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��ࡱ�>��	il����h�������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������g�	���|bjbjVV	.~r<r<�4����������PPPPP����ddd8��`<d~)r������(�(�(�(�(�(�($�*��-��(9P�(PP��H8)...~P�P��(.�(..!]!�����0��{��������)!�(N)0~)1!,,.��,.]!,.P]!h.�(�(.~)��������������������������������������������������������������������,.� :	AMYLOIDOSIS OF THE NASOPHARYNX AND NASAL CAVITY PRESENTING AS SEVERE EPISTAXIS AND SPHENOID SINUS DEHISCENCE
Sanaz Harirchian MD, Department of Otolaryngology - Head & Neck Surgery, University of Medicine and Dentistry of New Jersey  � New Jersey Medical School
Neena M Mirani, MD, Department of Pathology and Laboratory Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School
Soly Baredes, MD, Chairman, Department of Otolaryngology - Head & Neck Surgery, University of Medicine and Dentistry of New Jersey  � New Jersey Medical School
Institution: University of Medicine and Dentistry of New Jersey � New Jersey Medical School, Newark New Jersey USA

No financial support or disclosures
Conflict of interest: none
Corresponding author:
Soly Baredes, MD
90 Bergen Street
Suite 8100
Newark, NJ 07103
 HYPERLINK "mailto:baredeso@umdnj.edu" baredeso@umdnj.edu
tel: 9739724588
fax: 9739723767
Poster presented at Triologic Combined Sections Meeting, January 27-29th, 2011 in Scottsdale, Arizona 
Key Words: nasal amyloidosis, nasopharyngeal amyloidosis, amyloid head and neck 


















Abstract 
Background: Nasopharyngeal amyloidosis is rare, with only a few case reports in the literature. On Computed Tomography (CT) scan, these lesions usually present as a homogeneous, well defined soft tissue mass without any evidence of bony erosion. Methods: Case report and review of the literature. Results: We present a case of a 33 year old female who presented with persistent epistaxis despite surgical management and nasal packing. CT sinus revealed a soft tissue mass extending from the roof of the nasopharynx with associated dehiscence of the sphenoid sinus floor and unilateral sphenoid sinus opacification. Biopsies of the nasopharynx and right lateral nasal wall were consistent with amyloidosis. Conclusion: Otolaryngologists need to be aware of this rare clinical entity which may present with bony erosion and may be managed conservatively. 











Introduction:
Amyloidosis is a collection of diseases characterized by the extracellular deposition of the insoluble fibrillar proteinaceous material, amyloid. Its symptoms vary depending on whether the pathology is systemic or localized, and on the organ systems involved. While localized amyloidosis is rare, constituting 10-20% of amyloidosis cases, it most commonly affects the head and neck.1,2 Nasopharyngeal and nasal cavity amyloidosis is extremely rare, with only 14 prior case reports in the literature.3-5  It is typically treated with surgical resection and carries an excellent prognosis, despite recurrences. We present a patient with localized amyloidosis of the nasal cavity and nasopharynx who presented with severe epistaxis and sphenoid sinus dehiscence, and eventually had clinical resolution with conservative management. We will review the clinical and radiographic features of localized nasopharyngeal and nasal cavity amyloidosis, as well as its management and a review of the literature.  










Case report:
The patient is a 33 year old female with a past medical history of iron deficiency anemia and sickle cell trait who presented with a several month history of epistaxis, nasal congestion, and headaches. Noncontrast CT of the sinuses performed one month prior to admission noted bilateral anterior nasal cavity soft tissue masses, as well as a well circumscribed soft tissue mass along the roof of the nasopharynx. There was associated dehiscence of the sphenoid sinus floor and unilateral sphenoid sinus opacification (Figures 1). Retrospective review of a CT one year prior to presentation for complaints of nasal obstruction revealed the same radiographic findings.  
She was originally scheduled for sinus surgery by an outside otolaryngologist, however had worsening epistaxis requiring admission and nasal packing at an outside hospital. She was taken to the operating room for a septoplasty and biopsy of a right lateral nasal wall mass, however the surgery was terminated due to excessive bleeding. A posterior nasal pack was placed intraoperatively for hemostasis, and the patient was transferred to our institution for further management. 
Upon presentation to our institution, the patient was taken to the operating room for removal of nasal packing and possible cauterization and control of epistaxis. Nasal endoscopy revealed extensive soft tissue in bilateral nasal cavities, edematous and friable mucosa, and a large anterior septal perforation. A nonobstructive smooth well circumscribed tumor-like mass was noted along the roof of the nasopharynx, which was also biopsied. No clear source of epistaxis was found, and bilateral nasal septal splits were placed to prevent nasal stenosis. The patient was discharged on POD #2 without any significant recurrent epistaxis. The splints were removed on POD #7.
Pathologic examination of the right lateral nasal wall and nasopharyngeal biopsies revealed amorphous eosinophilic material in the subepithelial stroma, consistent with amyloid. The presence of amyloid was confirmed by Congo Red stain, and the presence of apple green birefringence with polarized lens (Figures 2-4). Systemic workup, including a chest radiograph, electrocardiogram, urine analysis, serum creatinine, liver function tests, serum electrophoresis, and a PET/CT scan, did not demonstrate any systemic disease.  Routine follow-up nasal endoscopy 6 months later did not demonstrate any nasal cavity or nasopharyngeal masses. 















