Allergy & Asthma Disease Management Center: Ask the Expert: Rhinitis

- Rhinitis -

12/14/2005 RE: Reactions to capsicum

A 50 year old male patient on insulin treatment is facing severe reaction to capsicum (fresh or dried )for the past 5 years or so. He starts to perspire immediately if he eats or smell food with capsicum (hot). The reaction is limited to perspiration of scull only, No perspiration in any other part of the body. He avoids going out & eating, it has made his life really miserable. He has to wash his head (hair) after every meal. The patient is of south Asian heritage & have been eating hot food all his life.

There are several plants in the capsicum pepper group. Some sweet peppers contain allergenic proteins to which some people become sensitive, particularly in occupational settings (see enclosed abstract). However, I suspect that you are referring to the "hot" chili peppers in which a major component is capsaicin, a chemical that is a potent stimulus of vanilloid receptors on sensory nerve fibers in the upper respiratory mucosa and the skin (see enclosed abstract). Some individuals appear to be inherently very sensitive to this capsaicin effect while in some others an increased sensitivity develops with time.

The simplest, most straight-forward approach for your patient would be complete avoidance of all foods containing chili peppers or their component parts. If the patient refuses to carry out such avoidance another possible approach (not guaranteed to be successful) is to try inducing tolerance to capsaicin by applying increasing amounts of capsaicin (starting with minute doses) under the tongue daily, as tolerated stopping at doses that elicit pain or other systemic symptoms (see enclosed abstract of a review article by Baraniuk).

Clin Exp Allergy. 2004 Nov;34(11):1739-46. Related Articles, Links
Characterization of cross-reactive bell pepper allergens involved in the latex-fruit syndrome.
Wagner S, Radauer C, Hafner C, Fuchs H, Jensen-Jarolim E, Wuthrich B, Scheiner O, Breiteneder H.
Department of Pathophysiology, Medical University of Vienna, Vienna, Austria.

BACKGROUND: Between 30% and 50% of individuals who are allergic to latex products are also allergic to specific plant foods, a fact that is well documented as the latex-fruit syndrome. Simultaneous sensitization to latex and bell pepper has been previously reported. Although bell pepper fruits are frequently consumed raw, cooked or as a spice, little is known about the cross-reactive allergens.
OBJECTIVE: In this study we wished to identify bell pepper allergens involved in the latex-fruit syndrome.
METHODS: Sera of four patients who displayed clinical symptoms to latex and bell pepper were used in immunoblot studies on protein extracts of three different cultivars of fresh bell pepper and fresh Hevea latex. Cross-reactive allergens were identified by inhibition experiments using recombinant Hev b 8 (latex profilin), and natural Hev b 2 (latex beta-1,3-glucanase) in addition to the protein extracts. A novel cross-reactive IgE-reactive 30 kDa protein was subjected to sequence analysis.
RESULTS: Three patients displayed IgE to profilins from bell pepper fruits and latex. Two patients possessed IgE to Hev b 2, a latex beta-1,3-glucanase, and a homologous protein in bell pepper. One patient possessed IgE reactive with a protein of 30 kDa identified by N-terminal sequencing as an l-ascorbate peroxidase and another patient to a protein of 38 kDa. Additionally, IgE binding proteins in two higher molecular weight ranges showed cross-reactive capacities.
CONCLUSION: Our findings show on the molecular level that bell pepper is part of the latex-fruit syndrome. For the first time we have identified the major latex allergen Hev b 2, a beta-1,3-glucanase, and the bell pepper l-ascorbate peroxidase as cross-reactive allergens. We were also able to show hat profilins are responsible for some of the IgE cross-reactivity.

J Allergy Clin Immunol. 1992 Dec;90(6 Pt 2):1045-50.
Sensory, parasympathetic, and sympathetic neural influences in the nasal mucosa.
Baraniuk JN.
Lung Biology Laboratories, Georgetown University, Washington, DC 20057.
Neural mechanisms contribute to many nasal symptoms and syndromes. Sensory nerve stimulation by irritants, mast cell products, and inflammatory mediators leads to sneezing and other systemic reflexes. Parasympathetic reflexes and sensory axon responses combine to increase nasal blood flow, fill venous sinusoids (which thickens the mucosa and reduces nasal patency), induce plasma extravasation, and stimulate glandular secretion of mucous and serous cell products.
These putative roles for nerves and neuropeptides in pathologic events open new therapeutic avenues. Anticholinergic agents, peptide neurotransmitter agonists and antagonists, drugs to reduce or modulate sensory or parasympathetic nerve function, potent topically applied glucocorticosteroids, and agents to inactivate inflammatory, secretory, or vascular cells may be of use. Ablation of sensory nerves by topical application of the chili pepper neurotoxin capsaicin has been successful in reducing the symptoms of refractory vasomotor rhinitis.

12/8/05 re: Vasomotor reaction and rosacea

I have a 53 year old man who has an 8 year history of recurrent and episodic allergy "attacks". His symptoms begin rather suddenly with clear rhinorrhea, sneezing, and eye watering, as well as nasal congestion, pain under the eyes, and "dizziness". He has previously been allergy tested for environmental allergies two times, and both tests were completely negative. His symptoms will often cause him to miss work. He has several episodes a year and they last variously from 12 to 48 hours, but do get better with oral decongestants. He has been given antihistamines, antibiotics, and intranasal corticosteroid sprays, all without measurable benefit. I can find nothing to suggest that this is food or drug related. I have suspected that these episodes are viral in nature, but by examination that theory is questionable. He does have rosacea with rhinophyma, and uses tetracycline orally.

I am thinking that this may be somehow related to the rosacea and vasomotor "instability". It does not appear to be cluster headaches or migraine. What do you think, and how would he be best treated?

Your description certainly suggests a vasomotor reaction. As you implied, vascular instability is a prominent and possibly causal manifestation in rosacea. Therefore, it is conceivable that whatever causes the rosacea might be responsible for the nasal and eye symptoms you describe. If there is a question whether respiratory allergies or NARES are playing a role, one can obtain nasal scraping specimens (not when the patient is treated with systemic or intra-nasal steroids) which are smeared and stained, looking for an increased frequency of for eosinophils

However, there are certainly unanswered questions if this thesis about vasomotor instability is correct. For example: 1) Why do not all patients with pronounced rosacea have the nasal/eye episodes you described? 2)why are such episodes infrequently episodic? These questions suggest that there may be other triggering factors involved. You did not mention whether the episodes are triggered by sudden weather changes, ethanol ingestion (which should be avoided anyway if rosacea is active),highly seasoned foods, stress, etc.

My therapeutic suggestions would be:

1) Aggressive treatment of the rosacea (besides the tetracycline) Some reports describe better results with doxycycline than regular tetracycline. However, sun avoidance is important. A trial of retinoids (local topical first, then systemic if topical not sufficiently helpful).

2) If nasal/eye episodes recur, start Atrovent nasal spray immediately, then repeat q6h as needed. Also use a long-acting oral decongestant preparation. Avoid sudden changes in environmental temperatures and eating highly seasoned foods during such episodes.

9/12/05 re: Allergy to newsprint

I recently saw a 77 year old woman with a history of new onset persistent rhinitis and episodic conjunctivitis who is otherwise healthy. She told me that her symptoms were caused by reading the newspaper or a paperback book. If she avoided either, her symptoms resolved. Her symptoms respond to antihistamines and she is not interested in an evaluation for aeroallergen sensitivity at this time. I am aware of some associations between printer ink and contact dermatitis and asthma. My question is: Is there a good source where I can find more info on the source of this patient's symptoms and is this a well described entity?

I have seen a moderate number of patients over the years who described the acute onset of rhino conjunctivitis, and occasionally asthma, after opening and starting to read a newspaper. In such cases, the newsprint was "wet" (not dried), leaving smudges of this ink on the hands when handling the newspaper. In most cases, the rhino conjunctivitis was prevented by having someone else open the newspaper and allowing it to stand in a warm area until the newsprint had dried. I have not seen any studies that characterized the chemical nature of the offender within newsprint that induces these respiratory symptoms. Therefore, it is not clear whether colophony., the agent thought to be mainly responsible for contact dermatitis to newsprint, also induces the rhino conjunctivitis. Therefore, I suggest that your patient have someone else open newspapers and books away from the patient and allow the print to thoroughly dry before attempting to read the material.

8/5/05 re: Non-allergic rhinitis

I have a patient with a chronic cough and a non allergic recurrent rhinitis. You are quoted on the American Journal of Respiratory and Critical Care Med June 1 2002, referencing an article Adverse reactions to nonsteroidal anti inflammatory drugs, Allergy Clinic North Am 1998, based on this quote the recommendation is to empirically treat patients with aspirin moderate dose as a trial therapy. I am not familiar with the science behind this recommendation Do you agree with this conclusion based on your article?

I referred your question to Dr. Donald Stevenson of the Scripps Clinic. His response is enclosed below.

