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Dr. Ted’s Blog

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.

Newborns Need Pain Relief ,Too

Pain Control Recommended for Newborns

Laurie Barclay, MD

November 11, 2009 — Feeding and breast-feeding newborns are found to be the most effective methods of pain relief during heel-lancing, according to the results of a prospective study reported in the November issue of Pediatrics.

“Pain experience can alter clinical outcome, brain development, and subsequent behavior in newborns, primarily in preterm infants,” write Amir Weissman, MD, from Technion-Israel Institute of Technology in Haifa, Israel, and colleagues. “The aims of this study were (1) to evaluate several simple, commonly used methods for pain control in newborns and (2) to evaluate the concordance between behavioral and autonomic cardiac reactivity to pain in term neonates during heel-lancing.”

During heel-lancing for routine neonatal screening of phenylketonuria and hypothyroidism, 180 term newborn infants were randomly selected to 1 of 6 groups: (1) control (no intervention for pain relief); (2) sucking without feeding; (3) holding by mother; (4) ingestion of oral glucose solution; (5) feeding with oral formula; or (6) breast-feeding. Response to pain was assessed with the Neonatal Facial Coding System score; duration of crying; and autonomic variables determined from spectral analysis of heart rate variability before, during, and after heel-lancing.

Compared with newborns in any of the 5 intervention groups, those in the control group with no pain intervention had the greatest levels of pain manifestation. Breast-feeding or feeding with oral formula appeared to be most effective vs all other groups, based on the lowest increase in heart rate (21 and 23 beats per minute, respectively, vs 36 beats per minute; P < .01), neonatal facial score (2.3 and 2.9, respectively, vs 7.1; P < .001), cry duration (5 and 13 seconds, respectively, vs 49 seconds; P < .001), and the lowest decrease in parasympathetic tone (–2 and –2.4, respectively, vs 1.2; P < .02). “Any method of pain control is better than none,” the study authors write. “Feeding and breast-feeding during heel-lancing were found to be the most effective methods of pain relief.” Limitations of this study include low sensitivity of the pain assessment methods, large variability of newborn response to painful stimuli, and the subjective nature of interpreting these data. “Neonatal pain prevention is the expectation of the parents and should be the goal of the medical staff; therefore, family members or staff may be recruited to help during these procedures, and nursing mothers should be encouraged to breastfeed during the procedure,” the study authors conclude. “If family members believe that they cannot withstand the procedure, hear their infant crying, or see the heel-lancing, then bottle-feeding seems to be a good alternative.” The study authors have disclosed no relevant financial relationships. Pediatrics. 2009;124:e921-e926.

WHO Urges Rapid Use of Antivirals in H1N1

New Guidelines on H1N1 Influenza Urge Quicker Use of Antivirals

Robert Lowes

November 12, 2009 — Updated treatment guidelines for H1N1 influenza from the World Health Organization (WHO) urge clinicians to administer antiviral medications as soon as possible to patients in at-risk groups with flu symptoms, patients with pneumonia, and those with uncomplicated influenza-like illness that worsens or fails to improve within 72 hours.

The reason for immediate antiviral therapy is that a mild case of H1N1 influenza can morph into a deadly disease such as pneumonia within 24 hours, according to the revised guidelines released Tuesday.

“The virus can take a life within a week,” Nikki Shindo, MD, a medical officer in WHO’s Global Influenza Programme, said during a press conference today. “The week of opportunity is very narrow in regard to the progression of the disease. The medicine needs to be administered before the virus destroys the lungs.”

Patients in at-risk groups who should receive antivirals once they experience flu symptoms include pregnant women, children younger than 2 years, and individuals with chronic illnesses such as respiratory problems, according to Dr. Shindo.

Dr. Shindo said that earlier WHO guidelines focused on treating severe disease stemming from the H1N1 virus. The updated guidelines, she explained, have more to say about preventing severe disease, especially with the use of antiviral medications. Initial guidance about antivirals had been more conservative because WHO “had almost no experience” in regard to their effectiveness and because supplies were limited, said Dr. Shindo. Now, WHO has more data about the safety and usefulness of the medicine, and supplies are more ample.

