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Turkiye Klinikleri J Dermatol 2017;27(3):142-6
142
elapsing polychondritis (RPC) is a rare immune-mediated condition,
which targets particularly the cartilaginous tissue. RPC frequently
attacks the ears, nose, eyes, joints and respiratory tract, but heart,
kidneys may also be affected. The diversity of the affected anatomic regions
and organs leads to a wide spectrum of clinical manifestations, which range
from an occasional auricular inflammation to aortic and/or mitral valvular
regurgitation or life -threatening tracheobronchomalacia.1RPC may coex-
ist with other diseases, such as systemic vasculitides, Graves’ disease or
myelodysplastic syndrome. As of today, there are no established clinical or
laboratory findings to predict the disease’s outcome.
Relapsing Polychondritis Misdiagnosed and
Treated as a “Soft Tissue Infection” and
a Brief Review of Diagnostic Clinical Clues
AABBSS TTRRAACCTT Relapsing polychondritis (RPC) is a rare immune-mediated disease, which targets par-
ticularly the cartilaginous tissue. At the initial stages of RPC, recurring mild-inflammatory attacks
targeting the ears, nose, eyes, joints and respiratory tract can be observed but as the disease pro-
gresses, aortic and/or mitral valvular regurgitation (AR/MR) or life-threatening tracheobroncho-
malacia (due to involvement of aortic, mitral valves and/or trachea) may occur, as well as severe
destruction of the ear, nose, etc. RPC may coexist with other diseases, such as systemic vasculitides,
Graves disease or myelodysplastic syndrome. Establishing an early diagnosis is of utmost impor-
tance to prevent the development of AR/MR, or tracheobronchomalacia by preserving the cartilage
tissue and also to diagnose a possible coexisting disease. Patients, particularly at the initial stages of
the disease may object to a skin biopsy due to concerns for visible scars. Therefore, a good grasp of
RPC’s clinical symptoms may facilitate to establish an early diagnosis.
KKeeyywwoorrddss:: Polychondritis, relapsing; otitis externa; diagnosis; diagnosis, differential
ÖÖZZEETT Tekrarlayan polikondrit (TP), özellikle kıkırdak dokuyu hedef alan, nadir görülen immün sis-
tem aracılı bir hastalık tablosudur. TP genellikle ilk aşamada kulak, burun vb. dokularda tekrarlayan
düşük şiddetli inflamatuar ataklara yol açarken ileri evrelerinde, hem bu dokularda ileri derecede
yıkıma sebep olabilir ve aynı zamanda aort, mitral kapak, trakea vb. dokuları etkileyerek aort/mit-
ral kapak yetmezlikleri ve trakeomalazi gibi hayatı tehdit edebilen tablolar oluşturabilir. TP’ye; Gra-
ves, sistemik vaskülitler, miyelodisplastik sendrom gibi başka hastalıklar da eşlik edebilir. TP’nin
erken tanınması kıkırdak dokunun korunarak aortik/mitral yetmezlikler, trakeomalazi gibi has-
talıkların gelişmesinin engellenmesi ve muhtemel eşlik eden diğer hastalıklara erken müdahale edi-
lebilmesi açısından faydalıdır. Çoğu hasta, erken evrelerde görünür iz kalabileceği endişesiyle
biyopsiye onay vermeyebilir. Bu yüzden TP'in klinik semptomlarının bilinmesi, erken ve ayırıcı
tanıyı kolaylaştıracaktır.
