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Reliable, easy-to-read patient information on common medical conditions โ€” written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Relapsing polychondritis

Introduction

Overview

Overview

Relapsing polychondritis is an immune-mediated chronic disease which involves the cartilaginous structure of different parts of the body, most commonly those of the ears, nose, and laryngotracheobronchial tree. The term relapsing polychondritis was first coined by Pearson in 1960. The majority of patients with relapsing polychondritis remain asymptomatic for several years. Early clinical features include ear pain, polyarthritis and other non-specific symptoms such as fever, weight loss and skin rash. The pathogenesis of relapsing polychondritis is unknown, however several studies have suggested the role of both cellular immunity and abnormal autoantibody in the pathogenesis of relapsing polychondritis. There are two different criteria to diagnose relapsing polychondritis which include Mc Adam criteria and modified Damiani criteria. There are no specific laboratory findings associated with relapsing polychondritis but certain antibodies are raised such as anti-type II collagen antibodies and antineutrophil cytoplasmic antibodies. Other abnormal laboratory findings include low haemoglobin, leukocytosis, eosinophilia, increased ESR, CRP, urinary glycosaminoglycans levels and urinary collagen type II neoepitope levels in active inflammation. Imaging such as chest x-ray is helpful to find out tracheal stenosis, however, CT scan is more useful to diagnose subglottic stenosis. MRI is useful to see the difference between edema, fibrosis, and inflammation. The mainstay of therapy for relapsing polychondritis is medical therapy. NSAIDs are used as an initial treatment of relapsing polychondritis. If NSAIDs are contraindicated or resistant, then steroids or dapsone can be used. Prednisone is used in the treatment of relapse. Treatment of life-threatening organ damage include prednisone and cyclophosphamide. Various surgical options include tracheostomy, cardiac valve replacement, aortic aneurysm repair, and saddle-nose deformity repair.

Historical Perspective

Historical Perspective

  • In 1923, Jaksch-Wartenhorst used the term polychondropathia to describe his first case about relapsing polychondritis.
  • In 1960, the term relapsing polychondritis was first coined by Pearson.
Classification

Classification

  • There is no established classification of relapsing polychondritis.
Pathophysiology

Pathophysiology

Differentiating Relapsing Polychondritis from other Diseases

Differentiating Relapsing Polychondritis from other Diseases

Also, Relapsing Polychondritis should be differenttieted form other causes of small-sized vessel vasculitis. Abbreviations: ABG= Arterial blood gas, ANA= Antinuclear antibody, ANP= Atrial natriuretic peptide, ASO= Antistreptolysin O antibody, BNP= Brain natriuretic peptide, CBC= Complete blood count, COPD= Chronic obstructive pulmonary disease, CRP= C-reactive protein, CT= Computed tomography, CXR= Chest X-ray, DVT= Deep vein thrombosis, ESR= Erythrocyte sedimentation rate, HRCT= High Resolution CT, IgE= Immunoglobulin E, LDH= Lactate dehydrogenase, PCWP= Pulmonary capillary wedge pressure, PCR= Polymerase chain reaction, PFT= Pulmonary function test.

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging Histopathology
Headache Fever Weight loss Arthralgia Claudication Bruit HTN Focal neurological disorder Biomarker CBC ESR Other CT scan Angiography Ultrasound/ Echocardiography Other
Small-Vessel Vasculitis ANCA-associated vasculitis Microscopic polyangiitis[2] + – – +/- – – – + Anti-PR3 antibody (C-ANCA) (40%), Anti-MPO antibody (P-ANCA) (60%) Leukocytosis, Normocytic anemia โ†‘ Proteinuria, Erythrocyte casts Suspected pancreatitis Mesenteric angiography for differentiating from polyarteritis nodosa – Bilateral nodular, and patchy opacities in CXR Glomerulonephritis with focal necrosis, crescent formation, and lack or paucity of immunoglobulin deposits Histological confirmation Rash, Hemoptysisย 
Granulomatosis with polyangiitis (Wegenerโ€™s)[3] + +/- +/- – – – – + Anti-PR3 antibody (C-ANCA) (90%), Anti-MPO antibody (P-ANCA) (10%) Leukocytosis, Normochromic normocytic anemia โ†‘ โ†‘Cr or BUN, Hypoalbuminemia Consolidation, Patchy or diffuse ground-glass opacities Occlusion or stenosis of LAD and RCA in coronary angiography – Single or multiple nodules and masses with cavitation in CXR Parenchymal necrosis, Granulomatous inflammation Histological confirmation Conjunctivitis,

