Bruce Miller, MD
Dr. Miller, a
Dermatologist,
is a Consultant for Diving Medicine Online. This is a lecture presented
to Medical Seminars, 2000
DOWNLOAD
THIS
ARTICLE ZIP.file
Download
pdf
format Requires 
Free
Download
Travel to the tropical climes can
often
aggravate preexisting skin problems as well as expose us to new
hazards.
Here is a review some of the more common ones and suggestions for some
treatment approaches.
Tropical Acne and
Hidradenitis
Suppurativa:
Heat and humidity, along with the
chafing
of the dive gear and wet suit, can aggravate a preexisting cystic acne
condition. Severe acne flares on the shoulders and back can be quite
painful
and lead to scarring. Large cysts in the groin and/or axillae can also
occur. If a diver has a history of cystic, conglobate acne, and/or
hidradenitis,
it would be wise to be sure that these conditions are in a state
of long-term remission. Otherwise, treatment with a course of
Accutane
should be considered well before the trip.
If a flare occurs while on the trip,
incision
and drainage under local anesthesia, intralesional steroid injections,
a short course of prednisone 40 mgm/day, and coverage with cephalexin
should
all be considered
Atopic Dermatitis,
Neurodermatitis,
and Xerotic Eczema:
All these eczemas are characterized by
dry, itchy skin. Paradoxically, repeated immersion in water, while
temporarily
hydrating the skin, in the long run dries it out because of loss of
oils
from the stratum
corneum. In addition the climate may
superimpose
a prickly heat problem on top of the dryness, causing more pruritus.
Treatment consists of mild soap,
don’t
over bathe, lubricate after your shower, and a good fluorinated topical
steroid once or twice a day. Severe flares can be managed with
prednisone
or 40 mgm of Kenalog and 1 cc of Hexadrol IM.
Allergic Contact
Dermatitis:
There are numerous opportunities for
exposure
to various allergens on dive trips. The prototypical eruption is the
weeping,
severely pruritic, edematous reaction from exposure to poison oak or
ivy.
However, there are other members of this family lurking in the
background.
Mango rinds, Japanese lacquer and cashew nut trees, and the marking nut
trees of India contain the catechol antigen (urushiol) and cause the
same
reaction.
Neomycin, benzocaine and its
relatives,
rubber accelerators in the neoprene rubber of your wet suit, and
delayed
hypersensitivity reactions to hydroid stings can all cause contact
dermatitis.Milder
cases may respond to a high-potency topical steroid (e.g., Ultravate,
Temovate,
or Diprolene). More severe reactions need to be treated with
prednisone.
It’s important not to chase the disease with the dose. A typical
regimen
would be 60 mgm QDX4, then 40 mgm QDX6 to start.
Fungal Infections
(Tinea
cruris, corporis, and pedis):
If you have preexisting “athlete’s feet”
(T. pedis) or “jock itch” (T. cruris), I can almost guarantee that
these
conditions will flare under the humid, soggy, wet conditions associated
with diving. Carefully drying the affected body parts after your shower
by using a hair dryer, followed by some talcum powder, and applying a
good
topical antifungal, such as Mentax, may well prevent a flare.If the
problem
won’t respond to topical therapy alone, add in an oral antifungal, such
as Sporanox or Diflucan. For persistent nail involvement
(onychomycosis),
use Lamisil QD for 90 days.
Tinea Versicolor:
A harmless superficial fungus know as
m. furfur, it is mainly of cosmetic significance. Areas of involvement
appear lighter than the surrounding skin in the summer due to blockage
of the tanning rays. During the winter, the situation is reversed and
the
involved spots are reddish-brown and darker than the surrounding
skin.Occasionally, people complain of itching, but usually this is
an
asymptomatic problem. Typically, heat and humidity aggravate the
condition.Treatment
consists either of a topical application of Selsun shampoo for 5
minutes
QD for 7-10 days or 2 weeks QD of one of the oral antifungals.How do
you
tell the difference? KOH prep shows “ spaghetti and
meatballs”=hyphae
and spores.
