Golden Wedding Anniversary Story

Well Linda and I celebrated 50 years of marriage on June 30th, 2023. We had plans to be on the road to North Star Lake, Minnesota to see family so the ‘celebration’ had to be on June 29th. I made reservations for 7:00 pm at our favorite restaurant, Angotti’s. During the hours before it took four visits to florists to find a corsage for her. I took the corsage to Angotti’s and gave it to the owner/chef, Ingrid. She was to give it to Linda upon arrival and she should the bouquet of roses setting at our table. Sounds like a great plan, right?

Then Mother Nature intervened. A rather impressive storm knocked out the power in downtown Columbus at about 4:30. We arrived for our date at about 6:50- Angotti’s was closed, and the entire area was dark. Linda had no idea what I had planned. I insisted we wait for a while. By 7:15 I realized this was not going to happen. I told her what was planned, and we went to Amazing Joe’s for steak.

She was amused by the story. We enjoyed our meal and when it was time to square up (pay the bill), the server said we were good to go, someone had paid for our dinner. We will never know who did that, but THANK YOU- it was a nice ending for a day that did not live up to expectations.

While on the road to Minnesota, Angotti’s sent a picture of the corsage.

Now that day was supposed to also be a ribbon-cutting Columbus Chamber of Commerce event or grand opening for Angotti’s (the weather knocked that out too). Yesterday, the ribbon-cutting event took place. While partaking in the festivities Ingrid told us that corsage was still there and brought it out. There was availability for dinner there and we returned at 7:00. Chianti, Ceasar salad, fresh bread, lasagna, chicken parmesan, NY cheesecake, and limoncello were enjoyed along with the staff and ambiance of Angotti’s. Pictures were taken and are on Linda’s Facebook page.

It took a while, but our 50th anniversary was quite eventful.

FEL July 14, 2023

Fenugreek and Legume Sensitivity

The case of Fenugreek

Up until a week ago, I had never heard of fenugreek.  On my first day back at Riley to start the 2009 new year, I had a young man, just under 2 years of age who presented with concerns about reactions to legumes. The list of suspects included peas, green beans, black beans, baked beans, and lentils. The mother also shared with me that during breast feeding she used ‘fenugreek’. This product is used to help nursing mothers. In our discussion, the mother brought up the concern that the fenugreek may have contributed to the legume reactions.

I had not heard of ‘fenugreek’ prior to this. I have been involved with allergy long enough to know that any food product ingested by mankind for as long as we have been on the planet has been implicated in an allergic response. I wanted to know more about this ‘fenugreek’.

I consulted my online food ‘Allergy Advisor’ regarding fenugreek and got a wealth of information to get me started. To my surprise later that week the Journal of Allergy and Clinical Immunology (JACI) had an article from a group in Norway regarding fenugreek.

Fenugreek (aka Greek hay, Greek fennel, Bird’s foot, Greek hay-seed) is a legume. It is used as a flavoring in many foods including curry, blends of spice, and even tea. As an herbal medication it has been touted as being helpful in initiating and maintaining milk production. There are references for its use in diabetes and hypertension. Importantly, it is a legume and many legumes share certain proteins and may be cross-reactive in some patients.

The purpose of the JACI article was to evaluate the allergenicity and antigenicity of the proteins in fenugreek. There were 29 patients in the study who had specific IgE antibodies to legumes, peanut, soy, pea, lupin, and fenugreek. These patients ranged from 1 to 53 years of age. High levels of antibody to both peanut and fenugreek were found in most patients and the sensitization to fenugreek was believed to be due to cross-reactivity in those patients with peanut allergy. In this study, the reactivity to the other legumes was weaker. Here the other legumes (specifically peanut) were implicated in causing sensitization to fenugreek. With the young lad that I saw I wondered if there is the possibility that the fenugreek may have worked in the opposite direction – fenugreek exposure causing sensitization to the other legumes.

I was not aware of this association: fenugreek and peanut. In my clinic notes I debated about doing the peanut test since he had no exposure, but since he reacted to a large number of the other legumes I had the skin test placed. His response was positive to peanut.

The world of IgE-mediated reactions to foods is growing significantly. Our diets are changing with significantly more opportunities for ingredients in foods from other lands becoming part of our lives. Herbal supplements may contain a variety of items that could lead to sensitization. It is important to inquire about the use of such products.