The updated guidelines state that clinicians should not delay antiviral treatment for patients with suspected H1N1 influenza for the sake of conducting tests to confirm the diagnosis. In addition, a negative result from some rapid influenza diagnostic tests should not justify withholding antiviral therapy because these tests “miss many infections with pandemic H1N1 virus.”

The first-line antiviral for treating the H1N1 virus is oseltamivir (Tamiflu), according to WHO. If oseltamivir is not available, it is not possible to administer it to a particular patient, or if the virus is resistant to oseltamivir, the guidelines recommend that clinicians use zanamivir (Relenza), which is inhaled.

To ensure easier access to treatment, public health authorities should distribute antivirals through general practitioners and not primarily through hospitals, said Dr. Shindo. “Patients should not have to visit the hospital to get antivirals prescribed,” she said. “This should help ensure that individuals get the care they need faster. This will leave hospitals freer to treat the more severe cases.”

Although Dr. Shindo emphasized the need for the earlier use of antivirals, she said that people not in the at-risk groups who are experiencing only mild flu symptoms do not need to take antiviral therapy. Nor should healthy individuals take it as a preventive measure.

WHO Guidelines Do Not Conflict With CDC Directives

The updated WHO guidelines specify watchful waiting for 72 hours for patients who have uncomplicated influenza-like illness and who do not have an underlying medical condition that puts them at risk. Hallmarks of progressive illness that warrant antiviral therapy include:

* Shortness of breath, hypoxia, and fast or labored breathing in children, which would suggest oxygen impairment or cardiopulmonary insufficiency.
* Altered mental status, unconsciousness, drowsiness, and seizures, which suggest central nervous system complications.
* Evidence of sustained virus replication or invasive secondary bacterial infection.
* Severe dehydration, expressed as decreased activity, dizziness, decreased urine output, and lethargy.

By necessity, this recommendation for follow-up requires patient education, Dr. Shindo said. Clinicians should instruct patients who initially present with uncomplicated influenza-like illness to return for another visit if they develop these or other symptoms of progressive illness — or do not get better — within 72 hours from the onset of symptoms, according to WHO.

The Centers for Disease Control and Prevention (CDC) have not issued any guidance on follow-up care for influenza patients that stipulates a 72-hour time frame, but the agency does advise patients who do not improve within a few days that they might have a complication like a secondary infection, said Anthony Fiore, MD, a medical epidemiologist with the CDC’s National Center for Immunization and Respiratory Diseases.

“I do not see the WHO recommendations as being in conflict [with the CDC directives],” Dr. Fiore told Medscape Infectious Diseases. CDC recommendations on administering antiviral medications are revised on average every 4 to 6 weeks, said Dr. Fiore. “We will look at the WHO guidance and the evidence base used to develop the guidance as part of [our] revision.”

The updated treatment guidelines are available on the WHO Web site.

CDC Update

At a CDC press briefing today, Anne Schuchat, MD, director of the CDC’s National Center for Immunization and Respiratory Diseases, provided an updated estimate of H1N1 cases using data extrapolated from the CDC’s Emerging Infections Program .

The CDC estimates that during the first 6 months of the pandemic (April through October 17, 2009), a total of 22 million people (range, 14 – 34 million) in the United States became infected with H1N1 influenza. Of these, 98,000 people (range, 63,000 to 153,000) were hospitalized; and 3900 (range, 2500 – 6100) died.

The data are also broken down by age group and highlight that fact that numbers of cases, hospitalizations, and deaths are disproportionately higher in people aged 64 years and younger than in older individuals.

These numbers will be updated every 3 to 4 weeks, she said.

Dr. Schuchat also discussed the effect of H1N1 influenza in patients with diabetes, which afflicts about 19% of adults hospitalized for H1N1. According to Dr. Schuchat, people with diabetes should be vaccinated (with the injectable vaccine not the nasal spray) against H1N1. People with diabetes who also have respiratory illness should receive antiviral therapy, which should be initiated prior to availability of test results. Patients with diabetes should also ensure that they have been vaccinated against pneumococcal infections.

