Seminars in Roentgenology
Volume 45, Issue 1 , Pages 36-42, January 2010

Sarcoidosis

  • Diem Quan Hoang, MD, FRCPC
    • ,
  • Elsie T. Nguyen, MD, FRCPC

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Elsie T. Nguyen, MD, FRCPC, Department of Medical Imaging-Cardiothoracic Division, General Hospital, University Health Network-Toronto, 585 University Ave, NCSB 1C567, Toronto, ON M5G 2N2

Department of Medical Imaging-Cardiothoracic Division, General Hospital, University Health Network-Toronto, Toronto, ON, Canada

Article Outline

 

Sarcoidosis is a systemic disorder of unknown etiology characterized pathologically by noncaseating granulomas. There are a variety of clinical and radiologic manifestations with mediastinal and pulmonary involvement occurring in 90% of cases. Extrathoracic sites of involvement include the skin, eyes, liver, spleen, lymph nodes, parotid glands, central nervous system, genitourinary system, muscles, and bones. Genetic, environmental, and immune etiologies of sarcoidosis have been proposed. The exact prevalence is unknown, but estimated to be 5-40 per 100,000, and is more common among the young and middle-aged, female, African-American, Scandinavian, and Japanese populations.1

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Clinical Features 

Diagnosis is based on recognition of clinical signs and symptoms, radiologic findings, and histology. Half of patients may be asymptomatic. Otherwise, signs and symptoms depend on the affected organ system but can also be nonspecific, such as fatigue, weight loss, fever, and night sweats.

Thoracic involvement by sarcoidosis can lead to functional impairment, gas exchange abnormalities, lung volume reduction, and respiratory failure.2 Common signs and symptoms include dyspnea, dry cough, and chest pain, whereas hemoptysis and digital clubbing are uncommon.3 Lung abnormalities have been known to spontaneously resolve, but can progress to fibrosis in 20%-25% of cases.4 Their severity can correlate with that of functional impairment, but there is poor correlation between chest radiographic staging and pulmonary function or histopathology. Lung fibrosis is typically associated with restrictive function, but there are reports of combined restrictive and obstructive, or even mainly obstructive pattern of lung function.2

The clinical course of the disease varies widely, and may be related to the mode of onset and extent at presentation.1 Two-thirds of patients undergo remission within the first decade, whereas one-third suffers from refractory disease. Recurrence beyond 1 year or more is uncommon. Recurrence may occur after lung transplantation despite immune suppression, but is often self-limited and associated with minimal radiographic abnormalities. Disease-related mortality is often due to pulmonary complications in the United States.1, 2, 5, 6

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Complications 

Pulmonary arterial hypertension can be a complication of sarcoidosis,7 most often the result of parenchymal fibrosis as in any other interstitial lung disease. Other proposed causes include granulomatous infiltration of the pulmonary arteries and direct compression by lymphadenopathy. True fibrosing mediastinitis is rare. Pulmonary thromboembolic events have been reported, but usually occur in the setting of coexistent abnormal coagulation factors.

In the last 2 decades, case reports have suggested an association between sarcoidosis and interferon treatment used for malignant and nonmalignant diseases, especially hepatitis C.8, 9, 10, 11, 12 Radiographic evidence of interstitial pneumonia in patients treated with interferon is very rare, and the true incidence of sarcoidosis among these cases is unknown.9, 12 Interestingly, interferons have been implicated in the pathogenesis of sarcoidosis, although no definite role has been established.8, 13 Clinical symptoms and radiographic abnormalities usually regress after discontinuation of therapy, further supporting a causal relationship.8, 9

Clinicians and radiologists must also be aware of the known association between chronic active sarcoidosis and both Hodgkin and non-Hodgkin lymphoma, also known as the “sarcoidosis-lymphoma syndrome.”14, 15, 16, 17 According to the Danish Institute of Clinical Epidemiology data, patients with sarcoidosis have up to a 5.5-fold increased risk of developing lymphoproliferative disorders compared with age-matched controls.15

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Diagnosis 

Biopsy specimens should be obtained from the most accessible organ, usually the lung or extrapulmonary sites, such as lymph nodes or liver.3 Transbronchial biopsy has a 70%-85% diagnostic yield. Characteristic findings at pathology are well-formed noncaseating granulomas with epithelioid cells and multinucleated giant cells.3, 18 CD4:CD8 ratio > 3.5 on bronchoalveolar lavage has a positive predictive value of nearly 80%.19

Blood CD4:CD8 ratio is usually decreased and hypercalcemia can also be observed.3 Angiotensin-converting enzyme level is no longer commonly used. These factors are not specific for sarcoidosis, but can be helpful. No definitive single test exists to establish the diagnosis of sarcoidosis and a combination of supportive findings is required. Initial assessment requires clinical history, physical examination, chest radiograph, pulmonary function tests, biopsy, electrocardiography, ophthalmologic evaluation, and complete blood count.

