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Autoimmune disorders of the larynx: Common conditions, symptoms, and treatments.


A wide variety of occupations require the continuous use of high intensity phonation. This group of professional voice users includes singers, actors, and teachers, among other occupations. Professional voice users suffer disproportionately from voice disorders compared with their peers in less vocally taxing professions. A study of patients visiting the voice clinic at the University of Wisconsin found that over forty percent of the clinical load was accounted for by teachers, singers, and salespeople. These data support the relationship between vocally taxing occupations and prevalence of voice disorders. (1) Singers are particularly affected by voice disorders, and singing teachers should know as much as possible about various voice maladies in order to help guide their students.

Voice disorders result from physiologic, anatomic, or functional changes that impair normal phonation and change voice production. These changes can affect professional voice users. (2) While vocal dysfunction can result from regular use, a number of medical problems can lead to serious voice impairment. Specifically, autoimmune diseases can lead to serious and permanent vocal deterioration. (3)

Autoimmune diseases are disorders that share a defect in the immune system leading to the body's inability to differentiate between normal and foreign components. Immune system components, including antibodies, identify normal tissue as foreign and incite an inflammatory response. The process of "autoreactivity" is attributed to a number of factors, including genetic predisposition, gender, and environmental exposure. Between three and nine percent of the general population are affected by autoimmune diseases, and the impact can be limited or systemic. Pathologic autoimmunity can lead to extensive damage to normal anatomy and potentially permanent loss of function. (4)

This review discusses the most common autoimmune diseases and their laryngeal sequelae, common signs and symptoms of vocal fold involvement, disease diagnosis, and effective treatment options. The information presented is especially important for professional voice users with autoimmune diseases. Awareness of the signs and symptoms of voice involvement can potentially limit time from symptom onset to first physician visit.


A thorough literature search was conducted to gather data to complete this review. For each autoimmune disorder presented, the search term "laryngeal manifestations of" preceded the disorder name. The search term was run through the PubMed database. Table 1 summarizes the search results found for each query. Initial filters were set between the years 2000 and 2014. Additional criteria for inclusion in the review were specific discussion of laryngeal manifestation of the autoimmune disorder and text written in English. Following initial review of collected literature, selected cited references were added as sources for this review.

Selected articles were organized subsequently into four groups. The groups included: (1) articles that discussed disease development, pathogenesis, and mechanism of laryngeal insult; (2) signs and symptoms found on exam, including classic and rare presentations; (3) current diagnostic modalities, with an emphasis on gold standard diagnostic tools; (4) current treatments and their efficacy as well as potential future treatments. Articles including a broad discussion of a specific disorder were placed in more than one group. This algorithm permitted adequate organization of resources and facilitated the identification of gaps in the literature.


Amyloidosis is an autoimmune disease characterized by the unnecessary secretion of protein into the extracellular environment. The disease becomes clinically apparent usually during the fifth and sixth decades of life, affecting men and women equally. The deposited protein, amyloid, is an insoluble fibrillar substance that can occur locally or throughout the body. (5) With the exception of laryngeal involvement, head and neck amyloidosis is often a sign of existing underlying malignancy.

Laryngeal masses caused by amyloidosis make up less than one percent of all benign laryngeal masses. (6) Laryngeal amyloidosis is rare and frequently occurs in the absence of systemic disease. The false vocal folds and ventricular space are affected most commonly, followed by the true vocal folds. Amyloid collects beneath the surface layer of epithelial cells and elicits a chronic inflammatory response comprised of lymphocytes and plasma cells. The precise cause of amyloidosis is not known. (7) A reaction to a self-antigen and the inability to clear protein produced by plasma cells are potential explanations. (8)

The most common presenting symptom is progressive hoarseness. Other complaints include dyspnea, stridor, vocal fatigue, and dysphagia. (9) The voice may sound high pitched, raspy, or coarse. (10) Dedo and Izdebski completed objective acoustic analysis on ten patients with laryngeal amyloidosis revealing increased breathiness and friction, decreased total voice range, diminished loudness, and decreased maximum phonation time. The same study found that symptoms were more severe when amyloid was deposited bilaterally on the undersurface of the true vocal folds and when amyloid extended from the false vocal folds to the true vocal folds. Patients with significant laryngeal involvement may be limited to a whisper and may suffer other changes to the voice. (11) Severe vocal impairment can prohibit patients from a variety of activities.

