Vitamin D3 is a general immuno-suppressant. Macrophages, monocytes, and other effectors cells of immune system have receptors for Vit D. At a recent Allergy meeting there was a poster presentation that showed supplementing Vit D reduced acute asthma exacerabations in the active group vs. placebo. Also, people high risk for developing MS nowadays are prescribed moderately strong doses of Vit D3. (2000 U/day)

The therapeutic-toxic gap of Vit D is much wider (unlike Vit A). Therefore relatively high doses are well tolerated. There is currently a proposal before FDA to raise the daily requirement of Vit D in an adult to 1-2000 units.

More time is spent indoor over the past 50 years, resulting in less sun exposure. And inadequate intake leads to vitamin D deficiency. Increases in TH2 balance leads to more asthma and allergies. I have not checked in my asthmatic patients, but I am thinking about it.

I think that some of the other information coming out about vit D deficiency and risk factors for other medical problems is interesting as well. D deficiency may be associated with increased risk for multiple sclerosis and insulin resistance.

I remember back in med school, learning that MS risk was greater in northern/colder climates, and the going theory was that “some kind of virus” that thrived in cold climates was responsible! Lack of sunlight or D deficiency was never suspected.

Today’s average sun exposure is far less than 20 or 30 years ago. Using a sunscreen of only 15 SPF blocks 95% of our skin’s ability to make vitamin D. Today people in general have far less unprotected sun exposure – between kids staying indoors and watching TV/playing video games/computer games, and more careful use of sunscreen by both kids and adults – people are just not making vitamin D with their skin the way we used to.

People with darker skin do not make as much vitamin D with sun exposure, and there is evidence that older skin does not make vit D as well either. Obese people are also more susceptible to D deficiency.

Vitamin D is not present in very many foods – cheese does not generally contain D, and yogurt rarely has much (unless it is fortified); the D in milk is destroyed when exposed to light.  All this means that the average person today has far lower D levels than people only 20 years ago.

I wonder if D deficiency and its associated insulin resistance is one more contributing factor to the obesity crisis (along with about a zillion other causes.) I have a question for anyone out there with a lot of experience with sarcoidosis. I have read that dark skinned people in Africa have low levels of sarcoidosis, but people of African ancestry who move to more northern climates have higher levels of sarcoidosis than the average population. I also understand that sarcoid nodules can actually PRODUCE vitamin D – and that countries with the highest level of sarcoidosis are Iceland and Sweden.

I’ve only recently started testing and treating, but I did have a new patient last week who was treated by his primary care doc last year, with marked improvement in his chronic tendonitis. The patient is a 35 year dentist, with naturally dark skin, who had been suffering from elbow tendonitis for over a year, despite NSAIDs and PT. After doing some reading about vit D, he asked his doc to check it. Level came back at 6. Post treatment level was 39 (8 weeks of weekly 50,000 IU of ergocalciferol/vit D2). Patient tells me that he was surprised that his symptoms resolved completely after treatment. Single case, but interesting.

How to replace— I like 1000-2000 u otc daily or.. 50000 units ergocalciferol weekly

Chondrodermatitis nodularis chronica helicis (also known as “Chondrodermatitis nodularis helicis”) is a small, nodular, tender, chronic inflammatory lesion occurring on the helix of the ear, occurring most often in men.