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Imaging Features 

Chest Radiograph 

Pulmonary manifestations occur in up to 90% of patients with sarcoidosis.3 There are 4 well-recognized stages based on chest radiographic findings1:

Stage 0 (10% of cases): No visible abnormalities

Stage 1 (50% of cases): Hilar or mediastinal lymphadenopathy only; radiographic abnormalities resolve in 65%

Stage 2 (30% of cases): Hilar or mediastinal lymphadenopathy associated with visible lung disease; radiographic abnormalities resolve in 50%

Stage 3 (10% of cases): Diffuse lung disease only; radiographic abnormalities resolve in 20%

Stage 4: End-stage fibrosis

Intrathoracic lympadenopathy is very commonly encountered in sarcoidosis, typically involving the right paratracheal area and both hila (the “1-2-3” pattern), and detected on chest radiograph in up to 95% of cases2, 3, 4, 20 (Figs. 1A and B). Although left paratracheal and aortopulmonary lymph nodes are also often enlarged, these are not well demonstrated on the chest radiograph.3

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  • Figure 1. 

    PA (A) and lateral (B) chest radiographs of a 43-year-old woman with sarcoidosis demonstrate bilateral hilar and right paratracheal lobulations (arrows), compatible with lymphadenopathy. The distribution is typical for sarcoidosis, referred to as the “1-2-3” pattern. PA (C) and lateral (D) radiographs 8 months later show, in addition to mediastinal and hilar lymphadenopathy, new reticulonodular opacities in the upper lobes. These findings represent progression to stage 2 sarcoidosis.

Lung involvement is seen in approximately 20% of patients with sarcoidosis,3 with a perihilar and upper-lung predominance. Nodules, well- or poorly defined and of variable sizes, are present in about half of patients on the chest radiograph, and a reticulonodular pattern occurs in an additional 25% of patients18 (Figs. 1C and D), but chest radiography remains relatively insensitive. Although radiographic abnormalities resolve in most patients, a reticular pattern indicating fibrosis persists in 15%,18 likely caused by endobronchial disease.3 This also has a central and upper-lung zone predominance.3, 18 On chest radiography, the fibrosis is illustrated by perihilar masses, upper-lobe volume loss with upward retraction of the hila, and areas of paracicatricial emphysema (Figs. 2A and B). Pleural abnormalities, such as effusion or thickening, also develop in 1% of patients with sarcoidosis.18

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  • Figure 2. 

    PA (A) and lateral (B) chest radiographs of a 71-year-old man show upper- and mid-lung coarse reticular and cystic changes and volume loss and upward displacement of the hila and main bronchi resulting from fibrosis. HRCT images at lung window settings (C-D) confirm bilateral extensive traction bronchiectasis, cystic spaces, and architectural distortion. CT image at mediastinal window settings (E) shows a left hilar lymph node with typical peripheral “eggshell” calcification (arrow). Coronal HRCT image (F) illustrates the upper lobe distribution of fibrosis and multiple calcified lymph nodes.

High-Resolution Computed Tomography 

High-resolution computed tomography (HRCT) shows, in decreasing frequency, nodal enlargement in the right paratracheal space, aortopulmonary window, hila, and subcarinal space18 (Fig. 3). Mediastinal lymphadenopathy without hilar involvement or only unilateral hilar lymphadenopathy is rare.18 Calcification may be present and may be amorphous, punctate, dense, or eggshell, and suggests chronic disease3, 18, 20 (Figs. 4A, 2E, and 2F). Internal mammary, paravertebral, or retrocrural lymphadenopathy has also been described, although it is less common.18

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  • Figure 3. 

    Contrast-enhanced CT image (A) of a 47-year-old man shows symmetrically enlarged bilateral hilar and subcarinal lymph nodes typical of sarcoidosis. Contrast-enhanced CT image obtained at a higher level (B) demonstrates right and left lower paratracheal node enlargement. The finding of isolated mediastinal and bilateral hilar lymphadenopathy in a fairly young patient is highly suggestive of sarcoidosis.

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  • Figure 4. 

    Unenhanced CT image (A) of a 62-year-old woman with sarcoidosis demonstrates faintly calcified subcarinal and hilar lymph nodes (arrows). This pattern of calcification or “egg-shell” calcification are very suggestive of, although it has also been reported with histoplasmosis. CT image at the same level in lung window setting (B) shows peribronchovascular and perifissural well–defined nodules in the right lower and middle lobes and left upper lobe.