Candidiasis (monilia,
yeast)
:
Usually seen in infants with diaper
dermatitis,
it can appear in adults. Diabetics and persons on broad-spectrum
antibiotics
are susceptible to this opportunistic organism, which is usually
peacefully
coexisting with the bacteria in our GI tract. Thrush, diarrhea,
candidal
vaginitis, and intertrigo can result from its overgrowth. The best
treatment
is an oral antifungal/yeast drug that will work within a few days,
(eg., Nizoral, Sporanox or Diflucan).How
do you tell the difference between these similar appearing intertrigos?
Do a KOH and culture..Actually, don’t do it yourself. send the patient
to a Derm.!
Erythrasma (a
corynebacterium):
Usually seen only in diabetics. The KOH
and culture are negative. Diagnosis is made by the process of
elimination
and characteristic fluorescence under Wood’s light. Treatment is oral
erythromycin
in any of its various forms.
Trichomycosis
Axillaris (
a gram positive organism):
Responds well to topical antibiotics,
e.g., cleocin-T.
Hot Tub Folliculitis:
Pseudomonas infection of the hair
follicles,
usually found only in poorly-maintained hot tubs in private settings.
It
can be quite extensive and uncomfortable, so I routinely treat it with
Cipro. 500 mgm BIDX1 week.
Pyodermas:
These are far and away the commonest
types
of skin infections I see on dive trips, not only in divers, but also in
the indigenous population.
a) Impetigo, the
most superficial of these infections, is usually caused by a gram +,
pencillin-resistant
staph. aureus, rather than beta-hemolytic strep., though occasionally
there
is a mixed infection. So here in the USA , I usually treat with
cephalexin
or dicloxacillin. In some of the less developed countries, where
antibiotics
are few and far between, almost any drug active against gram+ organisms
seems to work well. In Yap recently, I incised an axillary abscess in
one
of the dive guides and gave him some Keflex with
instructions to get more at the hospital
pharmacy. He ended up with Tegopen (cloxacillin) 500 mgm Q6H, the
poorly
absorbed predecessor to diclox.
b) Furuncles,
usually
due to staph., resemble small abscesses involving hair follicles,
usually
on the face or neck. If large enough, they should be incised and
drained,
as well as treated with antibiotics
c) Ecthyma is a
deeper
infection extending down into the subcutis and having draining sinuses.
Certainly a more severe infection and again usually due to staph.
aureus.
This needs to be treated aggressively to prevent a rapidly-developing
cellulitis
and possible bacteremia.
d) Cellulitis/erysipelas
is usually due to beta-hemolytic strep. and therefore can be treated
with
penicillin, but obtaining a culture is difficult. It often starts from
a small break or fissure in the skin. “Skip cellulitis”, of the lower
leg
is due to fissures between the toes from tinea pedis, serving as a
portal
of entry for the strep.
e) Abscess formation is
also
usually due to staph. This problem should be treated with surgical
drainage as well as cephalexin or dicloxacillin.
f) Pseudomonas otitis
externa.
This is a real mess that could have been prevented by prophylactic use
of Domeboro Otic after each dive. Be sure that the diver hasn’t been
using
Cortisporin Otic, which contains neomycin. I’ve seen allergic contact
dermatitis
to Neomycin with secondary infection look this bad. Treatment is
Domeboro
soaks and Cipro.
g) Some miscellaneous
skin
infections due to organisms peculiar to the ocean or aquatic
environment:
aeromonas hydrophilica, vibrio vulnificans, protothecosis, and
mycobacterium
marinum (swimming pool/fish tank granuloma).
Vibrio Vulnificus
is typically present in warm salt water. It can infect shellfish and,
when
ingested, can cause gastroenteritis or bacteremia in people with
hepatic
cirrhosis. It’s also an opportunistic infection that, after trauma to
the
skin, can result in a severe form of cellulitis.
Aeromonas hydrophilica is
present
in fresh or brackish waters. It’s a gas producing organism and
can cause cellultis with crepitus.
Both can cause cellulitis with bullae,
necrotic ulcers, and deeper soft tissue involvement, which can lead to
gram-negative sepsis.
Treatment consists of Cipro.
M. Marinum is an
acid-fast bacillus that can be identified by an AFB stain
on
biopsy. A good history and exam doesn’t hurt either. Treatment consists
of minocycline 100mgm BIDX30 Days or more.
