Dr. Ted’s Blog

This was taken from Medscape.com. It is an interview with Dr. Eric Hollander and reviews a lot of good information on what is currently known about autism. This interview IS nearly 5 years old, but if anything, the support for autism as a genetic entity and the complete lack of corroboration with vaccines as a cause is even stronger today. Read this and see for yourself, particularly if you are at all worried about vaccines and their refuted link to autism.

Autism: An Interview With Eric Hollander MD

From Medscape Psychiatry & Mental Health

Autism: An Expert Interview With Eric Hollander, MD
Published: 02/03/2005

Editor’s Note:
Requests for services related to autism are increasing, although there is controversy over whether this reflects a change in the prevalence of the disorder, better detection, or differences in definition. What is autism? How common is it? What are the best ways to treat it? What makes doing research on autism spectrum disorders exciting today? Elizabeth Saenger, PhD, Medscape Psychiatry & Mental Health, interviewed Eric Hollander, MD, Professor of Psychiatry, Director, Seaver and New York Autism Center of Excellence, Mount Sinai School of Medicine, New York, NY.

Medscape: How would you define autism?
Dr. Hollander: Autism is a developmental disorder that presents before the age of 3 years. It’s characterized by impairment in 3 core symptom domains, which include social deficits, communication difficulties, narrow restricted interests, and repetitive behaviors. In addition to that, there are also other associated symptoms that frequently coexist.

Medscape: What are those other symptoms?
Dr. Hollander: The other associated symptom domains can include factors like inattention and motor hyperactivity, impulsivity and aggression, mood instability, EEG abnormalities or seizure related type problems, and cognitive difficulties.

Medscape: How common is this disorder?
Dr. Hollander: It used to be felt to be very rare. The best estimates now are that about 0.6% of the population, a little under 1%, may meet criteria for the broader autism phenotype, or an autism spectrum disorder. Within that spectrum, we include autism, the Asperger syndrome, and pervasive developmental disorder or PDD NOS — not otherwise specified.

Medscape: How do you treat autism spectrum disorders?
Dr. Hollander: There are a few different treatment approaches. There are behavioral approaches, educational approaches, and medication approaches. We intervene early. There is some evidence that the earlier you pick up the problem and start to intervene with behavioral, educational, speech, and occupational therapy, the better the long-term developmental trajectory. So the idea now is to start to identify people at around 18 months if possible and often to slide people into the educational programs that incorporate a lot of speech and occupational therapy plus behavioral interventions like acute ABA-type treatments — applied behavioral analysis. And there is evidence that these kinds of treatments actually can be associated with better long-term outcome.
We are also finding that medicines may be very helpful in 2 types of approaches. One is a targeted treatment approach where we select a group of individuals who score high on a particular target symptom like lots of narrow, restricted interests, repetitive behaviors, self-stimulation-type behaviors, and compulsive behaviors, and then treat them, for example, with very low doses of selective serotonin reuptake inhibitors like fluoxetine or fluoxetine in a liquid form. We found that will significantly improve the core symptom domain and improve overall functioning.
Other treatment approaches involve stratifying the population, picking up the subgroup with a lot of disruptive behavior, such as impulsivity and aggression, tantruming, self-injury, and treating them with low doses of atypical antipsychotics, such as risperidone. We also have treatment approaches using the mood-stabilizing, anticonvulsant-type treatments like valproic acid or levetiracetam, finding that these medicines may be helpful in a lot of mood instability, a lot of the disruptive behavior like impulsive, aggressive, or self-injurious behavior. Sometimes for language-related functioning, and particularly those with some abnormal EEGs, patients have a very robust response to the anticonvulsant-type medicines.

Medscape: How successful are these interventions in helping people become what society generally considers normal?
Dr. Hollander: It probably depends on the baseline characteristics of the patient, because it turns out that autism is pretty heterogeneous. You have some individuals who have very high IQs and others with severe mental retardation. You have some individuals who have really outstanding verbal skills and others who have no language at all. You have some people who have accompanying seizure problems or other neurologic problems and others who don’t.
So as a group it’s fairly heterogeneous. And we know that individuals who start off with a higher IQ and better speech and language tend to have a better long-term outcome than those who have more severe impairment at baseline.
But we know that with early interventions, both behavioral and pharmacologic, people really can do a lot better, that the symptoms that cause distress can be significantly reduced and their overall functional ability can improve.

