International Journal of Rheumatic Diseases 2014; 17: 811–814
CORRESPONDENCE
Interstitial pneumonia as an initial manifestation in a patient with late-onset SLE
Dear Editor, Systemic lupus erythematosus (SLE) has the potential to affect any organ and the lungs are commonly involved later in the course of the disease. The most common pulmonary manifestation attributable to SLE is pleuritis. Parenchymal involvement includes chronic interstitial lung disease (ILD) and acute lupus pneumonitis (ALP). Pulmonary involvements except pleural effusion are uncommonly manifested as an initial presentation of SLE. SLE usually develops over 50 years of age in a small subset ranging from 3–18% of cases.1 These patients frequently show a more insidious onset with non-specific clinical features and less common occurrence of severe manifestations. Thus, diagnosis of late-onset SLE is often delayed and established after more extensive investigations. A 70-year-old Japanese man had productive cough and pain in the chest and back, in the middle of December 2011. Then, he had bilateral swelling and painful purpura of fingers and toes. He had a history of membranous nephropathy, Hashimoto’s thyroiditis and idiopathic thrombocytopenia at 55 years old. He had been treated with prednisolone for 2 years and 4 months; after then he had maintained remission. He had a history of normal pressure hydrocephalus at 64 years old. He was admitted to our hospital on January 27, 2012. On admission, his vital signs were body temperature 36.2°C, heart rate 87/min, blood pressure 115/ 66 mmHg, oxygen saturation by pulse oximetry (SpO2) of 98% on air. Fine crackles were heard throughout both lungs on auscultation. His initial laboratory findings are shown in Table 1. Forced vital capacity (FVC) was 90.4% predicted and forced expiratory volume percentage in one second (FEV1.0%) was 85.4%. Urine examination revealed positive reaction of proteinuria (0.2 g/day). A thoracic high-resolution computed tomography (HRCT) scan revealed patchy infiltrates bilaterally in lower lung zones. It clearly appeared on
the right side with infiltrative appearance (Fig. 1). He was diagnosed as having SLE because of arthritis, platelet depletion (72 9 109/L), hypocomplementemia (22.7 U/mL), positive anti-double-stranded DNA antibody (> 400 IU/mL) and anti-nuclear antibody titers of 1 : 320. The histological features of surgical lung biopsies showed a major pattern of nonspecific interstitial pneumonia (NSIP), along with a minor component of usual interstitial pneumonia (UIP). His symptoms improved after commencement of prednisolone (40 mg/day), proteinuria disappeared promptly, and thrombocytopenia and hypocomplementemia were gradually improved. At this time, 22 months after the diagnosis of SLE, he had no symptoms and interstitial pneumonitis is under control with a maintenance dose of 8 mg prednisolone. Pulmonary involvement occurs in up to 25% of patients with SLE.2 Pleural disease is the most frequent respiratory manifestation (30–59%) due to SLE. On the other hand, lung involvement is identified in 3% at the onset of SLE, and develops in an additional 7% over the period of observation.3 The onset of the symptoms of ILD is insidious in most cases, but may appear after one or more episodes of acute lupus pneumonitis.4 The histological pattern usually observed in ILD with SLE is that of NSIP. Because of different treatments and prognoses for NSIP and UIP, accurate diagnosis for these two diseases is critical.5 However, the differential diagnosis between them is hard for both clinicians and pathologists,6 especially between NSIP fibrotic pattern (NSIP-F) and UIP. In addition, cryptogenic organizing pneumonia (COP, formerly known as bronchiolitis obliterans organizing pneumonia: BOOP) has been reported in several patients with SLE.7–11 The current approach to the diagnosis of ILD is based on clinical, radiological and pathological data. Surgical lung biopsy is the most sensitive method for collecting accurate pathological data; however, this procedure is
© 2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd
Correspondence
Table 1 Initial laboratory findings Peripheral blood White blood cells Lymphocyte Red blood cells Hemoglobin Platelets
6.1 9 109/L 1.9 9 109/L 3,080 9 109/L 97 g/L 72 9 109/L
Biochemistry Total serum protein Albumin Aspartate aminotransferase Alanine aminotransferase Lactate dehydrogenase Blood urea nitrogen Creatinine Creatine kinase Krebs von den Lungen (KL)-6
72 g/L 33 g/L 36 IU/L 26 IU/L 228 IU/L 16.2 mg/dL 0.94 mg/dL 70 IU/L 839 U/mL (< 500)
Figure 1 Thoracic high-resolution computed tomography (HRCT) scan revealed patchy infiltrates bilaterally in lower lung zone. It clearly appeared on the right side with infiltrative appearance. After administration of 40 mg prednisone for 1 month, patchy infiltrates promptly disappeared.