Laryngeal amyloidosis must always be considered in patients with progressive hoarseness and voice impairment. (12) Definitive diagnosis can be made with biopsy of the lesion, staining with Congo Red, and exposing the tissue to polarized light to visualize the classic apple-green birefringence. (13) On electron microscopy, antiparallel beta pleated sheets can be observed. (14) Laryngoscopy permits visualization of the lesions, which range from edematous glottic strictures to protruding nodules. (15) The lesions may appear yellow, orange, or gray in color. (16) With significant false vocal fold involvement, the true vocal folds can be partially or completely obscured. (17) After diagnosing laryngeal amyloidosis, signs and symptoms of systemic involvement should be assessed. Traditionally, gastrointestinal and bone marrow biopsies are required to diagnose systemic amyloidosis. (18) More recently, less invasive blood tests have become accepted to assess kidney, liver, and hematologic health. (19)

There is no cure for amyloidosis; however, disease control is usually possible, and treatment often leads to excellent outcomes. Surgery often is recommended regardless of presentation, but it is especially important for patients presenting with substantial vocal impairment or evidence of airway obstruction. (20) Surgical extirpation followed by adjuvant radiotherapy can be used to treat isolated laryngeal amyloidosis. (21) This method putatively eliminates the pathologic plasma cells responsible for depositing the amyloid into the extracellular space, an approach that resembles the concept of chemotherapy for B-cell malignancies. (22) Truong et al. treated ten patients with head and neck amyloidosis using low dose radiotherapy to limit the potential for disease recurrence and reported disease control in eight of the patients. The dose of radiation used was low compared to that used for cancer treatment, leading to a limited side effect profile. (23) Further studies are needed to validate the true efficacy of radiation therapy for amyloidosis and the possible long-term adverse effects. (24) Patients with recurrent disease, submucosal lesions, or polypoid lesions should be treated surgically. (25) Although some authors believe that carbon dioxide laser excision is more precise and less traumatic to surrounding tissue compared with traditional surgical techniques, many other surgeons (including RTS) disagree and favor cold instruments especially for disease involving the true vocal folds. (26) Surgical treatment is often vocally restorative. Regardless of treatment choice, patients should be followed up regularly with serial laryngoscopies to assess for disease recurrence, and serial imaging also is valuable.


Relapsing polychondritis (RP) is a rare autoimmune disease that leads to recurrent inflammatory episodes within cartilage. The disease can manifest locally or systemically.

Onset occurs usually between the ages of 40 and 60; however, pediatric cases have been described. (27) While the etiology is unknown, a strong genetic relationship has been found between RP and the HLA-DR4 and HLA-DR B1 alleles. (28) Recent literature suggests that many RP patients have T inflammatory cells that react with type II collagen, the predominant protein in hyaline cartilage. (29) Chronic intrachondral inflammation leads to weakened structures, including vocal and airway support structures. Advanced disease can lead to airway obstruction, which is responsible for ten percent of all RP-related deaths. (30)

Compared with healthy control subjects, T cells from patients with RP increased almost five times the original number when exposed to type II collagen. (31) Navarro et al. recently published a pediatric case study in which a patient with RP was given exogenous type II collagen orally for 8 months apparently leading to complete disease remission. The authors propose that regular feedings with type II leads to induced tolerance. (32) These data suggest that RP results from an inappropriate reaction by the body's immune system to type II collagen.

RP is diagnosed classically using the McAdams Criteria, proposed in 1976. Table 2 outlines the qualifying signs and symptoms for diagnosis. A patient requires three of the six manifestations for definitive diagnosis. (33) While patients with RP may present with a variety of signs and symptoms associated with cartilage inflammation, a significant number of patients diagnosed with RP initially present with airway manifestations. Common laryngotracheal symptoms include cough, dyspnea, hoarseness, stridor, and wheezing. (34) Over time these symptoms can lead to airway stenosis and collapse, most pronounced with inspiration. Vocal fold masses may develop with severe disease. Stenosis, permanent deformity, and pneumonia are sources of morbidity and mortality. More recent literature demonstrates the existence of type II collagen antibodies and T cells reactive to type II collagen. (35) As more literature becomes available, serological evidence of RP could lead to improved ability to diagnose the disease.

RP is a progressive and fluctuating disease that often can be controlled with oral steroids and methotrexate. (36) Nonsteroidal anti-inflammatory medications can be beneficial. Severe disease exacerbation, including airway obstruction, requires emergency tracheotomy or endotracheal tube placement. If the patient is not in respiratory distress, high dose pulsed intravenous steroids may be effective. Under certain circumstances, RP may be refractory to standard therapy. Childs et al. described a patient with laryngeal RP complaining of dysphonia and airway difficulty refractory to standard treatment with steroids and methotrexate. A laryngeal mass was discovered on laryngoscopy. A pulsed-potassium-titanyl-phosphate (KTP) laser was used to treat the mass. Normal voice returned one-month following the procedure without evidence of a recurrent mass. (37) Mpofu et al. targeted the pro-inflammatory cytokine tumor necrosis factor (TNF) alpha to treat a patient with refractory laryngeal RP. Remicade (Janssen, Titusville, NJ), a medication used frequently for rheumatoid arthritis, binds and inactivates TNF alpha. After five doses of Remicade, the patient experienced substantial improvement. (38)


Sarcoidosis is a chronic granulomatous disease that commonly manifests in the respiratory tract. (39) In the United States, Hispanic and African American women are more often affected, compared with other ethnicities and men. (40) Laryngeal sarcoidosis is rare, and can lead to serious voice alterations especially concerning for professional voice users. Neel and McDonald studied over 2,000 patients with sarcoidosis between 1950 and 1981 and found laryngeal sarcoidosis in less than one percent of the study group. (41) The development of sarcoidosis involves an inappropriate immune response to an unknown antigen resulting in the formation of a granuloma, an attempt to wall off a foreign substance. The granulomas, which are noncaseating and without necrosis, may regress completely or become fibrous and hyalinized over time. (42)

Definitively diagnosing sarcoidosis requires tissue biopsy to visualize noncaseating, non-necrotic granulomas; however, a number of clinical manifestations can support the presence of laryngeal sarcoidosis. Hoarseness, dyspnea, dysphonia, and stridor are common presenting complaints. (43) Mayerhoff and Pitman described four patients to demonstrate the highly variable presentation of laryngeal sarcoidosis. The four cases differed in age of onset, presenting symptom, and timing of disease onset. The four cases included one pediatric patient and a variety of different chief complaints including dysphonia, globus, progressive snoring, and dysphagia. (44) A distinct "honking" vocal quality may be a diagnostic clue. A rapidly enlarging neck mass also may indicate the presence of disease. (45) Any airway symptom occurring in a patient already diagnosed with sarcoidosis should elicit immediate laryngoscopy to identify airway disease and prevent respiratory distress. (46) Pulmonary function testing can be helpful to identify extrapulmonary obstructive airway disease, the classic manifestation of laryngeal sarcoidosis.

Patients with symptoms highly suspicious for laryngeal sarcoidosis should receive routine blood tests, a chest radiograph to identify evidence of pulmonary involvement, and direct laryngeal visualization and biopsy when indicated. Biopsy is the gold standard for diagnosis. Laboratory and radiographic information serve a supportive role. Granulomas in the larynx are rare and may require multiple biopsies to confirm their nature when sarcoidosis is suspected. (47) The appearance of glottic structures during videolaryngoscopy can provide additional evidence suggestive of sarcoidosis. Turban-like supraglottic obstruction is often seen on endoscopic exam. Additionally, the true vocal folds and subglottis often appear nearly normal. Only with severe disease do these structures appear slightly erythematous and thickened. Vocal fold mobility is often normal. (48)

After establishing an open airway, the goal of treatment is to preserve or restore voice quality. First line treatment of laryngeal sarcoidosis involves oral steroids. More recent literature supports the potential use of topical or inhaled steroids to specifically treat laryngeal sarcoidosis. Dean et al. described a patient with longstanding, systemic sarcoidosis that presented with vocal manifestations. The patient was treated successfully with systemic steroids, but returned with isolated vocal manifestations. A trial of inhaled corticosteroids successfully led to sustained resolution of voice symptoms. (49) Another patient with progressive dysphonia, neck pain, and snoring diagnosed with extensive laryngeal sarcoidosis was treated with steroids unsuccessfully. The patient experienced rapid and sustained improvement with a trial of azathioprine, a cytotoxic agent specifically targeting T immune cells thought to be responsible for causing sarcoidosis. It is beneficial to avoid invasive surgical procedures in favor of medical treatment to avoid potentially permanent damage to the voice. (50) Surgical treatment should be considered in cases of failed medical treatment or severe disease. Debulking the airway provides significant symptomatic relief in patients with airway compromise.