To date, 41.6 million doses of H1N1 vaccine have become available. “This is more than we had before but not as much as we had hoped to have by today,” Dr. Schuchat said. Currently, 94 million doses of seasonal influenza vaccine have been distributed, with 114 million doses total expected by the end of the year.

Emma Hitt, PhD, contributed to this report.

H1N1 (Swine)Flu vaccines are now available to parents and caretakers!

We are now offering the H1N1(Swine)Flu vaccine to our patients parents and caretakers. There is a $20 admnistration charge for adults. If you are interested in recieving this vaccine please call the office to schedule an appointment.

Preservative free Swine Flu vaccine for ages 6 months – 35 months has arrived!

Our preservative free H1N1(Swine) Flu vaccines for age 6 months to 35 months has arrived. Please call the office to schedule your childs appointment. Please remember we are trying to accomodate many patients who want their children to have the vaccine and are doing our best to schedule everyone at the earliest time available. We are currently scheduling out 2-3 weeks. Thank you in advance for your understanding.

Cannabinoids Do Not Help Tics in Tourette’s Syndrome

Cannabinoids for Tourette’s Syndrome

Curtis A, Clarke CE, Rickards HE
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Summary
Cannabinoids for Tourette syndrome

Cannabinoid medication might be useful in the treatment of the symptoms in patients with Tourette’s syndrome. At the present time only two relevant studies have been conducted. Both studies used tetrahydrocannabinol (Δ9THC). In both studies Δ9THC was associated with tic reduction. However the sample size was small and a large number of multiple comparisons were made . There were only 28 participants in total, since eight participants took part in both studies. Possibly the patients who derived the greatest benefit and experienced the least adverse effects would be the most inclined to participate in further studies. There were a high number of drop outs/exclusions in the six week study and it is unclear whether intention to treat analysis (ITT) was performed. The results that are reported are analyses done on the patients who remained in the study on the study medication at the correct dose. In reality, patients do opt not to continue treatment if there is limited efficacy or unpalatable side effects. This introduces attrition bias. Whilst there were some significant results, the authors themselves accept that very few of these results are significant if a Bonferroni correction is performed. It is possible that cannabinoid medication has a beneficial effect which is too weak to be detected using ITT and such a small sample size. There is some weak evidence that cannabinoid medication may have an effect on obsessive compulsive behaviour but the measure used was an addition to the TSSL which has not been validated.There were no data on the effect of Δ9THC on quality of life.There is not enough evidence to support the use of cannabinoids in treating tics and obsessive compulsive behaviour in people with Tourette’s syndrome.

This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2009 Issue 4, Copyright © 2009 The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464-780X).
This record should be cited as: Curtis A, Clarke CE, Rickards HE. Cannabinoids for Tourette’s Syndrome. Cochrane Database of Systematic Reviews 2009, Issue 4. Art. No.: CD006565. DOI: 10.1002/14651858.CD006565.pub2

This version first published online: October 07. 2009
Abstract
Background

Gilles de la Tourette Syndrome (GTS) is a developmental neuropsychiatric disorder characterised by the presence of chronic motor and phonic tics. Drugs currently used in the treatment of GTS either lack efficacy or are associated with intolerable side effects. There is some anecdotal and experimental evidence that cannabinoids may be effective in treating tics and compulsive behaviour in patients with GTS. There are currently no systematic Cochrane reviews of treatments used in GTS. There is one other Cochrane review being undertaken at present, on the use of fluoxetine for tics in GTS.
Objectives

To evaluate the efficacy and safety of cannabinoids as compared to placebo or other drugs in treating tics, premonitory urges and obsessive compulsive symptoms (OCS), in patients with GTS.
Search strategy

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (in The Cochrane Library Issue 4 2008) , MEDLINE (January 1996 to date), EMBASE (January 1974 to date), PsycINFO (January 1887 to date), CINAHL (January 1982 to date), AMED (January 1985 to date), British Nursing Index (January 1994 to date) and DH DATA (January 1994 to date).