performed in less than 15% of patients.12 An accurate diagnosis of the histopathological subtype of ILD is important to guide prognosis and management. There are only a few reports on pathological investigation of ILD with SLE. To our knowledge, there are 11
812
Serology C-reactive protein IgG IgA IgM Antinuclear antibody Anti-dsDNA antibody Anti-Sm antibody Anti-SS-A antibody Anti-cardiolipin-b2-GPI antibody CH50 C3 C4 Arterial blood gas values pH PaCO2 PaO2
14.1 mg/L (< 3.0) 19.96 g/L (6.8–16.2) 6.95 g/L (0.84–4.38) 0.2 g/L (0.57–2.88) 1 : 320 (< 1 : 40) homogeneous pattern > 400 IU/mL (< 12) Negative Negative Negative 22.7 U/mL (23–46) 0.64 g/L (0.65–1.35) 0.07 g/L (0.13–0.35) 7.41 32 mmHg 104 mmHg
cases of SLE complicated with ILD, including ours (Table 2).7–11,13–15 COP7–11 was the most frequently reported in seven cases, and lymphocytic interstitial pneumonia (LIP),13 acute fibrinous and organizing pneumonia (AFOP)14 and desquamative interstitial pneumonitis (DIP)15 were reported, one in each case. It was reported that ILD with SLE is highly associated with the presence of anti-SS-A (Ro) antibodies, and 82% of patients (9/11) with lupus pneumonitis had anti-SS-A (Ro) antibodies.16 However, in the patients in Table 2, anti-SS-A antibody was positive in only one patient.13 ILD was the initial manifestation of SLE in five cases (45%), including our case.8,10,11 Prognosis seems to be favorable since 10 out of 11 cases (91%) displayed improvement. The clinical course of late-onset SLE is considered mild, rarely characterized by the occurrence of severe manifestations, such as renal or neuropsychiatric involvement. By contrast, serositis, lung involvement and secondary Sj€ ogren’s syndrome are more frequently detected in elderly lupus patients.1 The pooled analysis of the literature data showed significant decline of the female/male sex ratio observed with aging in SLE (4.4 in the late-onset group vs. 10.6 in the early-onset group). This probably reflects the relationship between SLE and estrogen status. The present report describes an unusual case of ILD in a patient with late-onset SLE. Clinicians should consider a surgical lung biopsy in patients with ILD. Further study is necessary to clarify the pathogenesis,
International Journal of Rheumatic Diseases 2014; 17: 811–814
International Journal of Rheumatic Diseases 2014; 17: 811–814
13 11
14
15
Filipek, 2004 Takada, 2005
Hariri, 2010
Esmaeilbeigi, 2012
70/M
23/M
47/M
34/F 16/F
34/F
21/F
33/F
83/F
54/M 28/F
Age/sex
1 : 320(< 1 : 40)
1 : 640
high
positive 1 : 2560 (< 40)
1 : 640
1 : 160
1 : 320
1 : 160
1 : 640 1 : 20
ANA
NS
22.7 U/mL (23–46)
> 400 IU/mL (< 12)
6.4 U/mL (30–40) 6.4 U/mL (30–40) NS 8 U/mL (20–50) NS
11 U/mL
NS
WNL WNL
Complement
Positive
Positive
NS 400 IU/mL (< 10)
88 IU/mL (< 20) 145 IU/mL (< 20)
160 U/mL
Positive
1 : 80 Positive
Anti-DNA antibody
Negative
Negative
NS
Positive NS
Negative
Negative
Negative
NS
NS Negative
Anti-SS-A antibody
NSIP, UIP
DIP
AFOP
LIP COP
COP
COP
COP
COP
COP COP
Histology
initial manifestation
6 years
initial manifestation initial manifestation 5 years initial manifestation 8 years
initial manifestation 19 months
7 months 2 months
Durations between SLE onset and lung involvement
PSL 50 mg AZP 150 mg PSL 40 mg
PSL 60 mg CPA 100 mg PSL 50 mg
PSL unknown PSL 60 mg
PSL 1 mg/kg
mPSL pulseX3 times, PSL 40 mg PSL 50 mg
