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Dr. Ted’s Blog

A Snapshot of ADHD in the US

Denise Mann
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.

CINCINNATI, Sept.4 — Almost 9% of U.S. children ages 8 to 15 meet standard diagnostic criteria for attention-deficit/hyperactivity disorder (ADHD), but less than half of them receive treatment.
Only 47.9% of the 2.4 million who met Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for ADHD had reportedly had their conditions diagnosed by a health care professional or been treated with medication, according to a report in the September issue of the Archives of Pediatrics & Adolescent Medicine.
A research team led by Tanya E. Froehlich, M.D., of Cincinnati Children’s Hospital Medical Center did a cross-sectional phone survey of the parents or caregivers of 3,082 eight- to 15-year old children who were participants in the National Health and Nutrition Examination Survey.
Survey respondents provided information about each child’s ADHD symptoms between 2001 and 2004. They also provided sociodemographic information and information about whether the child had ever been diagnosed with ADHD or taken medicine to treat the disorder.
The researchers found that 8.7% (95% CI; 7.3%-10.1%) met the DSM-IV criteria for ADHD in the year before the survey took place. An additional 3.3% of children did not meet the criteria, but had a parent-reported prior diagnosis and had been treated with an ADHD medication at some point during the previous year. The latter group, however, was not included in the main analysis.
More boys than girls met the diagnostic criteria for ADHD, 11.8% versus 5.4%, respectively (P<0.001), but girls were less likely than boys to have had the disorder recognized.
There were also discrepancies in ADHD rates by race and ethnicity. Non-Hispanic white children were more likely to meet criteria for ADHD than were Mexican-American children or children of other races/ethnicities, the study showed. These findings held in both bivariate and multivariate analyses.
The study authors could not explain why Mexican-American children had lower rates of ADHD, but they speculate that this may be related to “differences in the prevalence of causal risk factors, genetic susceptibility, and/or rates of reporting ADHD symptoms across cultures.”
Of the children who met the diagnostic criteria for ADHD, 38.8% had received medication to treat inattention, hyperactivity, or overactivity in the prior year and 32.0% had been taking medication for most of that year.
Regular medication use was more likely to be reported for older children than younger ones, the study showed.
Money also mattered in the new study. Children in the poorest quintile were more likely than those in the wealthiest quintile to have been diagnosed with ADHD (adjusted odds ratio [AOR] for PIR, first quintile vs fifth quintile, 2.3; 95% CI, 1.4-3.9)).
“Reasons for the increased likelihood of ADHD in poorer children may include the elevated prevalence of ADHD risk factors (i.e., premature birth and in utero or childhood exposures to toxic substances) in this group,” the study authors write.
“In addition, given the high heritability of ADHD and its negative impact on social, academic and career outcomes, it is plausible that families with ADHD may cluster within the lower socioeconomic strata.”
Although poor children were more likely to have ADHD, the poorest children were three to five times less likely to consistently receive medication when compared with their counterparts in other income groups, the researchers noted.
This finding “warrants further investigation and possible intervention to ensure that all children with ADHD have equitable access to treatment when appropriate,” the authors conclude.
The researchers also analyzed ADHD by subtypes. Specifically, 4.4% of the children met the criteria for ADHD-1A, 2.2% for ADHD-CT and 3.0% for ADHD-HI.
The poorest children were more likely to have ADHD-HI than their wealthier counterparts (AOR for PIR, first vs fifth quintile, 3.1; 95% CI, 1.2-8.3
In addition, African Americans and Mexican Americans were less likely to have ADHD-1A, compared to their non-Hispanic white counterparts, the study showed.

Allergies and "Allergic Shiners"

Hi Again,

I was also asked by Jennifer, one of our Moms here at Meyer Pediatrics, about allergic shiners, those dark and puffy circles under kid’s eyes that are often mistakenly thought to be due to lack of sleep. The’re not related to sleep at all. They are a sign of allergies, as are the creases under the eyes called Denny’s Lines and the raised pink bumps on the back wall of the throat called cobblestoning. If one parent has allergies, each child has about a 50% chance of having allergies (although what your child is allergic to is NOT inherited; that they have to do for themselves. Just because you are allergic to penicillin does not mean that your child is, or even ever will be). If both parents have allergies, then each child has about a 75% chance of having allergies.

I’m often asked when, or even if, a child should be tested for allergies. My short answer is that I would go through the relative trauma of skin testing (far more accurate than blood testing) only if the child’s life is being changed by the allergies. If they can’t go to a friends house because the friend has a dog, that may be a good reason to investigate.