Medscape: One thing I’m curious about is the paradox in a way of the idiot savant. Can you say something about that?
Dr. Hollander: What’s interesting is that within individuals you see a scattering of peaks and valleys in terms of skill levels. And you have some individuals who have extraordinary skills in certain areas. That may go along with their narrow restricted interests, where they become preoccupied with certain things and have all the information in the world about those things. And sometimes people can calculate statistics or memorize calendars or have some extraordinary mathematical or physics ability, or even certain visual/spatial abilities, musical abilities, verbal abilities. We think that there may be some positive attributes that may be coheritable with certain autism symptom domains. The idea is that either there are a number of these core and associated symptom domains that need to come together in order to produce the full syndrome of autism, and that in the first-degree family members, and even in the general population, we frequently see impairment in individual symptom domains. These individuals don’t have the full disorder, however, unless they get multiple domains coming together.
Some of the symptom domains that may make up the disorder may also be associated with high abilities in mathematical or visual, spatial, or musical abilities, and it’s not unusual to see in first-degree family members a high skill, for example, in physics, math, or computers. It’s also not unusual to see many family members who have extraordinary technical skills, for example. Within individuals with autism, you do see individuals with these islands of extraordinary skills also coupled with areas of the real impairment. And it seems that many people with autism have difficulties with the higher order of processing of information. They may be excellent in terms of their raw sensory information or their ability to manipulate the sensory information, but they have more difficulty with the higher-order processing or generating abstract conclusions from the sensory information.

Medscape: In other words, they would be like Raymond in the film, Rain Man, where Raymond could do difficult calculations involving the cards in the casino and win a lot of money or figure out how many toothpicks have been spilled on the floor, but in terms of figuring out how much change he would get if he went to the grocery store to buy something, he was a failure.
Dr. Hollander: Yes. I would say that often there are deficits in certain pragmatic skills — how to interact with the world in a social fashion to get what you want from the world — but that they can still have extraordinary specific skills.

Medscape: Can you tell us a little bit about your own research with people who have autism?
Dr. Hollander: Yes. Here at Mount Sinai we have the Seaver and New York Autism Center of Excellence. We have been doing business for over 10 years, initially funded by the Seaver Foundation and now funded by one of the NIH STAART Autism Centers of Excellence. We’re very focused on breaking autism down into the different core and associated symptom domains and finding relevant genes, understanding the specific brain circuits, and developing specific treatments for each of the different symptom domains. For example, we found genetic factors that may be associated with speech and language problems or with the repetitive behaviors. We’ve elucidated the metabolic activity in the limbic system associated with autism. And we have developed new treatments for the symptom domains, particularly the repetitive behaviors and the impulse of aggression. We’ve also been interested in peptides like oxytocin and the role that those peptides play in social attachment and in the repetitive behaviors; we have done some interesting alterations of that system and found that we can improve social attachment and repetitive behaviors by influencing the oxytocin system. We’ve also done research on immune abnormalities that may run in families, and related these immune abnormalities to different symptoms.
We’ve been very interested in the serotonin system and the role that that serotonin system plays in the repetitive behaviors and then how treatments for the serotonin system can improve the repetitive behaviors.

Medscape: This seems to tie into what you once said about the need to look at specific behaviors and then target them with specific medications to improve somebody’s behavior and life.
Dr. Hollander: That’s right. We think that there are basically 2 approaches with medicines. One is the targeted treatment approach where you stratify the population and you select individuals who have specific types of target behaviors that cause distress and interfere with functioning. You start with low doses of medicines and improve those target symptoms to see how that affects the overall level of functioning. Another approach that we’re starting to get into is early interventions to see if we can change the developmental trajectory. In a similar way, early behavioral interventions might improve IQ or social reciprocity with speech and language.