Highlights from the 2009 Allergy Meeting

I recently attended the 2009 annual meeting of the American Academy of Allergy, Asthma, and Immunology(AAAAI) in Washington, DC. There were five days of extraordinary educational activities (March 13-17, 2009). I thought that while I could still read my notes I would share with you a few things I observed, heard, and learned in the ever evolving world of allergy. I plan to adopt many of these changes in my practice.

The meeting’s agenda covered a wide variety of clinical conditions. It would have been impossible to attend every session. I chose sessions on the allergic environment, eczema, immunotherapy, food allergy, re-certification, headaches, and asthma. There are a number of ideas that are evolving and a number of things currently done in allergy/asthma care that need to change. Each and every one of these topics is truly worthy of more extensive review. I would be happy to use this blog to delve into topics in more detail (per request).

Atopic Dermatitis (aka Eczema)

I still need to be convinced regarding what to call this condition. Dr. Jeff Travers (chief of Dermatology at the IU School of Medicine) and I go back and forth on this topic. During the meeting I heard the concept of extrinsic and intrinsic atopic dermatitis. Extrinsic means from the outside and intrinsic from the inside. These terms have also been used for years to describe two presentations of asthma: extrinsic asthma due to allergy, and intrinsic asthma when no allergy is found. The word atopic means 1) the tendency to come from families with allergy, 2) to make the antibody seen with allergy (IgE, which would be elevated) and 3) to have positive allergy tests. Thus, Intrinsic AtopicDermatitis means no allergy demonstrated (intrinsic) in a condition associated with allergic sensitization (atopic). This blending of terms leads to confusion–why not stick with the simpler term of eczema?

I learned about the use of silver impregnated clothing to decrease the amount of bacteria on the skin. Skin bacteria can cause flaring of atopic dermatitis.

A number of  genes associated with atopic dermatitis have been discovered. These discoveries should increase our understanding on how this condition starts and hopefully how we can manage it better.

There was information on allergens that contain enzymes called proteases and how these protease containing allergens aggravate the skin.

Probiotics have been used to treat allergic conditions especially conditions related to food allergy. A review of studies on probiotics have not shown them to be effective in preventing or treating atopic dermatitis.

I listened to debates about being proactive in skin care therapy vs. being reactive. Proactive would be trying to prevent and reactive being treating only when there is a problem. This idea was particularly interesting. Atopic Dermatitis Guidelines and package inserts for a variety of medications used for atopic dermatitis treatment stress short courses of use, the reactive approach. The proactive debater posed the problem of a chronic disease that will have episodic flaring. The abnormality of the skin is there all the time requiring the need for medication to be used perhaps twice a week to avoid flares (those times when the skin is more itchy, more inflamed, and more broken down). Pediatrics deals extensively with disease prevention. My pediatric perspectives are preventative- proactive. All too often we (as patients) tend to be crisis-oriented or reactive to chronic conditions. I am obviously on the proactive side of this argument.

Therapies emphasized moisture and more moisture. Keep these kids wet! This is clearly a major step that is contrary to previous approaches that recommended the avoidance of frequent soaking/bathing. The avoidance of baths is clearly one of those long established principles of atopic skin care that has fallen by the wayside in contemporary skin care.

Foods are an issue in atopic dermatitis. The protease containing allergens such as molds, pets, and mites may have a role in triggering flares.

In Boston a program that has had success includes insuring compliance with the medications (taking them as prescribed), addressing the parents concerns about medication side-effects (helps with compliance), decreasing the itch, and increasing sleep. These are all essential elements to help with control of the condition.

Of note, we need to re-think the role of a specific therapy and make adjustments. Antihistamines are frequently used in atopic dermatitis. In allergic rhinitis and in hives, these products help control itch. However, in atopic dermatitis, the antihistamines have little effect on itch. The role of the anti-histamine is to sedate. Most of the scratching happens at night. A sedating antihistamine used at night works best.

Asthma

There were a number of new ideas regarding asthma. Look for vitamin D to have a possible role in treatment.

Current recommendations from evidenced-based asthma guidelines point out a difference between adults and children and the use of the long-acting bronchodilators in the two populations. These agents are called long-acting broncho-dilators (LABAs). In children, we should increase the dose of the inhaled corticosteroid before adding a LABA. This recommendation appears in two major asthma guidelines with type A evidence used to support the recommendation. This type of evidence (A) means that there are a substantial number of studies that support this statement.