At histology, well-formed noncaseating pulmonary granulomas are distributed along the lymphatic vessels in the peribronchovascular interstitial space, subpleural (including perifissural) interstitial space, and, to a lesser extent, interlobular septa.3, 18, 20, 21 This perilymphatic distribution of nodules is well illustrated at HRCT (Figs. 4B and 5). Nodules are typically small and well-defined. Their distribution can be patchy or focally localized in small areas of the lungs. Occasionally, they may be centrilobular or random in distribution and can undergo calcification. The pattern of perilymphatic distribution and predilection for the upper lung zones, combined with lymphadenopathy, is highly suggestive of sarcoidosis and helps differentiate from other lymphatic-centered lesions, such as lymphangitic carcinomatosis and lymphoproliferative disorders.3, 18 However, silicosis and berylliosis can present with imaging features identical to those of sarcoidosis.

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  • Figure 5. 

    In a 31-year-old patient with sarcoidosis, HRCT at the level of the superior segments of the lower lobes shows peribronchovascular nodules and thickening typical of sarcoidosis. Note also perifissural tiny nodules on the left (arrow).

Confluence of numerous interstitial granulomas can result in large, irregular, masslike opacities, with or without air bronchograms, resembling airspace consolidation.3, 18 This appearance has been referred to as alveolar sarcoid. HRCT demonstrates larger nodules and masses ranging from 1-4 cm in 15%-25% of patients.18 Small satellite nodules are often present at the periphery of these large nodules, termed the “galaxy sign” in comparison with a collection of stars18, 22 (Fig. 6A). These peripheral small nodules maintain their relatively distinct margins and the spaces between them are seen as low-attenuation spots.22 In a study of 59 patients with histologically confirmed sarcoidosis, this characteristic appearance was present in 27%.22 Of these patients, 2 showed central cavitation. This sign is proven by HRCT-pathologic correlation and is associated, but not specific to sarcoid, also seen in other granulomatous diseases and some cases of neoplasm. HRCT may also show patchy ground-glass opacities, with or without a background of interstitial nodules. Similar to alveolar sarcoid, these changes reflect the presence of large numbers of tiny granulomas.18

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  • Figure 6. 

    HRCT image (A) of a 49-year-old woman with sarcoidosis shows bilateral, central, masslike consolidation in the upper lobes, with air bronchograms. The findings are compatible with conglomerate fibrosis in end-stage sarcoidosis. Clusters of small peribronchovascular nodules are seen at the periphery, accounting for the term “galaxy sign.” Coronal CT image (B) illustrates the typical upper lobe, perihilar, and peribronchovascular distribution of fibrosis in sarcoidosis.

With fibrosis, HRCT shows early reticular opacities with posterior displacement of the main and upper-lobe bronchi. Progressive disease will lead to conglomerate fibrosis, characterized by central masses, with or without calcification, cavitation, architectural distortion, and traction bronchiectasis3, 18 (Figs. 2C, D, F and 6). Cysts and bullae may also be present.18 The presence of air bronchograms3 (Fig. 6A) may help differentiate from similar entities, such as complicated silicosis or coal workers' pneumoconiosis with progressive massive fibrosis. Honeycombing is uncommon and tends to involve the upper and mid lung and peribronchovascular spaces, in contrast to idiopathic pulmonary fibrosis.18 True cavitation is rare, more frequently associated with necrotizing sarcoid granulomatosis, a rare variant with angiitis.3, 23 Superimposed mycetomas can, however, complicate up to 10% patients of end-stage sarcoidosis cases18 (Fig. 7).

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  • Figure 7. 

    HRCT image of a 36-year-old woman with sarcoidosis shows a cavity in the right upper lobe with a thick and irregular wall. Within the cavity is a dependent, heterogeneous soft-tissue nodule separated from the cavity by an air crescent (arrowheads), representing a mycetoma. Bilateral peribronchovascular tiny nodules and irregular thickening in the left upper lobe are also present. Note the calcified right paratracheal lymph node (arrow).

The different HRCT findings in the setting of fibrosis may correlate with different patterns of functional impairment. For example, ventilatory restriction and low diffusion capacity are mainly associated with honeycomb cysts, whereas obstructive pulmonary function tests correlate with bronchial distortion, causing obstruction.4 Linear opacities alone generally translate into fewer pulmonary function test abnormalities.4 Superimposed nodular lesions are more frequently encountered with the linear or distorted fibrotic patterns, and rarely with honeycombing.4

Airway involvement is also commonly described, with HRCT showing nodular bronchial wall thickening, small endobronchial lesions, and findings of obstructive small airways disease (mosaic attenuation on inspiratory scans and air trapping on expiratory scans).2, 18 Nodular wall thickening of the trachea is another recognized finding.24, 25, 26 Bronchi can be obstructed by either endobronchial granulomas or extrinsic compression by enlarged lymph nodes, leading to atelectasis, particularly of the right middle lobe.18

Studies have shown that cigarette smoking confounds the correlation between the HRCT findings and pulmonary function test findings. Terasaki et al2 concluded that the extent of small nodules on inspiration correlated with restrictive lung function in nonsmokers only. In contrast, the extent of air trapping on expiration correlated with decrease in forced vital capacity in smokers. Cigarette use and emphysema were stronger determinants of airflow obstruction than sarcoidosis in their population study. Therefore, it is believed that smoking history should be taken into account when correlating the importance of lung findings on HRCT with functional impairment.

