Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (60)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baughman, R. P.
Right arrow Articles by Lower, E. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baughman, R. P.
Right arrow Articles by Lower, E. E.
(Chest. 2002;122:227-232.)
© 2002 American College of Chest Physicians

Thalidomide for Chronic Sarcoidosis*

Robert P. Baughman, MD, FCCP; Marc A. Judson, MD, FCCP; Alvin S. Teirstein, MD, FCCP; David R. Moller, MD and Elyse E. Lower, MD

* From the Department of Internal Medicine (Drs. Baughman and Lower), University of Cincinnati Medical Center, Cincinnati, OH; Division of Pulmonary and Critical Care Medicine (Dr. Judson), Medical University of South Carolina, Charleston, SC; Division of Pulmonary and Critical Care Medicine (Dr. Teirstein), Mount Sinai Medical Center, New York, NY; and Division of Pulmonary and Critical Care Medicine (Dr. Moller), Johns Hopkins University, Baltimore, MD.

Correspondence to: Robert P. Baughman, MD, FCCP, Holmes 1001, Eden Ave and Albert Sabin Way, Cincinnati OH 45267-0564; e-mail: Bob.Baughman{at}uc.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Thalidomide therapy has been shown to modify granulomatous diseases, such as tuberculosis and leprosy. Lupus pernio is a skin manifestation of sarcoidosis that does not remit spontaneously, and was used as a marker of efficacy of thalidomide for sarcoidosis.

Design: An open-label, dose-escalation trial of thalidomide.

Setting: Patients were seen at one of four specialized sarcoidosis clinics in the United States.

Patients: Fifteen patients with lupus pernio and other manifestations of sarcoidosis unresponsive to prior therapy were enrolled.

Interventions: Skin lesions were assessed with visual examination by the treating physician, and photographic evaluation by a blinded panel of physicians reviewing photographs of the lesions before and after therapy.

Measurements and results: Fourteen patients completed 4 months of therapy. All patients experienced some improvement in their skin lesions subjectively, and 10 of 12 evaluable patients showed improvement using photograph scoring. Five patients were better after 1 month (treated with 50 mg/d of thalidomide), seven more patients improved after 2 months (treated with 100 mg/d of thalidomide in the second month), and two patients required an additional month of 200 mg of thalidomide to achieve a response. Patients reported increased somnolence (n = 9), numbness (n = 7), dizziness (n = 2), constipation (n = 6), rash (n = 1), and increasing shortness of breath (n = 1). One patient discontinued therapy because of new-onset dyspnea, due to probably unrelated new-onset congestive heart failure.

Conclusion: Thalidomide was an effective form of treatment for chronic cutaneous sarcoidosis. The drug was well tolerated and may be a useful alternative to systemic corticosteroids.

Key Words: corticosteroids • lupus pernio • sarcoidosis • thalidomide • tumor necrosis factor


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Thalidomide was introduced in 1957 as a sedative and later an antiemetic. It was subsequently found to have teratogenic effects that led to the withdrawal of the drug. However, thalidomide has subsequently been found to be effective in treating the lepromatous reaction in leprosy,1 and it has been studied as an immumodulator for several conditions.2 3 4 It has also been shown to have antiangiogenic properties, which have led to its use in malignancy, especially multiple myeloma.5 In tuberculosis, it has been found to reduce the granulomatous response.6 7

Sarcoidosis is a granulomatous disease characterized by enhanced lymphocyte and macrophage activity,8 9 which is usually classified as a T-helper type 1 response. Among the inflammatory reactions is enhanced tumor necrosis factor (TNF)-{alpha} release by alveolar macrophages retrieved by BAL from patients with disease.10 11 Thalidomide attenuates the release of TNF-{alpha}.12 There have been case reports13 14 of the use of thalidomide for sarcoidosis.

Lupus pernio is a unique disfiguring skin involvement of the face characteristic of sarcoidosis.8 It is a chronic form of the disease and is associated with a low rate of resolution over 2 years.15 Patients with lupus pernio are usually treated with corticosteroids and other steroid-sparing agents with limited success.16 Lupus pernio is a form of cutaneous sarcoidosis that provides easy evaluation of therapeutic efficacy. Therefore, patients with lupus pernio were entered into an open-labeled, dose-escalation study of thalidomide.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients had known sarcoidosis and skin lesions consistent with lupus pernio unresponsive to previous treatment with corticosteroids. Patients were recruited from four medical centers, and all provided informed consent. All patients were counseled regarding pregnancy, with strict precautions instituted to avoid pregnancy while receiving the agent. Men were instructed to use barrier methods, and all women were at least 2 years postmenopausal or had surgical sterilization.