Medscape: The idea of improving IQ seems interesting. Can you tell us more about that?
Dr. Hollander: There are some behavioral treatment studies that suggest that early intervention with behavioral approaches will show an improvement in IQ if you follow individuals over long periods of time.
Some of those studies may be flawed because there wasn’t good randomization and people started with different IQ levels at baseline. But generally people feel that early intervention can be associated with improvement. And when you get clinical improvement, you also see a significant improvement in IQ.
Some of the studies that the STAART Centers are looking at now are early interventions with serotonin reuptake inhibitors that follow people over time to see if we can get improvement in IQ. Recently we’ve also been interested in looking at certain medicines that work on the glutamate system that are used specifically for cognition and memory to see if we can improve cognitive functioning and IQ with those approaches.

Medscape: You mentioned that early intervention in autism means catching a child or a baby at 18 months. How often is autism or potential autism recognized that early?
Dr. Hollander: It used to be very rare, so people usually identified it at around age 3 years when children weren’t talking. Nowadays, there’s a push to identify earlier problems like eye gaze, not interacting appropriately with other children or peers, or not having good joint attention with parents. And sometimes there can be subtle motor abnormalities that may be present at an earlier stage. There are suggested screening instruments, such as the Checklist For Autism in Toddlers — CHAT. Cure Autism Now has suggested that pediatricians routinely administer this to all children at 18 months to try to pick up people with developmental delays who should be screened more carefully afterwards.

Medscape: Are pediatricians doing that?
Dr. Hollander: I think that for the most part now, teachers, pediatricians, parents, and other mental health practitioners are doing a better job screening. There is a bit of a controversy in the field as to whether autism is dramatically increasing because the rates were much, much lower before. That may be because everybody is doing a better job screening, so we’re picking up the milder cases at an earlier stage. The alternative explanation is that there are environmental factors that interact with strong genetic factors to be associated with an increased risk for people presenting with these problems.

Medscape: I know that’s quite controversial. Can you tell us about some of the possible environmental factors that people are thinking about?
Dr. Hollander: Well, there’s been a lot of debate about vaccines — initially the MMR vaccine, and then more recently the thimerosal preservative, which is an ethylmercury preservative that was in certain multidose vials of vaccines. I think that the best available data really suggest that these vaccines are not associated specifically with an increased rate for autism. That’s because there have been good studies, for example, in England, shortly after the MMR vaccine was first introduced, that showed that there was no dramatic increase after it was introduced. The Institute of Medicine recently issued a report suggesting that it doesn’t look like vaccine played a role. It’s clear that mercury can be neurotoxic. It’s not good for the developing brain, but probably is not specifically related to the development of autism.
People have hypothesized all kinds of other factors. We were interested in the role that pitocin played in inducing labor and delivery as a possible risk factor. And other people have postulated that things like folate, for example, that are frequently given, may be an epigenetic factor that can turn on and turn off certain genes that could be associated with a greater risk.

Medscape: How did you get interested in this research area?
Dr. Hollander: Originally we were interested in other disorders that present with repetitive behaviors. And then we had the opportunity to partner with the Seaver Foundation and develop a new autism center.
Studying autism is really a great opportunity because if you understand what goes wrong in autism, you understand a little bit more about what makes people human. It gives you insight into issues around being able to see things from other people’s perspectives and issues around social attachment, which are really what make us human.

Medscape: What do you see on the horizon in terms of research on autism and social movements about autism?
Dr. Hollander: The media have been talking about autism a lot lately. There are a number of debates, for example, about funding issues in terms of ABA. It’s very costly. Does the existing database justify ABA, for example?
There are some controversies about whether autism — for example, Asperger’s disorder — is just an alternative way of being and whether trying to get rid of target symptoms is not allowing certain patients with Asperger’s to fully express who they are.My sense is that it’s pretty clear that if we can reduce certain target symptoms, then people will have significantly less distress and their overall level of functioning will improve.