There won’t be just one or 2 things that your child is allergic to and therefore you could just avoid. It likely will be a dozen or more things. In most cases, you could just treat the allergies and skip the whole testing phase. Obviously, if you think that your child has had a serious reaction to something, or perhaps may even have had a potentially fatal reaction to something such as having had difficulty breathing after eating shellfish, then of course you would want to have this checked by an allergist so that you can know for sure.

It depends on the child, but I often find that for kids with significant allergies it usually takes a combination of Singulair (a prescription medication for airway inflammation) plus an allergy nasal spray such as Omnaris or Nasonex or Nasocort, plus a once-a-day, non-sedating antihistamine (such as Allegra or Clarinex) to control the allergy symptoms well. One or two of those medications just doesn’t seem to work as well, in my experience.

I know that most parents don’t like the idea of their children taking mutliple medications, and I do prefer just letting the child live with mild symptoms, but if we’ve made the decision to treat allergies with medication, I think we might as well do it the right way. Go for the win.

As a preventative, Singulair once a day can often be used as a maintenance plan during the time of year when your child is most symptomatic, with antihistamines used on an “as needed” basis. When your child is fully symptomatic, however, you’re going to want to do everything, or nothing at all, in my opinion.

I hope that this little overview answered some of your questions about allergies. If not, or if there are other topics that you’d like to see me address, write me here at Dr. Ted’s Blog and I’ll try to get something written as soon as possible.

Does Your Four Year Old Still Wet the Bed?

I was asked about this in one of the comments, and I found that it is difficult to find my answer unless you already know where to look. So, I’m repeating myself here as a post to make it easier for everyone to find this information. We just started this blog about a month ago, and I’m still playing around with it to see how it all works. Below is my answer to Jennifer, one of our Moms here at Meyer Pediatrics who asked me about children who are late to get dry at night (and have never been dry before).

OK, at age 4, about 80% of all kids are dry at night. Those that aren’t are the “late” group, and they will slowly become dry over the next 10 or so years, at the rate of about 10% per year. SO, at 5 years old, about 90% of them are still wetting, and at 6 about 80% and so on. It’s NOT laziness or anything like that. It’s because, for reasons unknown to me, these kids are slow to get the night-time rise in a hormone called ADH (Anti-Diuretic Hormone, which is naturally secreted by our brains) that those of us who stay dry get. Ultimately, just about all of them WILL get this night-time surge and they will become dry.

There ARE rare other causes of night-time wetting (and I am ONLY describing kids who have ALWAYS wet the bed here, not kids who WERE dry and then started wetting later). At any rate, these kids should have a good physical exam one time to be sure that there is nothing else causing the enuresis (the medical term for night-time wetting) as there are several treatments available, at least for sporadic use, such as when your child wants to have a spend-the-night party without others finding out. In these cases, there is a prescription medication called DDAVP that is a chewable pill taken before bedtime that in over 80% of cases is successfully able to keep a child dry for that night.

Therefore, to answer your question, I would recommend the pullups until they aren’t needed anymore, whatever age that might happen to be. My patient who was the latest to get permanently dry was about 16 or 17. For the routine changeover from pull-ups to underwear, “big kid” underwear should be a reward, NOT an inducement. They should only be allowed to wear “big girl panties” when they can go a whole week without wetting.

Potty Training

Hi,

I was asked by Jennifer, one of our Moms, about potty training. Since I get asked about that a lot, I thought it made a good topic for a post. I often tell parents who ask that there are basically two ways to potty train a child; the slow and easy way or the fast but difficult way.

The slow but easy way is to wait until your child shows an interest in wearing “big kid underwear.” These should be a REWARD for staying dry, NOT an inducement to get dry, which does NOT work. The only downside of this approach is that the motivation for the kids to stop wearing pullups is being teased by their friends (“you’re a little baby wearing diapers”) which is obviously painful and embarrassing to your child.

The fast but difficult way involves removing yourself from the diaper equation. A child over 3 years of age is perfectly capable of being dry at night. They are choosing to be in diapers or pullups because it’s the “hot line” to Mommy. They can commandeer your time and attention simply by saying, “I gotta go NOW.” SO, to force the issue, tell the child that you no longer do diapers (as long as they at least 3 years old) and that you will only help them if they go on the potty. This ONLY works, by the way, if you NEVER cave in and help them with pullups. Say to the child, “Here are the pullups, here’s the toilet paper, here’s where the dirty diapers go. Knock yourself out, but don’t call me for ANY help unless you want to go on the potty. I don’t do diapers now that you are three. I only will come help if you go on the potty.”