Burt, If Dr. Ortiz is referring to patients with allergic or non-allergic rhinitis who do not have aspirin exacerbated respiratory disease (AERD), there are no published studies showing efficacy. There is some anecdotal experience with a few patients with nasal polyps who improve after aspirin therapy. If he is referring to patients with AERD (i.e. ASA or NSAIDs cause respiratory reactions), then there are 9 published studies showing efficacy of daily ASA 650 mg BID after aspirin desensitization. Five of these studies can be found on PUB MED under Stevenson DD

4/13/05 re: Allergy as a cause of epistaxis

I am a physician but am submitting a question about myself. Here is a brief overview. 2 years ago I relocated across town and began living at the edge of a wooded area. Contemporaneously I began having right nostril epistaxes that could not be controlled. After several courses of antibiotics from my ENT, he decided, based on MRI that there was a questionable cyst in the maxillary sinus causing the epistaxis. It was removed with no subsequent change in frequency of the nosebleed. HE then concluded that a piece of bone had been exteriorized and re-operated and also ligated a branch of the sphenopalatine artery. 6 months later the bleeding recurred; at the same time of the year of the original symptoms. I had moved from the woods side but still reside in the same state as I have for the last 30 years. Currently, my ENT is advising ligation of the Maxillary artery but I still feel as if there is an allergen basis. I requested, and am awaiting, results from allergy blood tests but have begun a course of OTC Loratidine. AS an aside, there has never been an on site identification of a bleeding site. I even saw the ENT on the same day I had an episode of Epistaxis but he could no see a site of bleeding.

Any thoughts to share with me??

In some individuals with allergic rhinitis, there is marked congestion of the nasal mucosa. This is due in part to considerable dilatation and congestion of the capacitance vascular plexus in the nasal mucosa (likely as a result of mediators released locally in the allergic reaction). Therefore, it is conceivable that epistaxis could result, particularly if the patient rubs the nose repeatedly or "picks" the nose to remove crusted secretions. However, I think that such epistaxis would almost always be preceded and accompanied by symptoms of a marked allergic reaction with prominent nasal congestion and perhaps watery nasal discharge and itching. I think that an allergic reaction would be a very unlikely cause of the isolated episodes of epistaxis without other nasal symptoms that you described.

You can explore this unlikely possibility of an allergic cause further by obtaining a specimen gently scraped from the nasal mucosa in the involved side using a plastic "hooked" speculum designed for that purpose. If that speculum is not available one can try using the wooden end of an applicator stick. The specimen (mostly mucus) should be smeared immediately on a slide, fixed in acetone for about 10 minutes, removed and allowed to dry, then stained with Giemsa solution and inspected under high power microscopy. If eosinophils are found (at least 20% of the inflammatory cells) in the specimen, the likelihood of allergic rhinitis is increased considerably.

Your description of recurrent epistaxis without an obvious bleeding point raises another possibility in my mind. Occasionally, such bleeding is thought to be due to a vascular anomaly in which there a local collection of increased numbers of small vessels (sort of analogous to vascular malformations seen elsewhere). I am no expert in such matters but wonder whether some of the newer, more sophisticated imaging techniques might detect such a vascular anomaly in the nasal mucosa.

6/28/03 re: Control of idiopathic sneezing

A patient was referred to me with myofascial pain syndrome, and stated that her facial pain is primarily triggered by sneezing. She has had thorough allergy, ENT, neurological and medical workups done without any medical/neurological conditions noted. Her allergy workups have been negative, and no oral medication or nasal sprays have been helpful (Astelin, Atrovent, INS), nor has saline irrigation been helpful. I use lidocaine, along with oxymetolazine, for rhinoscopic preparation, but was wondering whether a more diluted form of lidocaine spray could be used on a BID-QID basis to see if the sneezing could be reduced. Any suggestions would also be welcomed.

I assume from your comments that the patient manifests sneezing episodes fairly frequently with no obvious cause or sign of nasal inflammation. Such idiopathic paroxysmal sneezing has been considered an unusual disorder, most commonly seen in adolescent or young adult females (see enclosed abstract.) It is thought that many of such cases are psychogenic although the etiology is apparently not well-defined. Topical nasal anesthesia has been used successfully in some cases of such idiopathic sneezing without apparent adverse effects (see enclosed abstracts.) However, there may be a transient sense of local numbness, much as experienced by patients who have had nasal anesthesia induced before rhinoscopy.

You did not state whether the patient has any warning of impending sneezing episodes and how often such episodes occur. I mention this because the duration of the effect of lidocaine spray may not be that long if one has to use it daily for prophylaxis. Use of a 2% lidocaine gel may lead to a longer "protective" effect. If there is evidence to suggest a psychogenic component in the sneezing episodes, one might consider referring the patient to a reputable practitioner for instruction of the patient in self-hypnosis techniques.

J Otolaryngol. 1992 Dec;21(6):437-8.
Paroxysmal sneezing in children: two new cases.
Shapiro RS.
Department of Otolaryngology, McGill University, Montreal, Quebec, Canada.

Paroxysmal sneezing is an uncommon condition primarily affecting adolescents. Most of the reported cases were thought to be psychogenic, and only two were felt to be due to nasal sensitivity. This paper reports two adolescents with paroxysmal sneezing, neither of whom had apparent psychological or emotional problems. In one child the sneezing continued during sleep. The other child was successfully treated with topical nasal anesthesia. Both children were felt to have nasal sensitivity as the etiology of their paroxysmal sneezing. The evaluation of the patient with paroxysmal sneezing requires a thorough history and physical examination. One must not assume that every case of paroxysmal sneezing is of psychogenic origin. Topical nasal anesthesia should be tried for control of intractable paroxysmal sneezing.

J Laryngol Otol. 2002 Nov;116(11):958-9.
Intractable paroxysmal sneezing.
Gopalan P, Browning ST.
Department of Otolaryngology, Singleton Hospital, Swansea, UK.

Intractable paroxysmal sneezing is a rare disease primarily affecting teenage girls. We present the case of a 12-year-old girl who demonstrated the classical features of intractable paroxysmal sneezing of psychogenic origin. Most of the reported cases are psychogenic in origin, but a number of other conditions may cause an intractable paroxysmal sneeze. Apart from a detailed history, clinical examination and relevant investigations, topical nasal anesthesia should be tried for control of symptoms--that will help to differentiate psychogenic sneezing from organic sneezing. A timely diagnosis can avoid unnecessary medical trials, parental anxiety and poor school performance, as most of the patients are very young.

3/3/03 re: Chronic rhinnorhea in an infant

I have a 6 month old male in my practice that for the past 2-3 months has had a clear runny nose with occasional coughing and wheezing which has been documented by my exam. His mother had tried OTC Benadryl and she reports it relieves his symptoms for a couple of hours and then they come back. I thought I remembered from my days in med school that very young children/infants don't really develop allergic rhinitis? Is this true? And if they do develop allergic rhinitis, what is the recommended treatment? I have checked multiple sources, but haven't been able to find out much. Thanks.

I enlisted the input of Dr. Susan Schuval,of the Long Island Jewish Medical Center, New York, an expert in pediatric allergy and respiratory diseases to respond to your questions. Her response is enclosed below.
___________________________________________________

This infant has two problems which may or may not be related.

1. Recurrent cough/wheeze:
Has the child ever been treated with bronchodilators? If so, did he respond? Is there a family history of atopy or asthma? If so, the baby may have mild intermittent asthma which should be treated with PRN nebulized albuterol. He may require a chronic anti-inflammatory therapy (nebulized cromolyn or budesonide if he coughs/wheezes twice a week.

It is also possible that the infant's respiratory symptoms may represent a prolonged or recurrent infection (RSV, Chlamydia). I would definitely recommend a chest x-ray to rule out other pulmonary diagnoses.

Are there any associate growth issues? Diarrhea? Malabsorption? If so, consider cystic fibrosis.

2. Chronic Rhinitis:
The differential diagnosis of chronic rhinitis in a 6 month old infant includes: Infectious causes: congenital syphilis, URI, sinusitis, Anatomic bnormalities: choanal atresia, adenoidal hypertrophy, Allergic diseases: A 6 month old may have food allergies (to cow's milk formula or whatever formula he takes or to other foods in his diet (soy, eggs, wheat) which may cause nasal and/or pulmonary symptoms (any rash or atopic dermatitis?).

Although a 6 month old is generally not allergic to pollens (requires > 2 pollen seasons for sensitization), he may be sensitive to other environmental allergens such as dust mite, mold, or pet dander.

At this point, I would obtain additional history (family history, etc) and determine whether an allergy evaluation is indicated. I would also check a Chest x-ray.

11/12/02 re: Perennial allergic rhinitis reference

I am looking for a good article on all the signs and symptoms/treatments for perennial allergic rhinitis. Your assistance in this matter is appreciated.

