Should You Try a Colloidal Oatmeal Bath for Your Eczema…
Colloidal oatmeal baths can be a good natural remedy for reducing itch caused by eczema. Learn about how to make colloidal oatmeal at home and the science about how it reduces itch.
Published On: Mar 6, 2023
Last Updated On: Mar 6, 2023
Dandruff and cradle cap — these are terms you have likely heard before. Medically, they are part of seborrheic dermatitis (SD), one of the seven forms of eczema. SD is a common, chronic, relapsing form of eczema that typically affects the face and scalp but can appear in oily skin elsewhere on the body (including ears, H-zone of face, central chest, areas with dense body hair, et.). Common symptoms include flaking skin with visible skin inflammation, dandruff, patchy or flaky white or yellow scales on top of greasy skin, rash (sometimes ring-shaped) and itch. To date there is little research about the underlying causes of SD, but contributors include colonization of skin with a yeast called Malassezia and changes in a person’s immunity, skin barrier and sebaceous gland function (glands near hair follicles that secrete oil to lubricate hair and skin).1 Treatment options for SD include both over the counter approaches as well as topical drugs that have been approved for treating other diseases like psoriasis or atopic dermatitis (AD).2 In more severe and stubborn cases, oral medications may be used. While few treatments have been studied specifically for SD, a potential new topical therapy is on the horizon.
SD has been reported to exhibit peak incidence in three age groups: infancy within the first year, adolescence and young adults when sebaceous glands are changing during and after puberty and again between 30 and 60 years of age.1,2 During infancy, SD is often transient and known as “cradle cap”, appearing mostly on the scalp with yellowish, crusty lesions. In adolescents and adults, SD can become more persistent and appear as yellow, greasy, adherent scales with reddened skin on the scalp, face, ears and upper chest.1 The lesions can also be itchy. Dandruff, or flaking without visible skin inflammation, is thought to be present in between 15% and 50% of affected individuals.1 The global prevalence of SD is generally estimated to be about 3–5%, although this number may be affected by differences in rates of recognition and diagnosis. The burden of SD in different parts of the world was also recently reported with higher prevalence in Sub-Saharan Africa and North America, particularly the United States, and lower prevalence in Central Asia and Eastern Europe.3 The differences in SD incidence between geographic regions may be attributed to skin type, the type of Malassezia species present in the region and how the climate impacts the microbiome.2
The incidence of SD is higher in immunocompromised patients and patients with skin of color with incidence of 6.5% in African Americans.4 SD is one of the top five most common skin conditions in African Americans, but not White, Asian, or Hispanic populations.2 Misdiagnosis or delayed diagnosis of patients with skin of color can happen frequently.4 Changes in pigmentation, such as loss of color in the area (hypopigmentation), may be one SD symptom in patients with skin of color. As with other skin diseases that have been characterized by “redness” on white skin, SD may appear tan, gray or purplish on darker skin.5A few studies have highlighted the co-existence of SD with other skin conditions and other eczemas. For example, patients with SD have been reported to have lower incidence of allergy-induced contact dermatitis, but SD patients were often diagnosed as having contact dermatitis.6 Researchers discovered that the allergens underlying SD varied from those underlying contact dermatitis.6 Several reports helped explain to physicians how to differentially diagnose SD as opposed to other diseases including psoriasis7 and more rare skin disorders including pemphigus foliaceus.2 AD and SD are both prevalent in infants and can co-occur, particularly on the face and scalp, making them often difficult to distinguish from each other in infancy.8 Compared to SD, infants with AD are characterized by lack of sleep. Additionally, SD of infancy typically resolves before two years of age while AD can persist.
Colonization of skin with the yeast-type of fungus Malassezia has been the most attributed cause of SD, but other factors such as sebaceous gland activity, underlying genetics, immune factors, hormones and other components of the microbiome likely also play a role.9 No one knows exactly why Malassezia colonization contributes to SD, but sebum, the substance produced by sebaceous glands to moisten skin and hair, is one source of food for Malassezia. It may be that increased sebum production leads to an environmental advantage in which Malassezia can thrive. Immunocompromised individuals can struggle with increased colonization with Malassezia and therefore increased incidence of SD. For example, 40% of patients infected with HIV have SD while 3–5% of the general public have SD.3,10 Immunosuppression-using medication, for example after organ transplantation, can also be associated with higher incidences of SD.1 The fact that treatment with either antifungals or with topical steroids that modify the immune system work to treat SD means that certainly Malassezia is not the only factor contributing to SD pathology.1
The complex causes of SD have not been easy to study. Dr. Benjamin Ungar of Mount Sinai Hospital and Medical School said, “In order to understand the pathophysiology of SD, skin tissue sampling from patients with SD is needed to allow for molecular studies, similar to other inflammatory skin diseases. With the typical distribution of SD involving the face and scalp, this has historically been a challenge. The current understanding of molecular underpinnings of SD has been limited to only a few small studies.”