This works because the child is not attached to the pullups so much as attached to you and using the pullups to command your time and attention. From a young child’s perspective, NO ONE has EVER had enough attention, no matter how much they really get (and believe me, my patients typically get attention by the boat load). When forced to choose between you and diapers, a child will ALWAYS choose you, once they become convinced that you really mean it.

They will, of course, test you to see if you really mean it, but if you don’t cave, they likely will voluntarily switch over to “big boy underwear” within a day or so. I promise that this works IF you stick to your guns! Good luck!

Seasonal Flu shot for ages 3 years and older have arrived!

We have recieved the Seasonal Flu shots for ages 3 years and older. If you want to have your child recieve this vaccine please call the office to schedule an appointment. We also still have H1N1 (Swine Flu) vaccines available for ages 6 months and up. It is recommended that children recieve both the Seasonal and H1N1 vaccines.

Thanksgiving Holiday Hours

Meyer Pediatrics will be closed on Thursday, November 26th and Friday, November 27th. We will reopen at 8.30a.m. Saturday, November 28th. We are always available 24 hours a day by phone/answering service. I hope everyone enjoys the Thanksgiving Holiday!

Update for Patients with Cigna Insurance

Please note patients, if you have Cigna insurance you are required to have your laboratory tests sent to Lab Corp, Cigna’s preferred vendor. Labs included are Rapid Strep, Rapid Influenza A, Rapid Influenza B. However, you may choose to have the tests in our office with immediate results if you elect to self pay for the services. Rapid Strep is $25.00, Influenza A & B are $20.00 each.

Contact Dermatitis: More Than You Ever Wanted to Know

Contact dermatitis is simply inflammation that results from the interaction of skin and an external substance (even water) that comes in contact with it. It is an altered state of skin reactivity induced by exposure to an external agent. For the vast majority of people, these substances are harmless. “Eczema” and “dermatitis” are often used synonymously to denote a polymorphic pattern of inflammation of the skin. In all cases the lesions of contact dermatitis are primarily confined to the site of contact. Contact dermatitis can look – and itch – very much like eczema. It usually presents as a rash of tiny blisters, inflamed reddened skin, sometimes dry, or sometimes moist and oozing.

Contact dermatitis is produced through one of two major pathways: irritant or allergic.
Irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) are two of the most common dermatologic conditions in industrialized societies, with a prevalence of up to 10%. The two conditions are clinically indistinguishable and often both conditions co-exist. Many of the allergens causing ACD are also irritants.
Irritant contact dermatitis predominates, accounting for 80% of all cases of contact dermatitis. ICD is a non-immunologic skin reaction that does not involve immune system sensitization (previous exposure to the allergen). It can occur in all members of the population depending on the “irritancy” of the chemical, the duration of contact and individual susceptibility. Atopics (who invariably have dry skin) are more prone to irritant dermatitis. Water is one of the most common irritants; therefore atopics who do a lot of wet work will often get irritant hand dermatitis. Another reason atopics get irritant dermatitis is that the skin gets injured from chronic scratching, allowing the otherwise harmless chemicals in cosmetics to enter the skin. The most common skin irritants include acids, alkalis, detergents, and solvents that disrupt the barrier function of the skin. Common cosmetics / skin care products causing skin irritation include:

• Bath soaps & shampoos
• Eye shadow & mascara
• Make-up removers,
• Antiperspirants,
• Permanent hair-waving solutions.
• Water present in cosmetics and skin care products is the most common irritant to very dry skin.
Irritant contact dermatitis is a risk factor for allergic contact dermatitis, as the penetration of contact allergens is enhanced when the skin barrier function is disturbed.

Allergic contact dermatitis (ACD), on the other hand, is an immunologic skin reaction that occurs in a genetically predisposed individual. The allergic response occurs only when a person’s immune system is sensitized to the allergen. The more contact the individual has with the allergen the greater the risk of sensitization. In sensitized individuals, allergic contact dermatitis appears or is exacerbated 24 to 96 hours after contact with the causative allergen. ACD is usually accompanied by intense itching. The edges of the lesions are usually well demarcated, but unlike irritant dermatitis it may propagate beyond the site of contact. This reaction is also known as delayed hypersensitivity reaction, since the rash usually develops more than 12 hours after contact with the allergen. The reaction usually peaks about 48 hours after exposure. The number of chemicals known to be capable of causing ACD is said to be near 3000 and constantly increasing.