AAnnaahh ttaarr KKee llii mmee lleerr::Polikondrit, tekrarlayan; otitis eksterna; tanı; tanı, ayırıcı
Özgür GÜNDÜZ,a
Serkan DEMİRKAN,a
Güzin SAMAV,a
Hakan ARSLAN,a
Rebiye ÇAKARTAŞa
aDepartment of Dermatology and
Venerology,
Kırıkkale University Faculty of Medicine,
Kırıkkale
Ge liş Ta ri hi/Re ce i ved: 25.10.2017
Ka bul Ta ri hi/Ac cep ted: 11.12.2017
Ya zış ma Ad re si/Cor res pon den ce:
Özgür GÜNDÜZ
Kırıkkale University Faculty of Medicine,
Department of Dermatology and
Venerology, Kırıkkale,
TURKEY/TÜRKİYE
gunduzozgur@windowslive.com
Cop yright © 2017 by Tür ki ye Kli nik le ri
OLGU SUNUMU DOI: 10.5336/dermato.2017-58604
CASE REPORT
A 41-year old female presented with an earache
and a past medical history of recurrent ear infec-
tions. At the time of admission, she was noted to
have a red, painful, edematous swelling on her left
auricula, which spared the ear lobe (Figure 1). 10
weeks prior, she had developed transient cough.
Seven weeks later, an acute, painful, swelling oc-
cured on her left ear. She was evaluated by an oto-
laryngologist and diagnosed with
“swimmer’s ear”
and started on antibiotics. After two weeks, despite
the treatment with ciprofloxacillin, there was no
relief from her symptoms.
Her medical history revealed that the patient’s
complaints about her ears had started 3 years ago.
Initially, her right ear was affected. Her symptoms
were similiar to the current ones and she had been
treated with amoxicillin plus clavulanic acid com-
bination. Over the time, she started to have inter-
mittent episodes of cough and rhinorrhea,
intermittent painful redness in the eyes, recurrent
swellings on her right ear, which were diagnosed as
“otitis externa” and pain in the knees and ankles.
She was also diagnosed with arthritis and was pre-
scribed nonsteroid antiinflammatory drugs.
Laboratory tests revealed a sedimentation rate
of 67 mm/hr (0-20 mm/hr), a C-reactive protein
rate of 48.75 mg/L (0.15-5.0 mg/L), a mean corpus-
cular volume of 77.8 fL (78.0-105.0). Anti nuclear
antibodies, rheumatoid factor, creatinine, blood
urea nitrogen, liver enzymes were unremarkable.
Based on her history and clinical examination
(recurrent auricular inflammation on both ears,
nonerosive arthritis, recurrent ocular inflamma-
tion), her preliminary diagnosis was “recurrent
polychondritis”. She was consulted to departments
of physical therapy and rehabilitation, rheumatol-
ogy and started on methylprednisolone 40 mg/d.
After one week, the auricular inflammation was
significantly regressed.
DISCUSSION
RPC is an immune-mediated, multisystemic inflam-
matory disease that leads to degenerative changes in
the connective tissue. RPC may present within a
wide spectrum of diverse clinical manifestations, de-
pending on the extent and the severity of the affected
connective tissue. The etiology of RPC is unknown.
Various studies indicate an association between HLA-
DR4, HLA-DR6 and RPC.1,2 Hue-Lemoine and et al.
also identified a new set of genes, DQB1*0601,
DQA1*0103, to be associated with RPC.3Coexistence
of RPC and various other diseases; endocrine (Graves,
Hashimato thyroiditis, Diabetes mellitus, etc.) in-
flammatory bowel diseases, systemic vasculitides
(ANCA-associated, polyarteritis nodosa, Behcet’s dis-
ease, necrotizing vasculitis, etc) and an increased
prevalance of myelodisplastic syndromes are re-
ported.4-6 RPC is also reported to manifest after an in-
travenous injection of a mixture, which consisted of
hydrochloric acid, carburetor fluid, tap water, and in-
ternal matrix of a nasal inhaler.7Diversity of the clin-
ical symptoms, associated genes and coexistent
diseases indicate the possibility of RPC being a syn-
drome rather than a single, uniform disease.
Several study results point out a possible au-
toimmunity in RPC patients. Autoantibodies to type
II collagen, extracellular matrix components of car-
tilage have been identified and there are also reports
about a possible T cell-mediated reaction to cartilage
components in patients with RPC.8,9 Specific T-cell
clones for peptide corresponding to residues 261–273
of the type II collagen molecule has beeen reported
in a patient with RPC by Buckner et al.10 Imbalance
of T lymphocyte subsets has also been reported.11
Özgür GÜNDÜZ et al. Turkiye Klinikleri J Dermatol 2017;27(3):142-6
143143143
FIGURE 1: Erythema and edematous swelling of the left ear. The inflamma-
tion dominantly covers the helix and abruptly ends with a sharp demarcation
line, sparing the left lobule.