Research investigating the genetic contributors to SD has been very limited. A few mouse models have been developed that exhibit SD-like symptoms so that genetics and other underlying factors, such as immunologic factors, that contribute to disease can be studied.11-13 Genetic studies using these mouse models as well as human samples have identified around 11 genes that can be mutated in SD including five genes that control different components of the immune system and two genes that are important for skin cells to differentiate and create the barrier function of the skin.14 Mice missing one of these barrier genes, called Myelin Protein Zero Like 3 (MPZL3), developed SD-like features spontaneously without being immunocompromised.12 This model also revealed changes in the immune system including greater presence of immune cells in the mouse skin, linking the importance of the immune system and the skin barrier for development of SD. Further study of this model revealed that the cytokine (immune cell messenger) interleukin (IL)-17 was increased in SD-like mice, helping point the way toward a deeper understanding of which immune cells (T cells) may be involved in SD pathology.13
In addition to IL-17 increase found in the SD-like mouse model, a large number of inflammatory markers are increased in SD, including several other cytokines (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12) and other immune stimulators (TNF-α, beta-defensins, IFN-γ, nitric oxide and histamine).15 An immune response against Malassezia yeast on the skin is also thought to play a part in pathology.15
The microbiome (the spectrum of living organisms like bacteria, fungi and other species that live on skin) differs in SD skin beyond just the expansion of Malassezia.16 Again, only a few studies have been done, but several changes in bacterial levels on the skin and the balance between bacterial types were found in SD patients compared to those without SD.15 Environmental influences like hot or cold weather and hormone differences, such as between males and females, may alter Malassezia and other components of the microbiome. Diet, use of certain skin care products and growth of facial hair could also be a factor, although research is still needed to link these factors with microbiome changes.2 Some research is currently focusing on modulation of the microbiome using medication or over the counter (OTC) approaches. OTC probiotics may be useful for improving symptoms associated with SD.17 Certain species of bacteria are sensitive to topical ketoconazole, which is commonly used to treat SD. Another drug taken systemically, itraconazole, can reduce Malassezia and may have an impact on other components of the microbiome.16
Current treatment approaches for SD may vary considerably depending on the age of the individual and co-occurring diseases they may have. Treatments for infants and for adults with mild SD currently range from special OTC or prescription shampoos to creams, to topical antifungals and topical steroids, but there is not one uniform approach to SD treatment.18,19 Infants are generally treated with OTC baby shampoos enriched with emollients (shea butter, glycerin) or vegetable oils.9 Most adolescents and adults with SD are treated with a multi-pronged approach that can involve topical or systemic treatments.18 Dr. Andrew Blauvelt, MBA of the Oregon Medical Research Center said, “What has happened in the past is that topical drugs approved for other conditions like psoriasis or AD have been re-purposed for treating SD.” Indeed, topical corticosteroids and calcineurin inhibitors, both of which alter immune reactions, have been used to treat AD and SD.
Ketocoazole was introduced in 1979 as a systemic compound with activity against fungi through disrupting formation of fungal cell membranes. A topical form of ketoconazole 2% was FDA approved in 1990 as a prescription shampoo for scalp SD in patients 12 and over. In 1997 it was approved as an OTC 1% shampoo for dandruff or flaking scalp.9 Creams or gels containing ketoconazole were approved for treating other body sites in 2002 and 2006.9
Treating SD in patients with skin of color can also be challenging. Dr. Susan Taylor of the University of Pennsylvania said, “Scalp SD in these patients cannot be treated with prescription shampoos because they are very drying for tightly coiled hair, which leads to breakage. Education of healthcare providers on the presentation of SD in diverse populations and on hair care practices and customs may serve to improve outcomes for patients with skin of color.”
While there are currently limited treatment options for SD management, Dr. Blauvelt recently presented the results of a Phase III clinical trial (a step before the end of the process of seeking FDA approval for use of a specific drug to treat a specific disease) for a topical drug called roflumilast, which was already approved for psoriasis treatment. Dr. Blauvelt said, “80% of patients with moderate-to-severe SD treated with roflumilast foam experienced clearing (50% of treated patients) or partial clearing of their disease after 8 weeks of once daily applications. Study participants were extremely satisfied with the results. Studies of SD have been rare, even though the disease is very common, and most of the current therapies have drawbacks that can limit their use, so I think this new treatment is going to be very important for SD patients if it gets approved.”
Articles have called for both additional research into drug development and collaboration between patients and medical providers to determine the most appropriate treatment approaches for SD.18,19 It is important for affected individuals to be aware that SD can go away and come back again and that treatment may need to be long term, particularly in adolescents and adults.
Future studies are needed to understand wider factors underlying SD. Several articles have recently highlighted the higher percentage of patients with SD in African Americans compared to white individuals, meaning that the burden of this skin disease is higher in this population. Studies are needed to understand why this health disparity exists and if existing treatments, often borrowed from other diseases, are effective in diverse populations.
