OK Here is a googled cut/paste version of an article that was posted
on alt.support. arthritis in 2000. I can not find a link to the
article, so instead just cut and pasted it here. This should help
answer some of your questions.

ALLERGIC AND IMMUNE DISORDERS OF THE LARYNX
James A. Koufman, M.D.

(This article is reprinted from Koufman JA: Infectious and
inflammatory
diseases of the larynx, in Ballenger JJ, Snow JB, Eds.
Otorhinolaryngology Fifteenth edition, Chapter 30, pp. 535-555,
Williams
and Wilkins (Lea & Febiger) Philadelphia, 1996)

AUTOIMMUNE DISORDERS

This group of disorders is heterogeneous; however, altered immunity is
the common denominator.

Rheumatoid Arthritis

Rheumatoid arthritis is a systemic autoimmune disorder of unknown
cause,
which can affect any organ in the body. Its most common manifestation
is
symmetrical polyarthritis, but, it also can cause inflammation in
nonjoint structures, vasculitis, and pulmonary changes.3 Rheumatoid
arthritis may affect the larynx both directly and indirectly.

First, rheumatoid involvement of the cricoarytenoid joints may cause
hoarseness or airway obstruction. At post-mortem examination, up to
87%
of patients with rheumatoid arthritis have cricoarytenoid joint
changes,
but, based on laryngoscopy, only 17-33% of such patients have clinical
signs of laryngeal involvement, namely posterior laryngeal
inflammation
and decreased arytenoid mobility.4

Second, rheumatoid nodules may occur anywhere in the larynx or within
the substance of the vocal cord itself, leading to hoarseness. The
gross
appearance of rheumatoid laryngeal nodules is variable. They may
appear
as white submucosal nodules, as ulcerated friable polypoid lesions, or
as ill-defined masses deep within the substance of the vocal cords.
Occasionally, unsuspected rheumatoid nodules are discovered during
direct laryngoscopy by palpation of a nodule within the vocal cord.

Histologically, these lesions show a central area of fibrinoid
necrosis
surrounded by histiocytes, plasma cells, and lymphocytes. They can be
highly vascularized and hyalinized; they may have a fibrous capsule.
Frequently, rheumatoid nodules of the larynx are misdiagnosed as
pyogenic granulomas.5
Third, rheumatoid arthritis, like other collagen vascular diseases,
often involves the esophagus, causing esophageal dysmotility and
reflux
disease. Thus, patients with rheumatoid arthritis may have reflux
laryngitis, but it is not known whether such reflux contributes to the
arytenoid fixation.

The choice of treatment for rheumatoid airway obstruction secondary to
arytenoid fixation depends upon the patient's overall medical
condition.
Usually surgical rehabilitation of arytenoid function is not possible,
so that endoscopic arytenoidectomy is often the treatment of choice.
This procedure leaves the patient with an adequate airway and a
somewhat
breathy, dysphonic voice. Sometimes, the rheumatoid arthritis so
severely affects the neck that endoscopic exposure of the larynx is
not
possible. In such cases, an open surgical procedure, or simply a
tracheotomy, may be performed.

Because rheumatoid nodules of the larynx frequently lie within the
substance of the vocal cord and may be inflamed, the vocal cord may be
scarred after their removal. As a consequence, most patients with this
type of rheumatoid involvement have persistent hoarseness following
nodule removal.

Systemic Lupus Erythematosus

Lupus is a systemic, autoimmune disease of unknown etiology. It
affects
women more commonly than men, and it usually presents in the second
and
third decades of life. Patients with this condition may have
autoantibodies to a variety of different tissues, and head and neck
manifestations are common. While the most common manifestations of
lupus
are arthritis, malar rash, and photosensitivity, up to 40% of patients
have mucosal lesions of the aerodigestive tract as well.

The lesions may be varied, e.g., petechiae, ulcerations, or raised
nonulcerated lesions with erythematous borders. The palate and nose
are
commonly involved. Painless nasal septal perforations may also occur.
The larynx may be involved by these mucosal lesions, or by
cricoarytenoid arthritis.3

Laryngeal involvement usually occurs at times of acute exacerbation of
the systemic disease. Airway compromise is uncommon, but it does
occur.
Biopsy reveals a mononuclear cell infiltrate. Positive fluorescent
antinuclear antibody tests are important for diagnosis, and are a key
part of ARA criteria. Corticosteroids and symptomatic therapy are the
treatment.

Relapsing Polychondritis

Relapsing polychondritis is a rare idiopathic, generally progressive,
autoimmune disease that causes inflammation of cartilage. It can mimic
rheumatoid arthritis, and it sometimes occurs in patients with other
autoimmune diseases, such as Sjögren's syndrome, systemic lupus
erythematosus, and psoriatic and rheumatoid arthritis.

Relapsing polychondritis occurs in all age groups, having a
bell-shaped
distribution and a peak incidence in the fourth decade. Although only
10% of patients present with respiratory tract involvement (larynx and
trachea), more than 50% eventually develop such involvement, and 20%
require tracheotomy. Of the 20-30% of patients who eventually die of
the
disease, most die of respiratory complications.7

This disease is characterized by episodes of inflammation with
subsequent destruction of the cartilage of the ears, nose, and larynx.
Arthritis involving the large joints is also common. Laryngeal
involvement is manifested by hoarseness, dyspnea, stridor, cough, and,
sometimes, pain and hemoptysis.