Discussion: 
Amyloidosis is believed to result from immune dysregulation and the inability to break down the immunoglobulin and nonimmunoglobulin precursor proteins, with their resultant polymerization into an insoluble proteinaceous fibril which deposits in the extracellular space.5,6 The � pleated structural organization renders it resistant to proteolysis, and difficult to clear by native tissue. The two most common amyloid proteins are Amyloid associated (AA) and Amyloid light chain (AL). While AL is derived from plasma cells and contains immunoglobulin light chains, AA is a non-immunologic protein synthesized by the liver.
Systemic amyloidosis typically carries a poor prognosis due to vital organ infiltration and  is subtyped into 3 forms: 1) Primary amyloidosis (AL), which constitutes 75% of amyloidosis cases.4 This is associated with B cell or plasma cell dyscrasias, and results from the polymerization of monoclonal immunoglobin light chains into amyloid fibrils;  2) Secondary amyloidosis (AA), which is associated with chronic inflammatory conditions, such as Rheumatoid Arthritis, inflammatory intestinal disease, hypernephroma, and Hodgkin disease. 3) Familial amyloidosis is rare, comprising < 2% of systemic cases, with autosomal recessive transmission.7 
Although the localized form of amyloidosis is rare, it carries an excellent prognosis and frequently involves the head and neck.1,2 Many are focal areas of amyloid deposits, termed amyloidomas. Tissue involvement may be diffuse with submucosal infiltration, or nodular such as a tumorlike mass.  The larynx is the most frequently involved site of localized amyloidosis (61%), followed by the oropharynx (23%), trachea (9%), and orbit (4%).7 Nasopharyngeal and nasal cavity involvement is rare, with only 14 prior case reports in the literature.5 Due to its rarity, amyloidosis is not routinely considered in the differential of nasal cavity and nasopharyngeal masses. 
	Nasopharyngeal and nasal cavity amyloidosis typically presents with epistaxis, nasal obstruction or otologic symptoms due to Eustachian tube obstruction. Epistaxis is believed to be due to perivascular infiltration by amyloid and vascular wall fragility.3  Less common symptoms such as facial pain, epiphora, rhinorrhea, and chronic mouth breathing have also been reported.1  Although amyloidosis is typically a benign, slow growing, nondestructive process characterized by lack of bony erosion, there are a few case reports in the literature noting significant aggressive osteolysis.  Hegarty presented a case of nasopharyngeal amyloidosis with extensive skull base erosion and V-XII left sided cranial neuropathies.8  Although highly atypical, this case illustrates the possibility of an aggressive clinical course to this histologically benign lesion. Our patient also had isolated sphenoid sinus floor dehiscence, pointing to the potentially osteolytic behavior of amyloidomas. 
	Diagnosis is made with histological confirmation. Amyloid deposits are eosinophilic on hematoxylin-eosin staining and Congo red staining demonstrates apple-green birefringence under polarized microscopy. After diagnosis, a systemic workup is necessary due to the prognostic and therapeutic implications. The use of rectal biopsy (75% positive) has largely been replaced by aspiration of abdominal wall adipose, which has been shown to have a specificity of 92-100%, and a sensitivity of 75-90% in a diagnosis of systemic disease.5 If biopsies are negative and clinical suspicious remains high, organ directed biopsies may also be performed. Additional workup to exclude secondary or systemic amyloidosis includes serum protein electrophoresis, urinalysis, electrolytes, hemoglobin, erythrocyte sedimentation rate, and white and differential cell counts. 
Data on radiographic findings in localized amyloidosis is limited, making the diagnosis more challenging. The CT appearance of nasopharyngeal and nasal cavity amyloidosis is nonspecific, typically illustrating a well defined submucosal homogeneous mass with minimal, if any, contrast enhancement.4,7,8 Calcification is a common finding. Studies of  characteristics on MR have also been very limited, noting isointensity to surrounding skeletal muscle on T1-weighted images and iso- or slightly hyperintensity on T2-weighted images.7,8 Imaging currently does not add much to the diagnostic armamentarium besides better characterization of the extent of local disease, and the presence of bone destruction in those rare cases.  
	Due to the great rarity of cases of localized amyloidosis, it is difficult to predict the clinical outcome and optimal treatment algorithm. The mainstay of treatment is currently surgical, based primarily on experience with laryngeal amyloidosis. Local excision is performed, with emphasis on functional preservation. The necessary extent of surgical resection is not yet clear. However due to the benign histology, complete surgical excision should not be performed at the expense of significant functional deficits and morbidity.4  External beam radiation has been used postoperatively to clear residual laryngeal amyloidosis.9 Although surgical resection has variable results with recurrences reported in the literature, localized amyloidosis has an excellent prognosis. Our patient�s nasal cavity and nasopharyngeal disease appeared to show clinical resolution without treatment after 6 month nasal endoscopy highlighting the possibility of conservative management in this disease process if the patient�s symptoms are limited. That being said, the potential for the progression of localized to systemic amyloidosis is currently unknown and all patients with localized amyloidosis should be followed long-term for recurrence or systemic disease.




