Pathogenesis of RPC is unknown. Working
hypothesis proposes that following a damage of
connective tissue, particularly cartilage tissue, by
yet-unidentified factors, certain epitopes or anti-
genic molecules are exposed to the immune system
of genetically preconditioned individuals. This
leads to formation of antibodies to certain molecu-
lar components of cartilage and abnormal proin-
flammatory cytokine production, causing tissue
damage. Further support to this hypothesis comes
from the case reports, which describe development
of RPC after pinna piercing and glucosamine chon-
droitin ingestion.12,13
According to the aforementioned working hy-
pothesis, the initial antigens, are components of the
cartilaginous tissue. After exposure to the immune
system possibly due to a physical, infectious or bio-
chemical insult, they trigger an autoimmune reac-
tion. In several studies, various autoantibodies have
been detected against type collagen II (CII), ma-
trilin-1, cartilage oligomeric matrix proteins
(COMPs), and collagen type-IX (CIX), X, and XI in
RPC patients and animal models.8-10,14 Various re-
search groups succesfully recreated RPC models in
animals and observed a connection between CII
and several HLA groups.15,16 Bradley et al. showed
the development of auricular chondritis in HLA-
DQ6/8 double transgenic mice following the im-
munization with collagen-II.15 In a similar study by
Taneja et al. immunized transgenic mice express-
ing DQ8 (DQA1*0301, DQB1*0302) in a NOD
background lacking endogenous class II molecules
(Abetao) with CII and observed development of
polychondritis, auricular chondritis, and pol-
yarthritis, with clinical and histological similarities
to RPC in humans in 85% of NOD.DQ8 mice. CII-
immunized mice has also been found to develop a
T cell response and produce antibodies to type IX
collagen and self-CII. B10.DQ8 transgenic mice de-
veloped polyarthritis and antibodies to CII only.
The susceptibility to auricular chondritis in
NOD.DQ8 mice has been proposed as response to
CIX by the researchers. A higher number of acti-
vated cells, CD4+CD44(hi) CD62L(lo), and lower
regulatory cells CD4+CD152 +CD25+ in NOD.DQ8
mice compared with B10.DQ8 mice were also re-
ported.16 T lymphocytes in a young RPC patient
was found to have Th1cytokine profile.17 Lympho-
cytic activation seems to induce activation of
macrophage/monocyte system, since levels of
serum monocyte chemoattractant protein-1 (MCP-
1), macrophage inflammatory protein 1-beta (MIP-
1beta) and interleukin-8 (IL-8) has been observed
to increase during active inflammation in RPC.18
Epitope spreading seems also to play a role in
the RPC. At the initial stages, frequently one tissue
(ear, nose) is inflammed but at the later stages, other
organs, (i.e. heart, trachea, etc) can also be affected.
This can be attributed to occurence of new auto-an-
tibodies (i.e., autoantibodies to matrilin-1).
Clinical manifestations of RPC are very diverse.
Auricular chondritis, arthritis, nasal chondritis, la-
ryngeotracheal and ocular symptoms are the most
frequently encountered initial manifestations.19-21
Inflammation of the ear has been thought to be the
hallmark of the RPC.22 Chondritis of pinna is prob-
ably the most common and typical feature and is ob-
served in 91% of men and 78% of women with
RPC.20Overall 90% of the patients present with au-
ricular inflammation during the course of disease.14
Peripheral anatomic regions with profuse collagen
content are also the most affected organ systems in
RPC patients with advanced disease.
In addition, other systems such as large air-
ways, heart and nervous system, may be affected.
Particularly, large airway and heart involvement
may have very serious and fatal outcomes (eg., tra-
cheobronchomalasia, combined aortic and mitral
valve regurgitation and myocarditis, respectively).
