Acne Vulgaris and Hidradenitis Suppurativa



Acne Vulgaris and Hidradenitis Suppurativa


Mark S. Nestor

Alexandria B. Glass

Michael H. Gold



ACNE VULGARIS


BACKGROUND

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit and is the most common dermatological condition in the United States. The cost of treatment exceeds $3 billion annually, and at some point, 85% of all 12- to 24-year-olds are affected.1 This condition affects both genders equally and characteristically begins during puberty, peaks at 15 to 18 years of age, and frequently resolves during early adulthood. However, many adults, with women outnumbering men, are affected by acne well into their fifties.2,3,4


PRESENTATION

Acne vulgaris is generally located in areas with numerous sebaceous glands, such as the face, neck, chest, shoulders, and upper back. The open comedo, “blackhead,” can be seen as a flat or slightly raised papule with a central opening filled with darkened keratin. The closed comedo, “whitehead,” are skin-colored papules that sometimes can be visualized better by stretching the skin. The other 2 primary lesions are papules and pustules, which are larger and more prominent. Because these are due to inflammation, they can be painful, appear edematous and/or erythematous, and occasionally discharge yellowish or serosanguineous pus. In individuals with more severe acne, these papulopustules can
enlarge to form nodules and even coalesce to form sinus tracts under the skin. Patients with acne classically have a combination of all types of lesions in various states of resolution. When the inflammatory lesions resolve, they leave behind postinflammatory hyperpigmentation, which can appear dissimilar on different skin types. In light-colored skin, a reddish purple macule is generally seen compared with a dark brown/black macule in darker skinned individuals, which can take months to disappear. Larger lesions, especially those manipulated, can leave scars, which is why early detection and treatment is essential.2,4,5



PATHOGENESIS

The primary lesion in acne is the comedo, and its formation is multifactorial, but primarily due to 4 main factors: hyperproliferation of keratinocytes, excess sebum production, inflammation, and the activity of Propionibacterium acnes.1 First, hyperproliferation and abnormal differentiation of the keratinocyte occurs in the infundibulum of the hair follicle. Instead of normally being shed through the follicular ostium, the keratinocytes are retained owing to increased cohesiveness. This leads to hyperkeratosis, which creates a “plug” blocking the follicular opening. Additionally, during this time, there is a surplus of sebum production due to stimulation from increased circulating androgens. This increase transpires normally during puberty. Because the follicular opening is blocked, the lower infundibulum becomes dilated with entrapped sebum. This compressed unit creates an anoxic environment leading to an overgrowth of P acnes. The combination of keratin, sebum, and P acnes continues to expand and build pressure until the pilosebaceous unit eventually bursts discharging the contents into the dermis. Then, white blood cells such as neutrophils, lymphocytes, and foreign body giant cells are able to recognize the foreign lipoproteins. They do this through toll-like receptors (TLRs), which are transmembrane receptors that help immune cells and keratinocytes recognize pathogens. P acnes increases the expression of TLR2 and TLR4 on keratinocytes and also stimulates the release of proinflammatory interleukins, such as IL-6 and IL-8, resulting in inflammatory cell migration to the area. This reaction creates inflammatory acne lesions such as papules and pustules.2,3,4,5,6

The type of inflammatory response at the affected area can also determine the type of inflammatory acne lesion seen. If neutrophils compromise the majority of
the response, observed in earlier lesions, then a pustule is formed. Neutrophils can release enzymes creating reactive oxygen species (ROS), which may correlate to lesion severity. If a mixture of lymphocytes, foreign body-type giant cells, and neutrophils are seen, then papules, nodules, and cysts are more likely to form.3

Furthermore, P acnes plays a big role in the formation of acne. These anaerobic, gram-positive, nonmotile rods are found as part of the normal skin flora and in the lower infundibulum of the hair follicle. Increased organisms are found in patients with acne; however, the amount does not correlate with disease severity. The yeast, Malassezia furfur, is also part of the normal skin flora and can promote acne formation. They contribute to the inflammatory response by releasing ROS, proinflammatory mediators, and enzymes, such as lipases, that cause to comedo rupture.3,4

Hormones have been shown to influence acne, especially potent androgens such as dehydroepiandrosterone sulfate. Androgens are produced both by the sebaceous gland and by external sources such as the gonads and adrenal glands. In addition, androgen receptors, including testosterone and 5α-dihydrotestosterone, are found on the basal layer of the sebaceous gland and the outer root sheath of the hair follicle. Androgens stimulate the sebaceous gland to grow larger and produce more sebum. Androgen levels are increased in infants from birth to 6 to 12 months of age, decreasing around 1 year of age, and then remain stable until adrenarche. At the onset of puberty (typically occurring at the age of 10-11 years for females and 11-12 years for males), elevated levels of androgens lead to increased sebum production triggering acne formation, as previously mentioned. The increase in androgens explains why acne affects the majority of adolescents during puberty. In addition, this is the reason individuals in hyperandrogenic states, such as those with XYY karyotype, polycystic ovarian syndrome, hypercortisolism, and precocious puberty, tend to have more severe, resistant acne. Areas of skin that do not respond to androgens do not develop acne. Furthermore, giving estrogens may counteract the effects of androgens. Estrogens decrease sebum production but must be given in doses higher than those required for birth control. The ways these hormones influence sebum production provide additional therapies to treat acne.2,3,4,5

The relationship between diet and acne is controversial. In recent years, some studies have found that dairy, especially high intakes of skim milk may correlate with more severe acne. Also, some believe that a high-glycemic diet may worsen acne. However, these relationships are not widely accepted by all dermatologists at this time.2,3,4,5

Jun 29, 2020 | Posted by in Dermatology | Comments Off on Acne Vulgaris and Hidradenitis Suppurativa
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