Patients underwent an initial evaluation, including a focused history and physical examination to document sarcoidosis organ involvement using an organ-assessment instrument.17 Patients also underwent spirometry to measure FVC, and the predicted values were based on age, race, gender, and height.18

Patients received an open-labeled dose escalation of thalidomide for 4 months. The schedule was 50 mg at night for 1 month, and 100 mg at night during the second month. For the final 2 months, the dose was doubled to 200 mg at night. If toxicity developed, the dose was reduced by one level.

Patients’ skin lesions were assessed by three methods. A general impression was made by the treating physician and the patient as to whether the lesions were worse, the same, better, or resolved. The physician was also asked to draw the lesions of the face, the number of lesions were counted, and their properties, including color and depth, were noted. Finally, photographs were made using a digital camera. The images were stored, and the same views were compared from the initial visit and after 4 months of therapy. For each patient, a single image of the most obvious lesion was compared before and after therapy. The images were placed side by side in random order, and the investigators were asked to vote indicating which photograph was the initial lesion. Figures 1 , 2 show examples of a lupus pernio skin lesion on the face (initial images [left, A] and follow-up lesions [right, B]).



View larger version (76K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1. The skin lesions of a patient with chronic sarcoidosis and lupus pernio lesion across the nose and cheeks. Left, A: lesions prior to therapy. Right, B: the same view after 16 weeks of treatment with thalidomide (maximal dosage, 200 mg/d).

 


View larger version (96K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2. The skin lesions of a patient with chronic sarcoidosis below the left ear. Left, A: lesions prior to therapy. Right, B: the same view after 16 weeks of treatment with thalidomide (maximal dosage, 200 mg/d).

 
All patients were screened for toxicity. A specific series of questions regarding specific toxicities (eg, somnolence) were asked. Patients also reported all adverse events, whether likely to be drug related or not. Finally, patients were evaluated for peripheral neuropathy by a Vibratron II (Physitemp Instruments; Clifton, NJ). Vibratory threshold was determined before and after therapy using the same finger for all examinations.19

Statistical Analysis
Comparisons were made on paired data using paired Wilcoxon analysis. Calculations were made using software (MedCalc version 5.00; MedCalc; Mariakerke, Belgium). A p value < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Fifteen patients were enrolled into the study. All patients had previously received corticosteroids, and two patients were maintained on prednisone, 10 mg/d, during the course of the study. An additional patient was treated by her primary physician during month 3 with a 4-day course of prednisone, 40 mg/d, for an acute asthmatic bronchitis followed by prednisone at 5 mg/d. Although most patients had received one or more steroid-sparing agents in the past, no patients were receiving these drugs at the time of entry into the study. No patients had modifications of their regimen for sarcoidosis in the 3 months prior to study entry.

One patient received only 3 weeks of therapy (at 50 mg/d) before experiencing shortness of breath. The thalidomide was immediately discontinued, and he was subsequently found to have new-onset congestive heart failure secondary to a recent myocardial infarction, presumed to be due to his known hyperlipidemia. He was withdrawn from the study and excluded from further analysis.

The remaining 14 patients received thalidomide for 4 months. Table 1 summarizes the characteristics of the patients who completed the study. Most of the patients were African-American women. We included organ involvement in addition to skin disease. Definite or probable lung involvement was documented in 12 patients. Definite or probable sinus involvement was reported in 8 patients, over half of those studied. No other organ involvement was common; therefore, further analysis was not performed on the response of these organs to thalidomide.


View this table:
[in this window]
[in a new window]

  		Table 1. Characteristics of Patients Treated for 4 Months With Thalidomide

 
All patients treated for 4 months responded to treatment with reductions in their skin lesions reported by both the physician and patient. Five patients responded to 50 mg/d, seven more patients responded to 100 mg/d, while two patients did not respond until placed on 200 mg/d (third month of therapy). The number of skin lesions on the face were counted and compared. The individual patient counts are shown in Figure 3 . There was a significant drop from the initial counts (median, 7.5 lesions; range, 1 to 13 lesions) compared to counts after 4 months of therapy (median, 3.5 lesions; range, 1 to 10; p < 0.01). One month after therapy withdrawal, four patients had an increased number of lesions, but one patient noted further lesion reduction. The number of lesions counted 1 month after stopping therapy (median, 4.5 lesions; range, 1 to 10 lesions) was not significantly different from the count at the end of 4 months of therapy.