Herpes Simplex Virus
(HSV)
I and II: are frequently activated by sun exposure, colds,
stress, and who knows what else? These outbreaks can certainly make
your
trip miserable for a few days. If you’re susceptible to them, use chap
stick with a sun screen, although lipstick and zinc oxide work better
because
they stay on the skin. It’s also wise to carry a supply of Valtrex,
Famvir,
or Zovirax along with you on all trips. Start taking the drug at the
first
sign that you are developing an HSV outbreak
Insect bites:
Fleas,
mosquitoes, chiggers, bedbugs, no-see-ums, ticks, pediculosis, scabies,
biting flies, etc., are found all over the world and remain as a
constant
reminder that humanity does not always control Mother Nature. Aside
from
the rather dramatic bullous and hemorrhagic variants seen
particularly in children, they serve as
the vector for many unpleasant diseases.
Insect repellents, long sleeves, no
perfumes,
etc., all help but there is no way that you can completely escape. Most
bites cause some itching, which is self-limited. A good topical steroid
can help for the day or two it takes to resolve. Extensive bites can be
treated with prednisone.
Creeping Eruption:
This
is caused by the larvae of the dog/cat hookworm (ancyclostoma sp.)
that can’t complete its life cycle in humans.It’s endemic in certain
parts
of Florida. The message here is to wear sandals at all times and don’t
step in the shit.
Treatment consists of topical or oral
thiabendazol, a broad-spectrum
anti-helminthic.
Miliaria (prickly
heat):
This is due to eccrine sweat gland occlusion. It used to be a common
problem
in the tropics before the advent of widespread air conditioning.
Rupture
of the sweat gland at different levels creates the different clinical
presentations:
superficial leads to miliaria crystallina, deeper leads to more
inflammatory
lesions, miliaria rubra.
Treatment consists of moving the person
into a cool environment and possibly topical steroids.This condition is
mainly seen nowadays in infants whose parents overdress them for bed.
Cnidarians:
a) Phillipines box jellyfish-cubozoan
envenomation. During his tour of duty there, Dr. Reed reports
that
two children died from contact with this jellyfish while wading. Its
related
to the Australian box jellyfish, Chironex fleckeri, but usually not as
lethal. No anti venom is available.
b) Sea bathers eruption: caused by the
larvae of the thimble jellyfish (linuche unguiculata). This patient of
mine had been snorkeling off the Cozumel coast. Note the typical
distribution
under her bathing suit. It
consists of severely pruritic,
urticarial
papules. It’s also endemic off the coast of Florida.
Treatment is the same for all hydroid
stings: spraying the affected area(s) with alcohol or vinegar and
avoidance
of fresh water or trauma to the areas till the nematocysts have been
inactivated.
Dr. Auerbach has obliquely referred
to
this in several articles, but I want to emphasize that a delayed
hypersensitivity,
contact dermatitis, poison oak/ivy type of allergic reaction COMMONLY
develops
after exposure. If it’s the first time, it may take several days. If
it’s
a subsequent exposure, after you’ve been sensitized, this eczematous,
severely
pruritic reaction may appear within hours. At this point, treatment
usually
requires systemic steroids in the dose previously recommended.
Bruce Miller, MD
Dr. Miller, a
Dermatologist,
is a Consultant for Diving Medicine Online. This is a lecture presented
to Medical Seminars, 2000
DOWNLOAD
THIS ARTICLE in zip format
DOWNLOAD
in PDF format Requires Free
Download
A brief review of the
physics
and photobiology of ultraviolet radiation (UVR):
Transformation of H to He in sun’s
interior
liberates vast amounts of energy which reaches the earth’s surface in
the
form of electromagnetic radiation (EMR) : x-rays, cosmic rays, electric
waves, radio waves, infrared, visible light, and ultraviolet radiation
(UVR).
EMR travels in the form of waves
containing
packets of energy called photons. In the case of x-rays and cosmic
rays,
the wavelengths are very short, measuring only a few nanometers(nm):1
nanometer
= 1 billionth of a meter. On the other hand radio waves are very long,
measuring several kilometers (km):
1 km=1000 meters. The amount of energy
contained in EMR is inversely proportional to its wavelength. The
ozonosphere
blocks all EMR shorter than 297 nm (thank goodness!).