In response to your request, I have enclosed several recent references. The first, from Baraniuk's group describes well current concepts about the mechanism underlying perennial allergic rhinitis. The next article deals with perennial allergic rhinitis occurring in children and its link to co-morbid conditions. The third article deals with evidence-based treatment of allergic rhinitis. If you wish a "one stop" concise article about allergic rhinitis and can wait several months, you may wish to consult the "Primer on allergic and immunologic diseases" scheduled to be published as a supplement to the Journal of Allergy and Clinical Immunology in the first half of the year 2003.

Clin Allergy Immunol 2002;16:275-93
Mechanisms of allergic rhinitis.
Park YJ, Baraniuk JN.
Catholic University of Korea and St. Vincent's Hospital, Suwon, Korea.
_________________________________________________________

J Allergy Clin Immunol 2001 Jul;108(1 Suppl):S9-15
Pediatric allergic rhinitis and comorbid disorders.
Lack G.
Department of Pediatric Allergy and Immunology, St Mary's Hospital, London, UK.

Allergic rhinitis (AR) is rarely found in isolation and needs to be considered in the context of systemic allergic disease associated with numerous comorbid disorders, including asthma, chronic middle ear effusions, sinusitis, lymphoid hypertrophy with obstructive sleep apnea, disordered sleep, and consequent behavioral and educational effects. The coexistence of AR and asthma is complex. First, the diagnosis of asthma may be confounded by symptoms of cough caused by rhinitis and postnasal drip. This may lead to either inaccurate diagnosis of asthma or inappropriate assessment of asthma severity with over treatment of the patient. The term "cough variant rhinitis" is therefore proposed to describe rhinitis that manifests itself primarily as cough that results from postnasal drip. AR, however, also has a causal role in asthma; it appears both to be responsible for exacerbating asthma and to have a role in its pathogenesis. Postnasal drip with nasopharyngeal inflammation leads to a number of other conditions. Thus sinusitis is a frequent extension of rhinitis and is one of the most frequently missed diagnoses in children. Allergen exposure in the nasopharynx with release of histamine and other mediators can cause Eustachian tube obstruction possibly leading to middle ear effusions. Chronic allergic inflammation of the upper airway causes lymphoid hypertrophy with prominence of adenoidal and tonsillar tissue. This may be associated with poor appetite, poor growth, and obstructive sleep apnea. AR is therefore part of a spectrum of allergic disorders that can profoundly affect the well being and quality of life of a child. Prospective cohort studies are required to assess the disease burden caused by AR in childhood and to further assess the potential educational impairment that may result. Because AR is part of a systemic disease process, its management requires a coordinated approach rather than a fragmented, organ-based approach.

Curr Allergy Asthma Rep 2001 May;1(3):218-26
Evidence-based treatment of allergic rhinitis.
Pawankar R, Fokkens W.
Department of Otorhinolaryngology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan.

Allergic rhinitis is an extremely common disease worldwide, affecting 10% to 50% of the population. An increasing prevalence of allergic rhinitis over the past decades and its frequent association with asthma has raised concerns about treating the disease appropriately. New knowledge of the pathophysiologic mechanisms underlying allergic inflammation of the airways has resulted in the development of newer and better therapeutic strategies. This review focuses on evidence-based treatment of allergic rhinitis, highlighting the most recent international consensus and evidence-based guidelines on allergic.

9/5/02 re: Non-allergic rhinitis

I am researching the treatments for various causes of non-allergic rhinitis. According to the article of "Diagnosis and Management of Rhinitis: Complete Guidelines of the Joint Task Force on Practice Pentameters in Allergy, Asthma, and Immunology," there are certain conditions that may mimic symptoms of rhinitis, but I can not find any discussion about the management of these conditions. These include structural rhinitis (nasal tumors and choanal atresia), immunologic/inflammatory diseases (Sarcoidosis, Wegener's granulomatosis, midline granuloma, SLE, Churg-Strauss vasculitis, Sjogren syndrome, and relapsing polychondritis), and congenital defects (ciliary dyskinesia syndrome, cystic fibrosis, and Young's syndrome). Are these conditions categorized under non-allergic rhinitis? Can these rhinitis/conditions usually be management by primary care physicians? Or are they usually referred to specialist?

The conditions you have mentioned should sometimes be considered in the differential diagnosis of allergic rhinitis but they are not non-allergic rhinitis (NAR). NAR is usually considered to be an inflammatory/vasomotor reaction in the nasal cavity in which there is
no evidence of an allergic pathogenesis. Hormonal effects may play an important role in some cases. It is usually characterized by excessive nasal drainage (both anterior and post-nasal) and prominent nasal congestion. However, nasal itching and repetitive sneezing are much less common in NAR than in typical allergic rhinitis. In some cases of NAR, there is an associated inflammatory polyposis, usually bilateral and originating in the mucosa of the sinuses (although appearing in the nasal cavity). Some of those with nasal polyposis may be aspirin-intolerant or have cystic fibrosis. I separate NAR, as defined above, from infectious rhinitis, sometimes associated with ciliary dyskinesia or processes obstructing nasal/sinus drainage. The conditions you mentioned should be evaluated at least once by an ENT specialist. This is because fiber-optic rhinoscopy by an experienced observer is needed to identify conditions such as a structural abnormality or neoplasm that require surgical approaches. In such cases, as well as in some of the other conditions you mentioned, the assistance of an ENT surgeon in obtaining an adequate biopsy of a lesional area is needed.

5/14/02 re: Approach to possible allergic rhinitis with negative skin tests

I have referred several patients in the 5-10 yr old age category for allergy evaluations who have had negative skin prick test results. They have had classic symptoms of allergic rhinitis with wet, pale, swollen nasal mucosa, some sneezing, occasionally itchy eyes, frequently a seasonal pattern to their symptoms, and complications of sinusitis. One of these children has been tested 3 years in a row with no reactions to the prick tests.
Their parents seem appropriately concerned and assure me that the children were not on oral antihistamines at the time of their testing. (I regularly ask parents to alert the allergist's office regarding any medications and to ask for any special instructions regarding discontinuation of these meds prior to their appointments.)

What explanations are there for these results? Would RAST testing be appropriate or reliable? Any other suggestions? I have been recommending to most to continue treatment with antihistamines and occasionally nasal steroids, particularly when the children appear to do better and experience improvement of their symptoms when on these meds.

There are several possible reasons why an individual with a history suggestive of allergic rhinitis may have exhibited negative responses to allergy prick skin tests. These include:
1) Technical factors- I assume that you have referred your patients to highly qualified and experienced allergists whose skin testing techniques are very reliable

2) The skin of the individual is incapable of exhibiting a good whealing reaction (due to medication effects and other factors). Most of these factors can be eliminated from consideration if the patient exhibits strong whealing reactions to the "positive control" tests with appropriate concentrations of histamine and/or codeine. I assume that such positive controls were carried out in skin testing of your patients.

3) Skin testing with the particular offending allergens in those patients were not carried out. I assume that experienced allergist consultants seeing your patients will have tested for the unusual, as well as the common, aeroallergens in your region.

A suggested approach to the patients you mentioned:

1) Determine whether the seasonal rhinitis is truly allergic (a seasonal pattern does not always indicate allergic etiology). During the time period when the patient is particularly symptomatic, obtain a gentle scraping of the nasal mucosa (preferably, the middle turbinate area), smear gently on microscope slides, fix with ethanol and stain with special stains for eosinophils. This requires some experience and facilities to do this. I would suppose that the allergist seeing your patient should be set up to do this. In almost all cases of allergic rhinitis, particularly seasonal allergic rhinitis, there is a prominent eosinophilic inflammatory response (eosinophils at least 20% of the inflammatory cells in the scraping specimen). However, the patient must not have used nasal steroids for several weeks before the specimen is obtained since nasal steroids (but usually not antihistamines) may suppress the eosinophil inflammatory response However, an eosinophil accumulation in the nose can occasionally be seen in some non-allergic rhinitis, called by some as NARES (non-allergic rhinitis eosinophilia syndrome). However, in NARES, there is generally little sneezing or itching, two common features of allergic rhinitis. Also, there is usually not the history of typical allergies in parents and/or siblings seen in a large percentage of those with true allergic rhinitis.

2) If the history, as noted above, is strongly suggestive (including a family history of atopy) and there is a prominent eosinophil accumulation, but careful and thorough allergy skin tests yield negative responses, then a search with the RAST or ELISA techniques for specific IgE antibodies in the serum would be reasonable, provided:

a) These tests are done in a reliable lab. I have found that a number of commercial labs report overly sensitive or misleading results. You could ask your allergist consultant to assist you in this regard.

b) Do not draw too much implication from a modestly positive test (1+ or 2+ values). I have found that clinically verified positive RAST tests are usually in the 3-4+ ranges.

3) Meanwhile, your approach with therapeutic trials sounds very reasonable. However, I should emphasize that H1 antihistamines of any type or brand may help the sneezing or itching of allergic rhinitis, but do little to reduce the nasal congestion that becomes more prominent as the rhinitis becomes subacute/chronic. In my experience, added oral decongestants (usually pseudoephedrine) are helpful somewhat irregularly and only in some individuals, sometimes with stimulatory side effects (relatively narrow therapeutic index). Nasal steroids are usually more effective, controlling nasal congestion as well as sneezing and itching. However, they may take several days of use before any improvement is noted. Also, associated conjunctivitis will likely require additional therapy.