View larger version (22K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3. The number of skin lesions counted by the investigators initially, after 16 weeks of therapy, and 4 weeks after withdrawing therapy. The individual patients are connected by lines.

 
Comparative digital photographs were read blindly by three investigators unaware of the order of the slides (Fig 1) . Of the 12 patients with adequate pretherapy and posttherapy photographs, the photographs of 2 patients were deemed to show no differences by all three readers. Of the remaining 10 patients, the lesions appeared improved in the follow-up photographs.

Information on other organ manifestations from sarcoidosis was also collected. Not all patients underwent chest radiography on entry into the study. Of those patients who did undergo chest radiography, the findings of two were normal, four had hilar involvement alone, one had hilar and parenchymal disease, one had parenchymal disease alone, and two had significant fibrosis. There was no change in the chest radiograph during therapy for these patients. All patients had their FVC measured initially and after treatment. The mean FVC after therapy was 2.35 L (range, 1.61 to 4.19 L) was not statistically different from the pretreatment measurements (Table 1) . In only two patients did the treating physician report that lung involvement was better with therapy. Symptomatic sinus disease was reported by eight patients at the initial evaluation. The sinus disease was believed to be perhaps due to the sarcoidosis, since no other cause was identified. Four of these patients reported significant symptomatic improvement during thalidomide treatment. This was reflected by a reduction in the need for treatment with nasal steroids and antibiotics for sinus infection.

Table 2 summarizes the major toxicities associated with the use of thalidomide. We report the dosage at which they were first encountered. These complaints were specifically sought by questionnaire. Although several complaints were noted, only two patients required dose reduction, one for somnolence and the other for numbness in the hands. Both patients’ symptoms improved with the reduced dosage. Nine patients (64%) complained of daytime somnolence. Although many patients noted this even at the lowest dose of 50 mg, only one patient had the dose reduced because of somnolence. For four patients, continuation of drug was associated with reduction of daytime somnolence. Vibratron II readings (mean ± SD) were not significantly different between the initial readings (1.9 ± 0.92 vibration units) and follow-up readings at 4 months (1.7 ± 0.62 vibration units). There was no difference between baseline and when numbness was experienced. One patient had a pituitary adenoma detected during the course of the study. This was not believed to be related to thalidomide therapy.


View this table:
[in this window]
[in a new window]

  		Table 2. Summary of Side Effects Associated With Thalidomide Therapy*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The use of thalidomide was associated with significant subjective improvement in the skin lesion lupus pernio in patients with sarcoidosis. All patients had improvement in the number or size of their lesions, although all patients still had at least one lesion at the end of the study. Objective improvement was assessed using photographs of the lesions before and after therapy. In 10 of 12 evaluable cases, the lesions were scored as better after therapy by a panel blinded to treatment. Patients responded to 100 to 200 mg/d of thalidomide. Although side effects were commonly encountered, they rarely led to dose modification.

As previously reported for lupus pernio, all patients in this study had persistent lesions despite previous treatment with corticosteroids and other agents.8 15 This form of cutaneous sarcoidosis is especially difficult to treat, and alternative treatments are usually sought.16 Intralesional corticosteroids are not recommended for routine management because of the risk of skin and soft-tissue atrophy. In one patient, prior intralesional steroids had led to some disfigurement of the cheek. Unfortunately, the lupus pernio still recurred in the area of the injection, but did respond to thalidomide. Eight of the patients had sinus symptoms that were believed to be consistent with sarcoidosis of the upper respiratory tract (SURT). SURT has been associated with lupus pernio. SURT is also a chronic form of sarcoidosis15 that can be difficult to treat.20 21 Active SURT was diagnosed in eight patients, and half of these patients had significant improvement of their symptoms during the course of the study as assessed by patient complaints and use of medications for sinus disease.