Episcleritis,

Uveitis,

Optic nerve vasculitis

Eosinophilic granulomatosis with polyangiitis

(Churg-Strauss)[4]

+/- – – + – – – + Anti-MPO antibody (P-ANCA) (40%), Eotaxin-3 Eosinophilia, Anemia โ†‘ โ†‘Cr or BUN, Proteinuria, Erythrocyte casts, โ†‘IgE levels Significant enlargement of peripheral pulmonary arteries Myocardial ischemia and infarction in coronary angiography Congestive heart failure (CHF) in echocardiography Extensive air-space opacities in CXR Small necrotizing granulomas with eosinophilic core surrounded by macrophages and epithelioid giant cells Histological confirmation Allergic rhinitis,ย Asthma, Urticarial rash
Hydralazine-associated ANCA-associated vasculitis[5] – – – + – – – +/- Anti-MPO antibody (P-ANCA), Anti-histone antibodies Anemia – โ†‘Cr or BUN, Hypoalbuminemia Bilateral pulmonary infiltrates Aneurysms or occlusions of the visceral arteries – – Pauci-immune necrotizing and crescentic glomerulonephritis Histological confirmation Sinusitis, Hemoptysis
Immune complex small-vessel vasculitis Anti-glomerular basement membrane disease[6] + +/- – – – – + – Anti-GBM antibodies Hypochromic microcytic anemia, Thrombocytopenia – โ†“C3 level Pulmonary hemorrhage – Normal kidneys Alveolar infiltrates spreading from the hilum in CXR Cellular crescents in the glomeruli, Intra-alveolar hemorrhages Anti-GBM antibodies Hemoptysis, Hematuria
Cryoglobulinemic vasculitis[7] +/- +/- – + +/- – – – C4 component Leukocytosis,ย Anemia โ†‘ ANA, hypocomplementemia R/O underlying malignancy Stenosis or occlusions of the visceral arteries Bacterial endocarditis in echocardiography Interstitial involvement or pleural effusions in CXR HCV-associated proteins in vasculitic skin, Intraluminal cryoglobulin depositsย  Histological confirmation Acrocyanosis, Retinal hemorrhage, Purpura
Hepatitis C virus-associated cryoglobulinemic vasculitis[8] +/- +/- + + – – + +/- HCV RNA, Cryoglobulins Leukocytosis,ย Anemia โ†‘ โ†“Serum C4, Positive RF Increased hepatic echogenicity – Hepatomegaly, Splenomegaly Increased hepatic echogenicity in MRI Vasculitic skin, Antigen infilteration in lesions HCV RNA, Histological confirmation Palpable purpura, Microscopic hematuria
IgA vasculitis (Henoch-Schรถnlein purpura)[9] – – + + – – – – IgA Normochromic anemia, Leukocytosisย  โ†‘ Stool OB, โ†“C3, โ†“C4 – – Increased bowel wall thickness, hematomas, peritoneal fluid, and intussusception Dilated loops of bowel consistentย in abdominal X-ray Leukocytoclastic vasculitis in postcapillary venules with IgA deposition History and physical examination Hematuria, Palpable purpura
Hypocomplementemic urticarial vasculitis (anti-C1q vasculitis)[10] – – +/- + – – – – C1q Mild anemia โ†‘ ANA, โ†“C1q, โ†“C3, โ†“C4 – – Hepatomegaly, Splenomegaly – Deposits of immunoglobulins, complement, or fibrin around blood vessels Urticaria,

