Acneiform skin disorders: Pathology review

At the dermatology clinic, 31-year-old Lauren presents complaining of frequent flushing, mainly on the cheeks, nose, and forehead, for the past five months. She mentions that this seems to get worse after eating anything spicy or drinking alcohol. On examination, there are visible small, superficial, dilated blood vessels around the nares, while no comedones are seen. Based on the initial presentation, Lauren seems to have some form of acneiform skin disorder.

Okay, first, let’s talk about physiology real quick. Normally, the skin is divided into three main layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, containing hair follicles, nerve endings, glands, blood and lymph vessels. And above the dermis is the epidermis, which contains 5 layers of developing keratinocytes.

Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer.

Before we dive into the various acneiform skin disorders, there are several high yield terms to describe skin lesions. So, macules are flat, well circumcised lesions up to 1 centimeter in diameter, while patches are similar to a macule but are larger than 1 centimeter. Papules are raised bumps that are up to 1 centimeter in diameter, while plaques are like papules but larger than 1 centimeter. Finally, pustules are blisters filled with pus.

All right, onto acneiform skin disorders! Let’s begin with acne vulgaris, which is an extremely common and high yield skin disorder. The cause of acne is not completely understood, but there are a few main factors that contribute to its formation. First, when keratinocytes in hair follicles overproduce keratin, this may form keratin plugs which clog the opening of the hair follicle.

Second, sebaceous glands have androgen receptors, so if there’s increased androgen production like in puberty, there can also be increased sebum production as a response. The extra sebum can contribute to clogging up the follicles. Now, when there’s an excess in keratin plugs and sebum, they can start to fill up a hair follicle, but if part of the hair follicle still opens to the surface of the skin, then it’s called an open comedone, more commonly known as a blackhead.