Red facial rash with “granitos”

Causes and pathophysiology of rosacea

Although the cause of rosacea is unknown, its mechanism is understood to be nonspecific inflammation followed by dilation around follicles and hyperreactive capillaries. Oftentimes these dilated capillaries present as telangiectasias, which collectively exacerbate the red flushing. As the disorder progresses, diffuse hypertrophy of the connective tissue and sebaceous glands ensues.

Rosacea is more common in women than men (FIGURE 3). Men are typically more prone to the extreme forms of hyperplasia, which causes rhinophymatous rosacea (FIGURE 4)—eg,W C Fields’s nose.

Alcohol may accentuate erythema, but does not cause the disease. Sun exposure may precipitate an acute rosacea flare, but flare-ups can happen without sun exposure.

A significant increase in the hair follicle mite Demadex folliculorum is sometimes found in rosacea. It is theorized that these mites play a role because they incite an inflammatory or allergic reaction by mechanical blockage of follicles.

FIGURE 3
Papulopustular rosacea

FIGURE 4
Rhinophymatous rosacea

Stages of rosacea

There are 4 stages or subtypes of rosacea.

• Subtype 1: Erythematotelangiectatic rosacea. This stage is characterized by frequent mild to severe blushing with trace persistent central facial erythema in an individual.
• Subtype 2: Papulopustular rosacea (seen in FIGURES 1 , 2, AND 3). This is a highly vascular stage that involves longer periods of flushing than the first stage—often lasting from days to weeks. Minute telangiectasias and papules start to form by this stage, and some patients begin having very mild ocular complaints such as ocular grittiness or conjunctivitis.