Relapsing polychondritis

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

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

  • 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

  • There is no established classification of relapsing polychondritis.

Pathophysiology

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 ↑ 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, Hemoptysis 
Granulomatosis with polyangiitis (Wegener’s)[3] + +/- +/- - - - - + Anti-PR3 antibody (C-ANCA) (90%), Anti-MPO antibody (P-ANCA) (10%) Leukocytosis, Normochromic normocytic anemia ↑ ↑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 ↑ ↑Cr or BUN, Proteinuria, Erythrocyte casts, ↑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, Asthma, Urticarial rash
Hydralazine-associated ANCA-associated vasculitis[5] - - - + - - - +/- Anti-MPO antibody (P-ANCA), Anti-histone antibodies Anemia - ↑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 - ↓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, Anemia ↑ 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 deposits  Histological confirmation Acrocyanosis, Retinal hemorrhage, Purpura
Hepatitis C virus-associated cryoglobulinemic vasculitis[8] +/- +/- + + - - + +/- HCV RNA, Cryoglobulins Leukocytosis, Anemia ↑ ↓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-Schönlein purpura)[9] - - + + - - - - IgA Normochromic anemia, Leukocytosis  ↑ Stool OB, ↓C3, ↓C4 - - Increased bowel wall thickness, hematomas, peritoneal fluid, and intussusception Dilated loops of bowel consistent 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 ↑ ANA, ↓C1q, ↓C3, ↓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, ↑HCT -  ↑Amylase Bowel wall thickening, Intestinal pneumatosis, Portomesenteric thrombosis Mesenteric venous thrombosis  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 ↑ 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 Echocardiography (TTE) Janeway lesions, Osler nodes, Roth spots, Vertebral osteomyelitis
Leukocytoclastic Vasculitis[13] + - - + - - - + IgM, IgA, IgG Leukocytosis, Anemia ↑ Hypocomplementemia - Vascular stenosis and obstruction in visceral angiography - - Perivascular inflammatory infiltrate of neutrophils with leukocytoclasia (releasing nuclear debris) Histological confirmation Palpable purpura, Petechiae 
Pulmonary disease Langerhans Cell Histiocytosis[14] +/- - - + - - - - CD1a, CD207,BRAF-V600E Anemia ↑ 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,  PD-L1 Leukocytosis, Anemia ↑ 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 ↑ 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 ↑ 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, Reticulocytosis  ↑ ↑Lactate dehydrogenase (LDH), Hypercalcemia  Thalami, brainstem, or cerebellum abnormality Cerebral microangiopathy or hypertension Hypoechoic kidney  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, Proteinuria 
Chronic Lymphocytic Leukemia (CLL)[20] + + + + +/- - - +/- CD5, CD19, CD20, IgVH Absolute lymphocytosis, Smudge cells ↑ Flow cytometry Staging - - - Large atypical cells, cleaved cells, and prolymphocytes  Chromosomal and genetic testing Easy bruising
Multiple Myeloma[21] + - + + + + +/- +/- Ig light chain Anemia, Thrombocytopenia, Leukopenia ↑ Bone marrow aspiration and biopsy, ↑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 - ↑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, BCL2, BCL6, and TP53 Lymphocytosis, Anemia, Thrombocytopenia ↑ ↑Lactate dehydrogenase (LDH), Hypercalcemia  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 Leukopenia  ↑ Polyclonal gammopathy, ↑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 ↑ ↑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  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] + + + + - - - +/-  IL-2 and IFN-γ Mild anemia ↑ ↑ACE, ↑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 Leukocytosis with left shift, Thrombocytosis ↑ ↑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  Leukopenia, Lymphopenia, Anemia, Thrombocytopenia ↑ ↑Cr or BUN,

↑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 ↑ ↑Cr or BUN,

↑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 stenosis in CXR Chondrolysis, Chondritis, Perichondritis Clinical findings coupled with imaging Ear pain and redness, Polyarthritis

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

Common risk factors in the development of relapsing polychondritis include:

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

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 structures 
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