PSL 60 mg PSL 60 mg, CPA unknown mPSL 125 mg
Treatment
Improved
Improved
Recurrence
Improved
Improved Improved
Improved
Improved
Improved
Improved
Improved Death
Outcome
AFOP, acute fibrinous and organizing pneumonia; AZP, azathioprine; COP, cryptogenic organizing pneumonia; CPA, cyclophosphamide; DIP, desquamative interstitial pneumonia; LIP, lymphocytic interstitial pneumonia; NS, not specified; NSIP, nonspecific interstitial pneumonia; PSL, prednisolone; UIP, usual interstitial pneumonia; WNL, within normal limits.
This case
10
Min, 1997
9
Otsuka, 1996
10
8
Mana, 1993
Min, 1997
7 7
Ref.
Gammon, 1992 Gammon, 1992
Author, year
Table 2 Clinical features of SLE complicated with interstitial lung disease: literature review
Correspondence
813
Correspondence
clinical characteristics and prognosis of ILD associated with SLE. More attention to the pulmonary manifestations of late-onset SLE is warranted. Rumiko MIYAGI,1 Haruko IDEGUCHI,1 Takayoshi SOGA,1,2 Kazuhiro SAKAMOTO,3 Hitoshi NIINO,4 Takeki SHIINA,5 Atsuhisa UEDA6 and Yoshiaki ISHIGATSUBO6
6
7
1
Department of Rheumatology, National Hospital Organization Yokohama Medical Center, Yokohama, 2 Department of Rheumatology, Japanese Red Cross Shizuoka Hospital, Shizuoka, 3Department of Respiratory Surgery, 4 Pathology, 5Radiology, National Hospital Organization Yokohama Medical Center, Yokohama, and 6Department of Internal Medicine and Clinical Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan Correspondence: Haruko Ideguchi, M.D., Ph.D., Director, email: [email protected]
REFERENCES 1 Arnaud L, Mathian A, Boddaert J, Amoura Z (2012) Late-onset systemic lupus erythematosus: epidemiology, diagnosis and treatment. Drugs Aging 29 (3), 181–9. 2 Pego-Reigosa JM, Medeiros DA, Isenberg DA (2009) Respiratory manifestations of systemic lupus erythematosus: old and new concepts. Best practice & research. Clin Rheumatol 23, 469–80. 3 Cervera R, Khamashta MA, Font J et al. (1993) Systemic lupus erythematosus: clinical and immunologic patterns of disease expression in a cohort of 1,000 patients. The European Working Party on Systemic Lupus Erythematosus. Medicine 72, 113–24. 4 Matthay RA, Schwarz MI, Petty TL et al. (1975) Pulmonary manifestations of systemic lupus erythematosus: review of twelve cases of acute lupus pneumonitis. Medicine 54, 397–409. 5 American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias (2002) This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Execu-
814
8
9
10
11
12
13
14
15
16
tive Committee, June 2001. Am J Respir Crit Care Med 165, 277–304. Travis WD, Hunninghake G, King TE Jr et al. (2008) Idiopathic nonspecific interstitial pneumonia: report of an American Thoracic Society project. Am J Respir Crit Care Med 177, 1338–47. Gammon RB, Bridges TA, al-Nezir H, Alexander CB, Kennedy JI Jr (1992) Bronchiolitis obliterans organizing pneumonia associated with systemic lupus erythematosus. Chest 102(4), 1171–4. Mana F, Mets T, Vincken W, Sennesael J, Vanwaeyenbergh J, Goossens A (1993) The association of bronchiolitis obliterans organizing pneumonia, systemic lupus erythematosus, and Hunner’s cystitis. Chest 104, 642–4. Otsuka F, Amano T, Hashimoto N et al. (1996) Bronchiolitis obliterans organizing pneumonia associated with systemic lupus erythematosus with antiphospholipid antibody. Intern Med (Tokyo, Japan) 35(4), 341–4. Min JK, Hong YS, Park