Site of the skin reaction is usually the face especially around the eyes. In one study allergic contact dermatitis was found to be the cause in 74% of patients with eyelid dermatitis. In Saudi Arabia it is well known that men with dermatitis in the beard have an allergy to permanent hair dyes.
Common allergens in cosmetics and skin care products that cause contact dermatitis
Current reviews demonstrate that the most frequent allergenic groups causing cosmetic allergy are fragrances, preservatives, and paraphenylenediamine (PPD) found in permanent hair dyes.

Fragrance
The commonest allergen causing ACD is fragrance. More than 5000 different fragrances are used in cosmetics and skin care products. Seventy to eighty percent of fragrance allergy can be picked up by patch testing with Balsam of Peru and Fragrance Mix (which contains 8 common fragrances). Fragrance can also cause increased pigmentation of the affected skin, photodermatitis, or contact urticaria.
It is important to know that “unscented” does not mean “fragrance-free”. Some unscented products might contain a fragrance to mask other chemical odours. To indicate that no fragrance is added to a product it must be marked “fragrance-free” or “without perfume”.
In 1989, less than 10% of the patients patch tested in a multicentre project in Germany reacted to the fragrance mix (a mixture of 8 important fragrances). Between 1990 and 1994, a steady increase in the percentage of sensitizations diagnosed to more than 13% was noted (4).

Screening for Fragrance Allergy:
These are the fragrances tested in a standard patch test battery:
• Balsam of Peru
• Fragrance Mix:
1. Oak Moss
2. Cinnamic aldehyde
3. Cinnamic alcohol
4. Alpha amyl cinnamic alcohol
5. Geraniol
6. Hydroxycitronellal
7. Isoeugenol &
8. Eugenol

• Musk Ambrette and Moskene
In a worldwide multicenter investigation on fragrance contact dermatitis, reaction to fragrance mix occurred in 78% of patients patch tested
Balsam of Peru
Balsam of Peru (BP) is usually included in the standard screening patch-test series as an indicator of fragrance sensitivity. It is positive in 50% of cases of fragrance allergy. BP is a naturally occurring substance, obtained from fir trees. It is composed of many allergens including benzyl acetate, benzoyl alcohol, cinnamic acid, cinnamic alcohol, cinnamic aldehyde, eugenol, and isoeugenol.

Paraphenylenediamine (PPD) Hair dye Allergy
This is the most important dye used for permanent (oxidation) hair colouring and is the third most common ingredient after fragrances & preservatives that cause contact dermatitis from cosmetics. Permanent hair dyes are more sensitizing compared to other types of hair dye.
In most cases the reaction to the dye is itching of the scalp and some redness, but nothing more. These individuals might just think they have a bit of dandruff. In more severe cases the hair dye may trigger scaly skin & pain. The distribution of the affected skin can vary and may not match the exact area to which the dye was applied. In more severe cases there can be swelling around the eyes and scaly skin on the ears, face & neck. Sensitization to hair dye may gradually develop with repeated exposure.
In some European countries, PPD was banned because it was thought to be too hazardous. The regulations of the EEC, however, have allowed up to 6% PPD in hair dyes.
In the consumer, PPD produces acute dermatitis that involves the scalp, eyelids, face, and hairline and may extend to include the neck & upper portion of the trunk, but may spread to involve the whole body. In the hairdresser the most common region affected is the hand, but other exposed areas like the arms & face may be affected. Once the dye becomes fully oxidized it is no longer allergenic; thus dyed hair does not cause dermatitis.
Other damage to the scalp skin can make one more sensitive than normal to hair dye and other chemicals.

Substances related to PPD which should be avoided in PPD-sensitized people
• Benzocaine (found in some haemorrhoid preparations) & procaine – local anaesthetics.
• Azo dyes: used in temporary & semi-permanent hair dyes, pen inks,
• Textiles dyes – especially dark clothing & clothing made of synthetic fiber like polyester or nylon
• Some foods & pharmaceuticals coloured with azo dyes
• Sulfa drugs
• Para-aminobenzoic acid (PABA) – found in sunscreens

Hair dye open skin sensitivity Test (“Dab test”) or Open Patch Test
In many countries there is legislation that requires hair dye products to carry a warning about conducting patch test prior to using the dye. This is a precaution to make sure the individual is not sensitized to the dye.
Allergies to PPD can develop, even though there was no reaction during previous use. For this reason, it is important to take the allergy test 48 hours ahead of every use.
The test area used is either behind the ear or inside the arm at the elbow. A small amount of the “colour base” (or some companies recommend mixing the base with the developer first) is applied to the test area. Do not wash the test area. Wait 48 hours unless there is reddening, burning or other irritation. If there is no reaction on the unwashed patch test site after 48 hours, then one can proceed to the full application.
Three dermatological departments in Italy, Great Britain & Poland, have validated this test. They considered it an effective method to detect delayed hypersensitivity (contact allergy) to hair dyes, and as such are useful in the secondary prevention of hair dye allergy. (5)