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

  1. ↑ Lang B, Rothenfusser A, Lanchbury JS, Rauh G, Breedveld FC, Urlacher A, Albert ED, Peter HH, Melchers I (May 1993). "Susceptibility to relapsing polychondritis is associated with HLA-DR4". Arthritis Rheum. 36 (5): 660–4. PMID 8489544.
  2. ↑ Chung SA, Seo P (2010). "Microscopic polyangiitis". Rheum Dis Clin North Am. 36 (3): 545–58. doi:10.1016/j.rdc.2010.04.003. PMC 2917831. PMID 20688249.
  3. ↑ Kubaisi B, Abu Samra K, Foster CS (2016). "Granulomatosis with polyangiitis (Wegener's disease): An updated review of ocular disease manifestations". Intractable Rare Dis Res. 5 (2): 61–9. doi:10.5582/irdr.2016.01014. PMC 4869584. PMID 27195187.
  4. ↑ Keogh KA, Specks U (April 2006). "Churg-Strauss syndrome". Semin Respir Crit Care Med. 27 (2): 148–57. doi:10.1055/s-2006-939518. PMID 16612766.
  5. ↑ Keasberry J, Frazier J, Isbel NM, Van Eps CL, Oliver K, Mudge DW (2013). "Hydralazine-induced anti-neutrophil cytoplasmic antibody-positive renal vasculitis presenting with a vasculitic syndrome, acute nephritis and a puzzling skin rash: a case report". J Med Case Rep. 7: 20. doi:10.1186/1752-1947-7-20. PMC 3565908. PMID 23316942.
  6. ↑ McAdoo SP, Pusey CD (July 2017). "Anti-Glomerular Basement Membrane Disease". Clin J Am Soc Nephrol. 12 (7): 1162–1172. doi:10.2215/CJN.01380217. PMID 28515156.
  7. ↑ Ferri C, Mascia MT (January 2006). "Cryoglobulinemic vasculitis". Curr Opin Rheumatol. 18 (1): 54–63. PMID 16344620.
  8. ↑ Guo QY, Wu M, Wang YW, Sun GD (2017). "Hepatitis C virus-associated cryoglobulinemia with membrano-proliferative glomerulonephritis treated with prednisolone and interferon: A case report". Exp Ther Med. 14 (2): 1395–1398. doi:10.3892/etm.2017.4671. PMC 5525644. PMID 28810602.
  9. ↑ Farhadian JA, Castilla C, Shvartsbeyn M, Meehan SA, Neimann A, Pomeranz MK (December 2015). "IgA vasculitis (Henoch-Schönlein purpura)". Dermatol. Online J. 21 (12). PMID 26990342.
  10. ↑ Buck A, Christensen J, McCarty M (2012). "Hypocomplementemic urticarial vasculitis syndrome: a case report and literature review". J Clin Aesthet Dermatol. 5 (1): 36–46. PMC 3277093. PMID 22328958.
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  12. ↑ McDonald JR (2009). "Acute infective endocarditis". Infect Dis Clin North Am. 23 (3): 643–64. doi:10.1016/j.idc.2009.04.013. PMC 2726828. PMID 19665088.
  13. ↑ Einhorn J, Levis JT (2015). "Dermatologic Diagnosis: Leukocytoclastic Vasculitis". Perm J. 19 (3): 77–8. doi:10.7812/TPP/15-001. PMC 4500485. PMID 26176572.
  14. ↑ Margo CE, Goldman DR (2008). "Langerhans cell histiocytosis". Surv Ophthalmol. 53 (4): 332–58. doi:10.1016/j.survophthal.2008.04.007. PMID 18572052.
  15. ↑ Molina JR, Yang P, Cassivi SD, Schild SE, Adjei AA (2008). "Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship". Mayo Clin Proc. 83 (5): 584–94. doi:10.4065/83.5.584. PMC 2718421. PMID 18452692.
  16. ↑ Jackman DM, Johnson BE (2005). "Small-cell lung cancer". Lancet. 366 (9494): 1385–96. doi:10.1016/S0140-6736(05)67569-1. PMID 16226617.