Oral immunotherapy (OIT) for children’s peanut allergy may be a safe and effective approach, a new study has shown.
Findings from the phase 2 trial, published online January 29 in the Lancet, add to accumulating evidence that children can gradually build tolerance by ingesting increasing amounts of nut protein.
“To our knowledge, our findings provide the first well controlled and accurate estimate of the effect size, benefits, and risks of desensitisation with peanut OIT,” write Katherine Anagnostou, PhD, from the Department of Medicine, Addenbrooke’s Hospital, Cambridge, United Kingdom, and colleagues.
Previous results from small studies have suggested that peanut OIT might be an effective strategy for managing children with peanut allergy. However, until now, the approach had not been thoroughly evaluated in a sizable group of children.
Therefore, the investigators designed a 2-step, randomized controlled crossover trial testing OIT in 99 children aged 7 to 16 years. Children with all levels of peanut sensitivity were included in the trial.
In the first step, children were randomly assigned to 1 of 2 groups. One group received 26 weeks of OIT, which consisted of gradually increasing doses of peanut protein up to 800 mg daily. The other group was advised to avoid peanuts per usual, serving as controls. At the end of the 26 weeks, both groups underwent peanut challenge.
In the second phase, children in the control group were offered the 26-week OIT treatment followed by challenge.
“OIT successfully induced desensitisation in most children within the study population with peanut allergy of any severity, with a clinically meaningful increase in peanut threshold,” the researchers report.
“Peanut OIT raises the reactive threshold at least 25-times so that 84–91% of participants can tolerate daily ingestion of 800 mg protein.”
At the end of the first trial phase, 84% (95% confidence interval [CI], 70% – 93%) of the children in the active intervention group tolerated daily ingestion of 800 mg protein compared with none in the control group. In addition, 62% (95% confidence interval [CI], 45% – 78%) of the active intervention group had become desensitized, which was defined as having no reaction to ingestion of 1400 mg peanut protein (roughly equivalent to 10 peanuts).
After the second trial phase, 91% (95% CI, 79% – 98%) of children who had been assigned initially to the control group were able to tolerate ingestion of 800 mg protein daily, and 54% (95% CI, 35% – 72%) had become desensitized.
The authors point out that it would be unlikely for children to accidentally encounter 1400 mg of peanut protein.
About a fifth of the patients reported adverse reactions to OIT. However most were mild, with oral itching being the most common, occurring after 6.3% of doses (76 children). Gastrointestinal symptoms were also common, with 31 children reporting nausea, 31 reporting vomiting, and 1 reporting diarrhea. In addition, 41 children developed wheeze (0.41% of doses) and 1 child required intramuscular adrenaline.
Treat obstructive apnea events and prevent more serious events before they occur Auto-titrating PAP (APAP) technology from ResMed™ responds to flow limitation, which often precedes snoring and apneas. Review data from a recent studyInformation from Industry
In an accompanying comment, Matthew J. Greenhawt, MD, from the University of Michigan Food Allergy Center, Division of Allergy and Clinical Immunology, Ann Arbor, stressed that although the results of the study are promising, more high-quality data are needed before recommending the therapy to all child and adolescent patients with peanut allergy.
“It is important to understand that OIT research cannot be rushed, and is years away from routine clinical use,” Dr. Greenhawt notes. “Investigative groups need time to refine protocols, revalidate data, understand the mechanisms of OIT, and minimise adverse effects. This must be done without added pressure or heightened expectations to quickly produce a marketable therapy,” he concludes.
Support for this study was received from the Medical Research Council, National Institute for Health Research, United Kingdom. Two coauthors are inventors on a patent application that covers the protocol described in this study. The remaining authors have disclosed no relevant financial relationships. Dr. Greenhawt has reported that he is a member of the Educational Advisory Council for the National Peanut Board and has served as a consultant for Deerfield Industries.
Lancet. Published online January 29, 2014.

In 1979 the Federal Register of the FDA issued a final rule classifying a group of Bacterial Vaccines and Bacterial Antigens with “no U.S. Standard of potency” based on the review of a Panel Recommendations. Because they had insufficient data to support their safety and efficacy. The products never did studies as the manufacturers were not interested in the cost and they were withdrawn. Despite no documented scientific evidence supporting efficacy allergist had given these tablets for over 1/2 century without any adverse effects and many attested to there effectiveness at stopping recurrent upper respiratory infections. We knew most were viral but these bacterial antigens seemed to work.

In 2009 Dr. Bellanti produced a supplement to the Allergy Proceedings on new vaccine of ribosomal nature associated with glycoprotein cell walls from Klebsiella pneumoniae which served as an immunoadjuvant. From the articles it seems the ribosomes stimulate TLR2 and work on the innate immune system and boost the adaptive system.

If you live long enough you see a lot of old ideas recycled. I have some old vaccines from the 50’s and thought the younger allergist would get a kick out of seeing this stuff and a heads up to all of us to watch for a immunomodulator that may be coming soon.

While alkaline (battery) injuries are usually deeper and worse than acid injuries, it is because the alkali sets up a type of necrosis called liquefactive necrosis.  Acids cause coagulative necrosis.  Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small vessel thrombosis and heat production occurs.

Yesterday, the FDA Allergenic Products Advisory Committee supported approval for a new sublingual allergy tablets (Ragwitek) that work the same way allergy shots do… but instead is dissolved under the tongue at home instead of a shot in the arm in a medical office. Given this is only a panel recommendation, final “official” FDA approval may not occur for another year or so for sale/distribution under prescription in the United States.

Ragwitek is made by ALK-Abello and Merck and treats patients aged 18-65 years who are allergic to only short ragweed pollen. The way Ragwitek is taken is placement of 1 sublingual tablet daily starting 12 weeks before and continued until the end of the ragweed pollen season. The first dose is given in a medical office to ensure safety with all other doses taken at home. The tablet dissolves in less than 10 seconds.

Epipen needs to be available at home due to possible risk of anaphylaxis. As with allergy shots, patients on beta-blockers for high blood pressure are not eligible to undergo this treatment.

Ragwitek is similar to Oralair and Grastek which treat only grass allergy. Oralair and Grastek were both recommended by the FDA panel last year.