Medscape: Is there anything else you would like to add?
Dr. Hollander: I think this is an exciting time now. The NIH has taken a big interest in autism and launched STAART Autism Centers of Excellence. Many centers are working together to develop important new treatments. And integrated treatments are probably one wave of the future, integrating the behavioral and the medication treatments together.I think there is a lot of exciting work coming out on genetic findings. Mt. Sinai and the Seaver Center have started to actually see specific genes that may play a role in autism. It’s clear that there’s no single gene, but it may be that if you have a few of these different genes interacting together, you’re going to be at high risk for getting the syndrome. Each of the genes may code for the different symptom domains that need to come together to get the full syndrome.
I think that there are new imaging techniques, like functional MRIs, that are allowing us to design specific kinds of experiments to understand the specific neurocircuits that are involved in the different symptom domains of the disorder.
And finally, there’s a good partnership between academic medical centers and autism advocacy groups. I think the autism advocacy groups have been extremely effective — Cure Autism Now (CAN), National Alliance for Autism Research (NAAR), and Autism Society of America (ASA), for example — in terms of increasing awareness and increasing support for this important area.

Medscape: Thank you very much for sharing your thoughts with Medscape.
Supported by an independent educational grant from Janssen

I stole this from Snopes.com but I think the information is very good.

http://www.snopes.com/medical/toxins/aspartame.asp

Aspartame

Claim:   The artificial sweetener aspartame has been proved responsible for an epidemic of cancer, brain tumors, and multiple sclerosis.

Status:   False.

Origins:

To date, FDA has not determined any consistent pattern of symptoms that can be attributed to the use of aspartame, nor is the agency aware of any recent studies that clearly show safety problems.

Aspartame and the Internet   (The Lancet):
Our research revealed over 6000 web sites that mention aspartame, with many hundreds alleging aspartame to be the cause of multiple sclerosis, lupus erythematosis, Gulf War Syndrome, chronic fatigue syndrome, brain tumours, and diabetes mellitus, among many others. Virtually all of the information offered is anecdotal, from anonymous sources and is scientifically implausible.

ACSH Debunks Internet Health Hoax   (American Council on Science and Health):
Health scare artists have found a whole new medium for terrorizing the public — the Internet. Individuals in search of accurate health information may literally become caught in the Web, where health hoaxes and urban medical myths run rampant. The health scare messages are always the same — whatever it is, it will make you sick.

Beware The E-Mail Hoax: The Evils Of Nutrasweet (Aspartame)   (Dr. Dean Edell):
A highly inaccurate “chain letter” is being circulated via e-mail warning the reader of the health dangers of aspartame (Nutrasweet) diet drinks. There is so much scientific untruth in it, it’s scary. Be careful, because others know how to manipulate you by this. Just because something is beyond your comprehension doesn’t mean it is scientific.

FDA Statement on Aspartame   (FDA):
Analysis of the National Cancer Institute’s public data base on cancer incidence in the United States — the SEER Program — does not support an association between the use of aspartame and increased incidence of brain tumors.

Study Reaffirms Safety of Aspartame   (MIT News):
Even daily large doses of the high-intensity sweetener aspartame, also known as NutraSweet, had no adverse effect on study subjects’ health and well-being, a visiting scientist at MIT reported in the American Journal of Clinical Nutrition last week. “We conclude that aspartame is safe for the general population,” said Paul A. Spiers, visiting scientist in the Clinical Research Center (CRC).

A Web of Deceit   (TIME magazine):
A widely disseminated e-mail by a “Nancy Markle” links aspartame to Alzheimer’s, birth defects, brain cancer, diabetes, Gulf War syndrome, lupus, multiple sclerosis and seizures. Right away, the long list warrants skepticism. Just as no single chemical cures everything, none causes everything.

Last updated:   25 September 2007
The URL for this page is http://www.snopes.com/medical/toxins/aspartame.asp

Urban Legends Reference Pages © 1995-2008 by snopes.com.
This material may not be reproduced without permission.
snopes and the snopes.com logo are registered service marks of snopes.com.

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.

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.

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.

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!

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