Histological confirmation

Urticaria, Hematuria
Gastrointestinal disease Acute mesenteric ischemia[11] – +/- – – – – – – I-FABP, Alpha-GST, Ischemia-modified albumin (IMA) Leukocytosis,ย โ†‘HCT – ย โ†‘Amylase Bowel wall thickening, Intestinal pneumatosis, Portomesenteric thrombosis Mesenteric venous thrombosisย  Arterial stenosis or occlusion of the celiac or superior mesenteric arteries in duplex ultrasound Ileus with distended loops of bowel, Bowel wall thickening in abdominal X-ray Superficial mucosal hemorrhage, edema and necrosis History and physical examination Abdominal pain, Distension, Absent bowel sounds
Cardiovascular disease Infective Endocarditis[12] + + + – – – – + NT-proBNP Normochromic-normocytic anemia โ†‘ Hyperglobulinemia, Cryoglobulinemia Metastatic infections, such as splenic infarct, renal infarcts, or psoas abscess – Vegetation, abscess, or new dehiscence of a prosthetic valvein echocardiography Vertebral osteomyelitis in MRI Vegetation or intracardiac abscess demonstrating active endocarditis Echocardiographyย (TTE) Janeway lesions, Osler nodes, Roth spots, Vertebral osteomyelitis
Leukocytoclastic Vasculitis[13] + – – + – – – + IgM, IgA, IgG Leukocytosis, Anemia โ†‘ Hypocomplementemia – Vascular stenosis and obstruction in visceral angiography – – Perivascular inflammatory infiltrate of neutrophils with leukocytoclasia (releasing nuclear debris) Histological confirmation Palpable purpura, Petechiaeย 
Pulmonary disease Langerhans Cell Histiocytosis[14] +/- – – + – – – – CD1a,ย CD207,BRAF-V600E Anemia โ†‘ Hypercalcemia Pulmonary cysts and nodules, Bone lytic lesions – Hepatomegaly, Splenomegaly Cerebellum and pons hyperintensity in MRI Birbeck granules by electron microscopy Histological confirmation Brown to purplish papules, Eczematous rash
Non-Small Cell Lung Cancer[15] – +/- + – – – – +/- EGFR, ROS1, EML4-ALK, ย PD-L1 Leukocytosis, Anemia โ†‘ Hypercalcemia, Hyponatremia Pulmonary lesion or mass – Pulmonary marginal lesions Staging and response to treatment in PET-CT Adenocarcinoma, Squamous cell carcinoma High resolution CT-scan Cough, Hemoptysis
Small Cell Lung Cancer[16] – +/- + – – – – +/- p53, Thyroid transcription factor-1 (TTF1) Anemia โ†‘ Hyponatremia Large hilar mass with bulky mediastinal adenopathy – Endobronchial ultrasound (EBUS) Standard staging Spindled cells with dark nuclei, scant cytoplasm, and fine, granular nuclear chromatin High resolution CT-scan Cough, Hemoptysis
Pulmonary Infarction[17] +/- – – – – – + – D-dimer Mild leukocytosis, Mild anemia – Hypoxemia, Hypocarbia or Hypercarbia, Respiratory alkalosis Pulmonary embolism Low-density filling defect within the pulmonary artery Pericardial effusion in echocardiography Pulmonary infiltrates, atelectasis, and pleural effusions in CXR Infarct induced apoptosis Pulmonary artery angiography Cough, Hemoptysis
Renal disease Acute Poststreptococcal Glomerulonephritis[18] – – – + – – + +/- Antistreptolysin-O (ASO) titers Leukocytosis โ†‘ Hypocomplementemia – – Normal to slightly enlarged kidneys Central venous congestion in a hilar pattern in CXR Hypercellularity of endothelial and mesangial cells, Infiltration of the glomerular tuft with polymorphonuclear cells Histological confirmation Hematuria