UVA vs. UVB-what’s
the difference
and why it’s important:
UVR includes wavelengths of EMR
between
297-400 nm. Convention divides this spectrum into UVB = 297-320 and UVA
= 320-400. UVA may be further divided into UVA II = 320-340 and
UVA
I = 340-400. UVB is also known as the “sunburn spectrum” and is the
prime
factor in photo aging and photocarcinogenesis. UVA also contributes to
photo trauma but is the spectrum primarily responsible
for photosensitivity reactions because
of its deeper penetration into the skin.
UVB only penetrates into the epidermis
and the papillary (uppermost) dermis and is blocked by window glass.
UVA
penetrates into the reticular (deep) dermis and passes through window
glass
unchanged. Unlike UVB these rays don’t vary in intensity with the time
of day or the season. Compared to UVB, 100 times as many reach the
surface
of the earth.
Ozone depletion due to fluorocarbons
found
in aerosols, auto air conditioners, refrigerators, etc., pose a
significant
threat to us all in the form of an increased incidence of melanomas and
other skin cancers, depressed immunity, accelerated aging, etc., due to
high energy particles and increased UVR reaching the earth’s surface.
Under photosensitivity diseases, we
will
cover phototoxic and photoallergic systemic photoeruptions (mainly
drugs),
phototoxic and photoallergic contact dermatoses (mainly plants and
perfumes),
nature’s phototoxic diseases (the porphyrias), and a common photo
eruption
of unknown etiology, polymorphous
light eruption (PMLE).
Photoxic vs.
Photoallergic:
Fundamental to both is the absorption
of
photons of light by a chromophore. However, once this event occurs, the
mechanisms leading to cellular damage diverge.
In phototoxic reactions the
photosensitivity
is mediated by non-immunologic mechanisms. Absorption of photons of a
specific
wavelength (UVA in nearly all cases) by the photosensitizing
chromophore
results in electrons changing their orbits and creating unstable
singlet
or triplet states, which release
energy when the molecule returns to a
stable ground state. This energy causes cellular damage and the release
of products of inflammation, as well as free radicals, causing
cellular
damage and resultant erythema, edema, and occasionally vesiculation,
i.e.,
an exaggerated sunburn reaction, which is restricted to sun-exposed
areas.
This reaction can occur upon first exposure to the drug.These
chromophores
are typically polycyclic ring structures withalternating single and
double
bonds, and fluorination at critical sites onthe molecule. The
fluoroquinolones
are typical examples, as are the porphyrins. Apart from sunburn,
phototoxic
drug eruptions are the commonest photosensitivity reactions.
In photoallergic reactions, following
absorption
of the specific photons, a new compound is formed, which acts as a
haptene.
This molecule then combines with a protein to form a complete antigen,
which possesses immunologic properties. The mechanism of the host
response
is then similar to other forms
of delayed hypersensitivity and is
mediated
by T-lymphocytes. Morphologically, this response presents as an
eczematous
eruption, and while it may start in sun exposed areas, it may spread to
non-sun exposed parts of the body. These reactions are relatively
unusual
and require at least one prior exposure to the drug
Diseases such as discoid and systemic
lupus, PMLE, solar urticaria, and dermatomyositis may also fall into
this
category, although their morphologies vary widely.
List of drugs that
may cause
photosensitivity reactions
Sparfloxacin (Zagam) photox. as a
prototype.
Phototoxic reactions:
promethazine
HCTZ
tetracycline photox. eruption, photo
-onycholysis,
vesicles
PUVA photo-onycholysis
Tegritol
Thorazine
Photoallergic
reactions:
Thorazine
Lomotil (erythema multiforme)
Tetracycline (lichenoid)
Thorazine
PMLE (?)
Porphyria Cutanea
Tarda (PCT)
and Erythropoetic Protoporphyria (EPP):
These photoxic diseases are caused by
an
increased concentration of porphyrins in the blood. Porphyrins are
pyrimidines
arranged in a ring-shaped structure with alternating double bonds and
are
derived from the metabolic breakdown of old RBC’s. Due to enzymatic
defects,which
are probably hereditary in both types, porphyrins build up in the
bloodstream
and act as chromophores, absorbing UVA and causing cellular damage by
energy
transfer. Which type of porphyria develops depends on the specific
defect.
