First of all, I have no COIs with any makers of sunscreen! Even so, I'm going to avoid talking about any brands. Instead, we'll focus on the different factors you should consider when picking your favorite.
What is your current preference for sun protection (if any)?
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There's debate in the field right now about whether everyone even needs sunscreen. For this #tweetorial, I'm going to focus on those who've decided they need sun protection.
So 1st rec: The best sunscreen is one you'll actually put on. Doesn't matter if you won't use it!
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Ok, let's get into it. What is SPF?! Here's a nice website from the @US_FDA about what it is. In short, it's a measure of how MUCH UV your skin can take before it burns (compared to unprotected skin), NOT a measure of how long you can have UV exposure. 4/
Remember though that sunscreens are tested in ideal lab settings. That means that if you don't put enough of it on, you aren't getting to the same level of protection as "proven" in laboratory testing.
So while yes, SPF effect plateaus after 30, that was done in the lab! 5/
So how do we use this in the real world?
1) Pick a higher spf! I say minimum spf 50 b/c that way if you don't put enough on or don't reapply enough, you perhaps are getting to at least an spf30 equivalent.
2) Put enough on! One shotglass full with each application. 6/
So SPF blocks UVB, but what about UVA? We don't have a clear number to shoot for in terms of blocking UVA, so the best advice I can give is to make sure you pick a sunscreen that has "broadband" protection across the whole UV spectrum.
Remember
uvB ➡️ Burns
uvA ➡️ Aging
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But what about physical vs. chemical blockers?!
Physical blockers are the sunscreens whose main ingredient includes Zinc or Titanium.
Chemical blockers include ingredients that sound like they're in an orgo textbook😬
Both work as well as their SPF would suggest! 8/
The main drawback of physical blockers is how they look/feel when they go on. They are (usually) the ones that go on super white and can't be rubbed into the skin as easily.
In the article, the authors measured plasma levels after sunscreen use and found that the chemicals were absorbed at higher levels than previously thought. Importantly, they don't delve into downstream consequences, but this understandably made many nervous! 10/
So what does that mean? I'll just share that in our family, we make sure to use physical blockers on the kids, but my partner and I still use chemical blockers.
But I'm sure others of #dermtwitter have their own opinions! 11/
Okay, what about spray on versus smear on?
Tbh, I don't think there's a huge difference except real world outcomes. Those that use spray on often apply too little, and you can't as easily tell what areas you've missed. So be sure to apply enough if that's your preference! 12/
There was another sunscreen scare where a bunch of spray-on sunscreens were recalled because benzene (a known carcinogen) was found in them.
BUT, the concentrations were super low, and it wasn't a problem with the spray on sunscreen per se, but rather how it was made.
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And how should we actually apply it? I already went over how much to use, but the UV protection only lasts for ~2-3 hours, even shorter if it's when the UV index is super high!
So I advise my patients to apply every 2 hours, or more frequently if they are sweating/swimming! 14/
Finally - don't forget there are SO many ways other than sunscreen to protect yourself.
✅ Sun protective clothing that's well UPF rated.
✅ Avoiding sun between 10 am and 2pm.
✅ Using wide-brimmed hats that cover the ears! 15/
SUNSCREEN RECAP:
👉SPF is from ideal lab conditions. Use higher SPF and enough sunscreen (1 oz per application).
👉Use broadband protection to include UVA.
👉Physical blockers less likely to be absorbed, but downstream effects of chemical absorption unknown.
👉Avoid benzene!
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But at the end of the day, what does this mean for me and my family?
For us👇
Kids: Smear on physical blocker, at least SPF 50, applied every 2 hours, or more frequently with high UV, sweating, swimming.
My partner and I: Same as above, but okay with chemical blockers. 16/
Hope this #dermtwitter#tweetorial is helpful not just for counseling your patients, but also for you and your loved ones.
Let's start by establishing that Wilson Disease is a multisystem process wherein copper deposits in various tissues (liver, brain, eyes) because of improper transport.
A mutation in ATP7B causes this, and the depositional process leads to disease manifestations. 2/
Given the organs Cu2+ deposits in, you see neurologic effects, Kayser Fleischer rings in the eyes, and of course, liver disease.
While here👇, we see the always memorized, rarely seen, Kayser Fleischer rings, let's focus on the liver...
The primary lesion isn't enough to make the diagnosis. You're going to need the primary lesion AND time from rash onset to know what you should be expecting to see. 2/
The prodrome that occurs before the rash includes the typical ILI type symptoms of fever, malaise, headache, pharyngitis, and cough. Lymphadenopathy has been billed as a distinguishing feature of MPX from smallpox and Varicella.
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This is an autoimmune blistering disorder that can be triggered by drugs!
Hey #medtwitter, what do you think is one of common culprits for causing this eruption?
2/ You'd be correct if you said vancomycin!
Vanco triggers IgA to attack proteins in the hemidesmosome that holds epidermis to the basement membrane. That means this is a part of the PEMPHIGOID group.
So you get TENSE blisters with a NEGATIVE NIKOLSKY.
3/ For the #dermatology residents who need to memorize this, remember that the antigen that is targeted is the 97 kDa portion of the extracellular domain found in BPAg2.
For everyone, remember this is part of the pemphigoiD (D for deep) group, hence the exam findings.
2/ The "pemphigus" part of the name means we are similarly dealing with an EPIDERMAL blistering disease, much like it's better known cousin, "pemphigus vulgaris" (PV).
If you haven't had a chance yet, take a look at my prior #tweetorial on PV:
3/ Before we get into the nitty gritty details of PF vs PV, a reminder that in pemphiguS, we're dealing with a SUPERFICIAL desmosome antigen target, so compared with pemphigoiD (that's DEEP), you're still going to get the + nikolsky, flaccid bullae, etc.
2/ If you answered, "hands, feet, and ears," you're correct! This is tricky, and it wasn’t until dermatology residency that I learned it’s not palms and soles!
If you haven't yet, take a look at my old #tweetorial on acral rashes as a primer.