  17. ↑ Parambil JG, Savci CD, Tazelaar HD, Ryu JH (April 2005). "Causes and presenting features of pulmonary infarctions in 43 cases identified by surgical lung biopsy". Chest. 127 (4): 1178–83. doi:10.1378/chest.127.4.1178. PMID 15821192.
  18. ↑ VanDeVoorde RG (January 2015). "Acute poststreptococcal glomerulonephritis: the most common acute glomerulonephritis". Pediatr Rev. 36 (1): 3–12, quiz 13. doi:10.1542/pir.36-1-3. PMID 25554106.
  19. ↑ Corrigan JJ, Boineau FG (November 2001). "Hemolytic-uremic syndrome". Pediatr Rev. 22 (11): 365–9. PMID 11691946.
  20. ↑ Byrd JC, Stilgenbauer S, Flinn IW (2004). "Chronic lymphocytic leukemia". Hematology Am Soc Hematol Educ Program: 163–83. doi:10.1182/asheducation-2004.1.163. PMID 15561682.
  21. ↑ Michels TC, Petersen KE (March 2017). "Multiple Myeloma: Diagnosis and Treatment". Am Fam Physician. 95 (6): 373–383. PMID 28318212.
  22. ↑ Klion A (2009). "Hypereosinophilic syndrome: current approach to diagnosis and treatment". Annu. Rev. Med. 60: 293–306. doi:10.1146/annurev.med.60.062107.090340. PMID 19630574.
  23. ↑ Shankland KR, Armitage JO, Hancock BW (September 2012). "Non-Hodgkin lymphoma". Lancet. 380 (9844): 848–57. doi:10.1016/S0140-6736(12)60605-9. PMID 22835603.
  24. ↑ Lin RY (January 1986). "Serum sickness syndrome". Am Fam Physician. 33 (1): 157–62. PMID 2867672.
  25. ↑ Venugopal A (2014). "Disseminated intravascular coagulation". Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
  26. ↑ Nomura S (2016). "Advances in Diagnosis and Treatments for Immune Thrombocytopenia". Clin Med Insights Blood Disord. 9: 15–22. doi:10.4137/CMBD.S39643. PMC 4948655. PMID 27441004.
  27. ↑ Chiarchiaro J, Chen BB, Gibson KF (2016). "New molecular targets for the treatment of sarcoidosis". Curr Opin Pulm Med. 22 (5): 515–21. doi:10.1097/MCP.0000000000000304. PMC 5152532. PMID 27454074.
  28. ↑ Murdoch DR (January 2003). "Diagnosis of Legionella infection". Clin. Infect. Dis. 36 (1): 64–9. doi:10.1086/345529. PMID 12491204.
  29. ↑ Tsokos, George C. (2011). "Systemic Lupus Erythematosus". New England Journal of Medicine. 365 (22): 2110–2121. doi:10.1056/NEJMra1100359. ISSN 0028-4793.
  30. ↑ Scott JT (1991). "The gold standard in rheumatoid arthritis". J R Soc Med. 84 (9): 513–4. PMC 1293405. PMID 1682491.
  31. ↑ Emmungil H, Aydın SZ (2015). "Relapsing polychondritis". Eur J Rheumatol. 2 (4): 155–159. doi:10.5152/eurjrheum.2015.0036. PMC 5047229. PMID 27708954.
  32. ↑ Knipp S, Bier H, Horneff G, Specker C, Schuster A, Schroten H, Lenard HG, Niehues T (2000). "Relapsing polychondritis in childhood--case report and short review". Rheumatol. Int. 19 (6): 231–4. PMID 11063294.
  33. ↑ Belot A, Duquesne A, Job-Deslandre C, Costedoat-Chalumeau N, Boudjemaa S, Wechsler B, Cochat P, Piette JC, Cimaz R (March 2010). "Pediatric-onset relapsing polychondritis: case series and systematic review". J. Pediatr. 156 (3): 484–9. doi:10.1016/j.jpeds.2009.09.045. PMID 19880136.