Conclusion:
Nasopharyngeal and nasal cavity amyloidosis is a rare clinical entity which can present with persistent epistaxis and bony erosion on CT.  Our case highlights the possibility that nasopharyngeal amyloidosis may be managed conservatively. 


















References:
Pang KP, Chee LW, Busmanis I. Amyloidoma of the nose in a pediatric patient: a case report. American Journal of Otolaryngology 2001: 22: 138-141
Barnes, L. Miscellaneous orders of the head and neck. In: Barnes L, ed.  Surgical pathology of the head and neck. Vol 3, 2nd ed. New York: Marcel Dekker; 2001:2191-2193
Panda NK, Saravanan K, Purushotaman GP, Gurunathan RK, Mahesha V. Localized amyloidosis masquerading as nasopharyngeal tumor: a review. American Journal of Otolaryngology, Head & Neck Medicine and Surgery 2007; 208-211
Lim JS, Lebowitz RA, Jacobs JB. Primary amyloidosis presenting as a nasopharyngeal mass. American Journal of Rhinology 1999; 13: 209-212
Pearlman AN, Jeffe JS, Zynger DL, Yeldani AV, Conley DB. Localized amyloidosis of the nasal and paranasal mucosa: a rare pathology. American journal of Otolaryngology- Head and neck medicine and surgery 2010; 31; 130-131
Asaumi J, Yanagi Y, Hisatomi M, Konouchi H, Kishi K. CT and MR imaging of localized amyloidosis. European Journal of Radiology 2001; 39: 83-87
Gean-Marton AD, Kirsch CF, Vezina LG, Weber AL. Focal amyloidosis of the head and neck: Evaluation with CT and MR imaging. Radiology 1991; 181:521-525
Hegarty JL, Rao VM. Amyloidoma of the nasopharynx: CT and MR findings. American Journal of Neuroradiology 1993; 14: 215-218
Neuner GA, Badros AA, Meyer TK, Naji NM, Regine WF. Complete resolution of laryngeal amyloidosis with radiation treatment. Head Neck. 2010 Nov 10. 
Figure legend:
Figure 1. (A) noncontrast  coronal CT sinus demonstrating soft tissue mass along nasopharyngeal roof with sphenoid  sinus floor dehiscence and opacification (B) noncontrast coronal CT sinus illustrating bilateral nasal cavity soft tissue  masses L>R
Figure 2. (A) (H & E, 40X), Amorphous eosinophilic material in subepithelial stroma of nasopharynx (B) 400X, Congo red stain positive for amyloid (C) Congo red stain, birefringence on polarized microscopy










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