5/9/02 re: Saline lavage for rhinitis

I am assisting my colleague Nicole O'Kane, PharmD, in developing a rhinitis treatment guideline. We are looking for a reference for the treatment on mild symptoms with nasal saline sprays or lavages. Do you have such a reference?

There are a number of reports in this area which have come to somewhat varying conclusions about the efficacy of physiologic or hypertonic saline in the treatment of chronic rhinitis or rhinosinusitis. I have enclosed abstracts of several of these articles. My overall impression is that the findings are not definitive and better studies are needed. I consulted Dr. Eli Meltzer of San Diego, an internationally recognized expert in the treatment of rhinitis. His response is also enclosed below. I hope that this information is of assistance to you.

Arch Fam Med 1998 Jan-Feb;7(1):39-43
Comment in: Arch Fam Med. 1999 Mar-Apr;8(2):100.
A clinical trial of hypertonic saline nasal spray in subjects with the common cold or rhinosinusitis.
Adam P, Stiffman M, Blake RL Jr.
Riverside University Family Practice Clinic, University of Minnesota Department of Family Practice and Community Health, Minneapolis 55406, USA.

OBJECTIVE: To determine whether hypertonic saline nasal spray relieves nasal symptoms and shortens illness duration in patients with the common cold or acute rhinosinusitis.
DESIGN: Randomized trial with 2 control groups.
SETTING: Two family practice clinics.
PARTICIPANTS: One hundred forty-three adult patients with a cold or sinus infection. Patients with allergic rhinitis, symptoms for more than 3 weeks, or other respiratory diagnoses were excluded, as were those who had used topical decongestants.
INTERVENTION: Hypertonic saline or normal saline spray 3 times a day or observation. Subjects completed a 7-day symptom checklist that included a well-being question ("Do you feel back to normal?").
MAIN OUTCOME MEASURES: Nasal symptom score (sum of scores for nasal congestion, rhinorrhea, and headache) on day 3 and day of well-being (day of symptom resolution).
RESULTS: Data were collected for 119 subjects. No difference was found in either primary outcome when hypertonic saline was compared with either normal saline or observation. Mean day of well-being was 8.3 (95% confidence interval [CI], 6.9-9.7), 9.2 (95% CI, 6.9-11.43), and 8.0 (95% CI, 6.7-9.3) days in the hypertonic saline, normal saline, and observation groups, respectively. Day 3 mean nasal symptom score was 3.8 (95% CI, 3.0-4.5) for hypertonic saline, 3.7 (95% CI, 2.9-4.5) for normal saline, and 4.1 (95% CI, 3.5-4.7) for observation. Only 44% of the patients would use the hypertonic saline spray again. Thirty-two percent noted burning, compared with 13% of the normal saline group (P = .05).
CONCLUSION: Hypertonic saline does not improve nasal symptoms or illness duration in patients with rhinosinusitis

J Allergy Clin Immunol 1998 May;101(5):602-5
Treatment with hypertonic saline versus normal saline nasal wash of pediatric chronic sinusitis.
Shoseyov D, Bibi H, Shai P, Shoseyov N, Shazberg G, Hurvitz H.
Pediatric Department, Bikur Cholim Hospital, Hadassa Medical School, Jerusalem, Israel.

BACKGROUND: Chronic sinusitis (CS) is a common disease in children, especially those with allergies, that is caused by impaired drainage from the sinuses. Hypertonic NaCl solution has been shown to increase mucociliary clearance and ciliary beat frequency.
OBJECTIVE: We performed a randomized double blind study to compare the effect of nasal wash with hypertonic saline (HS) (3.5%) versus normal saline (NS) (0.9%) on CS.
METHODS: Thirty patients with CS aged 3 to 16 years were studied. They were randomly divided into two treatment groups matched by age and severity of the disease. Each individual was treated with either HS or NS for 4 weeks. All patients were evaluated by two clinical scores (cough and nasal secretions/postnasal drip [PND]) and by a radiology score at the beginning of the study and after 4 weeks.
RESULTS: The HS group improved significantly in all scores (average +/- SD): cough score, from 3.6 +/- 0.51 to 1.6 +/- 0.74; nasal secretion/PND score, from 2.86 +/- 0.35 to 1.6 +/- 0.74; and radiology score, from 8.06 +/- 1.28 to 2.66 +/- 1.04. The NS treatment group showed significant improvement only in the PND score (from 2.66 +/- 0.49 to 1.53 +/- 0.83) but no significant change in both the cough score (from 3.53 +/- 0.52 to 3.33 +/- 0.49) and the radiology score (from 8.13 +/- 1.25 to 7.86 +/- 0.91). Clinical observation 1 month after the end of the study showed no change compared with the end of the study in both groups.
CONCLUSION: HS nasal wash is an efficient treatment of CS.

Otolaryngol Head Neck Surg 2001 Jul;125(1):44-8
Nasal irrigation for the alleviation of sinonasal symptoms.
Heatley DG, McConnell KE, Kille TL, Leverson GE.
Division of Otolaryngology-Head and Neck Surgery, Department of Surgery,
University of Wisconsin School of Medicine, Madison, WI 53792-7375, USA.

OBJECTIVE: To determine the effect of nasal irrigation on sinonasal symptoms.
STUDY DESIGN AND SETTING: A total of 150 adult subjects with chronic sinusitis symptoms were recruited from the community and assigned to 1 of 3 treatment groups: nasal irrigation with bulb syringe, nasal irrigation with nasal irrigation pot, or control treatment with reflexology massage. Groups 1 and 2 performed daily hypertonic saline irrigation with 1 device for 2 weeks and then with the other device for 2 weeks. Group 3 performed reflexology massage daily for 2 weeks. Prospective data collected included pretreatment Medical Outcomes Study Short Form, pretreatment and posttreatment Rhinosinusitis Outcomes Measure, daily medication use, subjective treatment efficacy, and preference of irrigation method.
RESULTS: There was a significant and equivalent improvement in Rhinosinusitis Outcomes Measure 31 score after 2 weeks of intervention in each treatment group; 35% of subjects reported decreased use of sinus medication.
CONCLUSION: Daily nasal irrigation using either a bulb syringe, nasal irrigation pot, and daily reflexology massage were equally efficacious and resulted in improvement in the symptoms of chronic sinusitis in over 70% of subjects. Medication usage was decreased in approximately one third of participants regardless of intervention.

Laryngoscope 2000 Jul;110(7):1189-93
Clinical study and literature review of nasal irrigation.
Tomooka LT, Murphy C, Davidson TM.
School of Medicine, University of California San Diego, USA.

OBJECTIVES/HYPOTHESIS: Nasal disease, including chronic rhinosinusitis and allergic rhinitis, is a significant source of morbidity. Nasal irrigation has been used as an adjunctive treatment of sinonasal disease. However, despite an abundance of anecdotal reports, there has been little statistical evidence to support its efficacy. The objective of this study was to determine the efficacy of the use of pulsatile hypertonic saline nasal irrigation in the treatment of sinonasal disease.
STUDY DESIGN: A prospective controlled clinical study.
METHODS: Two hundred eleven patients from the University of California, San Diego (San Diego, CA) Nasal Dysfunction Clinic with sinonasal disease (including allergic rhinitis, aging rhinitis, atrophic rhinitis, and postnasal drip) and 20 disease-free control subjects were enrolled. Patients irrigated their nasal cavities using hypertonic saline delivered by a Water Pik device using a commercially available nasal adapter twice daily for 3 to 6 weeks. Patients rated nasal disease-specific symptoms and completed a self-administered quality of well-being questionnaire before intervention and at follow-up.
RESULTS: Patients who used nasal irrigation for the treatment of sinonasal disease experienced statistically significant improvements in 23 of the 30 nasal symptoms queried. Improvement was also measured in the global assessment of health status using the Quality of Well-Being scale.
CONCLUSIONS: Nasal irrigation is effective in improving symptoms and the health status of patients with sinonasal disease.

Laryngoscope 1997 Apr;107(4):500-3
Mucociliary clearance and buffered hypertonic saline solution.
Talbot AR, Herr TM, Parsons DS.
ENT Department, Sydney Hospital, Australia.