The mechanism of action of thalidomide in chronic granulomatous disease is unclear. It has been reported as useful in patients with sarcoidosis13 and tuberculosis.7 In a murine model of tuberculosis, thalidomide was associated with suppressed TNF release from the lung.22 In tuberculosis patients, treatment of patients with thalidomide was associated with reduction of TNF levels.7 In AIDS patients with aphthous ulcers, TNF release triggered by HIV was reduced by thalidomide.23 Other in vitro studies12 24 found thalidomide blocked the release of TNF from alveolar macrophages. Enhanced release of TNF by alveolar macrophages from patients with sarcoidosis has been reported.10 11 This release decreased after patients are treated with either corticosteroids or methotrexate.25 Increased levels of interleukin (IL)-12 have been reported in patients with sarcoidosis.26 Thalidomide has been found to suppress IL-12 released by peripheral blood monocytes stimulated with heat-killed Staphylococcus aureus and lipopolysaccharide,27 but not when stimulated by cross-linking T-cell receptor.28 27 There were no changes in IL-12 levels in the lung in the murine tuberculosis model.22

Side effects encountered in this study were similar but more frequent than that reported in other studies.5 23 29 An exception was rash, which occurred in only one patient in this study. Rash has been reported by > 20% of patients in other studies.5 23 These skin lesions included erythema nodosum, which was seen in patients with Behcet’s syndrome treated with thalidomide.29 Numbness was frequently reported in this study, but led to drug reduction in only one patient. The Vibratron II device had been suggested as a means to detect early neuropathy19 but was not useful in this study. The complaint of numbness was subjective and may have been overreported, since there was no placebo arm of the study. In the study of HIV-associated aphthous ulcers, peripheral neuropathy was encountered as frequently in the placebo group (5 of 28 patients) as in the treated group (7 of 29 patients).23

Studies5 23 29 of thalidomide have employed doses ranging from 100 to 800 mg/d. The dose necessary to treat sarcoidosis is unclear from the prior reports,13 14 which used various treatment regimens from 100 to 400 mg/d. We chose to start at a lower dose with a scheduled dose escalation. The onset of action of the drug was fairly rapid, and most patients have a response within 2 months. This response was more rapid than seen with methotrexate, which usually requires >= 6 months to become effective.30

In summary, thalidomide therapy was effective for lupus pernio in patients with chronic sarcoidosis. Its onset of action was relatively rapid and was well tolerated. Although thalidomide appeared effective for skin and sinus disease, its effect on pulmonary disease and other manifestations of sarcoidosis are not yet known. Given its low toxicity, thalidomide therapy should be considered as an alternative to corticosteroids and other agents for sarcoidosis.


   Acknowledgements
 
The authors thank Andrew Zeitlin and Celgene Corporation for helping to design safety monitoring and for financial support. We also thank Donna Winget, Susan D’Alessandro, Marilyn Marshall, Joanne Steimel, and Eileen Bowen for their technical support.


   Footnotes
 
Abbreviations: IL = interleukin; SURT = sarcoidosis of the upper respiratory tract; TNF = tumor necrosis factor

Supported in part by Celgene Corporation.

