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Month: August 2012

Flu shot value supercedes fear of many;

Flu shot value supercedes fear of many;

Dear Dr.K: I’ve never taken the flu shot because my father got Guillian-Barré syndrome from the 1976 swine flue vaccine. Now that I’m 50, I worry about getting really sick from influenza. Do you think I can take the flue shot?

In a word, “yes.”

For those readers who don’t know about Guillian-Barré, let me explain. Now that polio is almost non-existent, Guillian-Barré is the most common cause for acute paralysis worldwide. Even though fewer than 5 percent of affected people die, it still can be a very serious problem. Typically, the weakness (paralysis) starts in the peripheral muscles of the feet and hands and moves upward.

Most of the cases occur after a pre-existing respiratory tract infection or diarrheal illness. The single most common cause for Guillian-Barré is a G.I. bug caused by campylobacter jejuni (a bacteria known to be a main cause of bacterial food-borne disease in many developed countries). Other common pathogens capable of causing it are cytomagalo virus (an infection caused by a member of the herpes virus family); Epstein-Barr virus (which is very common and usually mild); varicella-zoster virus (chickenpox and shingles viruses), and mycoplasmas (stealthy bacteria that can cause acute and chronic diseases at multiple sites).

In 1976 there were a number of individuals who got Guillian-Barré after receiving the swine flu (H1N1) vaccine. Subsequent seasonal flu vaccines over the past 36 years have not been associated with this risk. In fact, in 2009, the National Institutes of Health and the Centers for Disease Control had some concern that the H1N1 vaccine that year might have the same potential as the 1976 H1N1 vaccine, but this turned out not to be the case.

The reason that an antecedent infection can trigger Guillian-Barré is because of a phenomenon called molecular mimicry. Lipooligosacchoride is a big word for a small molecule that is a major component of the myelin, which is the protective coating on our nerve fibers. Certain viruses and bacteria have the molecule in their outer membranes. When susceptible individuals who are infected mount an immune response to kill the infecting organism, they make antibodies against the lipooligosaccoride. Unfortunately, this also attacks the same molecule (molecular mimicry) found on the nerve sheaths.

Thus, the individuals’ nerves are attacked by their own immune system.

Luckily, there are modern immune therapies that can help slow and turn off this auto-immune attack, and thereby lessen the severity of the illness.

Egg Desensitization

Egg Desensitization

 Researchers at Duke University recently have completed a multi-year study of oral desensitization for egg allergy. They studied 55 children between five and eleven years of age with severe egg allergy.

Forty children were randomized to receive the oral vaccine while 15 received a placebo vaccine.

After 22 months of daily vaccine intake, all 55 children underwent a food challenge with egg. One-hundred percent of the placebo-treated children had an allergic reaction to the egg challenge; only 25 percent of the vaccine-treated children reacted allergically.

The vaccine therapy was discontinued after 22 months. Two months later the 40 children who received the true vaccine were re-challenged with egg. Of the children who had negative challenges at 22 months, half had a reappearance of their allergy. The children who were able to eat the egg challenge with no reaction, however, remained free of symptoms at 30 and 36 months. That is, they had a permanent resolution of the allergy that persisted even off the vaccine.

Don’t despair at urgent, post-meal, ‘uh-oh’ moments

Don’t despair at urgent, post-meal, ‘uh-oh’ moments

Postprandial Diarrhea Syndrome (PPDS) – the unexpected and urgent bowel movement shortly after eating a meal – was the topic of a recently review article in The American Journal of Medicine. The authors of this review (from the Mayo Clinic) commented that this condition is often given the all-embarrassing moniker of irritable bowel syndrome (IBS).

But they go on to say that unlike IBS, where no cause is known, PPDS can have a treatable cause. The most common of these are food allergy, celiac disease, maldigestion due to bile acid malabsorption, pancreatic deficiency or an a-glucosidase deficiency.

Food allergy is best diagnosed by allergy skin testing. The treatment is avoidance of the allergenic foods. Celiac disease is an immune (non-allergic) reaction to gluten and can be diagnosed by blood test or intestinal biopsy. Again, the treatment is avoidance of wheat and other grains.

Bile acid malabsorption is best diagnosed by an empirical trial of a taking a bile acid-binding resin. There are sophisticated GI tests that can be done, but these are usually only available in a research medical setting. If the bile-acid binding resin controls the symptoms, then it is continued as a maintenance therapy.

Pancreatic insufficiency (lack of the digestive enzymes produced by the pancreas) can be diagnosed by a fecal fat analysis. Treatment consists of taking replacement pancreatic enzymes orally.

A-glucosidase deficiency is the lack of one or more enzymes that break down certain sugars. The most common ones are deficiency of sucrase, glucoamylase, maltase and isomaltase. Treatment involves avoidance of foods that contain the specific sugars.

Before embarking on a diagnostic trip for PPDS it is important to have proper gastro-intestinal evaluation to rule out more serious underlying conditions, such as cancer, Crohn’s disease or other inflammatory bowel diseases.

White blood cell type counts

White blood cell type counts

An article in The American Journal of Respiratory and Critical Care Medicine discussed recent research of the heterogeneity or diversity of asthma. The thrust of the research project was to try to explain the variable benefit that asthmatics receive from inhaled corticosteroids.

It has been observed for quite some time that while many asthmatics show a marked improvement in their breathing with the use of inhaled steroids, there are others whose response to steroids is modest or nonexistent. Inhaled steroids have been a mainstay in asthma management for years. Because it is known that asthma occurs due to inflammation in the airways, steroids are potent anti-inflammatories and, hence, the predictable nature of their benefit.

Inflammation is defined as the incursion of white blood cells from the blood stream into the inflamed tissue. As it turns out, the type of white blood cell found in asthmatics determines how they respond to steroids. If the white blood cell is an eosinophil, then the patients have greatly benefitted by the inhaled steroids. If the white blood cell is a neutrophil, then steroids have been much less effective.

The researchers used a relatively test called sputum cytology. They collected multiple samples of sputa from a large number of asthmatics. These were sent to a special pathology lab to determine the type of anti-inflammatory cell: eosinophil or neutrophil. The researchers had already separated the asthmatics into groups of “steroid responders” and “steroid non-responders.” The two groups matched up perfectly with the cell type eosinophil or neutrophil respectively.