Nasal irrigations have been used for centuries without any scientific data to determine efficacy. For 10 years, the senior author has used buffered hypertonic saline nasal irrigation for patients with acute/chronic sinusitis and for those having undergone sinus surgery. A simple study was undertaken using volunteers without any significant sinonasal disease. Patients served as their own control using a saccharin clearance test before any nasal irrigation was used. Patients then used one of two solutions to irrigate their nose - buffered normal saline or buffered hypertonic saline - and were then retested. On a separate day, the control test was repeated, followed by irrigation with the alternate solution and a second saccharin clearance test. The outcome showed buffered hypertonic saline nasal irrigation to improve mucociliary transit times of saccharin, while buffered normal saline had no such effect

DR. MELTZER'S RESPONSE
I do not have any decent reference on the advantages and/or disadvantages of nasal lavage. I cannot document whether normal or hypertonic saline is better or worse. So much for what I do not have. Nonetheless, I think a good study would be valuable since, in some fashion, nasal saline lavage is commonly recommended for various forms of rhinitis and also rhinosinusitis. Our office regimen is as follows (no basis other than it seems, like chicken soup, to help):

Heat nasal airway with warm wash cloth over/under nose (can microwave 1-2 seconds on high if using tap water).

Blow nose to clear loose mucus or suction mucus out with bulb syringe.

Decongest stuffy side(s) with Afrin nasal spray (up to 5 days).

Repeat step 2.

Irrigate each nasal passage several times with saline (using solution listed below or store-bought saline). The drainage solution may exit from the same side, the opposite nostril or the mouth. The following alternative methods can be used on each side.
Squeeze commercial saline solution into one nostril and then gently sniff it in.

Sniff solution listed below from a cupped hand.

Using a bulb syringe, spray solution listed below gently toward outer side of nasal cavity.

Using a Water Pik with special nasal irrigation tip* spray solution toward outer side of nasal cavity.

Clean mucus out of nose by blowing or suctioning out with bulb syringe.

Clean edge of nostrils with Q-tip and warm water. If dry or irritated, use Vaseline or Bactroban.

Ingredients 1/4 tsp. salt, 1 cup warm water, "pinch" of baking soda

12/3/01 re: Meeting notes- 10/99

Where can I obtain a copy of: Data presented at the National Allergy Advisory Council Meeting (NAAC) titled "the broad spectrum of rhinitis: etiology, diagnosis and advances in treatment." St Thomas, US Virgin Islands, Oct 16 1999.

I am not sure which is the organization to which you referred when you mentioned the National Allergy Advisory Council (NAAC). The group with the name closest and most relevant to your description is the Advisory Council of the National Institute of Allergy and Infectious Diseases, (NIAID), a component of the NIH whose website is shown below. There was mention in this website of a meeting with a title similar to that stated by you. I did a search of the Internet using several search engines. There are many unrelated organizations that use the initials NAAC. However, I could not find reference to any meeting in 10/99 similar to that mentioned by you. Sorry that we cannot be of further assistance. I suggest that you contact the NIAID at the number suggested in their website to see if they know the information you requested.

8/13/01 re: Allergies in immunocompromised individuals

I am in the process of doing a research project on what types of precautions immunocompromised patients need to take in relation to their home environments. This encompasses such things as dust mites, mold, allergens, etc.
Do you have any information that I could have regarding what you recommend to AIDS or other immunocompromised patients?

In responding to your question, I will discuss the situation in AIDS separately from other immunocompromised states. Some previous studies have suggested that there may be an increased incidence of IgE-mediated allergic disorders in those with moderately advanced HIV infection. This possibility was raised by the quite high incidence of allergic reactions to TMP-sulfa treatment in HIV-infected individuals compared to age-matched individuals without HIV infection. Some studies found increased serum IgE levels at a time during HIV infection when there was a transient exaggerated humoral immune response. It was postulated that the HIV infection preferentially decreased Th1 type of immunity, skewing the immune response to the Th2-type responses associated with atopy and increased allergic responses to environmental agents such as pollens and dust mites. However, more recent surveys have found no evidence of increased allergic reactivity to food or airborne allergens in HIV-infected individuals (see enclosed abstracts). Therefore, it appears at this time that HIV-infected individuals are not particularly prone to have allergic reactions to environmental allergens. However, when these patients are profoundly immunocompromised, they could be susceptible to infections with microorganisms that sometimes contaminate particular environments such as very moldy dwellings or certain food preparations. In general, avoidance of such contacts would seem advisable.
In individuals with congenital defects in immune responsiveness (immunodeficient states) there does not appear to be an impressive increase in allergic reactions. The same would apply to those treated with "immunosuppressive" drugs such as cyclophosphamide or cyclosporine. Chronic treatment with high doses of corticosteroids actually decreases IgE levels and IgE-mediated allergies although the individuals may become susceptible to certain types of infections.

Laryngoscope 1999 Jun;109(6):939-44
Rhinosinusitis and atopy in-patients infected with HIV.
Garcia-Rodriguez JF, Corominas M, Fernandez-Viladrich P, Monfort JL, Dicenta M.
Department of Otolaryngology, Ciutat Sanitaria i Universitaria de Bellvitge, University of Barcelona, Spain.

HYPOTHESIS: Rhinosinusitis is common during HIV infection; its prevalence is uncertain and could probably be related to clinical features, immunoallergological status, and diagnostic criteria METHODS: Seventy-four patients hospitalized with HIV infection were prospectively evaluated for the presence of rhinosinusitis based on clinical findings, nasal endoscopy, or paranasal sinus computed tomography (CT). Immune status, nasal smear, features of atopy (based on the prick test), and its contribution to sinusal inflammatory pathology were also evaluated.

RESULTS: Most patients were severely immunosuppressed: CD4+ 155+/-201 cells/mL and 12+/-11% (mean +/- SD). Thirty-five percent of the patients presented at least two criteria of rhinosinusitis (clinical findings, nasal endoscopy, and CT: 35%; clinical findings and CT: 50%; nasal endoscopy and CT: 15%). CT scan showed multiple sinus involvement, pacification over 25% of the total volume of the maxillary sinus in 50% of patients, and pacification of the sphenoidal sinus in 40% of cases. Atopy was present in 18% of patients, a figure that reflects the expected prevalence in our geographic area. Two independent predictors were associated with a higher probability of rhinosinusitis: bilateral absence of maxillary infundibular patency (odds ratio, 7.5; 95% CI = 2.03-27.9) and low total count (odds ratio, 0.99; 95% CI = 0.99-1.00) or percentage of CD4+ (odds ratio, 0.93; 95% CI = 0.88-1.00).

CONCLUSIONS: There is a high prevalence of rhinosinusitis in HIV-infected individuals. This finding is related to a decreased cellular immunity, but it does not appear to be related to IgE-related immediate hypersensitivity. Nasal endoscopy should be the first-step diagnostic test. However, when clinical suspicion exists and endoscopy fails to explain symptoms, CT scan is a valuable adjunct to establish this diagnosis.

PMID: 10369287 [PubMed - indexed for MEDLINE]

Ann Allergy Asthma Immunol 1997 Feb;78(2):209-12
Food allergy in human immunodeficiency virus (HIV) infection.
Tubiolo VC, Vazzo LA, Beall GN.
Department of Medicine, Harbor-UCLA Medical Center, Torrance, California, USA.

BACKGROUND: Gastrointestinal complaints and pruritic skin conditions are common in-patients infected with human immunodeficiency virus (HIV). Because atopic disorders such as drug allergy, asthma, and allergic rhinitis are apparently increased, we hypothesized that food allergy may also be more common in-patients with HIV.

OBJECTIVE: The purpose of this study was to estimate the prevalence of food allergy in-patients infected with HIV. METHODS: Consecutive patients visiting our outpatient adult HIV clinic were screened for possible food allergy by use of a questionnaire. One hundred seventy-six patients responded. Sixty-two of these patients reported symptoms compatible with a possible food allergy. Follow up of the 62 subjects was possible in 40. Thirty-one patients were skin tested for foods thought to produce reactions.

RESULTS: Three patients (1.7%) described previous anaphylactic responses to specific foods and were therefore not skin tested or challenged orally. Six patients (3.4%) described very strong histories of food allergy but either refused or were too ill for testing. Twenty-nine of the 31 patients had negative skin tests. One of the two patients with a positive skin test to a suspected food also had a positive double blind, placebo-controlled food challenge (DBPCFC). There was no correlation between CD4 cell count and likelihood of food allergy. Based on a strong history alone, the maximal estimated prevalence of food allergy in this group was 5.7% (10 of 176). By using the more strict criterion of positive DBPCFC, the prevalence of food allergy in this patient population was 0.57% (1 of 176).

CONCLUSION: These results suggest that food allergy is an uncommon disease in patients with HIV infection with an estimated prevalence similar to that found in the general adult population.

8/9/01 re: Skin test reagent for investigating algae

I�m a lab technician, biologist. I�ve worked 10 years with asthmatic patients, today I work in Alentejo, one of the hottest regions of Portugal. Here the water of the lakes has blooms of cianophiceae (alg) that promote, sometimes, a lot of allergies. My question is: Is there any extract of cianobactery (Anabaena sp., Anphanizomenon, Microcistis) available to do allergic tests? I propose to do my master's in this area, it�s very important to discover a connection between the water that we drink and some allergies.

