Can hard water, softeners or chlorine in water affect your skin?
Published On: Jan 23, 2020
Last Updated On: Nov 2, 2020
In Ask the Ecz-perts, leading medical experts answer your most pressing questions about eczema and its related conditions.
A portion of this Q&A with Peter Lio, MD, originally appeared in Practical Dermatology® magazine. Visit PracticalDermatology.com to read more from Dr. Lio, including a discussion of gut health and the skin.
When we have eczema around the eye or on the eyelid, it’s somewhat difficult to treat because we have special considerations.
The skin around the eye is thinner and more delicate and some treatments could actually cause issues with the eye itself if they are too strong or overused.
This said, the principles are generally the same. We want to use a topical corticosteroid to cool things down briefly, and then switch to a noncorticosteroid-based cream as soon as we can.
We don’t want to use super strong topical steroids in the area around the eye ever, so we’ll start with either a mild or moderate steroid.
Once things are better, we can stop the steroid. If the case is mild enough, we might be able to avoid topical steroids altogether and just use one of our noncortisones.
With prolonged eczema flaring around the eye, the skin in this area can become damaged and thinned. It can actually get a stretchmark-type of appearance.
If people are rubbing a lot, you can also see a chronic thickening of skin around the eye that we call lichenification.
If we’ve overused topical steroids in this area, there can be a higher risk of cataracts and glaucoma. And these are two things we definitely want to avoid.
We continue to learn more at what seems like an ever-increasing pace, with numerous studies, publications, and products rapidly appearing.
In recent history, I would say that the thinking was that Staphylococcus aureus (staph) was a colonizer and an opportunist; it found the open, oozing skin of AD an apt home.
However, we are learning that staph may actually be a primary driver of skin disease for some patients, and this is altering our therapeutic approach, at least on the cutting edge.
Dr. Heidi Kong at the National Institutes of Health wrote a bold and impressive paper in 2012 that outlined the relationship between the microbiome and atopic dermatitis (AD) flares.
In short, it suggested that as staph became more dominant, the microbiome diversity decreased and this led to a flare. For recovery, the diversity increased again with staph correspondingly reduced, and then skin symptoms improved.
There is a bit of a chicken-and-egg problem here, but I am convinced that, in some instances, staph overgrowth (and loss of the erstwhile microbial diversity) can be a true cause of disease flares.
I feel very confident in saying that Staphylococcus aureus is the bad guy here. It dominates, makes a multitude of toxins and seems to have a verifiable effect on driving AD.
The good bacteria are a lot more complex. I think the most timeless answer, perhaps, would be to say that a strong diversity seems to reflect a healthy microbiome, and this may well be the priority over identifying one or several species as culprits.
I don’t think we really know for sure, but it certainly seems reasonable and likely. We know that gut microbial diversity in the first week of life is a strong predictive factor for developing AD and decreased diversity correlates with increased AD risk.
We also know that skin barrier dysfunction is an important independent risk factor for developing AD, such as filaggrin mutation and consequent filaggrin deficiency.
Thus, it follows that there are very likely to be microbiome abnormalities in newborn eczema, and, perhaps, if righted early enough, the disease could be halted.
There are many questions that need to be answered including the role of birth and home environment on the microbiome, better understanding differences in different body areas, better understanding prebiotics and postbiotics beyond just the organisms present.
I would say we are at the very beginning here and far from being able to understand how to manipulate the skin’s microbiome for therapeutic purposes at this point.
Even today, in late 2019, I’m not comfortable saying that any are reliably effective, but there are some studies that suggest oral Lactobacillus GG can have both a protective effect against developing AD and may have a slight (and variable) effect on existing AD.
There are several promising topical probiotics on the market, but I don’t feel we have seen enough data yet to routinely recommend them beyond personal explorations.
A so-called “microbiome transplant” with Roseomonas was recently published and seemed relatively convincing for an effect on AD severity, but, again, much more work needs to be done before we can confidently recommend such an approach.
Peter A. Lio, MD, is an assistant professor of clinical dermatology and pediatrics dermatology at Northwestern University Feinberg School of Medicine.