Scalp and hair disorders are among the most common concerns in patients of color, particularly African-Americans. Seborrheic dermatitis (SD) is a chronic, inflammatory condition that affects areas of high sebum production and is a common reason for dermatologic consultations in skin of color patients.1 A paucity of literature exists regarding the presentation and treatment of SD in this population. As more African-Americans seek dermatologic care, it becomes crucial for dermatologists to be trained in recognizing and addressing the concerns of diverse patient populations.The goal of this paper is to address the differences in the presentation and treatment of SD in skin of color patients. Highlighting these differences can allow for an effective approach and ultimately reduce the current disparities in the management of skin of color patients with SD.
Epidemiology and Causes
Seborrheic dermatitis (SD) is a common, chronic, benign inflammatory skin disorder of unclear pathophysiology affecting 3% to 12% of the population.2,3 SD may have slightly increased incidence among African Americans (6.5%)4 and West Africans (2.9-6%).5 In a study that compared the most common diagnoses for patients of various ethnic groups in a hospital-based dermatology practice, SD was among the five most common diagnoses observed in black patients.1 SD is prominent among black womenand can be exacerbated by excessive use of hair oil and pomade, and infrequent shampooing.6 Some of the recognized risk factors for SD include immunodeficiency (HIV), neurological (Parkinson’s disease) or cardiac disease, as well as alcoholic pancreatitis. Several factors have been proposed to play a role in the development of SD including the proliferation of the commensal yeast genus, Malassezia, the host immune response, and the composition of sebaceous gland secretions. The population density of Malassezia furfur has been shown to be highest in anatomic sites most highly populated with sebaceous glands,7 overlapping with areas where SD tends to occur. However, it is unclear if this has a direct impact on the pathogenesis of SD. In 1989, Bergbrant and Faergemann8 found no difference in the number of yeast cells in patients with SD and healthy controls, but several other studies since that time have suggested a positive correlation between yeast density and severity of SD.9,10 A study conducted by Nakabayashi et al9 compared lesional and non-lesional skin in patients with SD and healthy controls. The authors found that M. furfur and M. globosa were isolated at much higher rates from lesional skin on the face in SD patients than in healthy controls, which suggests that yeasts may have a pathogenic role in SD. Zaidi et al10 conducted a study that compared Malassezia yeast density to SD disease severity and found that when comparing SD patients, those with more severe clinical disease had a greater density of Malassezia yeast