I am not personally familiar with cianophiceae, the species of algae you mentioned. I also could find no mention of this organism when I did a Medline literature search. To try to obtain more information, I suggest that you contact the Research and Development Department, ALK-Abello, in Madrid, Spain, and try to speak to one of the staff investigators there. As you likely know, ALK-Abello is a very large company which deals with allergen preparation and characterization. Their division in Madrid may have a special interest in potential aeroallergens in the Iberian area. If you cannot locate someone in the Madrid offices of ALK-Abello, I suggest that you try contacting Dr. C. Schou in the main Research and Development offices of ALK-Abello in Horsholm, Denmark. Dr. Schou is very experienced in allergen characterization. If those approaches are not helpful, I suggest that you contact Dr. Sten Dreborg at the University of Uppsala in Sweden. Dr. Dreborg's group has studied individuals with sensitivity to green algae (see enclosed reference).
Tiberg E, Dreborg S, Bjorksten B., Allergy to green algae (Chlorella) among children. J Allergy Clin Immunol 1995; 96:257-9

6/6/01 re: Systemic mastocytosis and allergic rhinitis

I have a 33 year old new patient with allergic rhinitis to a variety of inhalants for many years and systemic mastocytosis by history and physical first manifesting itself 4 months ago with urticaria pigmentosa, tachycardia, flushing, near syncope, vomiting, and diarrhea. The episodes are occurring about every two weeks and last 2-4 hours before clearing. She feels fine between attacks. Screening by her PCP shows that her CBC and LFT's are normal, but she has an ANA of 1:320, homogeneous pattern, and a CRP of 9.1. I have placed her on allegra and zantac routinely and have given her an epipen. My questions to you are as follows: 1) How extensive an evaluation needs to be done at baseline? 2) Are the allergies in any way triggering the attacks? If so, is immunotherapy of benefit, or will it simply trigger more episodes? 3) Is there a role for leukotriene antagonists in the treatment of systemic mastocytosis? 4) How do you explain the ANA?

I have consulted Dr. Larry Schwartz, a highly respected authority about mast cells and their disorders. His responses are enclosed below. I will also add a few thoughts in response to your questions not responded to by Dr. Schwartz.

Dr. Schwartz's Comments
Regarding leukotriene antagonists in mastocytosis: I use them to help treat recurrent mast cell activation events. I know of no clinical trial assessing their efficacy, but there is a scientific rationale for using them. A diagnostic w/u for systemic mastocytosis should include a total serum tryptase level and appropriate skin/bone marrow biopsies. I do not typically obtain 24 h urine histamine measurements. Also, an additional tryptase level drawn within 2-3 hours of a possible mast cell activation event, e.g., hypotension and watery diarrhea, would reveal if mast cell activation had in fact occurred.

It is of interest that prominent allergic rhinitis (AR) is not a common feature in systemic mastocytosis. Therefore, I would approach the treatment of the AR in your patient as I would any patient with AR. This could include immunotherapy, if indicated. However, I would be much more cautious than usual when using this approach: 1) start with a lower dose than usual, particularly if the patient has high levels of IgE antibodies to the relevant allergens (you may have to obtain this information by in vitro assays since the skin may be non-specifically reactive to the trauma of a prick because of the increased number of skin mast cells); 2) build up the dose much more slowly than usual; 3) keep the patient under observation in your office for longer than the usual 20-30 minutes after each immunotherapy treatment.

I am not sure why the ANA was modestly positive in this patient. However, from my extensive experience teaching in the lab performing ANA assays in our hospital, I have been impressed with the greatly increased number of positive ANA in the 1:160-1:320 range found in patients with no clinical evidence of inflammatory connective tissue diseases since we (like many hospital labs) switched to use of the very sensitive ANA assay using Hep-2 cells as targets . If the patient has no clinical evidence to suggest lupus or other inflammatory connective tissue disease, I would not explore further with additional studies.

5/7/01 re: Facial rash in a small child

Nine-year-old boy with itchy, maculopapuar rash only around eyes, more prominent in summer. Has mild allergic rhinitis and also in the summer gets slightly hypopigmented areas on his face and exposed areas (his parents are of Indian origin).

Because I have not been involved in the care of small children for many years, I consulted Dr. Susan Schuval, a very experienced Pediatric Allergist and a member of our AADMC Advisory Committee. Her response is enclosed below.

The differential diagnosis for this patient includes:

Seasonal allergic rhinoconjunctivitis: Patient should have accompanying symptoms of conjunctival erythema, tearing, possible eye discharge, and ocular pruritus. Treatment would consist of topical antihistamines and/or mast cell stabilizers (cromolyn, ketotifen) with use of a systemic antihistamine (loratidine, cetirizine) if relief is not obtained.

Eyelid eczema: Patient should have atopic dermatitis affecting other areas of the body. Conjunctiva would be unaffected. Treatment would consist of very cautious application of low potency topical steroids +/- systemic antihistamine.

Pollen allergy: In very atopic individuals, such a rash may be secondary to contact of the skin with pollen grains. Treatment would consist of standard pollen avoidance measures and systemic antihistamines.

1/25/01 re: Best heating system for individuals with respiratory allergies, asthma

I would like to know if there is any opinion with respect to which home heating system is better for patients with allergic rhinitis and/or asthma: forced hot air, or baseboard hot water?

Although there are varied, and sometimes strongly expressed, opinions about the best heating system to use for individuals with respiratory allergies, I have found little published information from good studies to give a definitive response. I can tell you what I have recommended to patients and the reasons for such recommendations.
I recommend hot water heating systems for these reasons:

1) There is less excessive drying of the air with hot water than with hot air systems. Although several studies have shown that reduction of relative humidity (RH) below 50% is associated with significantly lower dust mite allergen levels, excessively dry air (less than 20% RH) is frequently irritating to the skin and respiratory tract. Such very dry air frequently results from continued use of hot air heating in cold weather regions. Insertion of a humidifier into the heating system may increase the humidity but the humidifier must be checked regularly for contamination of the water depot by molds, etc.

2) Forced air systems are sometimes associated with airborne circulation of irritants that get into the ductwork. Although there are now more efficient filters which can be inserted in forced air systems, such filters are relatively expensive may require fairly frequent replacement. Also, I have been told that "duct cleaning" approaches marketed aggressively in the lay media, are not really effective enough to warrant their cost.

I recognize that most homes constructed in the recent decades are equipped with forced air systems to allow central air conditioning as well as heating. Therefore, compromises may be required.

1/11/01 re: Cause of thick post-nasal discharge

What would cause nasal passage obstruction with thick dried mucus along with thick post nasal drip in the AM? This has also caused the patient to become a night time mouth breather causing snoring.

It is difficult to give a definitive response to your question without knowing additional clinical information not mentioned by you, including the presence or absence of other nasal symptoms such as sneezing, itching, the temporal pattern of symptoms, etc.
However, from your description, one would want to first investigate whether chronic sinusitis was present. Such investigation is best carried out by a careful endoscopic examination of the nasal cavity to see if the material in the post-nasal discharge is coming from one or more sinus ostia. Well-trained otolaryngologists and allergists have the experience to carry out such endoscopic exams. Plain sinus X-Rays give a limited amount of information about the maxillary and frontal sinuses, but may miss disease of the ethmoid sinuses, perhaps the most commonly involved sinuses in chronic sinusitis. Coronal view C.T. exams of the sinuses, though more expensive than plain X-Rays, are much better for detecting involvement of the osteo-meatal complex, the initial locus of most chronic sinusitis . Some experts reserve such C.T. exams for situations where anatomic abnormalities that may require sinus surgery are suspected. If chronic sinusitis is present, rather prolonged treatment with appropriate antibiotics may be necessary. Some studies have shown that concomitant treatment with intranasal steroid sprays may enhance the response to antibiotic therapy.

Other conditions that can lead to the picture you describe include chronic allergic rhinitis and chronic non-allergic (vasomotor rhinitis with/without nasal polyps). These can be distinguished by evaluation by an experienced allergist. Less common causes include cystic fibrosis, local granulomatous processes and others. You can obtain the names of certified allergists in your geographic region by checking the referral directory in the AAAAI website.

11/7/00 re: The Rhinoconjunctivitis Quality of Life Questionnaire

I need a copy of the "The Rhinoconjunctivitis Quality of Life Questionnaire" and or "Rhinitis Outcomes Monitoring System" . Can you direct me in finding a copy of the questionnaire. I would like to include this in the patients chart to better assess the symptoms.

J Allergy Clin Immunol 1999 Aug;104(2 Pt 1):364-9
Validation of the standardized version of the Rhinoconjunctivitis Quality of Life Questionnaire.
Juniper EF, Thompson AK, Ferrie PJ, Roberts JN
Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada.
BACKGROUND: In the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ), the 3 activity questions are selected by the patients themselves. For greater efficiency, a version with standardized activities is required.

OBJECTIVE: Our purpose was to develop and validate a standardized version of the RQLQ, the RQLQ(S).

METHODS: With use of 5 RQLQ databases, we identified the activities most frequently selected by patients and formulated 3 generic questions that would encompass the majority of these activities. The RQLQ(S) was tested in a 5-week observational study in 100 adults with symptomatic rhinoconjunctivitis. Patients completed the RQLQ(S), the RQLQ, and other measures of health status at baseline and 1 and 5 weeks.