Preservatives
Preservatives in cosmetics and skin care products are the second most common cause of skin reactions. Cosmetics that contain water must contain some preservative to prevent bacterial or fungal growth. Examples of cosmetics preservatives that cause allergy include:
• Parabens are the most commonly used preservatives in cosmetics
• Formaldehyde is an important sensitiser & is released by a number of biocides, it is mainly found in shampoos
• Imidazolidinyl urea (Germall 115)
• Quaternium-15 (Dowcill 200) is a formaldehyde releasing preservative found in many cosmetics including, eye makeup, foundations, shampoos, moisturizing lotions, sunscreens, body powders, and skin cleansers.
• Phenoxyethanol
• DMDM hydantoin (Glydant)

Cocamidopropyl Betaine (CAPB) was voted Contact Allergen of the year for 2004 by a committee of international experts. It is a non-ionic surfactant found primarily in rinse off cosmetics (shampoos, soaps, and bath gels). It is less irritating to the skin than older surfactants. For this reason patients may think that a less irritating product such as a baby shampoo is safer for the skin when it is more likely to cause allergic contact dermatitis.
A case was presented in the American Journal of Dermatology (Vol 15, No 1 (March), 2004: pp3-4) of a 37-year-old woman who presented with eyelid dermatitis that had been present for 5 months. She was instructed by her family doctor to apply baby shampoo to the eyelids daily (similar advice given in NZ as well). Patch testing revealed a + reaction to CAPB. CAPB was present in the baby shampoo she applied. Discontinuation of this product resulted in clearing of her allergic contact dermatitis.
CAPB is found in over 600 personal care products (according to FDA). The case of CAPB illustrates an important point regarding allergy to cosmetics. Because CAPB is “less irritating” than other surfactants, it may be preferred by consumers, manufacturers, and doctors. The fact that it is more allergenic came to light only after its widespread use.
The reported prevalence of allergic contact dermatitis (ACD) secondary to CAPB exposure ranges from 3.0 to 7.2% (6).

Lanoline or Wools alcohol
In North America lanoline was the fourth commonest cosmetic allergen (after fragrance, preservatives and PPD) causing contact dermatitis (7). It is felt that the prevalence of ACD to lanoline is decreasing because knowledge of its allergenicity has been known for a very long time.
It is a natural material obtained from the sebum of sheep. It is recovered from raw wool by solvent extraction. It is used in cosmetics because of its emollient, moisturizing, and emulsifying properties.
There are several allergens present in lanoline, and lanoline-sensitive patients can sometimes tolerate one lanoline preparation but not another.

Cosmetics containing lanoline include:

• Moisturizers, Hand creams, Protective creams
• Sunscreens
• Glossy lipsticks
• Makeup remover, Eye makeup
• Foundations, eye makeup
• Baby oils & diaper lotions
• Hair spray

Cosmetics with herbal ingredients
Virtually all-herbal remedies have been reported to cause either allergic sensitization or photosensitization.
In a recent study in Portland, Oregan, USA, 63% of patients with suspected cosmetics dermatitis that had used a skin product containing botanical extracts were patch test positive to a botanical extract. In New Zealand the true prevalence of contact allergy to botanical extracts in patients with cosmetics dermatitis is unknown, as most people who suffer from skin rashes do not seek medical help unless the rash is persistent.
Common herbal products causing contact dermatitis include plants from the Compositae family:
• Artichoke
• Chamomile (found in numerous shampoos & other hair treatment products)
• Daisy (Chrysanthemum)
• Dandelion (Taraxacum)
• Feverfew
• Marigold
• Pyrethrum
• Ragweed (Ambrosia)
• Thistle
Several plants in the Compositae plant family are regularly included in “natural skin care products” in New Zealand, especially shampoos and aromatherapy solutions. In some cases the reactions to Compositae is worsened by sunlight, often giving the appearance of a light-sensitive rash.

