REVIEW Influenza, hay fever and sinusitis: Know the differences Marnus Milne, BPharm, MSc(Pharmacology), PhD(Pharmacy), Senior Lecturer, School of Pharmacy, Sefako Makgatho Health Sciences University Tumelo Mokoena, BPharm, MPharm Candidate at Sefako Makgatho Health Sciences University Jade Du Toit, BPharm, MPharm Candidate at Sefako Makgatho Health Sciences University Zandile Dlamini, BPharm, MPharm Candidate at Sefako Makgatho Health Sciences University Natalie Schellack, BCur, BPharm, PhD(Pharmacy), Professor, School of Pharmacy, Sefako Makgatho Health Sciences University Correspondence to: Natalie Schellack, e-mail: [email protected] Keywords: Influenza, hay fever, sinusitis, common symptoms, differences Abstract Influenza, hay fever and sinusitis are all very different upper respiratory tract syndromes that share very similar symptoms. “Flu” is caused by the influenza virus and usually presents with headaches, myalgia, fever and body aches. Hay fever is an allergic response of the body to a trigger, more often treated by removal of the trigger. There is no place for antibiotic usage in flu or hay fever; there is no clinical evidence to suggest that using antibiotics alters the course of the disease or prevents secondary infection. Treatment is mainly symptomatic and includes many over-the-counter medicines, antivirals and herbal treatments. On the other hand, sinusitis is a common inflammatory condition defined by persistent symptomatic inflammation of the sinonasal cavities lasting from less than four weeks to longer than three months. Either a virus or bacteria may cause sinusitis. Appropriate use of medical therapies, including antibiotics for sinusitis is necessary to optimise patient quality of life and daily functioning and minimise the risk of acute inflammatory exacerbations. Patients often present at the pharmacy with complaints of “flu”. However, in many instances, symptoms may be confused with those of an allergy or sinusitis. It is important to know and understand the difference between influenza and allergies such as hay fever and sinusitis, in order to ensure correct diagnosis and offer appropriate therapeutic approaches. This article will review the clinical manifestations of influenza, allergic rhinitis (hay fever) and sinusitis, and highlight the differences between these three illnesses. © Medpharm S Afr Pharm J 2018;85(6):19-26 Introduction ALLERGIC RHINITIS (HAY FEVER) Allergic rhinitis – more commonly known as hay fever – sinusitis and influenza can be difficult to accurately distinguish based Hay fever, also known as allergic rhinitis (AR), is an IgE-mediated on symptoms presented, because they share so many common hypersensitivity response causing inflammation of the nasal 5 symptoms. Understanding the differences could assist in making passages. an accurate diagnoses and choosing the best treatment. This An allergic response is a hypersensitivity reaction mediated by the will decrease the unnecessary consumption of medications, adaptive immune system. The presence of a trigger, such as an and increase quality of life. Complications due to acute bacterial allergen or antigen, induces a humoral immunological response, sinusitis can be life threatening. It is for this reason critical to make which in turn initiates a complex immunological reaction. This an accurate diagnosis as early as possible to initiate the appropriate dysregulation in the immune function elevates the plasma levels antibiotic regimen, in order to prevent these complications.1 of immunoglobulin E (IgE). The release of IgE is followed by binding to the allergen or antigen, which in turn stimulates the mast cells Allergic diseases are complex diseases caused by a combination to degranulate and release several pro-inflammatory substances of genetic and environmental factors. Allergic diseases are on that include histamine, chemokines and numerous cytokines. the increase, affecting approximately 30% to 40% of the world’s population. They decrease quality of life and may have an immense There is vast evidence that shows that T-lymphocytes play a major 1,2,3 1)/T-helper cell influence on personal, social, and economic costs. role in allergic diseases. The T-helper cell type 1 (Th type 2 (Th2) paradigm has been extensively studied and seems to be Hay fever, allergies, sinusitis and influenza could all lead to the major pathological pathway in allergic diseases. The paradigm respiratory problems.3 It is important to accurately treat them explains the relationship between the Th1 and Th2 subsets of to avoid the preventable respiratory tract infections from the T lymphocyte. Th1 and Th2 subsets tend to differentiate from manifesting. This could decrease the frequency of antibiotic CD4+-naïve T lymphocytes. This means that