Eczema and Dermatitis are different words for the same skin condition

Skin condition : Eczema (Dermatitis)

What is it?

Eczema and Dermatitis are different words for the same skin condition. Both are derived from Greek. Eczema means ‘to boil over’ and Dermatitis means ‘skin (Derma) inflammation (itis)’.

To understand eczema you need to understand a bit about how the skin works. The top layer of skin is called the epidermis. This layer works as a barrier to prevent water evaporating out leading to dry skin and to prevent irritants such as bacteria, fungi, chemicals from getting in. All of the components within the epidermis  working together are known as the skin barrier. The skin barrier includes

  1. the keratinocyte cells ( the main skin cells)
  2. proteins that help to waterproof the skin such as fillagrin (more on this later)
  3. oil based substances that help to waterproof the skin such as cholesterols, ceramides and fatty acids.

In addition to the skin barrier the skin contains millions of immune cells. There are more immune cells in the skin than in the blood. There are many different types of immune cells but they can be roughly divided into four groups.

  1. Dendritic cells or antigen presenting cells. These cells detect foreign particles and show them to the immune system to see if a reaction is needed
  2. Regulatory cells- these cells control the reactions that occur. They can make an immune response larger or they can supress an immune response depending on the situation
  3. T cells- these trigger inflammation and produce chemicals that can kill bacteria and destroy foreign particles
  4. B cells- make antibodies. Antibodies can attack foreign substances, bacteria or viruses to kill them and promote their removal .

Eczema occurs when the skin barrier is not working properly and foreign antigens ( e.g microscopic proteins), which can be almost anything not normally found in the body, enter the skin.  These are detected by the immune system and an inflammatory response is triggered. The inflammation that occurs in eczema leads to:-

  1.  Fluid accumulation between cells ( seen as small blisters or vesicles)
  2. Increased blood flow to the area ( redness)
  3. Activation of itch nerves
  4. Increased growth of keratinocytes ( scaly, flaky skin or thickened areas of skin)

There are many different sorts of eczema but they are all due to a combination of a reduced skin barrier or an overactive immune response. A very poor skin barrier with a relatively normal immune response can lead to bad eczema as can a relatively normal skin barrier but a very overactive and sensitive immune response.

Why have I got it?

Anyone can develop eczema. The types of eczema are generally divided in to endogenous (due to genetic factors) and exogenous ( due to external factors).

Endogeonous eczema

These types of eczema are thought to be determined by inheriting a genetic susceptibility. There is often a family history. There may be associations with other diseases  such as the association between atopic eczema, asthma and hayfever.

All of the components of the skin barrier are determined to some degree by genetics. Every protein has a genetic code and in some cases there are variations in the codes. Gene variations can lead to proteins which do not work as well as they should. In 2010 researchers in Dundee discovered genetic variations in a protein called filaggrin which is an important component of the skin barrier.  They found that mutations in the filaggrin gene led to the production of an abnormal filaggrin protein that did not work as well resulting in a less effective skin barrier. Patients with severe eczema were found to be far more likely than unaffected patients to have filaggrin mutations. They also found that patients with a dry skin condition called icthyosis also had mutations in their filaggrin genes.

In addition to problems with filaggrin mutations they also found that we all have a different number of copies of the filaggrin gene. We all have between 20 and 24 copies of the fillagrin gene. Even if there are no mutations someone with only 20 copies is 2 to 3 times more likely to have dry skin and eczema than someone with 24 copies. This may well explain why many people who do not normally have eczema can develop problems when the skin barrier is put under stress either by too much hand washing or in the winter when the air is dry with low humidity.

Some doctors believe that genetic variations can lead to differences in the activity in the immune system in the skin. This is quite possible although the gene variations that determine this have not been identified.

Types of endogenous eczema include

  1. Atopic eczema
  2. Discoid eczema
  3. Seborrhoeic  dermatitis
  4. Varicose eczema
  5. Pompholyx eczema

Exogenous eczema

These eczema are generally triggered by exposure to external substances. Anyone can develop an exogenous eczema regardless of their genetic make up.

Types of exogenous eczema include

  1. Contact eczema ( also known as allergic eczema eg nickel allergy)
  2. Irritant eczema ( common on the backs of hands in people who do a lot of hand washing)
  3. Asteatotic eczema (dry legs often in elderly patients)


Comparing the treatment options


  1. If there is a trigger for your eczema that you have identified you will need to avoid it. Common triggers include
    1. The over use of detergent based washing products ie most soaps and  shower gels
    2. Wollen clothing
    3. With contact eczema it can be hard to identify a trigger but in some cases,  such as nickel allergy from jean buttons or cheap jewellery, it can be obvious.
  2. Moisturise the skin. One of the main causes of eczema is a poor  skin barrier which leads to dry skin and then eczema inflammation. Washing with moisturising products and using moisturisers regularly is essential to get eczema under control.
  3. Mild topical steroids. If you have previously had eczema and are confident that you have it again, weak topical steroids can be bought over the counter. However, these will often not be strong enough to settle the eczema and a visit to a GP or Dermatologist is often needed.

Help from your GP

If you are unsure of the diagnosis you must visit your GP or family doctor. Various other skin rashed can look like eczema. It is important not to confuse a fungal infection with eczema and equally important not to mistake psoriasis for eczema as the treatments are different.

Once a diagnosis of eczema has been established your GP may offer the following

  1. Stronger topical steroids
  2. Non steroid based eczema creasm such as tacrolimus ointment (protopic). This can be very helpful for difficult facial eczema.
  3. Antibiotics. The bacteria staphylococcus aureus is a normal part of our natural skin bacteria (microbiome) . When the skin barrier is not orkign well s. aureus can multiply and cause problems. The excess bacteria can lead to activation of the immune system. Sometimes a failure to respond to standard moisturisers and topical steroids can be due to s. aureus infection. In these situations antibiotics are needed.
  4. Antiseptics. Various antiseptic treatments can sometimes be used to reduce s,aureus levels. These include potassium permanganate added to the bath (messy) and Dermol lotion, a moisturiser which contains benzalkonium chloride and chlorhexidine hydrochloride which reduce levels of s. aureus.

Help from a Dermatologist

A visit to a Dermatologist is needed if there is any doubt about the diagnosis or if standard treatments given by the GP are not effective. Following diagnosis a Dermatologist may offer other options:-

  1. In patient or day unit based treatments. Intensive treatment by specialist Dermatology nurses in combination with education is often very effective.
  2. Phototherapy. Specialised light treatment known as narrowband UVB or TL-01 can be helpful for eczema.
  3. Immunosuppressive tablets. There are a range of different oral tablets that are effective for severe eczema. These tablets mainly work by supressing the immune system. Side effects can occur and careful consideration is required before starting. However, they can have a dramatic effect and lead to significant improvements. Medicines include ciclopsorin, methotrexate and azathioprine
  4. Diagnostic tests. A Dermatologist may offer tests such as prick tests or patch tests to help identify potential triggers.
  5. Biologic drugs. For very severe eczema some centres are now involved in clinical trials of new injected drugs that target specific molecules to treat eczema. It is likely that these drugs will become more commonly used over the next 5 to 10 years.

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