Tea Tree (Melaleuca alternifolia) Oil is increasingly being used in NZ in various cosmetics (soaps, deodorants, toothpaste, gargles & aftershave) and allergic contact dermatitis is being found related to this product throughout the world.
The leaves of the tea tree contain an essential oil, which contains turpentines (limonene, alpha-pinene, phellandrene). In one study in Honolulu limonene was the most common allergen causing allergic contact dermatitis from tea tree oil.
The ‘tea tree’ oil available in the Netherlands is distilled from the Melaleuca alternifolia and mainly contains eucalyptol. Eucalyptol is probably the most important allergen. The Photoaged Melaleuca is a stronger sensitiser than regular tea tree.
There have been recent reports of topical tea tree oil causing anaphylaxis (Allergy Asthma Proc. 2003 Jan-Feb; 24(1): 73-5)
Propolis
There are reports in the literature describing several individual cases of contact dermatitis in patients using propolis as a component of various cosmetic products, listing the most frequently sensitizing constituents of propolis. There are also reports of the existence of a cross-reaction between the components of Peruvian balsam and propolis constituents.

Henna Allergy
With the vigorous back-to-nature trend in Western countries, henna as a natural hair dye has become increasingly popular. This shift away from chemical dyes is enforced by the relatively high risk of sensitization to chemical dyes, in both hairdresser and their clients.
Henna is derived from a shrub Lawsonia inermis, which is native to the Middle East & North Africa.
There have been several reports in the literature of Immediate Allergic (& Anaphylactic) reaction to using Henna hair dyes. Most cases had sneezing, runny nose, cough, & shortness of breath instead of skin reactions. They were all diagnosed with the help of a positive skin prick test to henna extract. Most of these individuals were hairdressers who became sensitized from their work. It is felt that they became sensitized by inhalation of henna powder dispersed in the air.
Henna also causes allergic contact dermatitis.

Photosensitivity is the term used to describe skin disease caused by the interaction of UV radiation and an exogenously (externally) acquired chemical agent, which may be either a drug or food taken orally, or a substance applied to the skin. It can be divided into photodermatitis, also referred to as photoallergic dermatitis, and photoirritant contact dermatitis.

Plants that cause photodermatitis (Phytophotodermatitis)
Phytophotodermatitis produces reddening and blisters on first exposure followed by persistent hyperpigmentation (darkening of the skin). This darkening of the skin can last for months. The rash is produced via a phototoxic reaction, which simply means that the reaction renders the skin susceptible to damage by UV light, and symptoms include burning pain at the affected site. This is in contrast to the reaction produced by plants such as poison ivy, which is classified as allergic contact dermatitis, and involves symptoms such as intense itching.
Compounds related to furocouramins (psoralens) usually cause plant-related photosensitivity. Two requisites for initiation of phytophotodermatitis are contact with a sensitizing plant (e.g. furocouramin) and exposure to ultraviolet light (wavelength greater than 320 nm), usually sunlight. Therefore, this dermatitis is usually seasonal.

Common plants causing photodermatitis:

Common Name
Botanical Name
Family
Angelica
Angelica archangelica
Umbelliferae
Bergamot
Citrus bergamia
Rutaceae
Celery
Apium aurantium
Umbelliferae
Citron
Citrus medica
 
Dill
Anethum graveolens
Umbelliferae
Fennel
Foeniculum vulgare
Umbelliferae
Fig
Ficus carica
Moraceae
Lemon
Citrus lemon
Rutaceae
Lime
Citrus aurantifolia
Rutaceae
Parsnip
Pastinaca sativa
Umbelliferae
Wild Carrot
Dacus carota
Umbelliferae

In New Zealand many of these plants are also being added to “natural skin care products”.
Contact urticaria is a hives-like reaction occurring at the site of contact of the skin product and usually occurring within 15 minutes of the product touching the skin.

Diagnosis of skin rashes caused by cosmetics
Contact Urticaria is diagnosed by applying the product to the skin for 15 – 20 minutes and observing the skin for redness, swelling and itching or doing a skin prick test (applying the suspected allergen/s to the forearm and pricking the skin with a lancet & waiting 15 minutes for a bump like a mosquito bite at the site of the prick)

Contact Dermatitis is diagnosed by doing a patch test. The only way to obtain proof of allergic contact dermatitis is by patch testing. Patch testing is the universally accepted method for the detection of the causative contact allergens. The positive patch test reproduces an experimental contact dermatitis on a limited area of the skin. This is different from skin prick testing (which gives a positive response in 15 minutes) in that it is a delayed hypersensitivity response (it gives a positive response in about 48 hours).
The most frequently encountered contact allergens have been selected by various international contact dermatitis groups and included in standard patch test series. The chemicals are taped to the back in small chambers. The skin is not broken. The patches stay in place for 48 hours. You cannot shower or do any work or exercise that will wet or loosen the patches.
After 2 days, the patches are removed, and a reading is done. The patch sites are marked, and you may be asked to return for a final reading on another day. An experienced doctor can differentiate between allergic contact dermatitis and an irritant reaction on patch testing.