The exact frequencies of these manifestations re-
main unclear. 69% of patients are estimated to have
laryngeotracheal involvement.23 Costochondritis,
ocular inflammation manifested as conjunctivitis,
iritis, scleritis, retinopathy, even retinal detach-
ment, and polyarthritis affecting frequently inter-
phalangeal joints and knees have also been
reported.20,22-24 Early stages of large airway and heart
disease may be insidious. Therefore extra attention
must be paid to the examination of these systems
when RPC is included in the differential diagnosis.
There are no specific tests for RPC. McAdam et
al. proposed 6 criteria, of which 3 must be met to
eastablish the RPC diagnosis (Table 1).19 None of
Özgür GÜNDÜZ et al. Turkiye Klinikleri J Dermatol 2017;27(3):142-6
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Özgür GÜNDÜZ et al. Turkiye Klinikleri J Dermatol 2017;27(3):142-6
145145145
“The McAdams criteria” is pathogonomonic, so the
physician should have to exclude all the other possi-
ble causes for any of them. Also, some of these crite-
ria may not be overt, manifest slowly and even
subclinically, making them hard to recognize. An-
other set of proposed criteria (Table 2) include histo-
logic confirmation and positive response to steroids.25
Due to reluctance of some patients to undergo a skin
biopsy, an accurate diagnosis of RPC may depend on
the recognition of the clinical symptoms and on the
elimination of the other possible etiological factors
(Table 3). Honne et al. proposed fluorodeoxyglucose-
positron emission tomography/computed tomogra-
phy as a valuable diagnostic tool for the diagnosis and
evaluation of a RPC patient, who had not typical ear
and nose involvement.26Shimizu et al. reported that
inspiratory and expiratory three-dimensional com-
puted tomography and impulse oscillation with
three-dimensional color imaging may be used to
evaluate the airway involvement in the RPC patients
who can not perform (repeated) spirometry.27
Due to rarity of RPC, there is no established
therapy regiments.28 The treatment is largely em-
McAdam’s Criteria for Relapsing Polychondritis
Bilateral Auricular chondritis
Nonerosive, seronegative inflammatory polyarthritis
Nasal Chondritis
Ocular Inflammation (conjunctivitis, keratitis, scleritis/episcleritis,uveitis)
Respiratory tract chondritis (laryngeal and/or tracheal cartilages)
Cochlear and/or vestibular dysfunction
(neurosensory hearing loss, tinnitus, and/or/vertigo)
TABLE 1: McAdam’s Criteria for Relapsing Polychondritis”.
3 out of 6 criteria are required to
establish a diagnosis.19
Modified McAdam’s Criteria for Relapsing Polychondritis
At least three of McAdam ‘s diagnostic criteria
One or more of the clinical fndings with positive histologic confirmation
Chondritis at two or more seperate anatomic locations with
response to steroids and/or dapsone
TABLE 2: Modified McAdam’s diagnostic criteria for
“Relapsing Polychondritis”. 3 McAdam’s criteria,
1 McAdam’s criteria and histologic confirmation or
2 McAdam’s criteria and steroid and/or dapson responsive
multiple chondritis are required to establish a diagnosis.25
Clues for Differential Diagnosis of Relapsing Polychondritis (Excluding the Biopsy)
Disease Similar Clinical Findings Distinctive Clinical Findings Laboratory Findings
Soft Tissue Infection Auricular Inflammation Ear lobule affected Increased CRP, ESR
Possible peripheral lymphadenopathy Leukocytosis
No relapsing-remitting course
Tuberculosis (Lupus Vulgaris) Auricular Inflammation Usually Painless Positive culture (Löwenstein-Jensen)
Slow, asymptomatic progress PPD (+)
Frequently one ear is affected
Ear lobules
Leprosy Auricular Inflammation Usually seen in lepramatous leprosy M. leprae bacilli (+) microscopy
Saddle nose Deformity Accompanying numerous macules,
plaques and nodules
Various systemic manifestations
(hepatic failure, testicular involvement,
male gynecomasty etc)
Sensory neuropathy
Chondrodermatitis Nodularis Helicis Auricular Inflammation Solitary firm nodule located on helix or antihelix
Usually on the side patient lies on in the bed
Spares lobule
Stays stable for months
Wegener Granulomatosis Saddle Nose Deformity Mucosal Involvement of the Aformentioned Sites p-ANCA (+)
Tracheal Involvement Pulmonary Disease (+)
Eye Involvement Renal Involvement (RPGN)**
ANCA (+)* Neural system involvement (i.e., mononeuritis simplex)
Rheumatoid Arthritis Arthritis Erosive, symmetric arthritis High RF titers
Eye Inflammation High anti-cyclic citrullinated peptide titers
TABLE 3: Clinical and laboratory clues for the differential diagnosis of relapsing polychondritis.