Received for publication June 15, 2001. Accepted for publication November 16, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Sheskin, J (1965) Thalidomide in the treatment of lepra reaction. Clin Pharmacol Ther 6,303-306[ISI][Medline]
  2. Forsyth, CJ, Cremer, PD, Torzillo, P, et al (1996) Thalidomide responsive chronic pulmonary GVHD. Bone Marrow Transplant 17,291-293[ISI][Medline]
  3. Marriott, JB, Cookson, S, Carlin, E, et al (1997) A double-blind placebo-controlled phase II trial of thalidomide in asymptomatic HIV-positive patients: clinical tolerance and effect on activation markers and cytokines. AIDS Res Hum Retroviruses 13,1625-1631[ISI][Medline]
  4. Uthoff, K, Zehr, KJ, Gaudin, PB, et al (1995) Thalidomide as replacement for steroids in immunosuppression after lung transplantation. Ann Thorac Surg 59,277-282[Abstract/Free Full Text]
  5. Singhal, S, Mehta, J, Desikan, R, et al (1999) Antitumor activity of thalidomide in refractory multiple myeloma. N Engl J Med 341,1565-1571[Abstract/Free Full Text]
  6. Moreira, AL, Tsenova-Berkova, L, Wang, J, et al (1997) Effect of cytokine modulation by thalidomide on the granulomatous response in murine tuberculosis. Tuber Lung Dis 78,47-55[CrossRef][ISI][Medline]
  7. Tramontana, JM, Utaipat, U, Molloy, A, et al (1995) Thalidomide treatment reduces tumor necrosis factor {alpha} production and enhances weight gain in patients with pulmonary tuberculosis. Mol Med 1,384-397[ISI][Medline]
  8. Statement on sarcoidosis: Joint Statement of the American Thoracic Society (ATS), the European Respiratory Society (ERS) and the World Association of Sarcoidosis and Other Granulomatous Disorders (WASOG) adopted by the ATS Board of Directors and by the ERS Executive Committee, February 1999. Am J Respir Crit Care Med 1999;160,736-755[Free Full Text]
  9. Thomas, PD, Hunninghake, GW (1987) Current concepts of the pathogenesis of sarcoidosis. Am Rev Respir Dis 135,747-760[ISI][Medline]
  10. Pueringer, RJ, Schwartz, DA, Dayton, CS, et al (1993) The relationship between alveolar macrophage TNF, IL-1, and PGE2 release, alveolitis, and disease severity in sarcoidosis. Chest 103,832-838[Abstract/Free Full Text]
  11. Baughman, RP, Strohofer, SA, Buchsbaum, J, et al (1990) Release of tumor necrosis factor by alveolar macrophages of patients with sarcoidosis. J Lab Clin Med 115,36-42[ISI][Medline]
  12. Tavares, JL, Wangoo, A, Dilworth, P, et al (1997) Thalidomide reduces tumour necrosis factor-{alpha} production by human alveolar macrophages. Respir Med 91,31-39[CrossRef][ISI][Medline]
  13. Carlesimo, M, Giustini, S, Rossi, A, et al (1995) Treatment of cutaneous and pulmonary sarcoidosis with thalidomide. J Am Acad Dermatol 32,866-869[CrossRef][ISI][Medline]
  14. Lee, JB, Koblenzer, PS (1998) Disfiguring cutaneous manifestation of sarcoidosis treated with thalidomide: a case report. J Am Acad Dermatol 39,835-838[CrossRef][ISI][Medline]
  15. Neville, E, Walker, AN, James, DG (1983) Prognostic factors predicting the outcome of sarcoidosis: an analysis of 818 patients. Q J Med 208,525-533
  16. Baughman, RP, Lower, EE (1997) Alternatives to corticosteroids in the treatment of sarcoidosis. Sarcoidosis 14,121-130
  17. Judson, MA, Baughman, RP, Teirstein, AS, et al (1999) Defining organ involvement in sarcoidosis: the ACCESS proposed instrument. Sarcoidosis Vasc Diffuse Lung Dis 16,75-86[ISI][Medline]
  18. Hankinson, JL, Odencrantz, JR, Fedan, KB (1999) Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med 159,179-187[Abstract/Free Full Text]
  19. Gerr, FE, Letz, R (1988) Reliability of a widely used test of peripheral cutaneous vibration sensitivity and a comparison of two testing protocols. Br J Ind Med 45,635-639[ISI][Medline]
  20. Fenton, DA, Shaw, M, Black, MN (1985) Invasive nasal sarcoidosis treated with methotrexate. Clin Exp Dermatol 10,279-283[CrossRef][ISI][Medline]
  21. Zeitlin, JF, Tami, TA, Baughman, RP, et al (2000) Nasal and sinus manifestations of sarcoidosis. Am J Rhinol 14,157-161[ISI][Medline]
  22. Moreira, AL, Tsenova Berkova, L, Wang, J, et al (1997) Effect of cytokine modulation by thalidomide on the granulomatous response in murine tuberculosis. Tuber Lung Dis 78,47-55[CrossRef][ISI][Medline]
  23. Jacobson, JM, Greenspan, JS, Spritzler, J, et al (1997) Thalidomide for the treatment of oral aphthous ulcers in patients with human immunodeficiency virus infection: National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group. N Engl J Med 336,1487-1493[Abstract/Free Full Text]
  24. Rowland, TL, McHugh, SM, Deighton, J, et al (1998) Differential regulation by thalidomide and dexamethasone of cytokine expression in human peripheral blood mononuclear cells. Immunopharmacology 40,11-20[CrossRef][ISI][Medline]
  25. Baughman, RP, Lower, EE (1990) The effect of corticosteroid or methotrexate therapy on lung lymphocytes and macrophages in sarcoidosis. Am Rev Respir Dis 142,1268-1271[ISI][Medline]
  26. Moller, DR, Forman, JD, Liu, MC, et al (1996) Enhanced expression of IL-12 associated with Th1 cytokine profiles in active pulmonary sarcoidosis. J Immunol 156,4952-4960[Abstract]
  27. Moller, DR, Wysocka, M, Greenlee, BM, et al (1997) Inhibition of IL-12 production by thalidomide. J Immunol 159,5157-5161[Abstract]
  28. Corral, LG, Haslett, PA, Muller, GW, et al (1999) Differential cytokine modulation and T cell activation by two distinct classes of thalidomide analogues that are potent inhibitors of TNF-{alpha}. J Immunol 163,380-386[Abstract/Free Full Text]
  29. Hamuryudan, V, Mat, C, Saip, S, et al (1998) Thalidomide in the treatment of the mucocutaneous lesions of the Behcet syndrome. Ann Intern Med 128,443-450[Abstract/Free Full Text]
  30. Lower, EE, Baughman, RP (1990) The use of low dose methotrexate in refractory sarcoidosis. Am J Med Sci 299,153-157[ISI][Medline]