We also searched the reference lists of located trials and review articles for further information.
Selection criteria

We included randomised controlled trials (RCTs) comparing any cannabinoid preparation with placebo or other drugs used in the treatment of tics and OCS in patients with GTS.
Data collection and analysis

Two authors abstracted data independently and settled any differences by discussion.
Main results

Only two trials were found that met the inclusion criteria. Both compared a cannabinoid, delta-9-Tetrahydrocannabinol (Δ9THC), either as monotherapy or as adjuvant therapy, with placebo. One was a double blind, single dose crossover trial and the other was a double blind, parallel group study. A total of 28 different patients were studied. Although both trials reported a positive effect from Δ9THC, the improvements in tic frequency and severity were small and were only detected by some of the outcome measures.
Authors’ conclusions

Not enough evidence to support the use of cannabinoids in treating tics and obsessive compulsive behaviour in people with Tourette’s syndrome.

ADHD Represents Delayed, Not Abnormal Brain Maturation

by
Arline Kaplan MD

Cortical development in children with attention-deficit/hyperactivity disorder (ADHD) generally lags behind that in other children by several years, NIMH researchers reported recently.1 The greatest maturational delay occurs in prefrontal regions important for control of such cognitive processes as attention and working memory, they found.
There has been a long-standing debate as to whether ADHD is caused by a delay in brain development or is partly due to a complete deviation away from typical brain development, said Philip Shaw, MD, PhD, an NIMH staff clinician and leader of the research team.
To help resolve the controversy about the disorder that affects 3% to 5% of school-aged children, Shaw and his colleagues conducted a neuroanatomical MRI study and found evidence suggesting that ADHD is characterized by delay rather than deviance in cortical maturation.
“We looked at the development of the cortex, and we measured its thickness in 446 kids, half… with ADHD and half without the disorder,” Shaw told Psychiatric Times.
The researchers scanned the brains of most of the study participants at least twice at about 3-year intervals. While the participants included preschoolers and young adults, most ranged in age from 7 to 16 years. Among the participants with ADHD, 92% had combined-type ADHD at baseline.
Using computational neuroanatomical techniques, the researchers estimated cortical thickness at more than 40,000 cerebral points from 824 MRI scans. They focused on the age of attaining peak cortical thickness—when cortex thickening during childhood gives way to thinning following puberty, as unused neural connections are pruned for optimal efficiency during the teen years.
“While healthy kids reached peak cortical thickness at age 7 or 8, the kids with ADHD reached… peak cortical thickness a few years later, around age 10,” Shaw said.
The cortical maturation delay in ADHD was most prominent in the lateral prefrontal cortex, the region, according to the research team, that supports such cognitive functions as the ability to suppress inappropriate responses and thoughts, executive control of attention, evaluation of reward contingencies, and working memory. Delay was also found in the temporal cortex.
The only cortical area in which the ADHD group demonstrated slightly earlier maturation was the primary motor cortex.
“It is possible that the combination of early maturation of the primary motor cortex with late maturation of higher-order motor control regions may reflect or even drive the excessive and poorly controlled motor activity cardinal to the syndrome,” the research team wrote.
Although there was a delay in the young people with ADHD, the order in which the different parts of the cortex matured was similar in both groups.
Shaw was asked whether the findings indicate that children will eventually grow out of ADHD. The study findings cannot be interpreted to mean that in ADHD the brain normalizes at age 10 or 12, he said.
“The delay we showed is carried forward into adolescence,” he said. “Also we know from a host of other studies that there are very real persisting structural and functional differences between teenagers with ADHD and those who don’t have the disorder.” Frequently, he said, outcomes reported in previous studies depend on how ADHD is defined. If you use a strict definition, he explained, about one quarter of people who grow up with ADHD will still meet the definition in adulthood. If a broader definition is used, about two thirds of people with childhood ADHD will still have troublesome symptoms in adulthood.
Studies that measure brain volume or function also have detected differences between the brains of young people who have ADHD and those of individuals who do not have the disorder.