Systemic lupus erythematosus (SLE) is a multisystem inflammatory disease caused by the presence of circulating autoantibodies. (51) Upper airway disease can affect up to thirty percent of those diagnosed with SLE. (52) The fluctuating nature of the disease creates a mosaic of signs and symptoms. Laryngeal involvement is relatively rare in SLE. Three putative mechanisms have been proposed to explain laryngeal symptoms in SLE, each due to the inflammatory nature of the disease: (1) diminished blood flow to nerves supplying the larynx; (2) compression of laryngeal nerves due to pulmonary hypertension; and (3) mucosal edema and ulceration. (53)

Patients with laryngeal manifestations of SLE may complain of progressive sore throat, hoarseness, and dysphagia over weeks to months. (54) Dysphonia, foreign body sensation, and strained respirations are other likely complaints. (55) Rarely, acute airway obstruction can occur. (56) It is important to review patient medications, as various medicines may be associated with the development of lupus and laryngeal manifestations. Hari et al. described a patient with vocal dysfunction due to hydralazine-induced lupus. Hydralazine is a medication used commonly for severe hypertension. (57)

Direct laryngeal visualization is helpful in making a diagnosis. Diffuse laryngeal edema involving the aryepiglottic folds, vocal fold paralysis, and upper airway obstruction are all potential clinical findings in patients with laryngeal manifestations of SLE. (58) Vocal fold paralysis, edema, and vasculitis also may be present. (59) Structural changes can be seen with computerized tomography (CT). Laryngeal electromyography (LEMG) assesses the function of the nerves supplying the laryngeal musculature. If blood supply to the nerves is compromised, the function of these nerves may become compromised. (60) Serological data also should be obtained to confirm a diagnosis if not previously completed. Anti-double stranded DNA and anti-nuclear antibodies are both likely to be present in patients with SLE. (61) Additionally, assessment for other signs and symptoms should be completed, including mylagias and joint pain. (62)

Most cases of laryngeal lupus are treated effectively with corticosteroids. Teitel et al. presented four cases of patients with laryngeal manifestations of SLE with an accompanying review of 97 other case reports of similar patients. Steroid treatment was used successfully as monotherapy or in combination with other immunosuppressive or cytotoxic medications. (63) Occasionally, steroid therapy fails to completely treat symptoms, has no effect, or leads to undesired side effects. In such cases, alternative therapies may be employed. Increasing steroid dosing can improve symptoms in some cases. (64) Cyclophosphamide combined with prednisone has been used successfully to treat patients with more severe disease. Three patients refractory to steroids described by Teitel et al. were treated with the cytotoxic medication azathioprine. (65) More severe cases involving severe airway obstruction require intubation and mechanical ventilation.


Rheumatoid arthritis is a systemic inflammatory disease mainly affecting small synovial joints of the hands and feet; however, as the disease progresses, larger joints may become involved. Inflammation leads to the destruction of cartilage and erosion of bone. Over time, joints become deformed leading to severely diminished mobility. The cricoarytenoid joint (CAJ) in the larynx is a synovial joint surrounded by a fibrous capsule holding lubricating joint fluid. Good joint function is necessary for normal mobility of the vocal folds. Chronic inflammation leads to CAJ fixation and vocal fold adduction causing a narrowed airway. (66) The prevalence of RA is estimated to be one percent in the general population with women being affected twice as often as men. Most cases are diagnosed during adulthood. The incidence appears to increase with age until age 85, and then incidence declines. (67)

The laryngeal involvement with RA can impact voice quality. (68) Patients frequently present with dysphonia as well as dysphagia, foreign body sensation, odynophagia, sore throat, change in voice quality, referred otalgia, and respiratory symptoms. (69) Speyer et al. compared 160 patients with RA to 148 healthy controls and found that patients with RA are at increased risk of developing vocal dysfunction. RA patients experienced vocal symptoms more than three times more often than healthy patients. (70) Another study using the same tool to measure voice impairment examined patients with RA and also found an elevated incidence of vocal dysfunction. (71) Berjawi et al. studied a small cohort with RA and compared vocal quality with healthy patients. Almost all patients with RA experienced CAJ dysfunction that was absent in the healthy group. Those with RA also experienced decreased pitch and mean phonation time. (72) Respiratory symptoms may occur due to CAJ fixation, placing the vocal folds in the adducted position. Joint fixation can lead to airway obstruction and rapidly progressing dyspnea. (73)

Diagnosis of RA requires physical examination to identify small joint deformity and laboratory tests to assess for the presence of serologic markers of RA. The presence of circulating antibodies against rheumatoid factor and anticyclclic citrullinated protein are helpful in diagnosing RA. (74) To diagnose laryngeal involvement, a combination laryngoscopy and high-resolution computed tomography (HRCT) to inspect CAJ anatomy is advised. (75) In nearly fifty percent of patients with RA and voice symptoms, visible laryngeal changes can be observed. (76) Physicians and their patients with RA should be especially cognizant of subtle airway symptoms, which can precede acute airway obstruction.

