PlatformQ Health

 

Seasonal Allergies: Focus on Allergic Rhinitis

Allergic rhinitis (AR) is one of the major symptoms of seasonal allergies. When the nose is exposed to an allergen, an Ig-E mediated response ensues. Characteristic symptoms include watery rhinorrhea, nasal obstruction, nasal itching, and sneezing. In the US, approximately 60 million people suffer AR or 10-30% of the adult population and 40% of children.

The allergic sensitization that delineates AR has a very strong genetic component and the propensity to incite an IgE/mast cell/Th2 lymphocyte immune response is inherited in atopic individuals. Exposure to an allergen at threshold levels causes antigen presenting cells to assign the allergen to CD4+ lymphocytes. Interleukins IL-3,4 and 5 as well as other Th2 cytokines are released. These cytokines then drive certain proinflamatory responses, such as IgE production, against these allergens through actions of plasma cells, mast cells and eosinophils.

Mast cells are found on body surfaces and release chemical mediators that are stored in preformed granules once activated. After activation, leukotrienes and cytokines are made and can lead to very unpleasant symptoms. IgE is mostly found on the tissue of the mast cells that contain this receptor. Additionally, it can be found on circulating basophiles and activated eosinophils.  When these cells are activated at the site of the allergen or antigen entry, the release of these chemicals result in the recruitment of additional eosinophils and basophils.

There are two phases of the allergic response: the early and late phases. In the early stage response, in addition to the above, mast cell degranulation occurs when IgE is bound to FcεRI. Preformed mediators: histamine, heparin, tryptase, chymase, kikinogenase are released as well as inflammatory mediators: prostaglandin D2, sulfidopeptidyl leukotrienes C4, D4 and E4. When the latter occurs, blood vessels dilate and leak leading to mucosal edema and rhinorrhea. Mucosal glands release mucoglycococonjugates and antimicrobial compounds leading to fulling of the sinuses and nasal congestion.  Additionally, the chemical mediators stimulate sensory nerves leading to itching and sneezing.

In the late phase response, the chemical mediators released by the mast cells promote the expression of vascular cell adhesion molecules and E-selectin. This leads to the adhesion of circulating leukocytes to the endothelial cells. Chemoattractants such as IL-5 aid the infiltration of the mucosa with inflammatory cells. These cells are then activated leading to the release of inflammatory mediators reactivating many of the proinflammatory processes observed in the early phase reactions.  Eosinophilic mediators and leukotrienes can cause epithelial damage.  T helper cells release cytokines that promote IgE production, eosinophil chemoattraction,  eosinophil survival and mast cell recruitment. In the bone marrow, IL-5 promotes CD34+ synthesis leading to progenitor cells differentiating into mast cells. It plays a key role in mobilizing mast cells into the circulation, where they travel to tissue sites. Eosinophils are thought to possess both distinct and shared neutrophil adhesion pathways.

What are the symptoms of allergic rhinitis?

  • Rhinorrhea
  • Congestion
  • Itchiness in the nose, eyes, ears and/or palate
  • Sneezing
  • Postnasal drip
  • Headache
  • Ear ache
  • Excessive lacrimation
  • Red eyes
  • Eye swelling
  • Anosmia
  • Fatigue
  • Malaise
  • Drowsiness

Some possible complications of allergic rhinitis include acute and chronic sinusitis, otitis media, abnormal sleep, sleep apnea, dental problems, abnormalities of the palate, and Eustachian tube dysfunction. On physical exam, watery nasal secretions may be observed as well as a nasal crease. In chronic cases, the nasal septum may become deviated or perforated. The conjunctiva of the eyes may appear injected or swollen and the classic Dennis Morgan lines or allergic shiners may be seen. Cobblestoning may be present in the oropharynx. The tympanic membranes may be retracted or immovable.

The diagnosis of AR usually can be made from a careful history and physical. An environmental cause is suggested when certain triggers are identified. Family history is also very important as it is often hereditary. The utility of allergy testing should be reserved for times when it may change treatment. Empiric therapy is often appropriate without such testing. However, if the symptoms are unclear or the patient may be a potential candidate for immunotherapy, allergy testing can be a valuable tool. The most common tests utilized are the percutaneous skin tests or the IgE antibody test. Skin testing involves introducing tiny amounts of a possible allergen into the skin, which can identify both early and late phase allergic responses but the goal is to identify the immediate response which creates the diagnostic “wheal and flare” after 15 minutes.  Radioallergenosorbent testing (RAST) is useful when percutaneous testing is unavailable or the patient is taking a medication (such as an antihistamine) that can interfere with the skin testing results. RAST is very specific but not as sensitive as skin testing. It can be useful for identifying common allergens but not so much for food, venom or drug allergies.

Treatment of AR:

  • Allergen avoidance
  • Oral and topical antihistamines
  • Intranasal corticosteroids
  • Decongestants
  • Intranasal Cromolyn
  • Intranasl anticholinergics
  • Leukotrience receptor antagonists
  • Immunotherapy

The American Academy of Allergy, Asthma, and Immunology recommends starting with an intranasal corticosteroid for mild to moderate symptoms.  For more severe, second line treatments should be initiated. Intranasal corticosteroids act by decreasing the influx of the inflammatory cells and reducing the secretion of chemical mediators thereby reducing inflammation of the nasal mucosa. Their onset of action is 30 minutes, although peak onset to action may take hours to days. Maximum effectiveness is usually reached in 2-4 weeks. Many studies have found them to be more effective than oral and intranasal antihistamines. Second generation are now more commonly used than first generation ones due to improved side effect profile and less sedation.  Both generations have been shown to relieve the histamine related symptoms, such as sneezing, but don’t do much for the nasal congestion. School aged children using first generation antihistamines were found to have poorer school performance, probably due to the drowsiness. The onset of action is 15-30 minutes and are generally used on an as needed basis. Intranasal cromolyn is thought to act by inhibiting the degranulation of mast cells. Leukotriene receptor inhibitors were found to be better than placebo in many large studies but still not as effective as intranasal steroids or antihistamines. Many studies have concluded that combination therapy with antihistamines and intranasal corticosteroids is no more effective than using intranasal corticosteroids alone.

Allergy shots, or immunotherapy, work well for some. Both children and adults can receive allergy shots, though it is not generally used in children under the age of 5 years. Allergy shots work by gradually introducing the patient to increasing doses of the allergen. In the build-up phase, the patient usually receives the shots 1-2 times a week with incremental increases in the amount of the allergen. This phase generally lasts 3-6 months.  Once the effective dose is reached, the maintenance phase is started. Shots are typically given every 2-4 weeks depending on several factors, including the patient’s response to the therapy and are usually continued for 3-5 years.

About the Author

Linda Girgis MD, FAAFP is a family physician practicing in South River, New Jersey. She was voted one of the top 5 healthcare bloggers in 2016. Follow her on twitter @DrLindaMD.



Leave a Reply

Your email address will not be published. Required fields are marked *