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Author: Stephen J. Klemawesch, MD

Chicken or egg? 5-year-old not confused

Chicken or egg? 5-year-old not confused

Poets and philosophers long have argued chicken/egg algorithms. And scientists have argued food allergy/eczema scenarios. For years it was felt food allergy was the seminal event preceding eczema.

The natural history and logic of this position are hard to dismiss. Even a 5-year-old who recently completed his allergy testing to better understand his skin rash, (which showed strong positives to both egg white and egg yolk), asked me why he needed to have these tests for his “eggs-ema.” Wasn’t it obvious to the doc that eggs were the cause?

As it turns out, it’s the eczema that causes the food allergy. Or actually in more technical terms, it’s the loss in skin-barrier function that causes food allergy. The primary fault in eczema is a less-than-ideal barrier response of the skin, due to reduced production of a barrier protein called filaggrin. This allows skin absorption of food, which in turn leads to the development of food allergy. The loss of barrier function antedates the actual appearance of the eczema rash.

Ironically, once the food allergy develops, it becomes a strong driving force to worsen the eczema.

Allergenic children born that way

Allergenic children born that way

Infants who have food allergy display a pro-inflammatory profile at the time of birth in their umbilical cord blood.

So say research scientists at the University of Melbourne. They found that the length of a woman’s labor seemed to lead to greater numbers of white blood cells that produce inflammatory proteins (called cytokines). In other words: short labor also leads to less chance of food allergy; long labor leads to a greater chance of food allergy.

Dear Doc: How long can I count on my Epipen?

Dear Doc: How long can I count on my Epipen?

Dear Dr. K: I keep an Epipen for “just in case,” but so far I have never had to use it. I keep replacing it when it expires, but it is expensive. Is it possible to use it past its expiration date? 

The answer is “yes, probably.”

The “probably” is based on the clarity of the liquid. If, when you look through the syringe and the medicine is clear, then it’s both safe and effective. If the liquid is yellow or cloudy, then discard it.

The Medical Letter, which is a nonprofit academic resource for physicians and hospitals seeking non-pharmaceutical company-biased information, actually addressed these issues in their December issue. They actually cited their research studies done on epipens.

The first study looked at pens that were from 1 to 90 months past their expiration. This showed a percentage reduction in potency correlated with the number of post-expiration months; i.e., pens one-month past expiration had 1 percent reductions in potency, while pens 90 months past had 90 percent reductions.

A second study evaluated pens 36 months past expiration and found them to be from 84 to 100 percent potent.

A third study looked at epipens stored on EMS vehicles that were from one to 11 years expired. These devices retained from 3 to 31 percent of their potency. The Medical Letter pointed out that exposure to greater heat in the ambulances will speed the degradation of the active medicine.

Data from the U.S. Department of Defense/FDA Shelf-Life Extension Program, which tests the stability of drugs past their expiration dates, showed that in a study of 3,000 different drugs 88 percent of them remained stable and fully active 66 months past expiration. High heat and humidity do accelerate degradation of many drugs.

This publication did say that ophthalmic (eye) medicines should never be used beyond expiration, even though the medication may be stable, because bacterial contamination occurs with repeat use. Authors also pointed out that certain dry powder inhalers such as Advair Diskus slowly absorb moisture once the device is removed from its foil container. This “gums up” the delivery in devices past expiration.

Not allergy, but relief offered

Not allergy, but relief offered

Pityriasis rosea is not an allergic condition but is frequently seen by allergists as its main manifestation is a skin rash that looks “temptingly allergic” in nature.

This rash is preceded by a single spot called the “herald patch.” This clue is sometimes missed because it appears in a hidden spot on the body such as the back or armpit. Within one to two weeks of the herald, a generalized rash appears.

The spots are circular to oval in shape and about the size of a mosquito bite. There tends to be a little scaling of the skin from the pink/red spots.

On the trunk the rash often resembles a “Christmas tree” in distribution. It can occur at any age but is most common between 10 and 35 years of age.

Most patients don’t feel any sensation from the rash, but 10-15 percent feel mild itchiness. It can occur year-round, but is more frequent in the spring. Notably, in 69 percent of cases the rash is preceded by a simple upper respiratory infection.

Thought to be caused by reactivation of herpes viruses 6 and 7- which causes roseola in infants – the rash is usually the lone symptom, but some patients get a low-grade temp, headache, fatigue and nausea.

The rash is so typical it is usually diagnosed with a glance, but could be occasionally confused with Lyme disease, ringworm or psoriasis. It lasts three to 12 weeks and can be helped with the antiviral Acyclovir. Sunlight helps it heal, and moisturizers and antihistamines can be used by people who itch.

Long study of steroids in childhood asthma released

Long study of steroids in childhood asthma released

The results of a Harvard study done over the past 25 years on childhood asthma are somewhat distressing. The research was published in a recent edition of The New England Journal of Medicine. Known as CAMP – Childhood Asthma Management Program – the study allowed long-term outcomes to be determined.

It compared the use of a daily inhaled steroid versus placebo for the first 4.5 years. Then the children were returned to the care of their pediatricians and followed for 20+ years. As young adults, 11 percent of this group met the World Health Organization’s criteria for COPD (Chronic Obstructive Pulmonary Disease).

Also, there was no apparent long-term preventive value from the 4.5 years of daily steroid use during childhood. Development of chronic impaired lung function occurred equally in treated and untreated groups. Remember that despite this lack of long-term benefits, inhaled steroids are still the cornerstone of asthma management. Hundreds of studies have shown their benefit in controlling symptoms, improving quality of life and reducing ER visits and asthmatic deaths.

At least, there is a therapy known to prevent long-term loss of lung function in asthmatic children — that is immunotherapy (allergy shots). Of course, it only benefits children whose asthma is allergenic in nature. Fortunately, this is the majority of asthmatic children.

Infants who have food allergy display a pro-inflammatory profile in their umbilical cord blood at the time of birth.

So say research scientists at the University of Melbourne. They found that the length of a woman’s labor seemed to lead to greater numbers of white blood cells that produce inflammatory proteins (called cytokines).

Thus: short labor also leads to less chance of food allergy; long labor leads to a greater chance.

Q – Tips: phenylephrine

Q – Tips: phenylephrine

  • A recent double-blind study comparing phenylephrine to placebo showed no measurable difference in reducing nasal congestion. For people who need/use pseudoephedrine for their congestion, it is available “behind the counter” and must be signed for.
Dear Doc: Wheat, gluten, inflammation — baffling!

Dear Doc: Wheat, gluten, inflammation — baffling!

Dear Dr. K: I’ve had a blood test for gluten sensitivity, allergy tests for wheat and even an intestinal biopsy for celiac. All the tests are negative, but I still feel better when I avoid wheat. What gives?

What gives is that wheat is not good for you. No medical test is perfect. Even “gold standard” tests such as chest X-ray for pneumonia or cardiac catheterization for coronary blockage sometimes fail to demonstrate an existing abnormality. The bottom line is to listen to your body – it almost always gives reliable feedback.

I suspect you feel better wheat-free for one of two reasons: 1.) You are wheat-allergic or gluten sensitive, despite negative tests or, 2.) You are feeling metabolic and inflammatory buffeting from wheat.

Regarding the first possibility, the Mayo Clinic published research data from their GI department. They found that 15 percent of their patients with chronic GI problems improved on a wheat-free diet, despite negative tests for gluten sensitivity. They posited that perhaps a better test for gluten sensitivity needs to be invented.

With respect to the second possibility of metabolic and/or inflammatory problems, this case was probably best summed up by Dr. Daniel Lieberman, a Harvard social anthropologist, in his book, The Story of the Human Body. He maintains that the cultivation of wheat, starting 10,000 years ago, was both the best and worst step for humans. He contends the ability to farm allowed humans to move from sparsely populated hunter-gatherers to the burgeoning population of civilized humans who have covered the globe.