Repeated Open Application Test (ROAT) or Use Test
This is a simple test for new skin care products or products suspected of causing skin reactions. A small amount of the product is applied twice daily to a small area of normal skin, usually on the front of the elbow for 1 week. If no rash appears after 1 week the product is considered safe for that individual. This test simulates the everyday use of cosmetic products and can be used to define the clinical relevance of doubtful or positive diagnostic patch tests.
Photo-patch testing is patch testing with the addition of radiation to induce the formation of photoantigens. All photosensitive patients should be photo-patch tested.

Cosmetic Allergy & The Future
A recent Patch test study done in Austria (published in Paediatrics Dermatology 2003 Mar-Apr; 20(2): 119-23) showed that the overall sensitization rate was highest in children less than 10 years old (62%) and decreased steadily to be lowest among patients more than 70 years old. This coupled with the fact that appearance is so important to adolescents as they are bombarded with numerous cosmetic advertisements; they are significant consumers of toiletry & skin care products. Therefore we would expect the prevalence of cosmetic allergy to continue to increase.

References
(1) Allergic contact dermatitis to topical minoxidil solution: Etiology and treatment. J Am Acad Dermatol 2002; 46:309-12
(2) Dooms-Goossens A et al., Cosmetic products and their allergens. Eur J Dermatol 1992; 2: 465-8
(3) Kohl, et al, Allergic contact dermatitis from cosmetics. Retrospective analysis of 819 patch-tested patients. Dermatology. 2002; 204(4): 334-7
(4) Wolfgang Uter et al. Epidemiology of contact dermatitis. The information network of Departments of Dermatology. European Journal of Dermatology. Vol 8. Number 1. 36-40 Jan – Feb 1998
(5) Maya Krasteva et al. Contact Sensitivity to hair dyes can be detected by consumer open test. European Journal of derm. Vol. 12. Number 4, 322-6
(6) Joseph F. Fowler Jr et al. Allergy to Cocamidopropyl Betaine and Amidoamine in North America. Dermatitis, Vil 15, No 1 March, 2004: pp5-6
(7) Adams et al. A five year study of cosmetic reactions, J Am Acad Dermatol 13: 1062-1069, 1985
Contact & Occupational Dermatology by James G. Marks & Vincent A. DeLeo

Being Mom, by Anna Quindlen

If not for the photographs, I might have a hard time believing they
ever existed. The pensive infant with the swipe of dark bangs and the black button eyes of a Raggedy Andy doll. The placid baby with the yellow ringlets and the high piping voice. The sturdy toddler with the lower lip that curled into an apostrophe above her chin.

All my babies are gone now. I say this not in sorrow but in disbelief. I take great satisfaction in what I have today: three almost-adults, two taller than I am, one closing in fast. Three people who read the same books I do and have learned not to be afraid of disagreeing with me in their opinion of them, who sometimes tell vulgar jokes that make me laugh until I choke and cry, who need razor blades and shower gel
and privacy, who want to keep their doors closed more than I like.

Who, miraculously, go to the bathroom, zip up their jackets and move food from plate to mouth all by themselves. Like the trick soap I bought for the bathroom with a rubber ducky at its center, the baby is buried deep within each, barely discernible except through the unreliable haze of the past.

Everything in all the books I once pored over is finished for me now. Penelope Leach., T. Berry Brazelton., Dr. Spock. The ones on sibling rivalry and sleeping through the night and early-childhood education, all grown obsolete. Along with Goodnight Moon and Where the Wild Things Are, they are battered, spotted, well used. But I suspect that if you flipped the pages dust would rise like memories.

What those books taught me, finally, and what the women on the playground taught me, and the well-meaning relations –what they taught me, was that they couldn’t really teach me very much at all. Raising children is presented at first as a true-false test, then becomes multiple choice, until finally, far along, you realize that it is an endless essay. No one knows anything. One child responds well to positive reinforcement, another can be managed only with a stern voice and a timeout. One child is toilet trained at 3, his sibling at 2.

When my first child was born, parents were told to put baby to bed on his belly so that he would not choke on his own spit-up. By the time my last arrived, babies were put down on their backs because of research on sudden infant death syndrome. To a new parent this ever-shifting certainty is terrifying, and then soothing.

Eventually you must learn to trust yourself. Eventually the research will follow. I remember 15 years ago poring over one of Dr. Brazelton’s wonderful books on child development, in which he describes three different sorts of infants: average, quiet, and active. I was looking for a sub-quiet codicil for an 18-month old who did not walk. Was there something wrong with his fat little legs? Was there something wrong with his tiny little mind? Was he developmentally delayed, physically challenged? Was I insane? Last year he went to China. Next year he goes to college. He can talk just fine. He can walk, too.