SH et al. (1997) Bronchiolitis obliterans organizing pneumonia as an initial manifestation in patients with systemic lupus erythematosus. J Rheumatol 24, 2254–7. Takada H, Saito Y, Nomura A et al. (2005) Bronchiolitis obliterans organizing pneumonia as an initial manifestation in systemic lupus erythematosus. Pediatr Pulmonol 40, 257–60. Lynch DA, Travis WD, Muller NL et al. (2005) Idiopathic interstitial pneumonias: CT features. Radiology 236, 10–21. Filipek MS, Thompson ME, Wang PL, Gosselin MV, L Primack S (2004) Lymphocytic interstitial pneumonitis in a patient with systemic lupus erythematosus: radiographic and high-resolution CT findings. J Thorac Imaging 19, 200–3. Hariri LP, Unizony S, Stone J et al. (2010) Acute fibrinous and organizing pneumonia in systemic lupus erythematosus: a case report and review of the literature. Pathol Int 60, 755–9. Esmaeilbeigi F, Juvet S, Hwang D, Mittoo S (2012) Desquamative interstitial pneumonitis in a patient with systemic lupus erythematosus. Can Respir J 19, 50–2. Mochizuki T, Aotsuka S, Satoh T (1999) Clinical and laboratory features of lupus patients with complicating pulmonary disease. Respir Med 93, 95–101.
International Journal of Rheumatic Diseases 2014; 17: 811–814
Copyright of International Journal of Rheumatic Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
CORRESPONDENCE
Interstitial pneumonia as an initial manifestation in a patient with late-onset SLE
Dear Editor, Systemic lupus erythematosus (SLE) has the potential to affect any organ and the lungs are commonly involved later in the course of the disease. The most common pulmonary manifestation attributable to SLE is pleuritis. Parenchymal involvement includes chronic interstitial lung disease (ILD) and acute lupus pneumonitis (ALP). Pulmonary involvements except pleural effusion are uncommonly manifested as an initial presentation of SLE. SLE usually develops over 50 years of age in a small subset ranging from 3–18% of cases.1 These patients frequently show a more insidious onset with non-specific clinical features and less common occurrence of severe manifestations. Thus, diagnosis of late-onset SLE is often delayed and established after more extensive investigations. A 70-year-old Japanese man had productive cough and pain in the chest and back, in the middle of December 2011. Then, he had bilateral swelling and painful purpura of fingers and toes. He had a history of membranous nephropathy, Hashimoto’s thyroiditis and idiopathic thrombocytopenia at 55 years old. He had been treated with prednisolone for 2 years and 4 months; after then he had maintained remission. He had a history of normal pressure hydrocephalus at 64 years old. He was admitted to our hospital on January 27, 2012. On admission, his vital signs were body temperature 36.2°C, heart rate 87/min, blood pressure 115/ 66 mmHg, oxygen saturation by pulse oximetry (SpO2) of 98% on air. Fine crackles were heard throughout both lungs on auscultation. His initial laboratory findings are shown in Table 1. Forced vital capacity (FVC) was 90.4% predicted and forced expiratory volume percentage in one second (FEV1.0%) was 85.4%. Urine examination revealed positive reaction of proteinuria (0.2 g/day). A thoracic high-resolution computed tomography (HRCT) scan revealed patchy infiltrates bilaterally in lower lung zones. It clearly appeared on
