Antrochoanal polyp vs investing papillomatosis

Published в Inter finanzas forex | Октябрь 2, 2012

antrochoanal polyp vs investing papillomatosis

It may be confused with antrochoanal polyps on anterior rhinoscopy. J Clin Exp Invest Key words: Nasal obstruction, nasal polyp, paranasal si-. Non-neoplastic nasal polyps are common and tend to occur in certain Sinonasal or Schneiderian papillomas arise almost exclusively within the nasal. Its occurrence is extremely rare. They can be easily mistaken for antrochoanal polyp. Symptomatically, it is similar to antrochoanal polyp. BITCOINS KOPEN CONTANT

For the upper airway, there is clear evidence that remodeling is also present in chronic rhinosinusitis as well as allergic rhinitis [ 81 — 83 ]. Based on the differential expression of inflammatory cytokines and remodeling patterns, chronic rhinosinusitis with polyp formation CRSwNP can be distinguished from chronic rhinosinusitis without polyp formation CRSsNP. CRSsNP is typically showing more neutrophilic inflammation than CRSwNP, and also fibrosis formation of the extracellular matrix consisting of excessive collagen deposition and thickening of collagen fibers in the absence of pseudocysts.

This questions the link between inflammation and remodeling, as do findings of remodeling in early CRSsNP disease without signs of inflammation [ 85 ]. One striking feature is the relative lack of the transforming growth factor beta TGF- f1 signaling in CRSwNP and consecutively a lack of collagen production [ 86 ].

Remodeling is a dynamic process in both health and disease, balancing ECM production and degradation. In sinus disease, differing results and a multitude of MMP subtypes make it difficult to interpret data. In addition, MMP-9 was found to be involved in wound healing, and high levels predicts poor healing after sinus surgery [ 88 ].

Recent studies also found that the regulation of tissue-plasminogen activators u-PA and t-PA might contribute to tissue remodeling and pathogenesis of CRSwNP [ 89 , 90 ]. However, findings are partially contradicting, which might be due to a lack of correct sub-classification of the disease. Anti-inflammatory medications topical steroids being the gold standard have the potential to suppress inflammation and edema formation.

However, studies suggest that anti-inflammatory approaches alone are not successful in reversing changes such as collagen deposition, indicating that early treatment might be crucial for preventing disease progression. Antibiotics such as doxycycline also possess an anti-MMP effect, and have been shown to modify polyp size and healing after surgery [ 91 , 92 ]. Future studies are needed to optimize the usage of remodeling interventions in disease and after surgery.

These patients derive more benefit from maximal surgical options directed toward eliminating the inflammatory load and improving access for topical medication to retard or reverse the mucosal damage. Additionally, removal of irreversibly diseased mucosa allows healthy mucosa to regenerate in its place. Due to the complexity of disease in recalcitrant sinusitis, it is likely that multimodality treatment will serve these patients best [ 93 ].

Epithelial barrier and innate immunity The sinonasal mucosa serves as the site of interface with inhaled irritants, aero-allergens, commensal organisms and pathogens. Mucociliary clearance and apical junctional complexes AJCs between epithelial cells comprise a mechanical barrier between host and environment. Respiratory mucus, which is produced by goblet cells and submucosal glands, traps foreign material and moves it out of the sinuses and nasal cavity towards the nasopharynx.

Genetic defects in mucociliary flow are associated with a high incidence of CRS [ 94 , 95 ]; acquired mucociliary defects and increased mucus viscosity have also been suggested to underlie idiopathic CRS [ 96 , 97 ]. Sinonasal epithelial cells ECs , residing beneath the mucus layer, are linked by tight and adherence junctions AJCs , creating a relatively impermeable barrier.

Proteins comprising the AJC are subject to degradation by proteases, such as those found in allergens, bacteria and fungi. In CRSwNP, significantly altered levels of adhesion complex proteins have been identified [ 98 — ] as well as lower levels of intrinsic protective anti-protease activity [ , ]. Functional studies have also recently suggested that the epithelial barrier is more permeable in nasal polyps [ , ].

Taken together, these studies suggest that mucociliary dysfunction may play a role in the pathogenesis of CRS broadly, while a porous barrier has been more closely linked to CRSwNP. Environmental stimuli that breech the mechanical barrier may trigger an innate immune response. Sinonasal epithelial cells ECs and other cell types present express pattern recognition receptors PRRs that recognize pathogen associated molecular patterns PAMPs present on microbes [ , ]. Cellular damage is detected through damage-associated molecular patterns DAMPs [ , ] and the combined signal of foreign material plus cellular damage governs the release of host defense molecules, cytokines and chemokines.

Toll-like receptors TLRs are the best-studied PRR, with potential derangements contributing to the development of CRS, but data are thus far inconclusive [ , — ]. More recent evidence has indicated that classical taste receptors are also present on ECs functioning as PRRs by detecting microbial products and triggering enhanced mucociliary clearance and release of host defense molecules [ ].

Genetic variation in these taste receptors may play a role in CRS disease susceptibility [ ]. Nasal ECs secrete a vast arsenal of host defense molecules into the nasal mucus at baseline, with levels augmented upon PRR stimulation [ — ]. These innate responses in ECs are modulated in part by IL and its receptor ILR [ , ] which act in part through the transcription factor STAT 3, broadly mediating mucosal host defense and epithelial repair [ — ].

Decreased expression of some host defense molecules has been associated with CRS [ — ]. Regardless, the presence of diminished host defense molecules in CRS suggests the hypothesis that a primary sinonasal innate immune defect may contribute to local microbial proliferation fostering the development of CRS in a subset of patients [ ].

Beyond host defense molecules, ECs also secrete cytokines and chemokines in response to PRR which foster an inflammatory response and attract and activate innate effector cells [ , — ]. In addition, cytokine crosstalk between ECs, innate lymphoid cells ILCs and dendritic cells matches the appropriate innate and adaptive response to foreign stimuli.

In health, this maintains mucosal homeostasis with a tolerance of allergens and commensals and b defense against pathogens without the development of chronic inflammation. In support of this hypothesis, large numbers of Type 2 ILCs are present in nasal polyps [ ] and high levels of TSLP have been identified suggesting a key role for this cytokine in polyp pathogenesis [ — ].

In regard to IL, there is no current evidence for elevated expression or activity of this cytokine in CRS. EC chemokines play a major role in the attraction and activation of innate effector cells including eosinophils, mast cells, neutrophils and macrophages. The tissue changes associated with CRS are presumably secondary to toxic effects of excessive or persistent degranulation of these cell types [ 6 ]. In regard to CRS pathogenesis, most interest has centered on eosinophils [ ] and mast cells [ ] but elevated levels of neutrophils and macrophages are present and phagocytic activity may be impaired in CRS [ ].

ECs express enzymes involved in the generation of reactive oxygen species ROS and reactive nitrogen species RNS that are important in multiple epithelial processes including mucin production, epithelial repair, innate immunity and response to environmental toxins [ , ]. Variations in activity of these enzyme systems have been proposed to impair barrier function and innate immunity in CRS [ — ] but the clinical significance remains uncertain [ ].

EC enzyme systems also likely contribute to tissue levels of eicosanoids, which have been implicated in subtypes of CRSwNP [ — ]. Broadly speaking, CRS has been proposed as a disease characterized by a dysfunctional host-environment interaction at the sinonasal mucosa [ 6 ]. While the association of asthma and CRS is well established, the prevalence of other chronic inflammatory disorders in the CRS population was not found to be significantly above background [ ].

Diminished innate host defense coupled with a porous barrier should theoretically lead to increased microbial colonization, accentuated barrier damage and a compensatory adaptive immune response [ ]. This implies additional, as yet undetermined mechanisms, perhaps centered on EC and ILC signaling, that foster an inappropriate local, adaptive response in the sinonasal mucosa. Pathophysiology: acquired immunity, T cell signatures T cell patterns, Tregs, follicular structures, immunoglobulins.