whenever a raised 4 requirement associated with such respiratory tract complications. response towards either the Th1 or the Th2 subset occurs, the other S Afr Pharm J 19 2018 Vol 85 No 6 REVIEW 1-3 will be reduced. When there is a reduction in Th1 production, The most common antigens for allergic rhinitis are inhaled there are observed decreased levels of interferon gamma (IFN-g), allergens, of which dust mites, animal dander and pollen are interleukin (IL)-2 and tumour necrosis factor (TNF)-beta. This in the major ones of concern. When the patient is sensitised, an turn leads to elevated levels of Th2 effect, owing to a decrease in antigen comes into contact with the nasal mucosa. This leads 5,6,7 IgG production, which inhibits Th2 formation. to a cross-linking of IgE-mediated receptors on the mast cells. In turn, this leads to the degranulation of the mast cells, with a Allergic rhinitis can be classified either as seasonal, perennial resultant release of histamine and proteases from the preformed or episodic, according to the frequency of exposure to the granules. In addition, an array of early-phase pro-inflammatory stimulus. Table I differentiates between seasonal, perennial or episodic allergic rhinitis. Many different factors come into play molecules are synthesised and released, especially prostaglandins, when searching for the causative agent of allergy. Environmental leukotrienes, cytokines, tumour necrosis factor-alpha (TNF-α), influences that occur in pregnancy and early childhood can and IL-4. The release of these molecules causes oedema and alter the physiological, immune, structural and behavioural fluid secretion, which may result in congestion and other nasal development and thus transform response patterns that influence symptoms. The role of leukotrienes as mediators in allergic susceptibility to future diseases. Genetics also play a vital role in rhinitis is well-supported in the literature. Cysteinyl leukotrienes the susceptibility of an individual to an allergic disease. The most are able to facilitate the maturation of eosinophil precursors, common allergic conditions around the world include atopic and act as eosinophil chemoattractants, promoters of eosinophil dermatitis, rhinitis, asthma, rhinosinusitis, allergic conjunctivitis adhesion, and inhibitors of eosinophil apoptosis. The leukotrienes and, most recently, allergic oesophagitis. and thromboxane A2 (TXA2) are arachidonic acid derivatives. It has been shown in animal models that TXA agonists increase Allergic rhinitis affects approximately 20% of the world population 2 nasal airway resistance and vascular permeability. An acute- and is considered to be the most common chronic disease. AR is phase allergic reaction is also characterised by the production a type 1 allergic disease which reduces quality of life depending of prostaglandin D (PGD ), a major proinflammatory prostanoid, on the severity. Exposure to nasal allergens stimulates an 2 2 which results in vasodilation and bronchoconstriction, as well as a IgE-mediated type 1 hypersensitivity reaction, resulting in number of inflammatory biomarkers, such as N-α-tosyl-L-arginine symptomatic reactions to the allergen. The early characteristic methyl esterase (TAME)-esterase and eosinophil cationic protein symptoms of allergic rhinitis are rhinorrhoea, nasal congestion (ECP). PGD is also believed to be associated with hypertrophic and sneezing. AR can also be associated with various conditions 2 inflammation and acts as a recruiter of eosinophils. such as bronchial asthma, allergic conjunctivitis, rhinosinusitis and others.8,9,10 The late-phase or chronic inflammatory response involves cellular infiltration, which sustains tissue swelling and oedema, and Diagnosis further exacerbates congestion. The ensuing cytokine release A history of nasal symptoms after exposure to allergen and other results in the nasal mucosa being infiltrated with inflammatory physical signs related to this condition aid with the diagnosis, cells. These inflammatory cells, including eosinophils, neutrophils, however a skin prick test to determine if the reaction is IgE- basophils, mast cells and lymphocytes, sustain and intensify the mediated is preferred for a definitive diagnosis. An alternative, but nasal mucosal inflammatory reaction. The predominant cell type, less sensitive, is in vitro testing (blood). As asthma is an important namely the eosinophil, characterises the chronic inflammatory co-morbidity of allergic rhinitis, a spirometry test can be done to process which is present during the late-phase allergic response. assess pulmonary function.11 These eosinophils release a broad range of proinflammatory mediators, including the cysteinyl leukotrienes, ECP, eosinophil Pathophysiology peroxidase