Every part of raising children is humbling, too. Believe me, mistakes were made. They have all been enshrined in the, “Remember-When-Mom-Did Hall of Fame.” The outbursts, the temper tantrums, the bad language, mine, not theirs. The times the baby fell off the bed. The times I arrived late for preschool pickup. The nightmare sleepover. The horrible summer camp. The day when the youngest came barreling out of
the classroom with a 98 on her geography test, and I responded, What did you get wrong? (She insisted I include that.) The time I ordered food at the McDonald’s drive-through speaker and then drove away without picking it up from the window. (They all insisted I include that.) I did not allow them to watch the Simpsons for the first two seasons. What was I thinking?

But the biggest mistake I made is the one that most of us make while doing this. I did not live in the moment enough. This is particularly clear now that the moment is gone, captured only in photographs.

There is one picture of the three of them, sitting in the grass on a quilt in the shadow of the swing set on a summer day, ages 6, 4 and 1. And I wish I could remember what we ate, and what we talked about, and how they sounded, and how they looked when they slept that night. I wish I had not been in such a hurry to get on to the next thing: dinner, bath, book, bed. I wish I had treasured the doing a little more and the getting it done a little less.

Even today I’m not sure what worked and what didn’t, what was me and what was simply life. When they were very small, I suppose I thought someday they would become who they were because of what I’d done. Now I suspect they simply grew into their true selves because they demanded in a thousand ways that I back off and let them be.

The books said to be relaxed and I was often tense, matter-of-fact and I was sometimes over the top. And look how it all turned out. I wound up with the three people I like best in the world, who have done more than anyone to excavate my essential humanity.

That’s what the books never told me. I was bound and determined to learn from the experts. It just took me a while to figure out who the experts were….

Safety of H1N1 Vaccine Confirmed

FDA Commissioner Addresses H1N1 Vaccine Safety Concerns

Emma Hitt, PhD

Posted: 11/11/2009

November 11, 2009 — In a letter yesterday, the commissioner of the US Food and Drug Administration (FDA), Margaret A. Hamburg, MD, reassured healthcare professionals about vaccine safety and thanked them for their “extraordinary efforts” during the 2009 H1N1 influenza outbreak.

MedWatch, the FDA’s safety information and adverse event reporting program, announced the letter in a posting yesterday.

“Delays in vaccine delivery and the persistence of myths about vaccination have not made your job any easier,” she stated. “Thank you for rising to this public health challenge.”

Reassuring Patients About Vaccine Safety

Dr. Hamburg, who was confirmed on May 18, 2009 as the FDA’s new commissioner, described information about H1N1 that can be used to allay patient fears about vaccine safety.

She noted that some patients might think that the safety of the H1N1 vaccine is unconfirmed because the vaccine became available only 6 months after the 2009 H1N1 virus appeared. However, this fear is misguided because the H1N1 vaccine is produced in exactly the same way as the seasonal influenza vaccine.

“Companies began manufacturing the 2009 H1N1 vaccines in the same factories where they are licensed to manufacture seasonal influenza vaccines — using the same equipment and the same testing procedures,” she pointed out.

According to Dr. Hamburg, if the H1N1 virus had emerged a few months earlier, “it could have been included as 1 of the 3 strains in the 2009 seasonal vaccine. In this key respect, although the strain of the 2009 H1N1 virus is new, the 2009 H1N1 influenza vaccines are not.”

In addition, in National Institutes of Health–sponsored clinical trials of more than 3600 people, no serious adverse events have been attributed to the vaccine.

Dosing of the 2009 H1N1 influenza

Until recently, it was unclear how many doses of the vaccine would be needed. According to the letter, only a single dose of H1N1 vaccine is needed for healthy adults, the elderly, and older children. “For children ages 9 and younger, two doses of the H1N1 vaccine will likely be optimal, also similar to seasonal vaccine,” Dr. Hamburg said.

The letter is available on the FDA Web site. More information on H1N1 influenza is available here.

Adverse effects linked to any vaccine, including the 2009 H1N1 influenza vaccine, should be reported to the Vaccine Adverse Event Reporting System (http://vaers.hhs.gov/index).

Adverse events can also be communicated to MedWatch by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to 5600 Fishers Lane, Rockville, Maryland 20852-9787.
[CLOSE WINDOW]Authors and Disclosures
Journalist
Emma Hitt, PhD

Emma Hitt is a freelance editor and writer for Medscape.