Nasal Polyps Holistic Treatments
The reasons for lack of benefit from allergen immunotherapy include (1) inappropriate treatment with such therapy of non-IgE-mediated disease, such as chronic nonallergic rhinitis or vasomotor rhinitis (2) utilization of low-potency allergen vaccines (3) administration of inadequate doses of allergen (4) ineffective environmental control resulting in continued excessive exposure, for example, to cat or dog dander (5) a coexistent medical problem, such as sinusitis and nasal polyps, which accounts for most of the
Long-term, low dose macrolide therapy represents one attempt at controlling the inflammation associated with chronic sinusitis (80). Medicines that have anti-inflammatory properties and are well tolerated are sought to help ease the reliance on systemic corticosteroids that affect both the number and function of inflammatory cells. When used in a topical form, nasal steroid sprays have been shown to be safe and effective in reducing the symptoms of alleric rhinitis (81). Their use in patients with chronic sinusitis can decrease the size of nasal polyps, and diminish sinomucosal edema (82). There are no set guidelines for the duration of use, and the expected side effects from long-term use are not yet known. Experience in using oral steroids for the treatment of chronic sinusitis is only anectodal. The extended use of oral steroid may result in serious side effects that include muscle wasting and osteoporosis. Because of the side effects, steroids are tapered and given in short...
All patients should be asked if they can take aspirin or NSAIDs without ill effects, and this line of inquiry is even more important in patients with sinusitis or nasal polyps. Occupational asthma should be suspected if patient worsens early each week and then improves during the course of the week, or if asthma is worse during the week as com-
The mechanisms responsible for nasal symptoms associated with medications or hormones are variable. Antihypertensive therapies with p-blockers and a-adrenergic antagonists probably affect regulation of nasal blood flow. Oral a-adrenergic antagonists are also commonly utilized for symptom relief of prostate enlargement. Topical ophthalmic p-blocker therapy may also result in nasal congestion by the same mechanism. Nasal congestion and or rhinorrhea may also result from changes in estrogen, and possibly progesterone, either from exogenous administration, pregnancy, or menstrual cycle variations. Hypothyroidism is associated with nasal congestion, rhinorrhea, and a pale, allergic-like nasal mucosa. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) may result in congestion and rhinorrhea, primarily in subjects with aspirin triad. Subjects with intermittent symptoms associated with aspirin or NSAIDs may be part of the evolving spectrum of chronic, eosinophilic rhinosinusitis...
Nasal polyp view from the rhinoscope in the left nostril. The septum is on the left and the polyp is the pale soft tissue between the middle and inferior turbinate. Nasal polyps are associated with chronic inflammatory sinus disease, usually eosinophilic. Nasal polyps are not consistently found in subjects with allergic rhinitis but could explain persistent congestion. Cystic fibrosis is also associated with nasal polyps, although not generally with eosinophilic inflammation. Fig. 4. Nasal polyp view from the rhinoscope in the left nostril. The septum is on the left and the polyp is the pale soft tissue between the middle and inferior turbinate. Nasal polyps are associated with chronic inflammatory sinus disease, usually eosinophilic. Nasal polyps are not consistently found in subjects with allergic rhinitis but could explain persistent congestion. Cystic fibrosis is also associated with nasal polyps, although not generally with eosinophilic inflammation. described as...
It is estimated that 3-5 of asthmatics will reliably worsen after the ingestion of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Ingestion of aspirin or other NSAIDs may provoke either of two responses respiratory responses, including bronchorrhea, rhinorrhea, bronchospasm, conjunctivitis, lacrimation, and flushing or urticaria and angioedema. Rarely, combinations of the two patterns are seen. Aspirinsensitive patients may be recognized by the presence of nasal polyps, nonallergic rhinitis, persistent sinusitis, and asthma associated with moderate eosinophilia ( 1000 mm3). The frequency of NSAID sensitivity increases with age, although children and families have been described with clear-cut reactivity. There may be a wide range of associated allergies, but many subjects (about 50 ) are not allergic.
Chronic sinusitis is characterized by persistent mucosal inflammation, with histological evidence of edema and a mixed cellular infiltrate (eosinophils and lymphocytes). The marked thickening of sinus tissue observed microscopically, macroscopically, and radio-graphically has given rise to the term hyperplastic sinusitis. Nasal polyps, which are commonly identified in patients with chronic sinusitis, represent evaginations of sinus mucosa and are histologically identical to the tissue from which they originate. Although both aeroblic and anaerobic bacteria as well as fungi may be cultured from the sinus cavities of patients with chronic sinusitis, the true role of these organisms as infectious pathogens is unclear.
In the completely asymptomatic patient, results of chest examination will be normal, although head, eye, ear, nose, and throat examination may disclose concomitant serous otitis media, allergic conjunctivitis, rhinitis, nasal polyps, paranasal sinus tenderness, signs of postnasal drip, or pharyngeal mucosal lymphoid hyperplasia. Clubbing of the fingers is extremely rare in uncomplicated asthma, and this finding should direct the physician's attention toward diseases such as bronchiectasis, cystic fibrosis, pulmonary neoplasm, or cardiac disease. With an acute exacerbation, patients may be restless, agitated, orthopneic, tachypneic, breathing through pursed lips with a prolonged expiratory
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are important causes of anaphylactoid events. These reactions are not IgE-mediated. They apparently produce anaphylactoid reactions through the aberrant mechanism of arachidonic acid, with inhibition of cyclooxygenase and subsequent increased production of leukotrienes. However, some episodes may be caused by the direct degranulation of mast cells. Adverse reactions to aspirin typically include urticaria, angioedema, asthma, chronic rhinosinusitis, and nasal polyps in sensitive individuals. Because the sensitivity persists for life, management entails strict avoidance. Acetaminophen is the alternative recommended drug. Studies have suggested that the cyclooxygenase-2 inhibitors are safe in aspirin-sensitive asthmatics, but they do not have Food and Drug Administration (FDA) approval at this time. Salsalate, choline salicylate, magnesium salicylate, and propoxyphene hydrochlo-ride are the other drugs that can be used.
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