the right side with infiltrative appearance (Fig. 1). He was diagnosed as having SLE because of arthritis, platelet depletion (72 9 109/L), hypocomplementemia (22.7 U/mL), positive anti-double-stranded DNA antibody (> 400 IU/mL) and anti-nuclear antibody titers of 1 : 320. The histological features of surgical lung biopsies showed a major pattern of nonspecific interstitial pneumonia (NSIP), along with a minor component of usual interstitial pneumonia (UIP). His symptoms improved after commencement of prednisolone (40 mg/day), proteinuria disappeared promptly, and thrombocytopenia and hypocomplementemia were gradually improved. At this time, 22 months after the diagnosis of SLE, he had no symptoms and interstitial pneumonitis is under control with a maintenance dose of 8 mg prednisolone. Pulmonary involvement occurs in up to 25% of patients with SLE.2 Pleural disease is the most frequent respiratory manifestation (30–59%) due to SLE. On the other hand, lung involvement is identified in 3% at the onset of SLE, and develops in an additional 7% over the period of observation.3 The onset of the symptoms of ILD is insidious in most cases, but may appear after one or more episodes of acute lupus pneumonitis.4 The histological pattern usually observed in ILD with SLE is that of NSIP. Because of different treatments and prognoses for NSIP and UIP, accurate diagnosis for these two diseases is critical.5 However, the differential diagnosis between them is hard for both clinicians and pathologists,6 especially between NSIP fibrotic pattern (NSIP-F) and UIP. In addition, cryptogenic organizing pneumonia (COP, formerly known as bronchiolitis obliterans organizing pneumonia: BOOP) has been reported in several patients with SLE.7–11 The current approach to the diagnosis of ILD is based on clinical, radiological and pathological data. Surgical lung biopsy is the most sensitive method for collecting accurate pathological data; however, this procedure is
© 2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd
Correspondence
Table 1 Initial laboratory findings Peripheral blood White blood cells Lymphocyte Red blood cells Hemoglobin Platelets
6.1 9 109/L 1.9 9 109/L 3,080 9 109/L 97 g/L 72 9 109/L
Biochemistry Total serum protein Albumin Aspartate aminotransferase Alanine aminotransferase Lactate dehydrogenase Blood urea nitrogen Creatinine Creatine kinase Krebs von den Lungen (KL)-6
72 g/L 33 g/L 36 IU/L 26 IU/L 228 IU/L 16.2 mg/dL 0.94 mg/dL 70 IU/L 839 U/mL (< 500)
Figure 1 Thoracic high-resolution computed tomography (HRCT) scan revealed patchy infiltrates bilaterally in lower lung zone. It clearly appeared on the right side with infiltrative appearance. After administration of 40 mg prednisone for 1 month, patchy infiltrates promptly disappeared.
performed in less than 15% of patients.12 An accurate diagnosis of the histopathological subtype of ILD is important to guide prognosis and management. There are only a few reports on pathological investigation of ILD with SLE. To our knowledge, there are 11
812
Serology C-reactive protein IgG IgA IgM Antinuclear antibody Anti-dsDNA antibody Anti-Sm antibody Anti-SS-A antibody Anti-cardiolipin-b2-GPI antibody CH50 C3 C4 Arterial blood gas values pH PaCO2 PaO2
14.1 mg/L (< 3.0) 19.96 g/L (6.8–16.2) 6.95 g/L (0.84–4.38) 0.2 g/L (0.57–2.88) 1 : 320 (< 1 : 40) homogeneous pattern > 400 IU/mL (< 12) Negative Negative Negative 22.7 U/mL (23–46) 0.64 g/L (0.65–1.35) 0.07 g/L (0.13–0.35) 7.41 32 mmHg 104 mmHg
