Angioedema with life-threatening site is one of the most impressive and serious reasons for presenting to the ENT doctor. Among different causes (tumors, local infections, allergy reactions), an important cause is the side-effect of the angiotensin converting enzyme (ACE) inhibitors drugs. ACE-inhibitors-induced angioedema is described to be the most frequent form of bradykinin-mediated angioedema presented in emergency and also one of the most encountered drug-induced angioedema. The edema can involve one or more areas of the head and neck region, the most affected being the face, the lips, the tongue, followed by the larynx, when it may determine respiratory distress and even death.
There are no specific diagnosis tests available and the positive diagnosis of ACE-inhibitors-induced angioedema is an exclusion diagnosis. The authors performed a review of the most important characteristics of the angioedema caused by ACE-inhibitors and present their experience emphasizing the diagnostic algorithm.
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Polcalcins are highly cross-reactive calcium-binding allergen components specifically expressed in pollen from trees, grasses and weeds. The grass allergen component rPhl p 7, a recombinant non-glycosylated calcium-binding protein of 2-EF-hand type, is the most cross-reactive polcalcin and may be used as a polcalcin biomarker of IgE-mediated hypersensitivity. Polcalcin sensitization, which appears to be linked to geographical factors, level and time of pollen exposure, has to be assessed in allergic rhinitis patients with multiple pollen sensitizations and may be useful for a better targeted prescription of allergen immunotherapy.
The terminal nerve (cranial nerve zero, cranial nerve XIII, the nerve “N”) was discovered in fish in 1894. In the early 90’s, it was found in human embryos and human adults. In the anterior fossa, it courses on the inner side of the olfactory tract and bulb; it then spreads fibers through the cribriform plate to distribute beneath the nasal septum mucosa. Being provided with intrinsic ganglion cells, its functions are weakly suggested by studies in different species. It may be connected with the visual system, it could act upon the intracranial vascular system, or it could ensure the pathway for pheromone-mediated behaviours. The cranial nerve zero deserves a better attention equally from anatomists and ENT specialists.
Hereditary angioedema (HAE) is a rare autosomal dominant disease consisting of recurrent angioedema attacks, varying in severity, possibly life-threatening and with frequent involvement of the head and neck areas. The patophysiology of HAE differs from histamine-mediated allergic angioedema. Three types of reduced quality or quantity in various complement or coagulation factors, leading to massive release of bradykinin, increase vascular permeability and produce capilary leakage. Clinical manifestations of HAE include swelling located predominantly in the head and neck area, hands, feet and urogenital area and abdominal pain caused by edema of the gastrointestinal tract mucosa. Diagnosis requires laboratory tests for complement components and genetic tests. A timely and correct diagnosis in the emergency room is of utmost importance, the medical treatment of HAE being substantially different from that of allergic angioedema. Although new therapies are available and in development, airway intervention and surgery are still life-saving procedures and the ENT surgeon is an important part of the multidisciplinary team managing an HAE attack.
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