eMedicine Specialties > Neurology > Pediatric Neurology

Churg-Strauss Disease: Differential Diagnoses & Workup

Author: Robert Rust Jr, MD, Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, University of Virginia School; Clinical and Residency Training, Child Neurology, University of Virginia Hospital and Clinics
Contributor Information and Disclosures

Updated: Sep 28, 2006

Differential Diagnoses

Acute Inflammatory Demyelinating Polyradiculoneuropathy
Chronic Inflammatory Demyelinating Polyradiculoneuropathy
Polyarteritis Nodosa
Sarcoidosis and Neuropathy

Other Problems to Be Considered

Microscopic polyangiitis (microscopic polyarteritis)
Idiopathic hypereosinophilic syndrome
Essential cryoglobulinemic vasculitis
Strongyloidosis with hyperinfection syndrome
Loeffler syndrome (simple pulmonary eosinophilia)
Chronic eosinophilic pneumonia
Acute eosinophilic pneumonia
Allergic bronchopulmonary aspergillosis
Bronchocentric granulomatosis
Tropical pulmonary eosinophilia (wuchereriasis, brugiosis)

Workup

Laboratory Studies

  • The first (prodromal) phase of Churg-Strauss consists of asthma usually in association with other typical allergic features, which may include eosinophilia. During the second phase, clinical presentation with Churg Strauss disease, eosinophilia is characteristic (see below) and ANCAs with perinuclear staining pattern (p-ANCAs) are detected. Where possible, the diagnosis is confirmed by demonstration of angiographic abnormalities in affected organs and by pathognomonic biopsy findings. According to American College of Rheumatology criteria, clinical diagnosis is established when 4 of the following manifestations are documented: (1) allergic history, (2) asthma, (3) eosinophilia, (4) migratory pulmonary infiltrates, (5) paranasal sinus abnormality, (6) mononeuropathy or polyneuropathy, and (7) demonstration of extravascular eosinophilic infiltration of tissues on biopsy.
  • Eosinophil count
    • Once the second phase of Churg-Strauss disease is reached, eosinophilia (>1500/µL or >10% of total peripheral WBCs) is found on the peripheral blood film of at least 90% of untreated patients.
    • Mean values for absolute eosinophil counts are in the range of 5,000-9,000/µL, but, in rare instances, counts may exceed 100,000/µL. Thus, the history of asthma with the ensuing development of eosinophilia is highly suggestive of Churg-Strauss disease.
    • Treatment of asthmatic manifestations of the first stage of Churg-Strauss disease with corticosteroids may obscure this characteristic finding. The prompt resolution of eosinophilia with corticosteroid treatment is itself quite characteristic of Churg-Strauss disease.
    • Intermittent elevations of eosinophil counts during the third phase of Churg-Strauss disease may presage a relapse of systemic vasculitis.
  • Elevations of ANCA titers are found in 50-65% of cases of Churg-Strauss disease; these are predominantly p-ANCAs. In Churg-Strauss disease, the p-ANCAs usually are directed against myeloperoxidase antigens.
  • Serum IgE concentrations are elevated in three quarters of patients in the second or third phase of Churg-Strauss disease.
  • Erythrocyte sedimentation rate (ESR) and other indices suggestive of the presence of acute-phase reactants may be elevated.
  • Testing for rheumatoid factor is positive in approximately 70% of cases.
  • False-positive precipitin tests for syphilis have been reported.
  • Blood urea nitrogen and creatinine levels may be elevated in individuals who develop ANCA-associated renal vasculitis. Gross or microscopic hematuria and pyuria may be found and are due to inflammatory glomerulonephritis, although they may be misinterpreted as representing urinary tract infection. Dysmorphic red cells or red-cell casts in the urine sediment are consistent with the presence of glomerulonephritis; high-grade proteinemia is also suggestive, although the absence of proteinuria does not exclude glomerulonephritis.