The acquired immune system consists of T cell and B cell subsets, armed with different abilities to fight pathogens and orchestrate inflammation. CRSsNP and CRSwNP are characterized by specific compositions of lymphocytes; and specifically T helper cell signatures do have an important impact on the type of mucosal inflammation with respect to neutrophilic vs. The medial nasal and frontal processes give rise to the nasal septum, frontal bones, nasal bones, ethmoid sinus complexes, and upper incisors.

The lateral nasal and maxillary processes fuse to form the philtrum and columella. The cartilaginous nasal capsule forms deep to the nasal and frontal bones from the chondrocranium skull base during the 7th and 8th postovulatory weeks.

The paranasal sinuses develop from the lateral nasal walls at the sixth fetal week, and their growth continues after birth, throughout childhood and adolescence. The maxillary sinus is the first to develop, starting approximately at the 70th day of gestation from the lateral wall of the nasal cavities. The frontal sinuses derive from the region of the frontal recess of the nose, and the ethmoid sinuses originate as multiple separate evaginations from the nasal cavities, while the sphenoid sinuses take origin as evaginations from the posterior nasal capsule reaching the sphenoid bone.

Anatomy The nasal cavities are separated by the nasal septum and limited by a roof which is centrally formed by the cribriform plate of the ethmoid horizontal part , anteriorly by the frontal and nasal bones, and posteriorly by the body of the sphenoid. The floor is formed by the hard palate, which comprises the palatine process of the maxillary bone and the horizontal plate of the palatine bone [ 2 ]. The lateral walls have three turbinates or conchae and three horizontal spaces, or meatii, on each side.

The nasolacrimal duct opens in the inferior meatus, whereas the middle meatus receives drainage from the frontal, anterior ethmoid, and maxillary sinuses. Below the superior turbinate is the sphenoethmoid recess, with the openings of the sphenoid and posterior ethmoid sinuses. Each nasal cavity communicates posteriorly with the nasopharynx through the choanae and anteriorly with the nostril. The dilatation formed inside the aperture of each nostril is known as the vestibule.

The columella separates medially both vestibules. The paranasal sinuses are a group of cavities within the corresponding craniofacial bones maxilla, sphenoid, ethmoid, and frontal which communicate with the nasal cavities through an ostium. Histology The nasal vestibule shares similar histology with the skin. At the level of the limen nasi, the boundary between the osseous and cartilaginous walls of the nasal cavity, the keratinizing squamous epithelium gradually changes first to cuboidal or columnar epithelium and then to ciliated respiratory-type epithelium, which lines most of the nasal cavity and all the paranasal sinuses, with the exception of the roof [ 2 ].

Numerous goblet cells are interspersed in the respiratory-type epithelium. The lamina propria contains several seromucous glands, lymphocytes, monocytes, and a well-developed vascular network, particularly evident in the inferior and middle turbinate. The olfactory mucosa lines the horizontal part of the roof of the nasal cavity. The olfactory epithelium is predominantly made of columnar non-ciliated sustentacular cells, intermingled with scattered bipolar sensory neurons and basal cells; the olfactory serous glands of Bowman are located in the lamina propria.

Acute and Chronic Rhinosinusitis Acute Rhinosinusitis Definition Rhinosinusitis is an inflammatory condition of the nasal and paranasal sinus mucosa. Acute rhinosinusitis ARS is usually infectious and can be clinically characterized by purulent not clear nasal drainage anterior, posterior, or both lasting up to 4 weeks, accompanied by nasal obstruction, facial pain-pressure-fullness, or both [ 3 ].

In the immunocompetent patient, the etiology is predominantly viral or bacterial and less often fungal, whereas in immunocompromised patients, acute fungal sinusitis may occur. Synonyms Acute sinusitis and acute rhinitis Epidemiology The true incidence and prevalence of ARS are unknown, because a significant number of cases do not come usually to medical attention.