RESULTS: The activity domain of the RQLQ(S) consistently gave lower scores than did the activity domain of the RQLQ (P <.001). However, this made very little difference to the overall scores (RQLQ[S] = 2.36 +/- 1.23, RQLQ = 2.43 +/- 1.23), and overall concordance was high (intraclass correlation coefficient = 0.996). In patients whose rhinoconjunctivitis was stable between clinic visits, reliability (reproducibility and ability to discriminate between patients of different impairment) was high for both instruments and almost identical (intraclass correlation coefficient = 0.97). Responsiveness to change was also very similar and good (P <.001). Construct validity (correlation with other index values of health status) was strong for both the RQLQ(S) and the RQLQ.

CONCLUSIONS: The RQLQ(S) has strong measurement properties and measures the same construct as the original RQLQ. The choice of questionnaire should depend on the task at hand.

Clin Exp Allergy 2000 Jan;30(1):132-40
Development and validation of the mini Rhinoconjunctivitis Quality of Life Questionnaire.
Juniper EF, Thompson AK, Ferrie PJ, Roberts JN
Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada.

BACKGROUND: The 28-item Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) has strong measurement properties but for large clinical trials, surveys and practice monitoring, where high efficiency is important, a shorter questionnaire is needed.

OBJECTIVE: To develop and validate an abbreviated version of the RQLQ.

METHODS: Using five RQLQ databases, items with high item-item correlations were combined and then the highest scoring items were selected for the MiniRQLQ (14 questions). There are five domains: activity limitations (standardized), practical problems and nose symptoms, eye symptoms and other symptoms. The MiniRQLQ, which is self-administered, was tested in a 5-week observational study in 100 adults with symptomatic rhinoconjunctivitis. Patients completed the MiniRQLQ, the RQLQ, and other measures of health status at baseline, 1 and 5 weeks.

RESULTS: In patients whose rhinoconjunctivitis was stable between clinic visits, reliability (reproducibility and ability to discriminate between patients of different impairment) was very acceptable for the MiniRQLQ (ICC = 0.93) but not quite as good as for the RQLQ (ICC = 0.97). Responsiveness to change in clinical status was better with the MiniRQLQ than the RQLQ (P = 0. 044). Construct validity (correlation with other indices of health status) was strong for both the MiniRQLQ and the RQLQ. Concordance between the two instruments was high (ICC = 0.87).

CONCLUSIONS: The MiniRQLQ has strong measurement properties and measures the same construct as the original RQLQ. The choice of questionnaireshould depend on the task at hand.

11/10/00 re: Tree pollen sensitivity

Are pollen levels highest in the morning or the afternoon? Should I advise my pollen sensitive patients to exercise outside in the morning or the evening?
How far does tree pollen spread? Should tree sensitive patients be discouraged from planting maples etc. in their yards?

1.) There is no simple answer to your first question because the time for peak emission of pollen varies among the plants. However, if I had to pick one time when peak emissions are most likely, I would say early morning. Peak emission for some plants is in the late afternoon. If I had to make a choice between outdoor activities in the early morning or evening, I would recommend evening
2) The distance that tree pollen travels varies with the tree type. However, in general, the large majority of tree pollen falls to the ground surface close to the tree. The pollen weight, relative humidity, and wind speeds (up to 15-20 mph) affect airborne dispersal. With those factors in mind it can be said that some tree pollens can travel in the air for up to several miles. Although the pollinating season for trees may be relatively short in your area of Minnesota (with resultant short symptomatic periods) , it may be advisable to recommend planting of coniferous trees such as pines rather than trees such as maples. These coniferous trees can pollinate heavily but don't seem to cause clinical allergic reactions often.

11/10/00 re: Guidelines for allergic rhinitis in children

I am interested in knowing whether the Academy has guidelines for the management of allergic rhinitis in children, specifically, the appropriate use of nasal steroids vs. non-sedating antihistamines.

Although I have read articles about allergic rhinitis, I have not seen the exact guidelines to which you refer. Therefore, I consulted Dr. Estelle Simons, an outstanding Pediatric Allergist who has investigated extensively the treatment of allergic rhinitis with antihistamines and nasal steroids. Her response is enclosed below:

The Joint Task Force Document1 on rhinitis contains 3+ pages (Section 48, pages 513-516) on special considerations in children, but no direct answer to the specific question being asked, as there is little published information about intranasal corticosteroids versus non-sedating antihistamines in children under the age of 12 years with allergic rhinitis.

A recent meta-analysis2 of randomized, controlled trials comparing intranasal corticosteroids with oral antihistamines in allergic rhinitis did not include any pediatric studies.

1. Dykewicz MS, Fineman S (editors). Diagnosis and Management of
Rhinitis: Parameter Documents of the Joint Task Force on Practice
Parameters in Allergy, Asthma, and Immunology. Ann Allergy Asthma
Immunol 1998;81:463-518.

2. Weiner JM, Abramson MJ, Puy RM. Intranasal corticosteroids
versus oral H1 receptor antagonists in allergic rhinitis: systematic
review of randomised controlled trials. Br Med J 1998;317:1624-9.

9/11/00 re: Dysphonia due to inhalent allergies

Could be persistent disphonia caused by allergy to fungi and weeds pollen?

There have been occasional reports describing laryngeal pathology, including expression as dysphonia, frequently associated with allergic rhinitis (see below abstracts at www.medline.com). However, in my personal experience, dysphonia has generally been only an occasional problem, generally in those complaining of pronounced thick post-nasal discharge. There have also been case reports of laryngeal edema as apart of anaphylactic reactions to ingested pollen components ( as part of "health food" or "alternative medicine" remedies) in very sensitive individuals (see below abstract at www.medline.com). I am not aware of dysphonia as a particular manifestation of sensitivity to fungi. However, if an individual has the unusual disorder, allergic fungal sinusitis, it is certainly conceivable that post-nasal drainage of purulent material could induce dysphonia.
Of course, one must rule out the possibility that dysphonia is a complication of the use of inhaled steroids in the treatment of asthma or other lower airway inflammatory disease.

Otolaryngol Pol 1997;51(2):191-9
J Investig Allergol Clin Immunol 1996 May-Jun;6(3):208-9

6/20/00 re: Source of guidelines for rhinitis

Where can I find the most recent guidelines on the diagnosis and management of allergic rhinitis?

One of the best, and most detailed, sets of guidelines about rhinitis has been constructed by a Joint Task Force of specialists in the USA. It can be found on this website by going to the Current Literature section, then click on Practice Parameters, click on Rhinitis, then on Contents. Various aspects of diagnosis and management are covered separately for easy review.

6/2/00 re: Quality of life assessment for allergies

We are a multispecialty physician organization and our Otolaryngologists would like to do quality of life outcomes tracking for our allergy patient population comparing primary care and specialty care related to immunotherapy. Are there any current data collection tools out there that would be applicable (something similar to the OM-6 survey that collects information related to hearing and speech)?

The most extensively reported quality of life assessment approach used in allergic diseases and asthma is patterned after that described by Dr. Elizabeth Juniper in Canada. You can find an abstract describing use of the assessment questionnaire and others by looking under Dr. Juniper's name in a Medline search
REFERENCE
Eur Respir J 1999 Sep;14(3):591-6 www.medline.com

9/14/99 re: Safety of inhaled steroids in children

I would like to know how safe is to use inhaled steroids in children less 5 years who have allergic rhinitis.

The safety of inhaled steroids in children has been discussed extensively in recent years, with particular emphasis on effects on growth velocity. Most of the studies have involved use of inhaled steroids for asthma. However, there have been some studies of the effects of nasal steroids. I am enclosing below a brief summary of some of these reports which I wrote recently for the Academy News publication of the American Academy of Allergy, Asthma and Immunology. I suggest that you also consult these items in this AADMC website.

News section - ICS/Growth/Pro-con

Current Literature section - reviews of several articles about inhaled steroid side-effects

Adverse effects of inhaled steroids - the saga continues!
There has been a tremendous recent interest in possible adverse systemic effects of the inhaled steroids (Inh St) which have become a staple of asthma treatment. Concerns have been raised about the inhibition of growth velocity in asthmatic children on Inh St treatment (see Headline item in this AADMC web site). Yet varying conclusions have been drawn
about such adverse systemic effects in different studies, some of which have been reviewed in this Current Literature section of the AADMC.

Lipworth of the University of Dundee in Scotland has recently reported a meta-analysis of studies investigating possible adverse systemic effects of various Inh St preparations1. He concluded that both prominent HPA axis suppression and reduction in bone density is more common during chronic therapy with >750 mcg/day of fluticasone and >1500 mcg/day of
other Inh St. Medium-term growth velocity studies showed evidence of suppression at doses of >400 mcg/d for some Inh St although there has not yet been any evidence of significant reduction of final adult height. Long-term Inh St treatment increases the risk for posterior subscapular abstract, and to a much lesser degree, the risk for ocular hypertension
and glaucoma. In another report2, Li et al of the Mayo Clinic in Rochester, MN have
reported suppression of the HPA by prednisone 10 mgm/day but not by fluticasone in doses up to 400 mcg/day.