PCT causes elevated porphyrin levels in the serum. EPP causes elevated
levels within the
RBC’s.
Photocontact
dermatoses:
Phototoxic:
Usually caused by plants containing
furocoumarins
(psoralens) and called “phytophotodermatoses”. Also seen with perfumes
and colognes containing oil of bergamot -”berlock dermatitis”. Shalimar
perfume was a prime example. These phototoxic reactions are typically
blistering
and leave a brownish hyperpigmentation in their wake
Plants which can cause this are
parsnips,
fennel, dill, parsley, masterwort, celery, coriander, common rue, gas
plant,
bergamot, lime and other citrus, buttercup, mustard, blindweed,
agrimony,
yarrow, meadow grass, S. John’s wort, buckwheat, and ragweed. They all
contain furocoumarins. We’ve
frequently seen this in celery pickers
here in Oregon.
Photoallergic:
These reactions are now rare since
halogenated
salicylanilides were removed as antibacterial agents from soaps, and
people
learned to stop handling phenothiazine drugs.
PHOTO PROTECTION:
Review of the ideal characteristics
of
a sunscreen reveals that while there are many excellent products on the
market, they are primarily effective against UVB. Protection
against
UVA from 350-400nm has yet to be achieved, despite claims to the
contrary.
“The physical agents we tested provided
only weak UVA protection in both the shorter (320-340) and the longer
(340-400)
UVA ranges. Dibenzoylmethane derivatives (eg., parsol 1789) are much
more
efficient in the shorter but not in the longer UVA ranges. The best UVA
protection over the entire UVA range is, without doubt, provided by the
combination of real UVA filters (eg., benzophenones, parsol 1789,
eusolex
6300 and 8020, lawsone with dihydroxy acetone, diphenylacrylate, methyl
anthranilate, and octocrylene) and physical agents (eg., titanium
dioxide,
red petrolatum, talc, kaolin, and zinc oxide). The protection afforded
by this combination also appears to be cumulative.”
Roelandts R. Which components in
broad-spectrum
sunscreens are most necessary for adequate UVA protection? J Am Acad
Dermatol
1991;25:999-1004.
In a broad-spectrum sunscreen, the
UVA
filters are combined in varying combinations with UVB absorbing
chemicals:
PABA and its esters, methoxycinnamates, homosalate, salicylate,
sulfonic
acid, digalloyl trioleate, diphenyl acrylate, and lawson with
dihydroxyacetone.
Sun Protection Factor
(SPF).
If your burn time (MED=minimal erythema dose, defined as the minimum
amount
of energy required to produce a uniform, clearly demarcated erythema
response
at 24 hours) without a sunscreen is 10 minutes, then a SPF of 15 will
extend
your MED to 150 minutes. This does NOT mean you can stay out in the sun
all day. A SPF of 15 should be the absolute minimum level of
protection,
and we recommend higher numbers. The SPF only measures protection
against UVB. There is no analogous number available for UVA protection.
However, you should always use a “broad-spectrum” , UVA-UVB sunscreen
that
is labeled as WATERPROOF, not water resistant.
There are two new UVA filters :
Parsol
1789, aka “Avobenzone”, a dibenzoylmethane derivative, and octocrylene.
We are currently doing a study for
Galderma/L’Oreal
in PMLE using a combination sunscreen with two UVB and two UVA filters.
Mexoryl is the investigational UVA filter.
Photoprotective clothing is the only
sure
way to block the longer wavelengths.
For a catalog, write to:
Sun Precautions
2815 Wetmore Ave.
Everett, WA 98210
REFERENCES:
1. Gonzalez E, Gonzalez S. Drug
photosensitivity,
idiopathic photodermatoses,
and sunscreens.. J Am Acad Dermatol
1996;35:871-885.
2. Gould J, Mercurio M, Elmets C.
Cutaneous
photosensitivity diseases induced
by exogenous agents. J Am Acad Dermatol
1995;33:551-571.
3. Miller, B Sunning-and still having
fun.
Alert Diver 1996;Nov-Dec:37-39.