This article has been cited by other articles:


Home page
 ChestHome page
A. Thornburg, R. Abonour, P. Smith, K. Knox, and H. L. Twigg III
Hypersensitivity Pneumonitis-Like Syndrome Associated With the Use of Lenalidomide
Chest, May 1, 2007; 131(5): 1572 - 1574.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
Q. Ye, B. Chen, Z. Tong, S. Nakamura, R. Sarria, U. Costabel, and J. Guzman
Thalidomide reduces IL-18, IL-8 and TNF-{alpha} release from alveolar macrophages in interstitial lung disease
Eur. Respir. J., October 1, 2006; 28(4): 824 - 831.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
Y. S. Wasfi, C. S. Rose, J. R. Murphy, L. J. Silveira, J. C. Grutters, Y. Inoue, M. A. Judson, and L. A. Maier
A New Tool To Assess Sarcoidosis Severity
Chest, May 1, 2006; 129(5): 1234 - 1245.
[Abstract] [Full Text] [PDF]

Home page
 QJMHome page
R.P. Baughman and E.E. Lower
Fungal infections as a complication of therapy for sarcoidosis
QJM, June 1, 2005; 98(6): 451 - 456.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
J. D. Doty, J. E. Mazur, and M. A. Judson
Treatment of Sarcoidosis With Infliximab
Chest, March 1, 2005; 127(3): 1064 - 1071.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
W. J. Martin II, M. C. Iannuzzi, D. B. Gail, and H. H. Peavy
Future Directions in Sarcoidosis Research: Summary of an NHLBI Working Group
Am. J. Respir. Crit. Care Med., September 1, 2004; 170(5): 567 - 571.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
S. D. Roberts, D. S. Wilkes, R. A. Burgett, and K. S. Knox
Refractory Sarcoidosis Responding to Infliximab
Chest, November 1, 2003; 124(5): 2028 - 2031.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
N. Kaminski, J. A. Belperio, P. B. Bitterman, L. Chen, S. W. Chensue, A. M.K. Choi, S. Dacic, J. H. Dauber, R. M. du Bois, J. J. Enghild, et al.
Idiopathic Pulmonary Fibrosis
Am. J. Respir. Cell Mol. Biol., September 1, 2003; 29(3): S1 - 105.
[Full Text] [PDF]

Home page
 ChestHome page
R. P. Baughman and E. E. Lower
The Variability of Sarcoidosis: Can We Predict It?
Chest, May 1, 2003; 123(5): 1329 - 1332.
[Full Text] [PDF]

Home page
 Arch NeurolHome page
J. M. Katz, M. K. Bruno, J. M. S. Winterkorn, and N. Nealon
The Pathogenesis and Treatment of Optic Disc Swelling in Neurosarcoidosis: A Unique Therapeutic Response to Infliximab
Arch Neurol, March 1, 2003; 60(3): 426 - 430.
[Abstract] [Full Text] [PDF]

Home page
 Postgrad. Med. J.Home page
J N Gordon and P M Goggin
Thalidomide and its derivatives: emerging from the wilderness
Postgrad. Med. J., March 1, 2003; 79(929): 127 - 132.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (60)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baughman, R. P.
Right arrow Articles by Lower, E. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baughman, R. P.
Right arrow Articles by Lower, E. E.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS