Atopic Dermatitis = the decreased patchy cortisol production in epidermis?
Dr. Fukaya has posted a new article on his Japanese blog.
Atopic eczema can be the decreased patchy cortisol production in epidermis
The below picture is a dyed adrenal gland - the brown areas show that there are cortisol, which are found plenty in the cortical cytoplasm.
The picture below is dyed skin. Epidermis is certainly dyed, and in this case especially hair follicles are strongly tinted.
This one below is my skin. The epidermal cells are evenly dyed.
If you test on people with atopic eczema, however, some areas are not dyed at all. There are the parts where still produce steroids, but only in patches. This picture below is from a patient, who has withdrawn from topical steroids for a long time. This can explain the clinical condition of atopic dermatitis.
Steroids help to make skin thin and differentiated. Therefore, when epidermis stops producing steroids, it becomes thickened. Steroids are also thought to adjust and lessen reactions to external stimulus and allergens. So, without steroids, skin inflammation increases. It results in more intense immune reaction and non-specific hypersensitive reaction.
This picture below is from a different patient, who has been using topical steroids everyday for a few years to suppress atopic dermatitis. It shows that the epidermis isn't thickened, and cortisol production isn't patchy. Topical steroids are helping to increase the cortisol level in epidermal cells. As a result, the cortisol is evenly produced, although I think that the cortisol production would be patchy without using topical steroids. This is possibly the benefit of topical steroids treatment.
But, a different part shows the deficiency in the cortisol production as in the picture below.
It is noteworthy that another patient showed the patchy cortisol levels when his skin was worse,
but the cortisol production becomes even when his skin was improved (supposedly natural healing, as he has not been using topical steroids). This is only my hypothesis, but from all those cases, I think: Atopic eczema is the decreased patchy cortisol production in epidermis, therefore epidermis becomes thickened and cannot fully differentiated. Also, it cannot control external stimulus and allergens with self-produced cortisol, which results in skin inflammation.
Although topical steroids help to produce cortisol in epidermis and make skin seemingly normal, it could be the case that epidermis stops responding to topical steroids after a long term use.
When epidermis cells create more cortisol by application of topical steroids, nearby epidermis cells also respond to produce more cortisol. If epidermis stops corresponding to topical steroids, those nearby cells also function less and eczema would be worse. This can be interpreted as "rebound".
Also, the mechanism of natural healing can be the evenly produced cortisol. So-called "moisturiser withdrawal", which helps to increase the cortisol level in epidermis, may be working to make the cortisol production evenly. UVB radiation also helps to increase cortisol in epidermis, so it makes sense to use as a treatment for atopic eczema.
This hypothesis can explain various phenomana related to atopic eczema, but it is still a hypothesis. There are only a small number of cases yet and it requires further validation with testing on varied types of skin rash. --------------------
Dr. Fukaya is now looking into his hypothesis further, by calling for volunteer participants to collect more test cases in Japan. I will update when more info comes.