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Dr. Baughman is Professor of Medicine from the Division of Pulmonary and Critical Care Medicine, University of Cincinnati Medical Center; and Dr. Iannuzzi is Professor of Medicine from Pulmonary and Critical Care Medicine, Henry Ford Health Sciences Center.
Correspondence to: Robert P. Baughman, MD, FCCP, University of Cincinnati Medical Center, 231 Bethesda Ave, Room 6004, Cincinnati, OH 45267-0564; e-mail: bob.baughman{at}uc.edu
More than 120 years ago, Jonathan Hutchinson recorded the first case of sarcoidosis,1 which he called "a case of livid papillary psoriasis." Hutchinson’s patient presented with purplish skin lesions and "gout" and later died of renal failure. The renal failure was attributed to gout, but could have been caused by persistent hypercalemia, hypercalcuria, or multiple kidney stones due to sarcoidosis. Despite advances in diagnostic techniques made since Hutchinson’s time, the problem of distinguishing organ dysfunction due to sarcoidosis from other causes remains.
The diagnostic criteria for sarcoidosis, initially proposed in the 1950s by the International Sarcoidosis Association (now known as the World Association of Sarcoidosis and Other Granulomatous Diseases [WASOG]), included that granulomas be present in two or more organs with no agent known to cause a granulomatous response identified.2 This group also pointed out that a positive Kveim-Stilzbach test could also be used to support the diagnosis, and that false-positive Kveim-Stilzbach tests were infrequent. The histologic hallmark of sarcoidosis remains the finding of noncaseating granuloma, but unfortunately this is neither sensitive nor specific.3 Environmental and infectious causes of noncaseating granulomatous inflammation exist. In addition, some patients with sarcoidosis will have necrotizing areas within their granulomas, likely due to a more intense vascular inflammation.4 5 Furthermore, clinicians rarely go to the trouble of trying to demonstrate granulomas in more than one organ.
The most frequent biopsy sites are lung, lymph node, skin, and liver, but finding granulomas in any of these organs is never specific for sarcoidosis. In the liver, a necrotic granulomatous response to infection, even with Mycobacterium tuberculosis, is usually not seen.6 Also, granulomas isolated to the liver occur both from a variety of causes and of unknown significance.7 Thus, the finding of noncaseating granuloma in the liver is less specific than that in the lung.
How specific to sarcoidosis is the nonnecrotizing granuloma when found in the thorax? A nonnecrotizing granulomatous response of the lung is rarely seen in the lung in patients with tuberculosis or deep-seated fungal infections. These infections usually have a necrotizing component. Hypersensitivity pneumonitis may cause noncaseating granulomas, but the granulomas are usually less well formed.8 9 Lymph nodes, which are frequently enlarged in sarcoidosis, provide a convenient source of material for biopsy. However, a granulomatous response to malignancy, especially lymphoma, has been described.10 For this reason, the traditional approach to lymph node biopsy is to obtain a large enough sample in order to study lymph node architecture in which to place the context of a granulomatous response.11
In the current report by Tambouret et al in this issue of CHEST (see page 1004), the authors suggest that fine-needle aspiration biopsy (FNAB) appears to be underutilized in the diagnosis of sarcoidosis; when used in conjunction with radiologic and laboratory data, it is more cost-effective than excisional biopsy. The authors found FNAB to be reliable, with pathologists having a high degree of agreement on interpretation, and could replace the more costly surgical excision. The comments about interpreting a fine-needle aspirate suggest that a transbronchial needle aspirate would also be reliable. Transbronchial needle aspirate has been reported to increase yield of finding granulomas at the time of transbronchial biopsy, particularly in patients with stage I chest radiographs.12 13
The question raised by this report is how comfortable can we be with the diagnosis of sarcoidosis based on fine-needle aspirate? Until the cause or causes of sarcoidosis are identified, one will always have questions about the reliability of a diagnosis supported by histology. In actuality, there is no "gold standard" in diagnosis. There is only support for the diagnosis. This is why WASOG recommended the criteria of finding noncaseating granulomas in two or more organs.
Winterbauer et al14 reported several years ago that the finding of bilateral hilar adenopathy and right paratracheal node enlargement in an asymptomatic individual was specific for sarcoidosis. This has proved correct in > 95% of cases and remains a cost-effective method of approaching the asymptomatic individual.15 Patients with erythema nodosum, along with uveitis, and hilar adenopathy are very likely to have sarcoidosis. Other features that, when found together with a biopsy showing granulomas, make sarcoidosis highly likely are lupus pernio, uveitis, seventh-nerve paralysis (Bell’s palsy), and characteristic maculopapular skin lesions.16 Another factor that supports the diagnosis is the length of observation. The longer one observes a patient who presents with asymptomatic hilar adenopathy who remains asymptomatic, or is observed until radiograph resolution, the more convincing the diagnosis.
The diagnosis of sarcoidosis relies on the clinician putting together several pieces of information. This includes the clinical and radiographic patterns, histology, and a search for other potential causes of granulomas. The use of needle aspirate, either transbronchial or percutaneous, provides support but never absolute proof of diagnosis. It provides a peek into the patient’s inflammatory response. In some cases, a peek may be as good as a stare.
References
This article has been cited by other articles:
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  S. Garwood, M. A. Judson, G. Silvestri, R. Hoda, M. Fraig, and P. Doelken Endobronchial Ultrasound for the Diagnosis of Pulmonary Sarcoidosis Chest, October 1, 2007; 132(4): 1298 - 1304. [Abstract] [Full Text] [PDF]
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