REFERENCES
1. Arch Intern Med 1999;159:941-955
2. J Allergy Clin Immunol 1999;103:622-28

EDITOR'S COMMENTS
The findings in these reports add to the burgeoning body of information about possible systemic effects of Inh St. Taken together with information previously reviewed here (including J Resp Dis 1998;19:1023-1036; J Asthma 1998;36:307-311; News Section coverage of the Symposium on Inh St in the AAAAI meeting of 3/99) one can draw some
tentative conclusions:

Most data indicate that Inh St. in doses up to 400 mcg/day (perhaps 200 mcg/day for fluticasone) induce little if any adverse systemic effects.

The frequency of such adverse effects during higher dose therapy will vary with the study (population, outcome measurements, etc.). As speakers in the AAAAI symposium noted, the HPA axis suppression may be subtle and not recognized clinically but could represent a threat during any major stressful event such as severe infection, trauma or surgery.

Fluticasone may have greater anti-asthma efficacy on a mcg/mcg basis but possibly at the price of lower dose threshold for adverse effects.

These findings are particularly important because:

There is a much less prominent dose-dependency for anti-asthma efficacy of Inh St above certain doses (generally about 800 mcg/day) while the adverse effects are much more dose dependent at those levels.

Some authors strongly recommend "high dose" (over 1500 mcg/day) Inh St. as a "safe alternative" to low dose oral steroids in asthma.

Adding approaches such as inhaled salmeterol bid and possibly leukotriene antagonists (not yet proven) may help asthma control without increasing the daily doses of Inh St. above 400 mcg/day

There is often insufficient attention placed on controlling allergic factors in asthma pathogenesis even though such allergic reactivity has been shown clearly to be a major risk factor in many asthmatics. Such treatment approaches to the allergic component may help avoid going to higher doses of Inh. St. to control asthma

A recent report, also from the Univ. of Dundee, suggests greater systemic bioavailability of fluticasone delivered by an MDI with spacer than by a dry powder inhaler (Lancet 1999;353:2128)

It may take longer follow up of sizable patient study groups to draw firmer conclusions about the best approach to the treatment of asthmatics not well controlled on Inh St. doses of up to 400 mcg/day.

4/27/99 re: Pathogenic mechanism in beta-blocker induced nasal symptoms

Beta-blocker drugs are often included on the list of Vasomotor Rhinitis causes. Since mucosal congestion is mediated primarily through alpha-adrenergic receptors, what is the physiologic mechanism that mediates beta-blocker-induced VMR?

I was not aware that treatment with currently used beta-blocker agents commonly induced impressive nasal symptoms simulating rhinitis. I was able to find only one report of more than a single case. In that study from Scandinavia, most of the 5 patients were taking relatively non-selective beta-blockers. The nasal symptoms decreased markedly when patients were switched to more beta-1 specific blockers like the ones now commonly used in the USA.

6/1/98 re: anosmia

A 38-yr. old male, non-smoker has been suffering from mild to moderate degree of loss of smell for the past 7-8 years and feels that now there is almost complete anosmia. This is associated with heaviness of the head, stuffiness of the nose and lack of concentration. On X- Ray (OM view ) there is no deviation of the septum...PNS are clear except a mild ethmoiditis.

I had prescribed antihistaminics, nasal decongestants and a nasal steroid spray with a hope to relieve the possible edema of the olfactory region. However even after two months although the nasal stuffiness is better, the sense of smell has not improved. The patient has, however, developed tinnitus for which I have prescribed cinnarizine.

Please advise me regarding the possible cause and the future course of action that I must take.

Anosmia is a complex disorder in which there can be one or more of a number of etiologic factors. In a 38 year old individual, the most common underlying factors are:

inflammatory responses secondary to infection or allergic rhinitis

nasal polyposis

head trauma

local invasive malignancy

neuropsychologic- only considered after other factors ruled out

My approach would be:

Obtain a careful C.T. exam of the sinuses to look for a local mass and to see whether the olfactory cleft is patent. If the cleft is patent, this suggests that something else besides local obstruction to airflow is causal in the anosmia, often irreversible.

If there is any suggestion of obstruction at the cleft, try oral steroids (e.g.-30 mgm/day for 14 days). If there is considerable improvement in the sense of smell, a reversible inflammatory process is suggested.

If there is any suggestion of a local mass in the C.T. exam, the patient should be examined promptly by a physician very experienced in nasal endoscopy.

4/27/98 re: clinical efficacy of leukotriene receptor antagonists (LTRA) in chronic allergic rhinitis

Are leukotriene receptor antagonists showing any benefit in uncontrolled allergic rhinitis?

At least two recent studies have shown clinical efficacy of leukotriene receptor antagonists (LTRA) in chronic allergic rhinitis. However, from what I can tell, the patients studied were not those with poor symptomatic control by nasal steroids and antihistamines. Based on what we know about the broader anti-inflammatory action of steroids than LTRA, I would not expect the latter to be impressively efficacious in cases where intranasal steroid treatment had not controlled symptoms. It is possible that the nasal steroid sprays are not reaching the affected mucosal areas in a patient. There are approaches one can use to circumvent this problem. But it is reasonable to try LTRA for a period of several weeks.

4/14/97 re: recurrent anosmia

What is current Rx for this problem associated with post nasal drainage?

The treatment of anosmia with post-nasal drainage depends on the cause, which can be due to one or more factors. If the anosmia is pronounced, determine whether the patient has nasal polyps. If polyps are present,

Check for history of increased symptoms after aspirin, NSAID. If present (25% of cases), avoidance is very important. One group reports success with "aspirin desensitization."

If only on one side, refer to ENT specialist for Bx to R/O tumor.

If associated sinusitis, treat infection aggressively.

It is frequently necessary to treat with oral steroids for several weeks to significantly shrink prominent bilateral nasal polyps. Regular, daily use of intranasal steroid sprays may maintain this improvement.

Surgical removal of nasal polyps leads to improvement, often transient because of regrowth, sometimes rapidly. When surgery is indicated, additional endoscopic sinus surgery may be warranted.

If there is marked nasal congestion without polyps,

rule our allergic causes with appropriate consultation. Contact the American Academy of Allergy, Asthma and Immunology (800-822-2762) to get the names of certified allergists/immunologists in your area.

try intranasal steroids used regularly with the understanding that there may be a delay in onset of relief.

3/30/97 re: cat allergy

A young woman is allergic to cats but has a cat as a pet which she won't give up. She takes Claritin once a day and she keeps the cat out of her closed door bedroom at all times. She finds this generally satisfactory but occasionally has allergic symptoms. Is there anything else to recommend to her?

Other measures to reduce exposure to cat allergen:

There is a high concentration of Fel 1 (the major cat allergen) in cat saliva, and cats frequently groom themselves by licking. Therefore, frequent washing of the cat will reduce dissemination of cat allergen. Some cats do not like to be bathed; however, devices to do this have been marketed.

HEPA filters in an air filtration system and a high quality vacuum cleaner should reduce airborne cat allergen particles.

If the patient becomes more symptomatic with continued exposure and still refuses complete avoidance one can consider allergy injection treatment with standardized cat extract.
I suggest that you contact a certified allergist-immunologist in your region to assist you in managing this patient's problems. To get a list of such specialists in your region, contact the AAAAI Hot Line at 800-822-2762.

3/27/97 re: allergic rhinitis in pregnancy

I have a patient who has moderate to severe allergic rhinitis complaints in the first trimester of pregnancy. Beyond the recommendation to limit allergen exposure, what would you suggest, if anything, for pharmacologic control? I know that no medicine is best unless the benefit truly outweighs the risk. Perhaps you could provide me with a list of allergy medicines in order of their risk to the pregnancy.

The manufacturers of the more recent anti-allergy medications are generally very non-committal about their use in pregnant women, generally stating that no studies of the safety of the medication for the pregnant woman or fetus have been carried out. However, based upon what we know about:

the minimal systemic absorption of intranasal steroids sprays, and

the lack of convincing evidence of any adverse effects of small doses of oral steroids on the fetus, I would personally choose standard doses of the recent intranasal steroids. These agents are generally effective in reducing symptoms of allergic rhinitis. However, it should be noted that some women manifest "rhinitis of pregnancy", presenting mainly as nasal congestion, likely due to hormonal effects.

3/17/97 re: treatment for hay fever

Are steroids appropriate for Hay Fever?

In my experience, systemic steroid therapy is rarely indicated in uncomplicated seasonal allergic rhinitis (hay fever). However, appropriately used nasal steroid sprays are a valuable component of therapy, provided that they are used before nasal congestion becomes so pronounced that the spray does not penetrate adequately into the nasal cavity. The incidence of side-effects from nasal steroid spray therapy is quite low.

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