  34. ↑ McAdam LP, O'Hanlan MA, Bluestone R, Pearson CM (May 1976). "Relapsing polychondritis: prospective study of 23 patients and a review of the literature". Medicine (Baltimore). 55 (3): 193–215. PMID 775252.
  35. ↑ Damiani JM, Levine HL (June 1979). "Relapsing polychondritis--report of ten cases". Laryngoscope. 89 (6 Pt 1): 929–46. PMID 449538.
  36. ↑ Coppola M, Yealy DM (January 1992). "Relapsing polychondritis: an unusual cause of painful auricular swelling". Ann Emerg Med. 21 (1): 81–5. PMID 1539895.
  37. ↑ Kent PD, Michet CJ, Luthra HS (January 2004). "Relapsing polychondritis". Curr Opin Rheumatol. 16 (1): 56–61. PMID 14673390.
  38. ↑ O'Hanlan M, McAdam LP, Bluestone R, Pearson CM (1976). "The arthropathy of relapsing polychrondritis". Arthritis Rheum. 19 (2): 191–4. PMID 1259793.
  39. ↑ Balsa A, Expinosa A, Cuesta M, MacLeod TI, Gijón-Baños J, Maddison PJ (1995). "Joint symptoms in relapsing polychondritis". Clin. Exp. Rheumatol. 13 (4): 425–30. PMID 7586772.
  40. ↑ Foidart JM, Abe S, Martin GR, Zizic TM, Barnett EV, Lawley TJ, Katz SI (November 1978). "Antibodies to type II collagen in relapsing polychondritis". N. Engl. J. Med. 299 (22): 1203–7. doi:10.1056/NEJM197811302992202. PMID 714080.
  41. ↑ Ebringer R, Rook G, Swana GT, Bottazzo GF, Doniach D (October 1981). "Autoantibodies to cartilage and type II collagen in relapsing polychondritis and other rheumatic diseases". Ann. Rheum. Dis. 40 (5): 473–9. PMC 1000784. PMID 7030234.
  42. ↑ Papo T, Piette JC, Le Thi Huong D, Godeau P, Meyer O, Kahn MF, Bourgeois P (May 1993). "Antineutrophil cytoplasmic antibodies in polychondritis". Ann. Rheum. Dis. 52 (5): 384–5. PMC 1005055. PMID 8323388. Vancouver style error: initials (help)
  43. ↑ Passos CO, Onofre GR, Martins RC, Graff DL, Pagani EA, Sodré CT, Silva LC (July 2002). "Composition of urinary glycosaminoglycans in a patient with relapsing polychondritis". Clin. Biochem. 35 (5): 377–81. PMID 12270767.
  44. ↑ Kraus VB, Stabler T, Le ET, Saltarelli M, Allen NB (October 2003). "Urinary type II collagen neoepitope as an outcome measure for relapsing polychondritis". Arthritis Rheum. 48 (10): 2942–8. doi:10.1002/art.11281. PMID 14558101.
  45. ↑ Kempta Lekpa F, Piette JC, Bastuji-Garin S, Kraus VB, Stabler TV, Poole AR, Marini-Portugal A, Chevalier X (2010). "Serum cartilage oligomeric matrix protein (COMP) level is a marker of disease activity in relapsing polychondritis". Clin. Exp. Rheumatol. 28 (4): 553–5. PMID 20810035.
  46. ↑ Lee KS, Ernst A, Trentham DE, Lunn W, Feller-Kopman DJ, Boiselle PM (August 2006). "Relapsing polychondritis: prevalence of expiratory CT airway abnormalities". Radiology. 240 (2): 565–73. doi:10.1148/radiol.2401050562. PMID 16801364.
  47. ↑ href="https://radiopaedia.org/">Radiopaedia.org
  48. ↑ href="https://radiopaedia.org/cases/31793">rID: 31793
  49. ↑ Yoo JH, Chodosh J, Dana R (2011). "Relapsing polychondritis: systemic and ocular manifestations, differential diagnosis, management, and prognosis". Semin Ophthalmol. 26 (4–5): 261–9. doi:10.3109/08820538.2011.588653. PMID 21958172.

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