“One very striking thing about our findings is that they complement existing imaging studies from other groups that found structural and functional differences, and all of them are pointing to similar parts of the brain,” Shaw said.
Why the delay?
Discussing factors that might underpin the delay, the research team mentioned psychostimulants and genetic factors. Most of those with ADHD in the study were receiving standard treatment with psychostimulants, but there were not enough medication-naive children to analyze them as a separate group, according to Shaw. In the published report, the research team wrote “trophic effects of treatment with psychostimulants in the ADHD group are possible, but unlikely, given our previous reports of no effect of psychostimulants on gray matter volume.”
“Genetic factors will certainly play a role, with a perturbation in the developmental sequence of the activation and deactivation of genes that sculpt cortical architecture,” the team wrote. “In this context, neurotrophins, essential for the proliferation, differentiation, and survival of neuronal and nonneuronal cells, emerge as promising candidates.”
“The numbers needed to do genetic studies are enormous,” Shaw said. “Of course, there are very good multisite collaborative studies going on, which are helping us identify the key genes.”
There are a host of candidates and factors that could control neural growth, Shaw said, acknowledging that dopamine and other neurotransmitters in the brain also are important to the growth of the cortex.
While research continues on possible causes of ADHD, Shaw noted that his team would be using brain-imaging techniques to study what happens to children with ADHD as they grow older.
“There is a large cohort of children who have very persistent ADHD,” he explained. “We want to compare them with the kids who get better from ADHD. That involves scanning the kids a little bit later when they are in their mid-teens.”
Diagnosis and treatment
Brain imaging is not ready for use as a diagnostic tool in ADHD, Shaw said.”It is still too early to use neuroanatomical scans for diagnosis,” he said. “We had to scan hundreds of children to identify subtle differences. They [the differences] are very real, but they are subtle. So the scan of any one child will not tell you a great deal about whether [he or she has] ADHD or not. Currently, the diagnosis of ADHD remains clinical.”
What’s more, the brain imaging study was a “natural history study” and so it did not address treatment, he explained.
“We know the treatments that work for ADHD on the basis of very large clinical studies, including the Multimodal Treatment Study of Children With ADHD and the Treatment of Attention Deficit Hyperactivity Disorder in Preschool-Age Children study,” he said.
While the Shaw et al study is not relevant to issues of diagnosis and treatment, it is nevertheless important in providing another facet of our increasing knowledge about the neurobiology of this disorder, said F. Xavier Castellanos, MD, Brooke and Daniel Neidich Professor of Child and Adolescent Psychiatry and director of research for the New York University Child Study Center.
In his own work, Castellanos said, his group is pursuing some novel methods of functional MRI that may well have diagnostic implications.2,3
Also responding to the Shaw et al study was E. Clarke Ross, chief executive officer for Children and Adults With Attention Deficit/Hyperactivity Disorder, a national advocacy and support organization.
“In a time when a vocal minority denies the mountain of evidence showing ADHD to be a real disorder,” he said, “it is nice to watch brain scans light up on televisions across the country with images actually showing the structural differences in the brains of those living with ADHD.”

Be Aware of Fraudulent "Natural" Flu Treatments

FDA NEWS RELEASE

For Immediate Release: Oct. 19, 2009

Media Inquiries: Christopher Kelly, 301-796-4676 christopher.kelly@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA

FDA, FTC Issue Joint Warning Letter to Web Site Offering Fraudulent H1N1 Flu Supplements


Agencies continue effort to protect public health from illegal Web activity

On October 15, 2009, the U.S. Food and Drug Administration (FDA) and the Federal Trade Commission (FTC) issued a joint warning letter to a Web site marketing fraudulent supplements that claim to help prevent the spread of the 2009 H1N1 influenza virus.

The warning letter, the first to be issued jointly by the agencies, advises the owners of the site that they must discontinue the fraudulent marketing of their product or face legal action. The letter further advises the owners of the site that they have 48 hours to give the agencies a plan to discontinue their fraudulent marketing.