When laryngeal manifestations of RA are identified, medical, surgical, and speech language therapies are available and often necessary. Medical treatment includes oral steroids and NSAIDs to prevent permanent changes to anatomic structures. Like medical therapy, voice therapy should be initiated early to minimize permanent changes. Leflunomide, a DNA synthesis inhibitor, can be added to oral steroid treatment if symptoms persist. Severe RA exacerbations may require intravenous or intra-articular steroids to control symptoms, and cytotoxic medications are used commonly to treat RA. (77) Dyspnea associated with acute airway obstruction can be alleviated with a helium-oxygen mixture until definitive therapy can be selected. With severe disease, refractory symptoms, or acute airway obstruction a tracheotomy can be placed to ensure the airway remains patent. (78)


Scleroderma is an autoimmune disease characterized by chronic inflammation and progressive fibrosis throughout the body. Collagen is deposited in affected organs and vasculature. Early in the disease process inflammation is the predominant finding, comprised of CD4+ T lymphocytes and monocytes surrounding blood vessels. As the disease progresses, type I collagen and other structural proteins are deposited in the extracellular space causing architectural and functional changes to various organs. (79) In the United States, scleroderma is estimated to occur in 24 out of every 100,000 people. (80) Disease onset occurs usually between 35 and 40 years of age, with women being affected more often than men. Scleroderma is rarely seen before the age of 25. Older age of onset is associated with an increased risk of multiorgan disease, especially pulmonary manifestations. Onset appears to be later in white women compared with black women. (81)

Vocal changes are rarely the initial symptom in systemic sclerosis. The timing and pace of initial complaints is highly variable, and symptoms may arise abruptly or over the course of months. (82) Acute airway obstruction is the most severe consequence of systemic scleroderma. Viner et al. described a patient with a three-day history of vocal deterioration characterized by dysphagia and dyspnea. On physical examination the patient was tachypnic and in respiratory distress. (83) Sataloff et al. presented a case study describing a vocalist and physician who presented with no prior history of vocal dysfunction. The patient experienced sudden onset severe hoarseness while singing, which coincided with an exacerbation of previously diagnosed scleroderma. (84) Alternatively, Pepper et al. presented a case of slow-onset dysphonia over the course of three years. Increased severity ultimately led to complete loss of voice. (85)

Strobovideolaryngoscopy is the best tool to diagnose laryngeal involvement of scleroderma. Findings may include vocal fold hemorrhage, scarring, hypervascularity, and varicosities. (86) Evidence of physical and serological manifestations should also be assessed. History of gastroesophageal reflux disease, Raynaud's disease, and sclerodactyly may suggest existing disease. Over ninety-five percent of patients with systemic scleroderma are found to have serum antinuclear autoantibodies (ANA). Other autoantibodies commonly found in systemic scleroderma include anticentromere, antitopoisomerase I, and anti-RNA polymerase I/III. (87) Laryngeal scleroderma can be treated surgically and medically. Pepper et al. treated a patient successfully by resecting laryngeal nodules using a carbon dioxide laser followed by triamcinolone injections into the submucosa of the vocal fold. Follow-up after four months revealed slow improvement with persistent dysphonia despite voice therapy. (88)


(1.) Ingo R. Titze, Julie Lemke, and Dough Montequin, "Population in the US Workforce Who Rely on Voice as a Primary Tool of Trade: A Preliminary Report," Journal of Voice 11, no. 3 (September 1997): 254-259.

(2.) Suzanne M. Coyle, Barbara D. Weinrich, and Joseph C. Stemple, "Shifts in Relative Prevalence of Laryngeal Pathology in a Treatment-Seeking Population," Journal of Voice 15, no. 3 (September 2001): 424-440.

(3.) Gary S. Firestein, Ralph C. Budd, Sherine E. Gabriel, Ian B. McInnes, and James R. O'Dell, Kelley's Textbook of Rheumatology (Philadelphia: Elsevier Health Services, 2013), 281-195, 1059-1108, 1343-1365.

(4.) Ibid.

(5.) Lee M. Akst and Lester D. R. Thompson, "Larynx Amyloidosis," Ear, Nose & Throat Journal 82, no. 11 (November 2003): 844-845.

