Although prospective studies have shown an overall improvement in depression scores (indicating lessening in depression) in patients with severe acne taking isotretinoin, these studies were not powered to detect an increase in the incidence of depression or suicidal ideation. Given that retinoids readily cross the blood–brain barrier and that depression is common in the adolescent population and in patients with severe acne, it is prudent to counsel and monitor patients taking isotretinoin for the risk of depression at each visit.





Very common, affecting approximately 85% of young people.


Puberty; may appear first at 25 years or older.


More severe in males than in females.


Lower incidence in Asians and Africans.



Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


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