However, the prevalence of rhinosinusitis in the general population is considered to be high, and it is estimated that more than 24 million cases of acute bacterial rhinosinusitis occur annually in the United States [ 4 ]. ARS is more common in children than adults.

The prevalence of this disease is increased in women. It is generally thought that the process starts in the nasal mucosa and spreads through the ethmoidal prechambers to the frontal and maxillary sinuses. Swelling of the mucosa may cause obstruction of a sinus ostium, with subsequent secondary bacterial infection acute bacterial sinusitis. The most commonly involved agents are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis [ 5 , 6 ].

Allergic rhinitis hay fever is part of an inherited syndrome which also may manifest as atopic eczema and asthma. In allergic rhinitis, airborne particles, such as grass pollens, molds, and animal allergens, are deposited on the nasal mucosa giving rise to acute and chronic reactions. Allergens combine with the IgE antibodies produced by the plasma cells of the nasal mucosa which are avidly bound to the Fc-epsilon receptors on mast cells. This triggers degranulation of mast cells and releases the inflammatory mediators of the type I hypersensitivity reaction, causing rhinorrhea and nasal obstruction.

A further type of rhinitis is the non-allergic form non-allergic rhinitis, NAR , which is defined by exclusion as a chronic nasal inflammation which is not caused by systemic IgE-dependent mechanisms [ 7 ]. Their recognition is important in order to choose the appropriate treatment. Macroscopy The mucosa is thickened and edematous, and there is a prominent exudate, which is purulent in bacterial forms.

Necrotic tissue is obtained from debridement procedures in case of acute fungal sinusitis. Microscopy In ARS, histopathologic examination is rarely requested. The sinonasal mucosa demonstrates extensive inflammation, with neutrophil-rich infiltrate. In some cases, hemorrhage and necrosis may also be noted.

In acute fungal sinusitis, fungal hyphae can be recognized with appropriate staining methods. The fungus has a tendency to invade blood vessels causing thrombosis and may spread through the perineural spaces [ 8 ]. The affected tissues exhibit coagulative necrosis and hemorrhage, while the inflammatory reaction is scant [ 9 ].

In allergic rhinitis, the nasal mucosa shows numerous eosinophils, abundant plasma cells, and in some cases increased number of mast cells. There is goblet cell hyperplasia of the respiratory epithelium, and the basement membrane, which is destroyed in the acute phase, appears considerably thickened in the chronic phase. Differential diagnosis Clinical data are usually sufficient to separate ARS from other inflammatory conditions.

Histochemical stainings for fungi are helpful to recognize acute fungal sinusitis. Treatment and prognosis The treatment of ARS is medical and depends upon the viral or bacterial etiology. Acute bacterial rhinosinusitis usually resolves with antibiotic therapy. Complications are rare and include contiguous infectious involvement of the orbit or central nervous system and can be potentially life-threatening.

They include epidural abscess, subdural empyema, and cerebral abscess. The incidence of these complications seems to peak in early adolescence.

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Huge Nasal Polyps Removal By Dr. Shahriyar Yahyavi


There are no pathognomonic signs in the Magnetic Resonance imaging MRI but often shows as T1 hypointense and hyperintense in T2 with a peripheral enhancement in the cystic part when intravenous contrast is administered [ 32 ]. Figure 2: Coronal CT scan of a patient with a right ACP Antrochoanal polyp ; A Shows a full right maxillary sinus with a free main ostium with co-incidence of left posterior ethmoid opacification; B Axial CT scan; C Sagittal CT scan showing the homogenously opacified mass extending thru the choana without any infiltration or bone resorption.

View Figure 2 Differential Diagnosis The differential diagnosis for an ACP must include the Juvenile nasopharyngeal angiofibroma, an uncommon vascular tumor, almost exclusively found in young male patients years that starts with unilateral nasal obstruction and epistaxis. Imaging studies shows a highly enhanced mass with tissue destruction and bone remodeling [ 33 ]. Another tumor that must be excluded is the Rhabdomyosarcoma, this malignant tumor has a bimodal distribution among years and years, when the nasopharynx is affected its signs and symptoms can be unilateral nasal obstruction with or without nasal discharge, at MRI it shows as an isointense T1 and iso- to hypointense signal on T2 with variable contrast enhancement.