Imaging Studies

  • Chest radiographs
    • Chest radiographs demonstrate pulmonary infiltrates in at least half of the patients in the second phase of Churg-Strauss disease and a greater percentage in the third phase of the disease. Typically, these are transient patchy alveolar infiltrates, usually without preferential, lobar, or segmental distribution. In some instances, a diffuse interstitial infiltrative pattern may be apparent.
    • Lungs may be hyperinflated.
    • Nonsegmental reticulonodular opacities without cavitation may be found. These may be solitary but may be multiple in more advanced cases. In some patients with advanced disease, quite striking bilateral reticulonodular opacities are observed.
    • Bronchial walls may be thickened.
    • Enlarged intrapulmonary lymph nodes may be found in some cases. This unusual finding suggests Churg-Strauss disease in asthmatic patients who have no history of heavy smoking.
    • Pleural effusions are not common. Pulmonary hemorrhage is a particularly suggestive and ominous sign in Churg-Strauss disease.
    • Imaging of the heart may reveal cardiomegaly or pericardial effusion.
  • CT scan of lungs
    • CT scan of lungs demonstrates the above-mentioned findings of Churg-Strauss disease even more clearly. In most cases of advanced disease, thin-section lung CT scan also reveals the highly suggestive finding of bilateral, ground-glass pulmonary opacity.
    • Subpleural airspace consolidation is an additional feature in about half of cases, while more widespread consolidation is discerned occasionally.
    • Occasional finding of centrolobular nodular densities within the background ground-glass opacity also is highly suggestive of Churg-Strauss disease. This change is much more apparent on CT scan than on plain radiographs, as is the thickening of interlobular septi and bronchial wall.
    • Increased vascular wall caliber also may be discerned.
    • Enlarged hilar or mediastinal lymph nodes also are apparent on pulmonary thin-section CT scan in many patients with Churg-Strauss disease, representing an opportunity for diagnostic biopsy.
    • Pleural or pericardial effusions occasionally are detected.
  • Results of abdominal or renal angiography usually are negative in Churg-Strauss disease. However, Churg-Strauss disease may account for less than 5% of all cases of ANCA-associated renal vasculitis, while MPA accounts for approximately half, and WG approximately one third of such cases.
  • MRI imaging of brain in patients with CNS manifestations may reveal vascular territory infarction, with or without hemorrhage. Areas of bright signal on T2-weighted MRI suggestive of vasculitis also may be found.

Other Tests

  • Electrophysiological studies
    • Electrophysiological studies of peripheral nerves may reveal deficits referable to both myelinated and unmyelinated sensory and motor fibers, especially those subserving the lower extremities.
    • Abnormalities in the findings of electrophysiological studies of the sciatic nerve (including tibial and peroneal branches) typically are more profound than those in the radial, median, and cubital nerves. The absence of conduction blocks may be helpful in distinguishing Churg-Strauss mononeuritis multiplex from chronic inflammatory demyelinating polyneuropathy.
    • Patients may be found to manifest acute-onset reduction or absence of sensory nerve action potentials.

Procedures

  • Procedures that may be valuable in the diagnosis of Churg-Strauss disease have been reviewed and include the following:
    • Biopsy of skin, hilar lymph nodes, lung parenchyma, or peripheral nerve demonstrates the characteristic vasculitis. Kidney biopsy may show segmental necrotizing glomerulonephritis with crescent formation, possibly including highly characteristic eosinophilic infiltration of the renal interstitium.
    • Electrophysiological studies of peripheral nerves

Histologic Findings

  • Histopathologic studies of a biopsy of affected skin areas reveal small-vessel arteriopathy with granuloma formation in the vascular walls. The region of arteriopathic change chiefly consists of a central eosinophilic core surrounded by an inflammatory exudate consisting of macrophages, epithelioid cells, and giant cells. Similarly constituted inflammatory exudate may infiltrate the perivascular surround. Fibrinoid necrosis of the vascular media also may be discerned.
  • Enlarged intrapulmonary, hilar, or mediastinal lymph nodes or pulmonary nodules, if biopsied, may reveal similar characteristic histologic abnormalities.
  • Biopsy of lung parenchyma may show tissue injury and eosinophilia without necrotizing vasculitis or the presence of extravascular granulomata.
  • Nerve biopsies reveal vasculitic epineural necrosis in more than half of patients with clinical neuropathy. As has been noted, the predominant cell type within the epineural inflammatory exudate is lymphocytes expressing CD8+ or CD4+ T-cell markers. Lesser numbers of eosinophils also are found, with small numbers of CD20+ B cells. Scarce deposits of IgG, IgE, and C3d antibodies may be detected.
  • Kidney biopsy may disclose eosinophilic interstitial pauci-immune segmental glomerulonephritis. Occasionally, glomerulonephritis with IgA deposition is found.

Staging

Lanham divided the clinical evolution of Churg-Strauss disease into 3 phases (see History).

More on Churg-Strauss Disease

Overview: Churg-Strauss Disease
Differential Diagnoses & Workup: Churg-Strauss Disease
Treatment & Medication: Churg-Strauss Disease
Follow-up: Churg-Strauss Disease
References
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Further Reading

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Keywords

syndrome of allergic granulomatosis and angiitis, allergic angiitis and granulomatosis, allergic granulomatosis, Churg-Strauss syndrome, CSS, Churg Strauss disease, allergic granulomatous angiitis, eosinophilic angiitis, eosinophilic granulomatosis

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Contributor Information and Disclosures

Author

Robert Rust Jr, MD, Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, University of Virginia School; Clinical and Residency Training, Child Neurology, University of Virginia Hospital and Clinics
Robert Rust Jr, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Robert Baumann, MD, Program Director, Professor, Departments of Neurology and Pediatrics, University of Kentucky
Robert Baumann, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American College of Epidemiology, American Epilepsy Society, and Child Neurology Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kenneth J Mack, MD, PhD, Senior Associate Consultant, Department of Child and Adolescent Neurology, Mayo Clinic
Kenneth J Mack, MD, PhD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, Phi Beta Kappa, and Society for Neuroscience
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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