Recently SD has gained interest in the research community since receiving attention in the mainstream media. Masks worn to avoid COVID-19 illness were associated with an increase in SD incidence.2 Dr. Taylor said, “I believe that when attention is given to any disease entity, it sparks interest regarding research and development of agents to address the disease. Pharmaceutical companies are always searching for unmet needs in medicine and articles and news segments highlight unmet therapeutic needs in diseases that they may not be aware of.”
Overall, this is an exciting period in history for understudied skin diseases as there are new, non-invasive skin sampling techniques and new technologies that allow characterization of all the cells playing roles in a specific disease. With revolutionary new treatments occurring for multiple skin diseases, this common form of eczema may be getting some long overdue attention, as well as much needed research and treatment options.
Dr. Benjamin Ungar, in addition to providing insight into why SD has been so difficult to study, also provided great optimism for the future. He said, “This is a very exciting time for research in SD, because newly developed minimally invasive skin sampling techniques now offer the ability to collect samples from large numbers of patients without biopsies that leave scars, enabling gene and protein expression studies. Furthermore, with new non-steroidal treatments for SD on the horizon, there is an opportunity not only to characterize the SD disease state itself, but also to tease out the immune pathways that are modulated with different treatments that lead to clinical responses. Huge advances will be made in understanding SD pathogenesis in the upcoming months and years.”
References:
1. Wikramanayake TC, Borda LJ, Miteva M, Paus R. Seborrheic dermatitis-Looking beyond Malassezia. Exp Dermatol. 2019;28(9):991-1001.
2. Jackson JM, Alexis A, Zirwas M, Taylor S. Unmet needs for patients with seborrheic dermatitis. J Am Acad Dermatol. 2022.
3. Buja A, Miatton A, Cozzolino C, et al. The global, regional, and national burden of seborrheic dermatitis: results and insights from the Global Burden of Disease 2019 Study. Arch Dermatol Res. 2022.
4. Chatrath S, Bradley L, Kentosh J. Dermatologic conditions in skin of color compared to white patients: similarities, differences, and special considerations. Arch Dermatol Res. 2022.
5. Elgash M, Dlova N, Ogunleye T, Taylor SC. Seborrheic Dermatitis in Skin of Color: Clinical Considerations. J Drugs Dermatol. 2019;18(1):24-27.
6. Silverberg JI, Hou A, Warshaw EM, et al. Allergens in patients with a diagnosis of seborrheic dermatitis, North American Contact Dermatitis Group data, 2001-2016. J Am Acad Dermatol. 2022;86(2):460-463.
7. Gisondi P, Bellinato F, Girolomoni G. Topographic Differential Diagnosis of Chronic Plaque Psoriasis: Challenges and Tricks. J Clin Med. 2020;9(11).
8. Siegfried EC, Hebert AA. Diagnosis of Atopic Dermatitis: Mimics, Overlaps, and Complications. J Clin Med. 2015;4(5):884-917.
9. Dall’Oglio F, Nasca MR, Gerbino C, Micali G. An Overview of the Diagnosis and Management of Seborrheic Dermatitis. Clin Cosmet Investig Dermatol. 2022;15:1537-1548.
10. Chimbetete T, Buck C, Choshi P, et al. HIV-Associated Immune Dysregulation in the Skin: A Crucible for Exaggerated Inflammation and Hypersensitivity. J Invest Dermatol. 2023;143(3):362-373.
11. Oble DA, Collett E, Hsieh M, et al. A novel T cell receptor transgenic animal model of seborrheic dermatitis-like skin disease. J Invest Dermatol. 2005;124(1):151-159.
12. Wikramanayake TC, Borda LJ, Kirsner RS, et al. Loss of MPZL3 function causes seborrhoeic dermatitis-like phenotype in mice. Exp Dermatol. 2017;26(8):736-738.
13. Wikramanayake TC, Hirt P, Almastadi M, et al. Increased IL-17-expressing gammadelta T cells in seborrhoeic dermatitis-like lesions of the Mpzl3 knockout mice. Exp Dermatol. 2018;27(12):1408-1411.
14. Karakadze MA, Hirt PA, Wikramanayake TC. The genetic basis of seborrhoeic dermatitis: a review. J Eur Acad Dermatol Venereol. 2018;32(4):529-536.
15. Adalsteinsson JA, Kaushik S, Muzumdar S, Guttman-Yassky E, Ungar J. An update on the microbiology, immunology and genetics of seborrheic dermatitis. Exp Dermatol. 2020;29(5):481-489.
16. Tao R, Li R, Wang R. Skin microbiome alterations in seborrheic dermatitis and dandruff: A systematic review. Exp Dermatol. 2021;30(10):1546-1553.
17. Carmona-Cruz S, Orozco-Covarrubias L, Saez-de-Ocariz M. The Human Skin Microbiome in Selected Cutaneous Diseases. Front Cell Infect Microbiol. 2022;12:834135.18. Desai S, McCormick E, Friedman A. An Up-to-Date Approach to the Management of Seborrheic Dermatitis. J Drugs Dermatol. 2022;21(12):1373-1374.
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