Scintigraphy 

Scintigraphic findings of sarcoidosis are well described. Gallium-67 scanning classically shows the “lambda sign” in the chest: an uptake pattern of right paratracheal and bilateral hilar areas.14, 27 In addition, the “panda sign” refers to uptake in the lacrimal and parotid glands. When both patterns are seen simultaneously, it becomes highly specific for sarcoidosis.14, 27 18-Fluorodeoxyglucose (FDG)-positron emission tomography also shows increased uptake in active sarcoidosis, but both the intensity and distribution of FDG uptake are nonspecific, and can mimic malignancy, particularly lymphoma and metastases.14 Although not widely used for clinical assessment, FDG- positron emission tomography in conjunction with computed tomography can play a role in monitoring response to therapy.

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Necrotizing Sarcoid Granulomatosis 

This rare variant is thought to represent a vascular manifestation of sarcoidosis. Often asymptomatic, it may only be detected incidentally by chest imaging. These include multiple, bilateral, often confluent lung nodules (Fig. 8). In contrast to the classic sarcoidosis, necrotizing sarcoid granulomatosis does not usually present with enlarged hilar and mediastinal lymph nodes. Diagnosis is confirmed by core or surgical lung biopsy, and there is good response to corticosteroid treatment.18

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  • Figure 8. 

    (A) and (B) HRCT images of a 62-year-old woman with necrotizing sarcoid granulomatosis show multiple, bilateral, peribronchovascular, and peripheral nodular foci of consolidation with air bronchograms. Courtesy of Jeffrey P. Kanne, MD (Madison, WI).

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Immune Restoration Syndrome 

Cases of sarcoidosis have been described after the administration of highly active antiretroviral therapy in treating human immunodeficiency virus infection.28, 29, 30 It has been proposed that the rapid increase in T lymphocytes and restoration of pathogen-specific immunity after highly active antiretroviral therapy results in sarcoidosis as a manifestation of this immune restoration.28 The pathologic features and HRCT findings are identical to classic sarcoidosis.21, 28 However, cases of sarcoidosis in immune restoration syndrome tend to present with perilymphatic lung nodules without mediastinal lymphadenopathy.28, 29, 30

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Cardiac Sarcoidosis 

Cardiac involvement, observed in up to 25% in autopsy series,31 may only translate to electrocardiographic abnormalities without any signs or symptoms, and myocardial involvement only occurs in 5% of patients.5 A spectrum of cardiac pathologies and events has been described and includes cardiomyopathy, ventricular arrhythmias, valvular lesions, heart block, congestive heart failure, and sudden cardiac arrest.3

Besides the occasional cases of myocardial thinning, computed tomography is generally insensitive and is surpassed by magnetic resonance imaging (MRI) for detection of granulomas within the myocardium. Cardiac MRI can detect abnormal signal intensity at the sites of affected myocardium (increased signal intensity on T2-weighted images and/or delayed enhancement on contrast-enhanced inversion recovery prepared T1-weighted gradient recalled echo images),32 focal thickening and segmental wall motion abnormalities. Gallium-67 scintigraphy, although not highly sensitive, may be helpful in detecting and following disease activity when MRI is not possible, but is not widely used in clinical practice.33

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Therapy 

The standard treatment regimen includes corticosteroids,3 which aim to suppress inflammation, decrease granulomas and prevent fibrosis. Alternatives in refractory cases include immunosuppressants, such as methotrexate, azathioprine, and cyclophosphamide although few studies guide their use.3 Tumor necrosis factor-α inhibitors, such as infliximab have also been used in the treatment of sarcoidosis.34, 35, 36 There are no guidelines as to when treatment should be initiated. Standard practice is to start treatment when there is organ compromise, after weighing the risks against the benefits. Optimal dose and duration of therapy have not been studied in a randomized controlled trial.

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Conclusion 

Sarcoidosis is a systemic disorder of unknown etiology, characterized by noncaseating granulomas, which can involve multiple organs. However, morbidity and mortality result mostly from pulmonary disease, with lung involvement being present in 90% of patients, and hilar and mediastinal lymphadenopathy being the most common finding. Therefore, familiarity with the radiologic thoracic features plays an important role in clinical diagnosis and treatment.

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References 

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PII: S0037-198X(09)00071-6

doi:10.1053/j.ro.2009.07.007

Seminars in Roentgenology
Volume 45, Issue 1 , Pages 36-42, January 2010

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