QUESTIONS:
1. Electomagnetic radiation below 297
nm does not reach the earth’s surface
due to:
a) smog
b) clouds
c) the Van Allen belt
d) the ozonosphere
e) rap music
2. The following drugs have been
associated
with photoeruptions:
a) penicillin
b) cephalosporins
c) amiodarone
d) fluoroquinolones
e) tetracycline
3. Phototoxic drug reactions most
resemble:
a) eczematous dermatitis
b) hives
c) an exaggerated sunburn
d) psoriasis
e) none of the above
Answers:
1. c
2. c, d, e
3. c
SUNLIGHT,
SKIN CANCER AND AGING
PHOTODAMAGE,
PHOTOPROTECTION AND SUNSCREENS
|
Bruce H.
Miller,
M.D.
* Lecture presented
Bruce
Miller, MD, Medical Seminars, Palau, 1996
Download
this Article in zip format
DOWNLOAD
in pdf format Requires Free
Download
Humanity evolved on earth, bathed in
solar
radiation from our star, the sun. The nuclear reactions in its
interior
transform hydrogen atoms into helium, liberating vast amounts of energy
in the process. This energy reaches the earth in the form of
electromagnetic
radiation (EMR) and includes x-rays, cosmic rays, electric waves, radio
waves, infrared, visible light and ultraviolet radiation (UVR).
Without
the effects of EMR on the earth's surface, life itself could not have
begun,
and our planet may have been covered by oceans of liquid nitrogen and
enveloped
in an atmosphere of methane. Sunlight also plays a crucial role
in
a wide range of photobiological processes, touching all forms of life
on
earth. However, under certain circumstances, the same sunlight
that
has given us life can also cause significant morbidity in the form of
sunburns,
drug reactions, exacerbation of photosensitive diseases and
photoaging.
In addition, recurrent episodes of phototrauma over a lifetime can lead
to the development of skin cancers.
Current scientific thinking holds
that
EMR travels in the form of waves that contain packets of energy called
photons. These wavelengths can be very short, measuring only a
few
manometers (a manometer, NM = I billionth of a meter) in the case of
cosmic
and x-rays or very long, measuring several kilometers (kilometer = 1000
meters), in the case of radio waves. The shorter the wave length,
the more energy the EMR contains.
The wave lengths that concern us lie
in
the ultraviolet range, specifically ultraviolet B (UVB) from 290 - 320
NM, and ultraviolet A (UVA) from 320 - 400 NM. Fortunately for
us,
the ozone layer in our atmosphere, the ozonosphere, blocks all EMR
below
290 NM so these high energy particles can't reach the earth's
surface.
For many years photobiologists and sunscreen manufacturers have
concentrated
on UVB, also known as the "sunburn spectrum". Recently,
increasing
attention has focused on UVA, also known as "long wave UV", and its
additive
role in photodamage when combined with UVB. UVA also seems to be
primarily responsible for causing photodrug eruptions and exacerbating
photosensitivity in diseases. In recognition of this increasing
awareness,
many sunscreens now contain UVA blockers.
The ability of a sunscreen to protect
the
user from UVB is defined as its Sun Protection Factor (SPF). The
SPF is the ratio between the time it usually takes your skin to sunburn
and how long it takes if you've applied that sunscreen. For
example,
an SPF of 15 will provide 15 times the amount of protection you'd get
without
using anything. Thus, if 10 minutes in the sun is enough to turn
you red, your sunscreen would allow you to stay out for 150 minutes
before
burning. An SPF of 15 filters approximately 92% of the sunburning
rays. For UVA the degree of protection is defined as the
Phototoxic
Protective Factor (PPF). These values are much lower, ranging
from
1.5 - 4.8, because the energy contained in UVA is so much less.
PPF's
have yet to make it out of the laboratory.
How should you select your
sunscreen?
Divers should use sunscreens that are water proof, broad spectrum
(UVA/UVB)
screens, and that have an SPF of at least 15. Next, you should
determine
your skin type (Table 1). Then you need to take into account such
environmental factors as time of year, geographical location, altitude,
reflecting surfaces, time of day, air pollution, water immersion,
proximity
to the equator, clothing (or lack thereof), and exposure time.