*Anti neutrophil cytoplasmic antibodies **Rapidly progressive glomerulonephritis.
Özgür GÜNDÜZ et al. Turkiye Klinikleri J Dermatol 2017;27(3):142-6
146
piric and based on case reports. A combination of
immunsupressive drugs are usually preferred.
Arthralgias, mild auricular and/or nasal involve-
ments are preferentially treated with non-
streroidal anti-inflammatory drugs.29,30 Dapson is
also reproted to be beneficial for the cardiorespira-
tory involvement.30 Severe acute attacks with a risk
of end-organ damage, i.e. systemic vasculitis, se-
vere laryngeobronchial and/or ocular involvement,
should be treated with systemic steroids.29,30 Simi-
lar to the the treatment of autoimmune diseases,
steroid-sparing agents, methotrexate, azathioprine
and cyclosporine have been used in the treatment
of RPC and reported tohave beneficial effects.30,31
Tumor necrosis factor-α antagonists may also be
used in RPC. Improvement of laryngotracheal,
nasal and auricular chondritis was reported in 18
of 31 RPC patients treated wit infliximab. Etaner-
cept and adalimumab was also reported to benefi-
cial. Improvement obtained with etanercept was
reported to last between 9 months and 3 years.32
As conclusion, this case highlights a prolonged
diagnostic phase (approximately 3 years) of a RPC
patient and aims to familiarize the physicians with
RPC. A good grasp of RPC’s common manifesta-
tions may enable an early diagnosis, intervention
and subsequently prevent serious organ-damage
and improve the disease outcome.
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Authors declared no conflict of interest or financial support.
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IIddeeaa//CCoonncceepptt::Özgür Gündüz, Serkan Demirkan, Güzin Samav,
Hakan Arslan, Rebiye Çakartaş; DDeessiiggnn::Özgür Gündüz, Serkan
Demirkan, Güzin Samav, Hakan Arslan, Rebiye Çakartaş; CCoonn--
ttrrooll//SSuuppeerrvviissiioonn:: Özgür Gündüz, Serkan Demirkan, Güzin Samav,
Hakan Arslan, Rebiye Çakartaş; DDaattaa CCoolllleeccttiioonn aanndd//oorr PPrroocceessssiinngg::
Özgür Gündüz, Serkan Demirkan, Güzin Samav, Hakan Arslan, Re-
biye Çakartaş; AAnnaallyyssiiss aanndd//oorr IInntteerrpprreettaattiioonn:: Özgür Gündüz, Serkan
Demirkan, Güzin Samav, Hakan Arslan, Rebiye Çakartaş; LLiitteerraattuurree
RReevviieeww::Özgür Gündüz, Serkan Demirkan, Güzin Samav, Hakan Ar-
slan, Rebiye Çakartaş; WWrriittiinngg tthhee AArrttiiccllee:: Özgür Gündüz, Serkan
Demirkan, Güzin Samav, Hakan Arslan, Rebiye Çakartaş; CCrriittiiccaall
RReevviieeww:: Özgür Gündüz, Serkan Demirkan, Güzin Samav, Hakan Ar-
slan, Rebiye Çakartaş.
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