Why Eczema Occurs and How We Can Treat it
- Abigail Simpson
- 12 minutes ago
- 5 min read
Eczema, or atopic dermatitis, is a common inflammatory skin condition affecting people of all ages, characterised by red, inflamed, dry, itchy and broken skin, with many people experiencing persistent flare ups that make it difficult to manage. Unfortunately, this condition is complex and is influenced by genetic, immune and environmental factors, meaning there is not a single miracle treatment to cure it, and recovery often can take months while the skin fully heals.
Patients have a disrupted skin barrier, and their skin loses moisture easily and becomes a lot more sensitive to irritants and allergens, as skin barriers are the first defence against anything foreign entering the body, which can cause immune reactions and infections. In many people affected by this disease, it becomes chronic rather than acute, and can last months or even years.
Factors
Endogenous factors are those that come from within the body to cause eczema, such as genetics, an overreactive immune system and hormonal influences.
Eczema often runs in families, meaning in a lot of people there is a genetic cause. The filaggrin gene (FLG) is a gene that codes for the production of the filaggrin protein, which is needed for building and upkeep of the outer layer of skin and creates a strong barrier which is naturally moisturised. This protein helps keep the skin strong, compact, and an effective defence against microbes or irritating molecules. In people with eczema, this gene is often mutated, meaning the filaggrin protein is deficient, and as a consequence, the skin barrier is not as strong as it should be, and becomes leaky, weaker, drier, and cannot keep out foreign bodies [1].
It is often that mutation that allows the immune system to overreact and worsen the eczema. With a deficient and broken skin barrier, molecules that are foreign, like irritants, now are free to enter the skin, and encounter the immune system. The immune system will mistake the substances for a dangerous invader, and produces an innate and adaptive immune response consisting of immune cells called T-helper cells, which release inflammatory cytokines, contributing to the inflammation, damage, and itchiness of the skin [2]. Many people experience such intense itches that are difficult to resist, but help to break down the skin barrier even further. This is often caused by a cytokine called IL-31, released from T-helper immune cells, which activate sensory neurons and cause an itch [8]. This process is the body doing what it thinks is right for the health of the person, but actually exacerbates the process of eczema.
In women, hormonal influences can affect their eczema. Many women report their eczema gets worse in the week before their period, when progesterone levels rise and oestrogen levels drop. This is thought to occur because oestrogen maintains the skin barrier function and lock in moisture, so a decrease in oestrogen impacts eczema negatively. Progesterone can also trigger inflammatory responses in the skin, contributing to eczema, but this occurs more in the rare disorder of autoimmune progesterone dermatitis [3].
Exogenous factors are those that occur from outside of the body. Irritants like soap, chemicals or excessive hand washing can strip skin of its moisture, allowing the skin barrier to disintegrate, and allows further allergens like pollen or certain foods, to enter, causing an immune reaction, causing the further stripping of the skin barrier along with intensive inflammation and itchiness [1]. The cold and dry air we experience in winter can also drain moisture from skin and lead to dryness however sweating from hot weather can also be an irritant. Skin infections from bacteria such as Staphylococcus aureus can occur more in people with eczema as the damaged skin barrier allows this bacterium to survive and reproduce, releasing toxins to further cause inflammation [4].
Common treatments
So what treatments are effective for this? Different medications are going to work differently on everyone, and an examination from a doctor is the best way to ensure a patient will get the best treatment.
Generally, the options available include emollients and moisturisers, which create a very oily layer on top of the eczema that traps moisture in the skin that the skin desperately needs, which helps restore the skin barriers function and helps the flaky and dry skin heal. These are available in many forms like lotions, creams, gels, and more the oily the treatment, the more effective it will be at locking in moisture. These generally do not have many adverse side effects unless a patient has an allergic reaction to one of the products in the skin [5].
Topical corticosteroids are steroid creams that are effective at controlling eczema as they work at the cellular level, regulating gene expression in the nucleus of cells at the site of eczema. This means that the steroid cream is effective at reducing pro-inflammatory responses by cells, so inflammation and immune cell activity is reduced in the area, allowing the skin to heal without the interruption and damage caused by immune cells [6]. These creams are usually very safe, but can cause adverse effects such as local skin thinning, which may bruise or tear easier, or small red bumps or rashes on the skin. An extremely rare consequence of mild hydrocortisone creams is steroid withdrawal, which happens more with stronger and more potent steroid creams. When this withdrawal happens, the patient can get a rebound eczema that is far worse than the original condition, with very intense redness, burning, itching and peeling of skin layers [7].
When treating eczema effectively, it is important to keep consistent with treatment, and apply ointments or creams often and over a period of several days to weeks, until the skin has fully had a chance to heal and to restore the skin barrier function which will in turn reduce inflammation and intense itchiness. Steroid creams should be used only short term over a small number of weeks to reduce flare-ups. Women who experience more intense eczema before menstruation may need to take extra precautions with their skin in this period and may need to apply additional treatments.
Future treatments
Researchers are currently studying different more targeted therapies for eczema, including a medication called nemolizumab, a drug which disrupts the signalling of the itch cytokine IL-31, to hopefully reduce inflammation and itchiness, to help the skin heal [9]. Other treatments being studied involve a treatment called rocatinlimab, which targets a receptor called the OX40 receptor, which reduces the immune T cells which are contributing to the inflammation and eczema [10]. Researchers have gained promising results so far, for both of these therapies, and hopefully these become accessible to those struggling with eczema.
References:
Weidinger S, Novak N. Hand eczema. The Lancet. 2024 Nov;404(10470).
Pan Y, Wang Y, Xu M, Zhong M, Peng X, Zeng K, et al. The roles of innate immune cells in atopic dermatitis. Journal of Innate Immunity. 2024 Jul 18.
Nguyen T, Razzaque Ahmed A. Autoimmune progesterone dermatitis: Update and insights. Autoimmun Rev. 2016;15(2):191-197.
Mayo Clinic. Atopic dermatitis (eczema) - Symptoms and causes [Internet]. Atopic dermatitis (eczema). Mayo Clinic; 2023. Available from: https://www.mayoclinic.org/diseases-conditions/atopic-dermatitis-eczema/symptoms-causes/syc-20353273
NHS . Overview - Atopic Eczema [Internet]. NHS. 2024. Available from: https://www.nhs.uk/conditions/atopic-eczema/
Gabros S, Zito PM. Topical Corticosteroids [Internet]. PubMed. Treasure Island (FL): StatPearls Publishing; 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532940/
Mohta A, Sathe NC. Topical Steroid Withdrawal (Red Skin Syndrome) [Updated 2024 May 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK603718/
Datsi A, Steinhoff M, Ahmad F, Alam M, Buddenkotte J. Interleukin-31: The "itchy" cytokine in inflammation and therapy. Allergy. 2021;76(10):2982-2997. doi:10.1111/all.14791
Ruzicka T, Hanifin JM, Furue M, Pulka G, Mlynarczyk I, Wollenberg A, et al. Anti–Interleukin-31 Receptor A Antibody for Atopic Dermatitis. New England Journal of Medicine. 2017 Mar 2;376(9):826–35.
Guttman-Yassky E, Simpson E, Bissonnette R, et al. ROCKET: a phase 3 program evaluating the efficacy and safety of rocatinlimab in moderate-to-severe atopic dermatitis. Immunotherapy. 2025;17(2):83-94. doi:10.1080/1750743X.2025.2464528
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