Journal: Current allergy and asthma reports
Mast cell activation syndrome (MCAS) is a condition with signs and symptoms involving the skin, gastrointestinal, cardiovascular, respiratory, and neurologic systems. It can be classified into primary, secondary, and idiopathic. Earlier proposed criteria for the diagnosis of MCAS included episodic symptoms consistent with mast cell mediator release affecting two or more organ systems with urticaria, angioedema, flushing, nausea, vomiting, diarrhea, abdominal cramping, hypotensive syncope or near syncope, tachycardia, wheezing, conjunctival injection, pruritus, and nasal stuffiness. Other criteria included a decrease in the frequency, severity, or resolution of symptoms with anti-mediator therapy including H(1) and H(2)histamine receptor antagonists, anti-leukotrienes, or mast cell stabilizers. Laboratory data that support the diagnosis include an increase of a validated urinary or serum marker of mast cell activation (MCA), namely the documentation of an increase of the marker above the patient’s baseline value during symptomatic periods on more than two occasions, or baseline serum tryptase levels that are persistently above 15 ng/ml, or documentation of an increase of the tryptase level above baseline value on one occasion. Less specific assays are 24-h urine histamine metabolites, PGD(2) (Prostaglandin D(2)) or its metabolite, 11-β-prostaglandin F(2) alpha. A recent global definition, criteria, and classification include typical clinical symptoms, a substantial transient increase in serum total tryptase level or an increase in other mast cell derived mediators, such as histamine or PGD2 or their urinary metabolites, and a response of clinical symptoms to agents that attenuate the production or activities of mast cell mediators.
Acute otitis media (AOM) is a polymicrobial disease, which usually occurs as a complication of viral upper respiratory tract infection (URI). While respiratory viruses alone may cause viral AOM, they increase the risk of bacterial middle ear infection and worsen clinical outcomes of bacterial AOM. URI viruses alter Eustachian tube (ET) function via decreased mucociliary action, altered mucus secretion and increased expression of inflammatory mediators among other mechanisms. Transient reduction in protective functions of the ET allows colonizing bacteria of the nasopharynx to ascend into the middle ear and cause AOM. Advances in research help us to better understand the host responses to viral URI, the mechanisms of viral-bacterial interactions in the nasopharynx and the development of AOM. In this review, we present current knowledge regarding viral-bacterial interactions in the pathogenesis and clinical course of AOM. We focus on the common respiratory viruses and their established role in AOM.
Intranasal medication for eustachian tube dysfunction (ETD) is an established practice in otolaryngology through the effects of steroids, decongestants, antihistamines or a combination of the above in reducing tubal oedema. The author has previously argued that a double-blind, randomised control trial would be helpful in determining effectiveness of treatment, if a standardised head position, chiefly Mygind or Ragan, was adopted to maximise intranasal drop delivery into the eustachian tube orifice. One recent paper suggests that intranasal treatment is not very effective, but ultimately does not state whether a standardised head position was adopted. Although a large body of evidence supports the hypothesis that the nasal passages are the route to middle ear disease, there is as yet no paper that has been published that has specifically addressed this issue, therefore the author must conclude that evidence to support intranasal treatment for ETD is still lacking and further research is desirable.
Allergic rhinitis is the most common atopic disorder seen in ENT clinics. It is diagnosed by history, physical exam and objective testing. Patient education, environmental control measures, pharmacotherapy, and allergen-specific immunotherapy are the cornerstones of allergic rhinitis treatment and can significantly reduce the burden of disease. Current treatment guidelines include antihistamines, intranasal corticosteroids, oral and intranasal decongestants, intranasal anticholinergics, intranasal cromolyn, and leukotriene receptor antagonists. In the mechanism of allergic rhinitis, histamine is responsible for major allergic rhinitis symptoms such as rhinorrhea, nasal itching and sneezing. Its effect on nasal congestion is less evident. In contrast, leukotrienes result in increase in nasal airway resistance and vascular permeability. Antihistamines and leukotriene receptor antagonists are commonly used in the treatment of allergic rhinitis. The published literature about combined antihistamines and leukotriene antagonists in mono- or combination therapy is reviewed and presented.