Other common differential diagnosis are the variations of the ACP, the choanal polyps arising from the ethmoid, or sphenoid sinus [ 34 , 35 ] and the common SNP. Although not common in the pediatric age other diagnosis that should be though are the Inverted Papilloma IP , a benign tumor of the sinunasal cavities that can arise from the maxillary sinus, most commonly diagnosed in the fifth and sixth decade of life [ 36 ], IP can be found as a reddish-gray lobulated tumor, more firm and friable than an inflammatory polyp [ 37 ], IP may be associated to bone lysis by CT scan, in MRI is hypointense in T1, with homogeneous enhancement and a cerebriform aspect in T2 [ 38 ].

Other rare pathologies the olfactory neuroblastoma, meningo- encefalocele, lymphoma or hemangioma [ 39 ]. Treatment The excision of the polyp by functional endoscopic sinus surgery FESS with the concomitant treatment of the obstructed sinus complex, a safe procedure with relatively minor complications, like synechiae or epistaxis, is the cornerstone for the resolution of ACP in all ages [ 14 ]. The external approaches as the Caldwell- Luc procedure CWL , Mini Caldwell-Luc or transcanine sinuscopy could also be used for the definitive treatment, however currently are used if the origin of the ACP cannot be found or in revision surgery in a combined approach.

Routine office nasal endoscopy is suggested, as in any FESS, to prevent and treat synechiae, to minimize complications. Recurrences have been reported from 6 months to 3 years after surgery, with reports of a higher recurrence in the pediatric age group compared to the adult group [ 41 ].

These differences could be explained by the difficulty to find the ACP origin, FESS without angled endoscopes and instruments, and the narrow nasal anatomy of the pediatric group. Conclusions The ACP is a benign tumor of the maxillary sinus that prolapse to the nasal cavity in a variable extent, almost always unilateral, more common in children, without gender difference in this age group, with a male predisposition in the adult age group.

Although highly researched the exact physiopathology of the ACP is still unknown, so still there is no way of prevention. The image studies help for surgery planning and differential diagnosis, but still the standard diagnosis is clinical. The only treatment is surgery, including the total removal of the polyp, treating the associated obstructed sinus complex, preferably by functional endoscopic sinus surgery.

The patient follow up should be of at least 2 years, there is no standard in how the patient should be followed. However, this procedure has fallen from favor due to potential complications, such as facial paresthesia, injury of the infraorbital nerve and risk of damaging the maxillary growth centers in children.

This procedure involves removal of both the solid nasal and cystic antral portions of the polyp. This technique minimizes the risk of complications and recurrence, with some studies showing complete resolution. She has received follow-up care from ENT specialists who have noted no evidence of recurrence of the antrochoanal polyp. Our patient will continue to receive routine follow-up care over this span, and her prognosis is excellent. The risk factors leading to its etiology are unclear.

Comprising nasal mucosa, it originates in the maxillary sinus and can cause symptoms of nasal obstruction. The polyp can be definitively diagnosed on CT. Treatment involves surgery and recurrence is rare if the entire polyp is removed. Nasal polyps in the pediatric population. Antrochoanal polyp: analysis of cases. Acta Otorhinolaryngologica Italica. Characteristics of antrochoanal polyps in the pediatric age group. Ann Thorac Med. Evaluation and Management of Antrochoanal Polyps.

Clin Exp Otorhinolaryngol. Histologic structure of antrochoanal polyps. Acta Otolaryngol. Antrochoanal polyps. Antrochoanal polyps: How long should follow-up be after surgery? Int J Otolaryngol. Antrochoanal polyp. Appl Radiol.

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Rhinology : Huge Antrochoanal ( AC ) polyps

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