Asthma may be related to bacterial colonization at birth and to the occurrence of the common cold virus later in life. Evidence was also presented regarding the observation from large population studies that the process of airway inflammation starts well before actual symptoms. We heard about diet, viruses, stress, ozone, and endotoxin having a role in the development of asthma. The gene or genes for asthma need to be present. These genes then need to be activated or expressed for the child to show the signs and symptoms of disease. Bacterial colonization and a variety viruses may have a role in activating the genes.

Headaches

This was a great session. The audience heard from an ENT surgeon, an allergist, and a neurologist regarding their approach to headaches. The consensus was that migraine is the biggest player in these situations. The connection of allergy to headache has always been a concern. However, headache is not a manifestation of allergy. There are many studies that have looked at this. People with headaches can have positive allergy tests but does that make the allergen the cause of the headache? Think about other conditions or associations. Could there be an allergic cause for an appendicitis?

I heard of the concept of ‘allergic appendicitis’ during this presentation. It was very odd to hear about this in a headache session, but a valid point was made. This concept of the allergic appendix was compared to allergic headaches. Follow along; data from a national health survey from 1994 indicated that 50% of the population reported that they had allergy. So if someone who had problems with the appendix was allergy tested, the chances are very high that allergy would be found. This however does not make the inflammation of the appendix due to allergy. You can find a significant number of positive allergy tests, be sure of why the tests are being ordered. Think migraine more often as a reason for headache. Allergy is not a major reason for headaches.

Food Allergy

The biggest news from the meeting was the work done by Wes Burks at Duke on peanut allergy. This is exciting and long awaited for those who have peanut allergy and for the families who have someone with peanut allergy. Immunotherapy for peanut trials have allowed the equivalent of about 12 peanuts to be eaten without any problems/reactions. This would certainly take the fear from accidental exposure to peanut especially from tabletops at school cafeterias. I have to check my note again, but I had written down the treatment would be a suppository(?).

There was a very popular abstract (a quick presentation of work in progress prior to it being published in a journal) on food allergy and the over- use of panels for food allergy (pet peeve). A New York Times article a few months ago reported that food allergies were being over diagnosed. Dr. Sears at National Jewish Hospital in Denver, Colorado reported on over one hundred children seen at their center who had food allergy as determined by blood test panels. The average number of food allergies reported were six. After undergoing food challenges the number decreased to only 2 foods. 88% of the foods this group of children were told to avoid based on RA ST panels were added back into the diet. Using a food challenge, no one with meat ‘allergy’ had a positive food challenge (where meat caused a problem), 88% of the grain ‘allergic’ children were negative on challenge, and 83% of the fruit and vegetable group were also negative after a food challenge. Bottom line- the use of these panels is giving falsely positive information and leading to a misdiagnosis of food allergy.

Allergy Testing

I learned that I should no longer use the word RAST. The term is outdated and refers to a technology not used. The blood tests for allergens should no longer have a 0-6 grading scale and should only be reported in what is actually measured kU/l of serum. The test measures a concentration of a specific antibody in the blood. The relationship of that concentration to clinical activity needs to be determined by the clinician. I predict that the interpretation of the blood test results may be a huge issue.

A new in vitro or blood test for specific IgE in the blood is called an ISAC chip. This technology will help with cross-reacting proteins. We see the problem of cross-reactivity with multiple positive allergy tests to legumes (peanut, soy, beans, and peas). I think this will be a very worthwhile test in allergy.

There are three blood tests out there for detecting specific IgE. These are the Immunolite, ImmunoCap, and Hytec. Each of these measure something different. They measure a different population of IgE antibodies and may not be comparable. Caution was advised regarding the blood tests for specific IgE. The physician should know the method used, the validity of the assay, the performance of the laboratory in doing the assay, and realize that no test for allergy is infallible.

Conclusions

Each and every one of these topics could stand alone for more detail and interpretation and I would be most happy to elaborate in more detail. Let me know if you would like more information by adding a comment. If there continues to be an increase in the use of specific IgE panels (as advocated by those who market these tests) we will be doing significantly more food challenges in our office. Usually we are doing food challenges for those who may have outgrown a food allergy. We certainly can offer a food challenge for a child who has been told that food allergy exists based on blood test results. One of my tasks upon my return to the office is to look at our track record of doing food challenges. I hope to report on our successes and failures for our food challenge experience with milk, egg, soy,wheat, and of course peanut.