cases of SLE complicated with ILD, including ours (Table 2).7–11,13–15 COP7–11 was the most frequently reported in seven cases, and lymphocytic interstitial pneumonia (LIP),13 acute fibrinous and organizing pneumonia (AFOP)14 and desquamative interstitial pneumonitis (DIP)15 were reported, one in each case. It was reported that ILD with SLE is highly associated with the presence of anti-SS-A (Ro) antibodies, and 82% of patients (9/11) with lupus pneumonitis had anti-SS-A (Ro) antibodies.16 However, in the patients in Table 2, anti-SS-A antibody was positive in only one patient.13 ILD was the initial manifestation of SLE in five cases (45%), including our case.8,10,11 Prognosis seems to be favorable since 10 out of 11 cases (91%) displayed improvement. The clinical course of late-onset SLE is considered mild, rarely characterized by the occurrence of severe manifestations, such as renal or neuropsychiatric involvement. By contrast, serositis, lung involvement and secondary Sj€ ogren’s syndrome are more frequently detected in elderly lupus patients.1 The pooled analysis of the literature data showed significant decline of the female/male sex ratio observed with aging in SLE (4.4 in the late-onset group vs. 10.6 in the early-onset group). This probably reflects the relationship between SLE and estrogen status. The present report describes an unusual case of ILD in a patient with late-onset SLE. Clinicians should consider a surgical lung biopsy in patients with ILD. Further study is necessary to clarify the pathogenesis,
International Journal of Rheumatic Diseases 2014; 17: 811–814
International Journal of Rheumatic Diseases 2014; 17: 811–814
13 11
14
15
Filipek, 2004 Takada, 2005
Hariri, 2010
Esmaeilbeigi, 2012
70/M
23/M
47/M
34/F 16/F
34/F
21/F
33/F
83/F
54/M 28/F
Age/sex
1 : 320(< 1 : 40)
1 : 640
high
positive 1 : 2560 (< 40)
1 : 640
1 : 160
1 : 320
1 : 160
1 : 640 1 : 20
ANA
NS
22.7 U/mL (23–46)
> 400 IU/mL (< 12)
6.4 U/mL (30–40) 6.4 U/mL (30–40) NS 8 U/mL (20–50) NS
11 U/mL
NS
WNL WNL
Complement
Positive
Positive
NS 400 IU/mL (< 10)
88 IU/mL (< 20) 145 IU/mL (< 20)
160 U/mL
Positive
1 : 80 Positive
Anti-DNA antibody
Negative
Negative
NS
Positive NS
Negative
Negative
Negative
NS
NS Negative
Anti-SS-A antibody
NSIP, UIP
DIP
AFOP
LIP COP
COP
COP
COP
COP
COP COP
Histology
initial manifestation
6 years
initial manifestation initial manifestation 5 years initial manifestation 8 years
initial manifestation 19 months
7 months 2 months
Durations between SLE onset and lung involvement
PSL 50 mg AZP 150 mg PSL 40 mg
PSL 60 mg CPA 100 mg PSL 50 mg
PSL unknown PSL 60 mg
PSL 1 mg/kg
mPSL pulseX3 times, PSL 40 mg PSL 50 mg
PSL 60 mg PSL 60 mg, CPA unknown mPSL 125 mg
Treatment
Improved
Improved
Recurrence
Improved
Improved Improved
Improved
Improved
Improved
Improved
Improved Death
Outcome
AFOP, acute fibrinous and organizing pneumonia; AZP, azathioprine; COP, cryptogenic organizing pneumonia; CPA, cyclophosphamide; DIP, desquamative interstitial pneumonia; LIP, lymphocytic interstitial pneumonia; NS, not specified; NSIP, nonspecific interstitial pneumonia; PSL, prednisolone; UIP, usual interstitial pneumonia; WNL, within normal limits.
This case
10
Min, 1997
9
Otsuka, 1996
10
8
Mana, 1993
Min, 1997
7 7
Ref.