Hematologic disease Hemolytic-Uremic Syndrome[19] + + – + – – + + C5b-9, ADAMTS13 Anemia, Thrombocytopenia, Reticulocytosisย  โ†‘ โ†‘Lactate dehydrogenase (LDH), Hypercalcemiaย  Thalami, brainstem, or cerebellum abnormality Cerebral microangiopathy or hypertension Hypoechoic kidneyย  Abnormal hyperintensity in the brain cisterns in MRI Microthromboses include fibrin thrombi that may occlude the glomerular tuft Clinical findings coupled with laboratory abnormalities Hematuria, Proteinuriaย 
Chronic Lymphocytic Leukemia (CLL)[20] + + + + +/- – – +/- CD5, CD19, CD20,ย IgVH Absolute lymphocytosis, Smudge cells โ†‘ Flow cytometry Staging – – – Large atypical cells, cleaved cells, and prolymphocytesย  Chromosomal and genetic testing Easy bruising
Multiple Myeloma[21] + – + + + + +/- +/- Ig light chain Anemia, Thrombocytopenia, Leukopenia โ†‘ Bone marrow aspiration and biopsy, โ†‘Cr Osseous involvement and lytic lesions Peripheral zone of increased vascularity in lesions – Punched-out lesion in skull X-ray Clonal proliferation of plasma cells Protein electrophoresis plus conventional X-rays Constipation
Hypereosinophilic Syndrome[22] +/- +/- – – – – – – IgE, CD117 with CD2 Eosinophilia – โ†‘Serum tryptase Lymphadenopathy and splenomegaly – Intracardiac thrombi in echocardiography – Reticulin stain for myelofibrosis and tryptase staining for mast cells Clinical findings coupled with laboratory abnormalities Splinter hemorrhages, Raynaud phenomenon
Non-Hodgkin Lymphoma[23] + + + + +/- +/- +/- +/- MYC,ย BCL2,ย BCL6, andย TP53 Lymphocytosis, Anemia, Thrombocytopenia โ†‘ โ†‘Lactate dehydrogenase (LDH), Hypercalcemiaย  Enlarged lymph nodes, Hepatosplenomegaly, Filling defects in the liver and spleen – Hepatosplenomegaly Mediastinal lymphadenopathy Small cleaved or noncleaved, intermediate, or large cell with a follicular or diffuse pattern Surgically excised tissue biopsy Easy bruising, Testicular mass, Skin lesion
Serum Sickness[24] + + – +/- +/- – – +/- IL-1, IL-6, TNF Leukopeniaย  โ†‘ Polyclonal gammopathy, โ†‘Cr, Cryoglobulinemia – – – – Arteritic lesions are focal, necrotizing, and inflammatory involving all layers of the artery Clinical findings coupled with laboratory abnormalities Hematuria, Skin rash
Disseminated Intravascular Coagulation[25] +/- + – +/- – – + + Fibrin degradation product (FDP) Thrombocytopenia, Schistocytes โ†‘ โ†‘D-dimer, aPTT and PT Intracranial hemorrhage – – – Ischemia and necrosis due to fibrin deposition in small and medium-sized vessels Clinical findings coupled with laboratory abnormalities ย Acral cyanosis, Hemorrhagic skin infarctions
Idiopathic Thrombocytopenic Purpura[26] + +/- – + – – – + FC gamma receptors (FCGR) IIb Anemia, Thrombocytopenia – HIV, ANA R/O other causes – R/O splenomegaly – Increased number of normal morphologic megakaryocytes Clinical findings coupled with thrombocytopenia Easy bruising, Purpura
Systemic disease Sarcoidosis[27] + + + + – – – +/- ย IL-2 and IFN-ฮณ Mild anemia โ†‘ โ†‘ACE, โ†‘1, 25-dihydroxyvitamin D Active alveolitis or fibrosis – Hepatosplenomegaly Bilateral hilar adenopathy Noncaseating granulomas (NCGs) Histological confirmation Heart block, Ocular lesion
Legionella Infection[28] + + + + – – – +/- Inflammatory cytokines Leukocytosisย with left shift, Thrombocytosis โ†‘ โ†‘D-dimer, FDP, Hyponatremia Pleural effusion – – Nonspecific and indistinguishable CXR Intra-alveolar inflammation, Microabscesses in the parenchyma Sputum culture Cough, Diarrhea
Systemic lupus erythematosus[29] + + + + – – + + Anti dsDNA, ANA ย Leukopenia, Lymphopenia, Anemia, Thrombocytopenia โ†‘ โ†‘Cr or BUN,