Now you need to think about
protection
from UVA as well. Are you taking or contacting any of the
medications
or substances in Table 2? Do you have any of the diseases listed in
Table
3 that are aggravated by sun exposure, If so, you need an effective UVA
sunscreen as well!
Why should you use a sunscreen?
Isn't
a tan "healthy"? Prolonged and repetitive sun exposure causes
phototrauma
(sunburn and cellular damage) which, over a period of time, causes
photodamage:
coarse wrinkling, mottled hyperpigmentation ("age" or "liver" spots),
roughness,
sagging, yellowing, broken blood vessels, and skin fragility. In
addition, prolonged sun exposure causes skin cancers: basal cell
carcinomas,
squamous cell carcinomas and melanomas (malignant moles). In
1990,
over 600,000 new cases of skin cancer were diagnosed, afflicting more
people
than all other cancers combined. Of this group, there were 8,800
deaths, 6,300 from melanoma and 2,500 from squamous cell
carcinomas.
The incidence- of melanoma is doubling every decade! By the year
2000, it is estimated that one in every 90 people will develop a
melanoma,
if our UVR exposure patterns remain unchanged. What can you do to
prevent these undesirable side effects from sun exposure? Follow
these guidelines:
1. Avoid sun exposure from 10:00 a.m.
to
3:00 p.m.
2. Beware of cloudy days and
reflecting
surfaces: snow,, water, sand and concrete. YOU CAN STILL BURN.
3. Wear tightly knit, dry clothing
and
a hat. Wearing sun-protective clothing is a good idea.('Solumbra').
4. Ban chlorofluorocarbons!
These
compounds are destroying the ozonosphere and permitting more UVB to
reach
the earth's surface.
5. Stay away from tanning beds.
6. Stop all elective photosensitizing
medications
while on vacation (e.g. Tetracycline and Retin-A for acne). If
you're
unable to stop your medications, use the most effective UVA blocker
available
currently "Parsol 1789" (Butylmethoxydibenzoyl methane). People with
photosensitivity
diseases should follow the previous recommendations and avoid UVR
exposure,
if at all possible. They should use a screen of the highest SPF that
also
contains Titanium dioxide, a physical screen.
8. Regularly apply a sunscreen that
you
find cosmetically acceptable and will prevent you from sunburning
whatever
your skin type and wherever you are. Preferably this sunscreen
will
resist washing off and will contain a UVB blocker with an SPF of at
least
15 and a UVA blocker with a PPF of at least 1.5 (benzophenones) to 4.8
(Parsol 1789). You can tan through your sunscreen, and stay young
and beautiful.
Table I
| Skin Type |
Sensitivity to the Sun |
Risk of Skin Type |
Photodamage |
| Type 1 |
Always burns easily |
High |
never tans |
| Type 2 |
Always burns easily |
High |
tans minimally |
| Type 3 |
Burns moderately |
Moderate |
tans gradually and uniformly
(light brown) |
| Type 4 |
Burns minimally |
Moderate |
tans well (moderate) |
| Type 5 |
Rarely burns |
Low |
tans profusely (dark brown) |
| Type 6 |
Never burns |
Low |
deeply pigmented (black) |
Table 2.
|
Drugs |
1. Tetracyclines
Declomycin Vibramycin
2. Thiazide Diuretics:
Diuril,
Hydrodiuril,,
Hygroton,
Dyazide,
etc.
3. Hypoglycemic agents
(Antidiabetics)
4. Sulfonamides
5. Phenothiazines:
Phenergan,
Thorazine,
Stelazine,
Compazine,
etc.
6. Nalidixic Acid
7. Quinidine and Quinine
S. Lomotil
9. Griseofulvin
10. Psoralens |
| Topical
Photosensitizers: |
1. Oil of Bergamot - perfumes,
cologne
2. Deodorant soaps
3. Plants - figs, lines, celery,
parsnips |
Table 3.
|
Photosensitivity Diseases
|
1. Herpes Simplex
2. Porphyrias:
Erythropoietic Proto-porphyria,
Porphyria Cutanea Tarda
3. Discoid and Systemic
Lupus Erythematosus
4. Polymorphous Light Eruption
5. Xeroderma Pigrnentosa
6. Solar Urticaria
7. Dermatomyositis
8.
Actinic Reticuloid
|