Balloon dilation technology (BDT), also known as balloon sinuplasty, has been in clinical use since September, 2005. Prior to BDT, surgeons performed a procedure called FESS, or functional endoscopic sinus surgery, for patients with chronic sinusitis. As is true with any new technology or procedure in medicine, a debate often ensues between early adopters and mainstream practitioners. Over the past 7 years, much has been discussed, debated, and learned about BDT. What follows is a review of the origins of the BDT: the theory, technology, indications and applications; and a review of the pertinent outcomes literature. Independent of how one feels about BDT, the evidence strongly supports its safety, efficacy, and growing popularity among patients and physicians alike.
Empty nose syndrome (ENS) is a rare, late complication of turbinate surgery. The most common clinical symptoms are paradoxical nasal obstruction, nasal dryness and crusting, and a persistent feeling of dyspnea. Little is known about the pathogenesis of ENS, though it is speculated that anatomical changes leading to alterations in local environment, disruption of mucosal cooling, and disruption of neurosensory mechanisms are strongly implicated. The diagnosis is clinical, though often difficult to make due to the poor correlation between subjective and objective findings. Medical therapies include mucosal humidification, irrigations, and emollients. Surgical therapy should be reserved for refractory cases and may involve turbinate reconstruction, most commonly using implantable biomaterials. Ultimately, prevention of this feared complication through turbinate-sparing techniques is essential.
To compare the prevalence of sensitization in different countries based on specific IgE values and to evaluate the use of isolated native or recombinant allergens for diagnosis.
Anaphylaxis is a severe allergic reaction that is rapid in onset and may cause death. Since it is unpredictable and potentially fatal, prompt recognition and treatment are vital to maximize a positive outcome. The occurrence of anaphylaxis is increasing across all ages in the United States, with increased risk of worse outcome in teenagers/young adults and in those with comorbid conditions such as asthma. Gaps in the assessment of patient-specific risk factors, identification and prevention of triggers, recognition of signs/symptoms, and pharmacologic treatment of anaphylaxis have been identified at the physician and caregiver/patient level. A PubMed literature search (January 2000-December 2011) was conducted to identify publications on childhood anaphylaxis using the following terms: food allergy, food allergens, food hypersensitivity, epinephrine, epinephrine auto-injectors, anaphylactic triggers, and anaphylaxis. This review will critically appraise these key issues and highlight strategies that might result in improved management of anaphylaxis in children.
Developed societies, although having successfully reduced the burden of infectious disease, constitute an environment where metabolic, cardiovascular, and autoimmune diseases thrive. Living in westernized countries has not fundamentally changed the genetic basis on which these diseases emerge, but has strong impact on lifestyle and pathogen exposure. In particular, nutritional patterns collectively termed the “Western diet”, including high-fat and cholesterol, high-protein, high-sugar, and excess salt intake, as well as frequent consumption of processed and ‘fast foods’, promote obesity, metabolic syndrome, and cardiovascular disease. These factors have also gained high interest as possible promoters of autoimmune diseases. Underlying metabolic and immunologic mechanisms are currently being intensively explored. This review discusses the current knowledge relative to the association of “Western diet” with autoimmunity, and highlights the role of T cells as central players linking dietary influences to autoimmune pathology.
The avoidance of wheat- and gluten-containing products is a worldwide phenomenon. While celiac disease is a well-established entity, the evidence base for gluten as a trigger of symptoms in patients without celiac disease (so-called ‘non-celiac gluten sensitivity’ or NCGS) is limited. The problems lie in the complexity of wheat and the ability of its carbohydrate as well as protein components to trigger gastrointestinal symptoms, the potentially false assumption that response to a gluten-free diet equates to an effect of gluten withdrawal, and diagnostic criteria for coeliac disease. Recent randomized controlled re-challenge trials have suggested that gluten may worsen gastrointestinal symptoms, but failed to confirm patients with self-perceived NCGS have specific gluten sensitivity. Furthermore, mechanisms by which gluten triggers symptoms have yet to be identified. This review discusses the most recent scientific evidence and our current understanding of NCGS.