Grass Pill

Angioedema (or Quincke’s edema) is inflammation of the deep dermis or submucosa. It is non pitting, non dependent, non tender, non erythematous, usually assymmetric.  The term angiioneurotic oedema was a misnomer as it was initially thought to be a nervous system disorder. It can be life threatening if it involves the airway. It can be congenital, idiopathic, or drug induced. Ace inhibitor blood pressure medications are common offenders causing this condition. NSAIDS and food allergies are the other big culprit. A thorough allergy history and testing are paramount. Exciting new drugs are on the horizon for this condition.

Heinrich IrenaeusQuincke (26 August 1842 – 19 May 1922) was a German internist and surgeon who internist and surgeon.  He was perhaps the first (1882) to recognize angioedema which is often referred to as “Quincke’s edema”.[1] “Quincke’s pulse”, with redness and pallor seen under the fingernails, is one of the signs of aortic insufficiency.“Quincke’s puncture” is a somewhat outdated eponym for lumbar puncture, used for the examination of the cerebrospinal fluid in numerous diseases such as meningitis and multiple sclerosis. In 1893 he described what is now known as idiopathic intracranial hypertension, which he labeled “serous meningitis”.

Discoveries

He was perhaps the first (1882) to recognize angioedema which is often referred to as “Quincke’s edema”.[1] “Quincke’s pulse”, with redness and pallor seen under the fingernails, is one of the signs of aortic insufficiency.[2] “Quincke’s puncture” is a somewhat outdated eponym for lumbar puncture,[3][4] used for the examination of the cerebrospinal fluid in numerous diseases such as meningitis and multiple sclerosis. In 1893 he described what is now known as idiopathic intracranial hypertension, which he labeled “serous meningitis”.[5]

Congenital or Hereditary Angioedema is relatively rare. It usually shows up in childhood. It is essentially caused from either absent of non functioning complement factors. Primarily C1 Esterase Inhibitor. Acquired or hereditary angioedema do not typically respond to antihistamines or steroids, so the fact that he got better with these medications argues against this. It is bradykinin mediated and inflammation peaks in about 12 hours. Also, Hereditary Angioedema does not Urticate (No Hives). Nevertheless, checking labs would put these (remote) possibilities to rest. A good laboratory screen would be aC2, C3, C4, C1q, and C1-INH level and function, ESR, ANA, RF, hepatic transaminases, TSH, T4, anti-thyroglobulin antibodies, anti-thyroid peroxidase antibodies, CBC/diff and CU index (available thru Quest and Labcorp).  If your patient has had a recent reaction, then simple doing a C4 assay will rule out a hereditary etiology.  I have yet to diagnose a case of this.  The drug company that manufactures cinryze is a human derived C1 esterase inhibitor and has to be given IV every few days and cost nearly 300k per year.  Given androgens on a regular basis is the other option for this chronic condition.

The vast majority of Angioedema is idiopathic and often drug induced. It is essentially a deeper (subdermal or submucosal) version of urticaria and is similarly most often idiopathic. It usually manifests in adulthood. Medications started within the past several months are most likely. However, ACE inhibitors are notorious for causing these reactions even after years of safe use. Aspirin and NSAIDs are also frequent causes or exacerbating factors. Less commonly, underlying problems like thyroid disease, liver disease, autoimmune disease or occult malignancy can be responsible. About half of patients with otherwise “idiopathic” chronic urticaria/angioedema make IgG autoantibodies against the high affinity IgE receptor on mast cells. Foods are uncommon offenders, but should be considered. Routine allergy testing and diet diary are appropriate.  Non hereditary forms are histaminic and thus respond better to allergy medications such as antihistamines, epinephrine, and steroids.

Treatment is largely symptomatic. Symptoms wax and wane for weeks and even months. Unfortunately up to 95% of patients will never find the etiology. I often suggest a daily 24 hour acting antihistamine to prevent/suppress episodes, such as Zyrtec 10 mg qd. If symptoms persist, you can add Allegra 180 mg qam and take Zyrtec 10 mg qhs. If symptoms STILL persist, you can continue Allegra and switch Zyrtec to Atarax, titrated as needed to suppress episodes while minimizing (hopefully) daytime sedation. I also often add a type 2 antihistamine such as Zantac. Steroids of course are helpful, however one should be cautious of rebound inflammation.

Denervation as a therapy for vasomotor rhinitis has often been considered.  With the advent of topical therapies, Dr Templer referred to this a complex procedure in search of an indication.  By transecting the Sphenopalatine Artery, we are in essence dividing the more distal nerve and thus attaining our objectives.

Most of us give our patients oral steroids such as prednisone or methylprednisolone.  Convenience, compliance, and side effects are the reasons we might consider injecting over oral administration.  60 mg of Kenalog seems to give patients a good measure of relief with very little side effects.  There is also no question of compliance with this.  The site of injection seems to matter very little, however, as we see with our tip rhinoplasty patients local atrophy is real and might actually be a beneficial side effect if we consider the inferior turbinate.  Safety in regards to micro emboli need to be considered, however, this seems very unlikely with our improved techniques and visualization.