โ†‘ALT or AST, Proteinuria

Interstitial lung disease, Pneumonitis, Pulmonary emboli, Alveolar hemorrhage Aneurysms Pericardial effusion, pulmonary hypertension, or verrucous Libman-Sacks endocarditis in echocardiography Central nervous system (CNS) lupus white-matter changes in MRI Staging lupus nephritis Anti-dsDNA antibody test Skin rashes or photosensitivity
Rheumatoid arthritis[30] – – + + + + – – RF, Anti-CCP antibody Anemia โ†‘ โ†‘Cr or BUN,

โ†‘ALT or AST, ANA

Microfractures Aneurysms Effusions in joints Basilar invagination with cranial migration of an eroded odontoid peg in MRI Influx of inflammatory cells into the synovial membrane, with angiogenesis, proliferation of chronic inflammatory cells Clinical findings coupled anti-CCP antibody Rheumatoid nodules
Relapsing polychondritis[31] – +/- +/- + + – – – – Leukocytosis, Anemia – Cryoglobulins, ANA, C-ANCA Calcification of cartilaginous structures Aortic root dilatation Aortic root dilatation and degree of aortic regurgitation in echocardiography Tracheal stenosisย in CXR Chondrolysis, Chondritis, Perichondritis Clinical findings coupled with imaging Ear pain and redness, Polyarthritis
Epidemiology and Demographics

Epidemiology and Demographics

  • The incidence of relapsing polychondritis is approximately 4 per 100,000 individuals in Minnesota.

Age

  • Relapsing polychondritis is more commonly observed among patients aged 40 to 60 years but it can also occur in childhood.[32][33]

Gender

  • Relapsing polychondritis affects men and women equally.

Race

  • Relapsing polychondritis usually affects Caucasian.
Risk Factors

Risk Factors

Common risk factors in the development of relapsing polychondritis include:

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

  • The majority of patients with relapsing polychondritis remain asymptomatic for several years.
  • Early clinical features include ear pain, polyarthritis and other non-specific symptoms such as fever, weight loss and skin rash.
  • Common complications of relapsing polychondritis include collapsing of cartilage which causes facial abnormalities, deformities of the ear, eye, and destruction of the thyroid gland.
  • Relapsing polychondritis has the relapsing and remitting course, Prognosis depends upon the type of organ involvement, stage of the disease.
Diagnosis

Diagnosis

Diagnostic Criteria

Mc Adam diagnostic criteria for relapsing polychondritis[34]
Criteria Requirement
Recurrent chondritis of both auricles 3 out of 6 features

are required for definitive

diagnosis of relapsing

polychondritis

Non-erosive inflammatory polyarthritis
Nasal chondritis
Inflammation of auricular structuresย 
Chondritis of the respiratory tract
Cochlear and/or vestibular damage

According to modified Damiani criteria, there should be one of the following findings to diagnose relapsing polychondritis:[35]

  • There should be three of McAdam’s diagnostic criteria.
  • One or more of the clinical findings of McAdam’s diagnostic criteria and positive histologic confirmation.
  • Chondritis at two or more separate anatomic locations with a response to glucocorticoids or dapsone.

Symptoms

Symptoms of relapsing polychondritis may include the following:[36][37][38][39]

Physical Examination

Laboratory Findings

Imaging Findings

Relapsing polychondritis
Source: Case courtesy of Dr Charlie Chia-Tsong Hsu[47][48]
Other Diagnostic studies

Other Diagnostic studies

Treatment

Treatment

Medical Therapy

  • The mainstay of therapy for relapsing polychondritis is medical therapy.
  • NSAIDs are used as an initial treatment of relapsing polychondritis.[49]
  • Preferred regimen: Naproxen 500 mg PO q12h or ibuprofen 800 mg PO q6h x 7 to 10 days.
  • If NSAIDs are contraindicated or resistant then following regimens are used:
    • Preferred regimen: Dapsone 50 to 100 mg PO q24h x 4 months depending on the severity of the disease.
    • Preferred regimen: Prednisone 30 to 60 mg PO q24h in divided dose.

Treatment of relapse:

Treatment of life-threatening organ damage:

  • Preferred regimen: Initial therapy is the combination of prednisone 1 mg/kg PO q24h and cyclophosphamide 2 mg/kg PO q24h.
  • Maintenance therapy depends on the renal function of a patient.
  • Patient without nephritis, Preferred regimen: Methotrexate 15mg PO once weekly.
  • Patient with nephritis, Preferred regimen: Azathioprine – dose is adjused according to GFR.

Surgery

Medical therapy is the mainstay of therapy for relapsing polychondritis, however various surgical options include:

Prevention

There are no primary preventive measures available for relapsing polychondritis.

References

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ,Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]