(6.) Carla R. Penner and Susan Muller, "Head and Neck Amyloidosis: A Clinicopathologic Study of 15 Cases," Oral Oncology 42, no. 4 (April 2006): 421-429.

(7.) Robert T. Satalofff, Mona Abaza, Nabil A. Abaza, Amy Markiewicz, and Mary Hawkshaw, "Amyloidosis of the Larynx," Ear, Nose & Throat Journal 80, no. 6 (June 2000): 369-370; Akst and Thompson.

(8.) Geoffrey A. Neuner, Ashraf A. Badros, Tanya K. Meyer, Nahid M. Nanajii, and William F. Regine, "Complete Resolution of Laryngeal Amyloidosis with Radiation Treatment," Head and Neck 34, no. 5 (November 2012): 748-752; Firestein et al.

(9.) Herbert H. Dedo and Krzysztof Izdebski, "Laryngeal Anyloidosis in 10 Patients," The Laryngoscope 114, no. 10 (October 2004): 1742-1746; Satalofff et al.; Neuner et al.

(10.) Gregory J. Gallivan and Helen K. Gallivan, "Laryngeal Amyloidosis Causing Hoarseness and Airway Obstruction," Journal of Voice 24, no. 2 (March 2010): 235-239.

(11.) Dedo and Izdebski.

(12.) Gallivan and Gallivan.

(13.) Akst and Thompson.

(14.) Ibid.; Sataloff et al.

(15.) A. Alaani, A. T. Warfield, and J. P. Pracy, "Management of Laryngeal Amyloidosis," The Journal of Laryngology & Otology 118, no. 4 (April 2004): 279-283.

(16.) Fatih Celenk, Cengiz Durucu, Elif Baysal, Zeynel A. Karatas, Mustafa Polat, Kemal Bakir, Semih Mumbuc, and Muzaffer Kanlikama, "Management of Upper Aerodigestive Tract Amyloidosis," Annals of Otology, Rhinology & Laryngology 122, no. 8 (August 2013): 535-540.

(17.) Sataloff et al.; Gallivan and Gallivan.

(18.) Akst and Thompson.

(19.) Celenk et al.

(20.) Dedo and Izdebski.

(21.) Minh T. Truong, Lisa A. Kachnic, Gregory A. Grillone, Harry K. Bohrs, Richard Lee, Osamu Sakai, and John L. Berk, "Long-Term Results of Conformal Radiotherapy for Progressive Airway Amyloidosis," International Journal of Radiation Oncology 83, no. 2 (June 2012): 734-739; Celenk et al.; Neuner et al.

(22.) Neuner et al.

(23.) Truong et al.

(24.) Gallivan and Gallivan; Neuner et al.

(25.) Celenk et al.

(26.) Gaetano Motta, Francesco A. Salzano, Sergio Motta, and Stefania Staibano, "C[O.sub.2]-Laser Treatment of Laryngeal Amyloidosis," The Journal of Laryngology & Otology 117, no. 8 (August 2003): 647-650.

(27.) Tobias Lahmer, Matthias Treiber, Alexander von Werder, Frauke Foerger, Andreas Knopf, Uwe Heemann, and Klaus Thuermel, "Relapsing Polychondritis: An Autoimmune Disease with Many Faces," Autoimmunity Reviews 9, no. 10 (June 2010): 540-546; M. J. Navarro, G. C. Higgins, K. M. Lohr, and L. K. Myers, "Amelioration of Relapsing Polychondritis in a Child Treated with Oral Collagen," The American Medical Sciences 324, no. 2 (August 2002): 101-103.

(28.) Jane H. Buckner, Megan Van Landeghen, William W. Kwok, and Laura Tsarknaridis, "Identification of Type II Collagen Peptide 262-273-Specific T Cell Clones in a Patient with Relapsing Polychondritis," Arthritis & Rheumatism 46, no. 1 (January 2002): 238-244.

(29.) Ibid.

(30.) Goohyeon Hong and Hojoong Kim, "Clinical Characteristics and Treatment Outcomes of Patients with Relapsing Polychondritis with Airway Involvement," Clinical Rheumatology 32 (April 2013): 1329-1335.

(31.) Buckner et al.

(32.) Navarro et al.

(33.) Lawrence P. McAdam, Michael A. O'Hanlan, Rodney Bluestone, and Carl M. Pearson, "Relapsing Polychondritis: Prospective Study of 23 Patients and a Review of the Literature," Medicine 55, no. 3 (May 1976): 193-215.

(34.) Lesley F. Childs, Scott Rickert, Oscar C. Wengerman, Robert Lebovics, and Andrew Blitzer, "Laryngeal Manifestations of Relapsing Polychondritis and a Novel Treatment Option," Journal of Voice 25, no. 5 (September 2012): 587-589; Lahmer et al.; Hong and Kim.

(35.) Buckner et al.; Childs et al.

(36.) Hong and Kim.

(37.) Childs et al.

(38.) S. Mpofu, C. Estrach, J. Curtis, and R. J. Moots, "Treatment of Respiratory Complications in Recalcitrant Relapsing Polychondritis with Infliximab," Rheumatology 42, no. 9 (September 2003): 1117-1118.

(39.) Yuri Agrawal, David A. Godin, and Peter C. Belafsky, "Cytotoxic Agents in the Treatment of Laryngeal Sarcoidosis: A Case Report and Review of the Literature," Journal of Voice 20, no. 3 (September 2006): 481-484.

(40.) Carole M. Dean, Robert T. Sataloff, Mary J. Hawkshaw, and Edmund Pribitkin, "Laryngeal Sarcoidosis," Journal of Voice 16, no. 2 (June 2002): 283-288.

(41.) H. B. Neel and T. J. McDonald, "Laryngeal Sarcoidosis: Report of 13 Patients," Annals of Otology, Rhinology, and Laryngology 91, no. 4 (July/August 1981): 359-362.

(42.) H. M. Tucker, The Larynx (New York: Thieme Medical Publishers, Inc., 1987), 45-46.

(43.) Dean et al.

(44.) Ross M. Mayerhoff and Michael J. Pitman, "Atypical and Disparate Presentations of Laryngeal Sarcoidosis," Annals of Otology, Rhinology & Laryngology 119, no. 10 (October 2010): 667-671.

(45.) Enrique Palacios, Andrew Smith, and Neel Gupta, "Laryngeal Sarcoidosis," Ear, Nose and Throat Journal 87, no. 5 (May 2008): 252-254.

(46.) Anne-Kathrin Brill, Eberhard Seifert, Thomas Geiser, and Sebastian R. Ott, "A Red Flag in Sarcoidosis: Laryngeal Obstruction," Respiration 84, no. 5 (August 2012): 429-430.

(47.) Tucker.

(48.) Neel and McDonald.

(49.) Dean et al.

(50.) Agrawal et al.

(51.) Murat K. Ozcan, Secil Bahar, Ibrahim Ozcan, Lale Pasaoglu, Engin Sennaroglu, Yasar Karaaslan, and Huseyin Dere, "Laryngeal Involvement in Systemic Lupus Erythematosus: Report of Two Cases," Journal of Clinical Rheumatology 13, no. 5 (October 2007): 278-279.

(52.) Jose M. Pego-Reigosa, Dina A. Medeiros, and David A. Isenberg, "Respiratory Manifestations of Systemic Lupus Erythematosus: Old and New Concepts," Best Practice & Research Clinical Rheumatology 23, no. 4 (August 2009): 469-480.

(53.) Michael Hughes and Jason Hill, "Left Vocal Cord Paralysis in Sytemic Lupus Erythematosus," Modern Rheumatology 19, no. 4 (May 2009): 441-442.

(54.) Ariel D. Teitel, C. Ronald MacKenzie, Richard Stern, and Stephen A. Paget, "Laryngeal Involvement in Systemic Lupus Erythematosus," Seminars in Arthritis and Rheumatism 22, no. 3 (December 1992): 203-214.

(55.) Ozcan et al.

(56.) Yuki Nanke, Shigeru Kotake, Koichi Yonemoto, Masako Hara, Makoto Hasegawa, and Naoyuki Kamatani, "Cricoarytenoid Arthritis with Rheumatoid Arthritis and Systemic Lupus Erythematosus," The Journal of Rheumatology 28, no. 3 (March 2001): 624-626.

(57.) C. K. Hari, S. Ali Raza, and M. I. Clayton, "Hydralazine-Induced Lupus and Vocal Fold Paralysis," The Journal of Laryngology & Otology 112, no. 9 (September 1998): 875-877.

(58.) Teitel et al.

(59.) Yutaka Imauchi, Yukitomo Urata, and Kazuya Abe, "Left Vocal Cord Paralysis in Cases of Systemic Lupus Erythematosus," Journal for Otorhinolaryngology and its Related Specialties 63, no. 1 (January/February 2001): 53-55.

(60.) Jung Hwan Lee, In Young Sung, Jin Hong Park, and Jong-Lyel Roh, "Recurrent Laryngeal Neuropathy in a Systemic Lupus Erythematosus (SLE) Patient," American Journal of Physical Medicine and Rehabilitation 87, no. 1 (January 2008): 68-70.

(61.) Hari et al.

(62.) Lee et al.

(63.) Teitel et al.

(64.) Nanke et al.

(65.) Teitel et al.

(66.) Benjamin Fisher, Kathleen Dolan, Lesley Hastings, Catherine McClinton, and Peter Taylor, "Prevalence of Subjective Voice Impairment in Rheumatoid Arthritis," Clinical Rheumatology 27, no. 11 (November 2008): 1441-1443.

(67.) Athena Linos, John W. Worthington, Michael O'Fallon, and Leonard T. Kurland, "The Epidemiology of Rheumatoid Arthritis in Rochester, Minnesota: A Study of Incidence, Prevalence, and Mortality," American Journal of Epidemiology 111, no. 1 (January 1980): 87-98.

(68.) Mario A. Ferrari de Castro, Rogerio A. Dedivitis, Elio G. Pfuetzenreiter, Ana P. Brandao Barros, and Debora dos Santos Queija, "Videolaryngostroboscopy and Voice Evaluation in Patients with Rheumatoid Arthritis," Brazilian Journal of Otorhinolaryngology 78, no. 5 (September/October 2012): 121-127.

(69.) A. L. Hamdan and D. Sarieddine, "Laryngeal Manifestations of Rheumatoid Arthritis," Autoimmune Diseases 2013, no. 6 (June 2013): 1-7.

(70.) Rene Speyer, Irene Speyer, and Marielle A. Heijnen, "Prevalence and Relative Risk of Dysphonia in Rheumatoid Arthritis," Journal of Voice 22, no. 2 (March 2008): 232-237.

(71.) Fisher et al.

(72.) Ghina Berjawi, Imad Uthman, Lorice Mahfoud, Sami T. Husseini, Jihad Nassar, Aghiad Kotobi, and Abdul-Latif H. Hamdan, "Cricothyroid Joint Abnormalities in Patients with Rheumatoid Arthritis," Journal of Voice 24, no. 6 (November 2010): 732-737.

(73.) Yoshihiko Kumai, Daizo Murakami, Masako Masuda, and Eiji Yumoto, "Arytenoid Adduction to Treat Impaired Adduction of the Vocal Folds Due to Rheumatoid Arthritis," Auris Nasus Larynx 34, no. 4 (December 2007): 545-548.

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Adam R. Szymanowski, MS is a medical student at Drexel University College of Medicine in Philadelphia. He was formerly a middle school science teacher with the New York City Department of Education. Mr. Szymanowski holds an undergraduate degree from the University of North Carolina at Chapel Hill in biology and a master's degree in teaching from Pace University in New York City, New York.

Amy L. Rutt, DO, is an Instructor in the Department of Otolaryngology-Head and Neck Surgery at Drexel University College of Medicine in Philadelphia, Pennsylvania. Dr. Rutt attended King's College, where she graduated with a Bachelor of Science and Physician's Assistant degree. She received her medical degree from the Philadelphia College of Osteopathic Medicine in Pennsylvania. Dr. Rutt completed her Otolaryngology-Head and Neck Surgery Residency at the Detroit Medical Center in affiliation with Michigan State University. She then completed an internationally renowned fellowship in laryngology and care of the professional voice at the prestigious American Institute for Voice and Ear Research in Philadelphia, in affiliation with Drexel University College of Medicine. Dr. Rutt will be practicing laryngology at the Mayo Clinic in Jacksonville, Florida.

TABLE 1. PubMed search results.

Autoimmune Disorder          Results Produced from
                                 PubMed Search

Amyloidosis                           19
Relapsing Polychondritis              31
Sarcoidosis                           27
Systemic Lupus Erythematosus          12
Rheumatoid Arthritis                  25
Scleroderma                            6

TABLE 2. Summary of the McAdams Criteria.

Bilateral auricular chondritis
Nonerosive inflammatory polyarthritis
Nasal chondritis
Ocular inflammation (conjunctivitis, scleritis, uveitis)
Respiratory tract chondritis (laryngeal and tracheal cartilages)
Vestibulocochlear dysfunction (hearing loss, tinnitus, and
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Author:Szymanowski, Adam; Rutt, Amy L.; Sataloff, Robert T.
Publication:Journal of Singing
Geographic Code:1USA
Date:Jan 1, 2015
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