Respectfully submitted,

Fred Leickly

Farewell to Pontiac

 

I write this entry with a tear in my eye. In the Sunday Indianapolis Star I read the following story ‘Alas, the Pontiac- R.I.P..

My 1967 Lemans-May 3, 2009
My 1967 Lemans-May 3, 2009

Mr. Dan McFeely noted on the next line that ‘Aficionados lament General Motors’ decision to end production of the brand now likely to be a hot classic’. The obituary noted that GM life support for Pontiac was pulled on April 27th, 2009. Pontiac (nee the Oakland Motor Car Company) was born in 1926 in (appropriately) Pontiac, Michigan. Pontiac was the proud parent of GTO, Firebird, Catalina, Grand Prix, Bonneville, the Chief, the Star Chief, Fiero, and my beloved Lemans (just to name a few ).

I  owned a 1967 Pontiac Lemans convertible in 1973. I had that car for six months before it became car number five in a six car sandwich. The car was totaled in April in Cleveland, Ohio. I never had a chance to put the top down and enjoy it. I owned it for six months of which only one month was considered spring (I lived in Cleveland at the time).

In 2001 I thought I had seen a ghost. Appearing on the internet was the exact same car. It was the same color, the same year, the same make, the same everything. It was for sale in Southern California by its second owner who enjoyed driving the car to the beach with his surf board in the back.

Friends of mine looked at the car and I made the purchase. For the past eight years I have an exact copy of my 1967 Lemans (as I remember it from 1973).

I am sure you have all heard of the GTO and perhaps not so much about the Lemans. The Lemans has been called the poor man’s GTO. It has a very similar shape and look. This is my toy.

1967 Lemans

1967 Pontiac Lemans and home.                                                       

 lemans05141

 1967 Lemans – top down and ready to go cruising for burgers.

lemans05151

No 1967 muscle car would be complete without a hula girl on the console. This was courtesy of ‘Old Blue’s’ previous owner.

Fred Leickly

Teaspoons vs. milliliters- It does matter!

I receive the journal Contemporary Pediatrics. I have found the articles to be very practical for everyday use. For the most part the authors are reviewing a specific topic of interest. An author will condense a large volume of literature into a very readable format. Back in the day, I was asked to write an article about chronic hives for Contemporary Pediatrics.  I titled that article ‘When the road gets bumpy, chronic urticaria’.  I enjoy reading Contemporary Pediatrics and I have used interesting findings in this blog (see my note on the ‘Patient History’)

I always scan the articles and a while back I came across a little quip that caught my attention. It made me wonder about the many times I had suggested using a teaspoon measure of medication.

When we prescribe medications we all have the tendency to use the teaspoon/tablespoon measure of delivery. Our assumption is that a teaspoon is five milliliters (mls) and a tablespoon is three teaspoons so that would equate to 15 mls. The question was asked whether or not teaspoons are standardized. I discovered that they clearly are not and the use of teaspoons for dosing could lead to more overdosing as opposed to under dosing.

So the question is, do you use mls or teaspoons?

The article was amazing- It was a clinical tip about the timely death of the ‘teaspoon’ at least for giving medications. The work was done by Alvin N. Eden, MD, and Mohammad Mir, MD Department of Pediatrics, Wyckoff Medical Center Brooklyn, N.Y. and appeared in the November 1, 2008 Contemporary Pediatrics.

The background is that more than 50% of liquid preparations given to children are written as a number of teaspoons. This small research project looked at the volume of 53 teaspoons brought in by physicians, nurses, and the receptionists at a general pediatric practice. Only one of the teaspoons actually measured 5 milliliters. The range was 4.3-12.9 mls! Based on these findings, using the tsp format could result in overdosing by 2.5 times the intended dose.

This made me think about the use of oral steroids for our children who have a flare of their asthma. The medications are 15 mg per 5 mls and the dose would be 2 mg/kg of body weight per day. If a teaspoon that measured 12.9 mls was used, then 38.7 mg were given and not the intended 15 mg!  Steroid side-effects could occur due to the over-exposure via generous teaspoons.

Due to this extreme variability in volume and the chance of an overdose, the milliliter format was suggested as the proper way to administer liquid medications.

Go metric- ask for how many milliliters and use the proper dosing apparatus.

Fred Leickly