The FDA and the FTC remind consumers to be cautious of promotions or Internet sites offering products for sale that claim to diagnose, prevent, mitigate, treat or cure the 2009 H1N1 influenza virus. Fraudulent H1N1 influenza products come in many varieties, including dietary supplements, as well as products purporting to be drugs, medical devices or vaccines. Since May 2009, the FDA has warned more than 75 Web sites to stop the sale of more than 135 products with fraudulent H1N1 influenza virus claims.

“Products that are offered for sale with claims to diagnose, prevent, mitigate, treat or cure the 2009 H1N1 influenza virus must be carefully evaluated,” said Commissioner of Food and Drugs Margaret A. Hamburg, M.D. “Unless these products are proven to be safe and effective for the claims that are made, it is not known whether they will prevent the transmission of the virus or offer effective remedies against infection. Furthermore, they can make matters worse by providing consumers with a false sense of protection.”

The FDA and the FTC also warn consumers to take extreme care when buying products over the Internet that claim to diagnose, prevent, treat or cure the H1N1 influenza virus because, in addition to being fraudulent, they could be dangerous.

In collaboration with the FTC, the FDA will continue to work aggressively to identify, investigate and take regulatory action against individuals or businesses that wrongfully promote purported 2009 H1N1 influenza products.

This will include taking joint action, when appropriate, such as the issuance of last Thursday’s warning letter. Additional legal action could include an injunction or issuance of an administrative order by the FTC or seizure of products, an injunction or criminal prosecution by the FDA.

“The FDA continues to consider the sale and promotion of fraudulent H1N1 influenza products to be a possible threat to the public health and in violation of the Federal Food Drug and Cosmetic Act,” said Michael Chappell, acting associate commissioner for regulatory affairs. “The FDA has an aggressive surveillance program to detect fraudulent H1N1-related products and will take prompt action to stop the marketing of fraudulent H1N1 influenza products and will hold those who are responsible for doing so accountable.”

To view the warning letters, visit: http://www.fda.gov/ICECI/EnforcementActions/WarningLetters/2009/default.htm.

There are two antiviral drugs approved by the FDA for treatment and prophylaxis of the 2009 H1N1 influenza virus – Tamiflu (oseltamivir phosphate) and Relenza (zanamivir). Tamiflu and Relenza, in addition to their approved labeling, have been issued Emergency Use Authorizations by the FDA that describe specific authorized uses during this public health emergency.

H1N1 Flu Fraud Widget

This week, the FDA enhanced its efforts to warn the public about potentially deceptive H1N1 influenza products and to report suspected criminal activity with the release of an H1N1 flu fraud widget.

The portable application, embedded in a Web page that can be copied onto any other Web site or blog, will allow the public to play an active role in preventing flu fraud, and is available at http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm186340.htm

Consumers are urged to report any suspected fraudulent products or criminal activity relating to FDA-regulated products associated with H1N1 influenza virus, including the names of Web sites that may be offering these products for sale, to the FDA by visiting: http://www.accessdata.fda.gov/scripts/email/oc/oci/flucontact.cfm

Consumers are urged to purchase and consume only FDA-approved or authorized medical products to diagnose, treat, prevent, or cure infections caused by the H1N1 virus. Consumers also are urged to contact their health care provider if they have any questions or concerns about medical products or personal protective equipment.

For more information:

FDA 2009 H1N1 (Swine) Flu Page
http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm150305.htm

Centers for Disease Control and Prevention – 2009 H1N1 Flu (Swine Flu)
http://www.cdc.gov/h1n1flu/

Fraudulent 2009 H1N1 Influenza Products List
http://www.accessdata.fda.gov/scripts/h1n1flu/

Influenza Antiviral Drugs and Related Information
http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm100228.htm

The Federal Government’s Influenza Web site
http://www.flu.gov/

FTC Warns Internet Peddlers that Potentially Bogus H1N1 Influenza Products May Violate Federal Law—Press Release, May 5, 2009
http://www2.ftc.gov/opa/2009/05/swineflu2.shtm

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