Gammon, 1992 Gammon, 1992
Author, year
Table 2 Clinical features of SLE complicated with interstitial lung disease: literature review
Correspondence
813
Correspondence
clinical characteristics and prognosis of ILD associated with SLE. More attention to the pulmonary manifestations of late-onset SLE is warranted. Rumiko MIYAGI,1 Haruko IDEGUCHI,1 Takayoshi SOGA,1,2 Kazuhiro SAKAMOTO,3 Hitoshi NIINO,4 Takeki SHIINA,5 Atsuhisa UEDA6 and Yoshiaki ISHIGATSUBO6
6
7
1
Department of Rheumatology, National Hospital Organization Yokohama Medical Center, Yokohama, 2 Department of Rheumatology, Japanese Red Cross Shizuoka Hospital, Shizuoka, 3Department of Respiratory Surgery, 4 Pathology, 5Radiology, National Hospital Organization Yokohama Medical Center, Yokohama, and 6Department of Internal Medicine and Clinical Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan Correspondence: Haruko Ideguchi, M.D., Ph.D., Director, email: [email protected]
REFERENCES 1 Arnaud L, Mathian A, Boddaert J, Amoura Z (2012) Late-onset systemic lupus erythematosus: epidemiology, diagnosis and treatment. Drugs Aging 29 (3), 181–9. 2 Pego-Reigosa JM, Medeiros DA, Isenberg DA (2009) Respiratory manifestations of systemic lupus erythematosus: old and new concepts. Best practice & research. Clin Rheumatol 23, 469–80. 3 Cervera R, Khamashta MA, Font J et al. (1993) Systemic lupus erythematosus: clinical and immunologic patterns of disease expression in a cohort of 1,000 patients. The European Working Party on Systemic Lupus Erythematosus. Medicine 72, 113–24. 4 Matthay RA, Schwarz MI, Petty TL et al. (1975) Pulmonary manifestations of systemic lupus erythematosus: review of twelve cases of acute lupus pneumonitis. Medicine 54, 397–409. 5 American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias (2002) This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Execu-
814
8
9
10
11
12
13
14
15
16
tive Committee, June 2001. Am J Respir Crit Care Med 165, 277–304. Travis WD, Hunninghake G, King TE Jr et al. (2008) Idiopathic nonspecific interstitial pneumonia: report of an American Thoracic Society project. Am J Respir Crit Care Med 177, 1338–47. Gammon RB, Bridges TA, al-Nezir H, Alexander CB, Kennedy JI Jr (1992) Bronchiolitis obliterans organizing pneumonia associated with systemic lupus erythematosus. Chest 102(4), 1171–4. Mana F, Mets T, Vincken W, Sennesael J, Vanwaeyenbergh J, Goossens A (1993) The association of bronchiolitis obliterans organizing pneumonia, systemic lupus erythematosus, and Hunner’s cystitis. Chest 104, 642–4. Otsuka F, Amano T, Hashimoto N et al. (1996) Bronchiolitis obliterans organizing pneumonia associated with systemic lupus erythematosus with antiphospholipid antibody. Intern Med (Tokyo, Japan) 35(4), 341–4. Min JK, Hong YS, Park SH et al. (1997) Bronchiolitis obliterans organizing pneumonia as an initial manifestation in patients with systemic lupus erythematosus. J Rheumatol 24, 2254–7. Takada H, Saito Y, Nomura A et al. (2005) Bronchiolitis obliterans organizing pneumonia as an initial manifestation in systemic lupus erythematosus. Pediatr Pulmonol 40, 257–60. Lynch DA, Travis WD, Muller NL et al. (2005) Idiopathic interstitial pneumonias: CT features. Radiology 236, 10–21. Filipek MS, Thompson ME, Wang PL, Gosselin MV, L Primack S (2004) Lymphocytic interstitial pneumonitis in a patient with systemic lupus erythematosus: radiographic and high-resolution CT findings. J Thorac Imaging 19, 200–3. Hariri LP, Unizony S, Stone J et al. (2010) Acute fibrinous and organizing pneumonia in systemic lupus erythematosus: a case report and review of the literature. Pathol Int 60, 755–9. Esmaeilbeigi F, Juvet S, Hwang D, Mittoo S (2012) Desquamative interstitial pneumonitis in a patient with systemic lupus erythematosus. Can Respir J 19, 50–2. Mochizuki T, Aotsuka S, Satoh T (1999) Clinical and laboratory features of lupus patients with complicating pulmonary disease. Respir Med 93, 95–101.
International Journal of Rheumatic Diseases 2014; 17: 811–814
Copyright of International Journal of Rheumatic Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