On examination of the larynx, severe glottic and subglottic edema and
inflammation are seen. No laboratory test is diagnostic, although
patients with active disease usually have an elevated erythrocyte
sedimentation rate, and most patients with this disorder also have
autoantibodies to type II collagen. Relapsing polychondritis is
therefore a clinical diagnosis that is confirmed by cartilage biopsy.

Initially, most patients present with bilateral involvement of the ear
cartilage. Typically, the ears suddenly become red, swollen, and
tender.
With or without treatment, the condition may subside within 5-10 days.
The next most common sites of involvement are the nose and the costal
cartilages. On occasion, there may be involvement of the eye.

Histologically, the normal cartilage is replaced by an eosinophilic
material, and acute and chronic infiltrates of lymphocytes and plasma
cells are present. The usual basophilic appearance of the cartilage
matrix is lost; lacunae are interrupted; and fibrous tissue replaces
cartilage. As the disease progresses, fibrosis and chondronecrosis
become marked.

Treatment includes corticosteroids and anti-inflammatory medications
such as dapsone; tracheotomy may be necessary in the later stages of
the
disease. Corticosteroid and immunosuppressive medications are used for
patients with severe, recalcitrant, or rapidly progressive disease,
especially when the larynx or other airway structures are involved.

Sjögren's Syndrome

Sjögren's syndrome is an idiopathic autoimmune disorder characterized
by the clinical triad of xerostomia (dry mouth), conjunctivitis sicca
(dry eyes), and rheumatoid arthritis. Patients with Sjögren's syndrome
have a relatively high chance of developing lymphoma. There is also a
"limited" form of the disease, occurring without the arthritis, which
is
called "sicca syndrome."

Although the cause (or causes) of these syndromes is unknown, both the
limited and the full blown forms have in common autoantibodies to
glandular tissue in the eyes, nose, oral cavity, and laryngopharynx.
In
addition to the lacrimal glands and the major salivary glands, minor
salivary and seromucinous glands are usually affected throughout the
aerodigestive tract.

The diagnosis is made clinically using a Schirmer's test to document
the
dryness of the eyes, and by salivary gland biopsy. In the major
salivary
glands, the histological picture demonstrates (1) an intense lymphoid
infiltrate, especially in periductal areas; (2) glandular atrophy; and
(3) myoepithelial hyperplasia.

Although the salivary glands are virtually always affected, biopsy of
a
major salivary gland is rarely necessary. Instead, biopsy of minor
salivary gland tissue (lip biopsy) is usually sufficient to make the
diagnosis. The histopathological features seen in minor salivary
glands
are similar to those seen in the major salivary glands, although the
myoepithelial hyperplasia is absent. The seromucinous glands of the
larynx may be involved, leading to inflammation of the larynx similar
to
that seen in the salivary glands.

Clinically, this involvement produces edema, erythema, dryness,
crusting, and hence, chronic hoarseness. Laryngeal Sjögren's syndrome,
however, does not occur in isolation; that is, patients with laryngeal
signs and symptoms of Sjögren's syndrome also have other
manifestations of the disease.8

In some cases, the mucosa of the posterior commissure appears so
hypertrophic that the clinician must consider the possibility of
tumor;
on examination, there is intense erythema and hypertrophy of the
posterior commissure, as well as dry, tenacious mucus between the
vocal
cords.

Biopsies of the larynx reveal histological findings similar to those
seen in the salivary glands. In addition, patients with Sjögren's
syndrome often have impaired esophageal function and gastroesophageal
reflux. Treatment is symptomatic, and antireflux and anti-inflammatory
medications are sometimes prescribed.

References
1. Werber JL, Pincus RL. Oropharyngeal angioedema associated with the
use of angiotensin-converting enzyme inhibitors. Otolaryngol Head Neck
Surg, 101:96-98, 1989
2. Wahle D, Beste DJ, Conley SF. Laryngeal involvement in toxic
epidermal necrolysis. Otol Head Neck Surg 107:796-799, 1992
3. Campbell SM, Montanaro A, Bardana EJ. Head and neck manifestations
of
autoimmune disease. Am J Otolaryngol 4:187-216, 1983
4. Jurik AG, Pedersen U, Nrgård A. Rheumatoid arthritis of the
cricoarytenoid joints: A case of laryngeal obstruction due to acute
and
chronic joint changes. Laryngoscope 95:846-848, 1985
5. Friedman BA, Rice DH. Rheumatoid nodules of the larynx. Arch
Otolaryngol 101:361-363, 1975
6. Hanson RD, Olsen KD, Rogers RS, III. Upper aerodigestive tract
manifestations of cicatricial pemphigoid. Ann Otol Rhinol Laryngol
97:493-499, 1988
7. McAdam LP, O'Hanlan MA, Bluestone C, Pearson CM. Relapsing
polychrondritis: prospective study of 23 patients and a review of the
literature. Medicine 55:193-215, 1976
8. Barrs DM, McDonald TJ, Duffy J. Sjögren's syndrome involving the
larynx. Report of a case. J Laryngol Otol 93:933-936, 1979
© Copyright, Center For Voice Disorders of Wake Forest University

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