The trade-off, he says, is a dramatic increase in the “civilized” diseases of metabolism and inflammation. Ghrelin, leptin, adiponectin and insulin are crucial to proper metabolism and weight management, and all four are adversely affected by wheat. He points out the phytic acid (phytate) in wheat severely reduces absorption of essential micronutrients and vitamins.

With respect to inflammation, gluten is pro-inflammation; in addition, wheat contains the lectin WGA (wheat germ antibody). Lectins are proteins that bind to the glycoproteins and glycolipids found in many cells in the body. These include: skin, respiratory system, GI tract, nerves, cartilage, connective tissues, prostate, kidneys, pancreas, liver, uterus and thyroid. This binding serves as a promoter of inflammation in these tissues. Lieberman draws a direct parallel between the increased consumption of wheat and the appearance of “modern” diseases such as diabetes, heart disease, autoimmune diseases, allergy and cancer.

Drug hypersensitivity genetic?

Drug hypersensitivity genetic?

The most common cause for drug allergy is from IgE-mediated (allergic) reactions, such as having hives from penicillin. New research is discovering a second mechanism for drug reaction being called “drug hypersensitivity,” as it is mediated by T-lymphocytes. The reactions are different from the arch-typical “allergy” in that they tend to be somewhat delayed and different types of rashes. Examples are measles-type bumps, the life-threatening skin condition Steven-Johnson Syndrome or liver irritation.

Of great interest is that there seems to be a genetic predisposition to react to certain individual drugs. Following is a list of certain HLA (genetic) types and the drug that reacts:


Genetic Type


HLA A 31:01


HLA   A 33:03


HLA   A 68:01


HLA   A 02:06

Cold Medicines

HLA   B 56:02


HLA   B 58:01


HLA   DRB 1 11:01


HLA   DRB 1 13:02


HLA   C 04:01



Because this research is new there are lots of uncertainties. Genetic testing is expensive, and everyone with the implicated gene won’t react to the medicine. It’s too early to recommend across-the-board testing, but an awareness of possibilities, along with finding less expensive ways to do this testing, may soon lead to “genetic profiling” of all of us.

‘Magic Bullet’ antibodies beef up to meet today’s need

‘Magic Bullet’ antibodies beef up to meet today’s need

In the early 1900s, German scientist and Nobel Laureate Paul Ehrlich pioneered an antiserum to help combat diphtheria. His anti-serum saved many lives in the pre-antibiotic era. He also popularized the concept in medicine of a “Magische Kugel” (Magic Bullet).

His idea was to find treatments that were so specific that they only worked on their specific targets without any collateral effect or damage to the body. In 1975 Cesar Milstein and Georges Kohler (also Nobel Laureates) invented hybridoma technology which allows the production of large quantities of antibodies specific for a single target also known as monoclonal antibodies.

Roughly 10 years later the first therapeutic antibody was made: monoclonal antibodies (muromonals), with a target of the CD-3 receptor on T -lymphocytes. You see, by inactivating CD-3, it prevents rejection of organ transplants, and it revolutionized transplant medicine by allowing better survival with less need for high-dose steroids.

Since 1985 the floodgates have opened up with more than 35 monoclonal antibodies that have been approved by the Food & Drug Administration (FDA) for use in medicine. Hundreds more are being researched. These antibodies are used to treat a variety of diseases. Some examples which include the antibody, the target and the disease follow.







Rheumatoid arthritis



Crohn’s disease








Gp11b/111a on platelets

Prevent clots

after coronary stenting



Breast cancer


Two other strategies being worked on are using monoclonal antibodies as vaccines and making an antibody-drug conjugate. The idea is to couple an antibiotic or an anti-cancer drug to the “magic bullet” so only the target receives the medicine. This would allow high concentrations of the drug to be used.

As far as vaccine therapy goes, there actually is one already in use: palivizumab, which targets the F protein found on RSV (Respiratory Syncytial Virus). It is given once a month to high-risk infants to prevent their catching RSV.

Similar efforts are underway to develop a vaccine for HIV, and also one for influenza.