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Decreased DLCO

MedGen UID:
892993
Concept ID:
C4073175
Finding
Synonym: Decreased diffusing capacity
 
HPO: HP:0045051

Definition

Reduced ability of the lungs to transfer gas from inspired air to the bloodstream as measured by the diffusing capacity of the lungs for carbon monoxide (DLCO) test. [from HPO]

Term Hierarchy

Conditions with this feature

Niemann-Pick disease, type B
MedGen UID:
78651
Concept ID:
C0268243
Disease or Syndrome
The phenotype of acid sphingomyelinase deficiency (ASMD) occurs along a continuum. Individuals with the severe early-onset form, infantile neurovisceral ASMD, were historically diagnosed with Niemann-Pick disease type A (NPD-A). The later-onset, chronic visceral form of ASMD is also referred to as Niemann-Pick disease type B (NPD-B). A phenotype with intermediate severity is also known as chronic neurovisceral ASMD (NPD-A/B). The most common presenting symptom in NPD-A is hepatosplenomegaly, usually detectable by age three months; over time the liver and spleen become massive in size. Psychomotor development progresses no further than the 12-month level, after which neurologic deterioration is relentless. Failure to thrive typically becomes evident by the second year of life. A classic cherry-red spot of the macula of the retina, which may not be present in the first few months, is eventually present in all affected children. Interstitial lung disease caused by storage of sphingomyelin in pulmonary macrophages results in frequent respiratory infections and often respiratory failure. Most children succumb before the third year of life. NPD-B generally presents later than NPD-A, and the manifestations are less severe. NPD-B is characterized by progressive hepatosplenomegaly, gradual deterioration in liver and pulmonary function, osteopenia, and atherogenic lipid profile. No central nervous system (CNS) manifestations occur. Individuals with NPD-A/B have symptoms that are intermediate between NPD-A and NPD-B. The presentation in individuals with NPD-A/B varies greatly, although all are characterized by the presence of some CNS manifestations. Survival to adulthood can occur in individuals with NPD-B and NPD-A/B.
Familial pulmonary capillary hemangiomatosis
MedGen UID:
90956
Concept ID:
C0340848
Disease or Syndrome
Pulmonary venoocclusive disease-2 is an autosomal recessive subtype of primary pulmonary hypertension (PPH; see 178600). It is characterized histologically by widespread fibrous intimal proliferation of septal veins and preseptal venules, and is frequently associated with pulmonary capillary dilatation and proliferation. The disorder can cause occult alveolar hemorrhage. High-resolution CT imaging of the chest shows patchy centrilobular ground-glass opacities, septal lines, and lymph node enlargement (summary by Eyries et al., 2014). For a discussion of genetic heterogeneity of pulmonary venoocclusive disease, see PVOD1 (265450).
Autosomal recessive inherited pseudoxanthoma elasticum
MedGen UID:
698415
Concept ID:
C1275116
Disease or Syndrome
Pseudoxanthoma elasticum (PXE) is a systemic disorder that affects the elastic tissue of the skin, the eye, and vascular system. Individuals most commonly present with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage and/or characteristic papules in the skin. The most frequent cause of morbidity and disability in PXE is reduced vision due to complications of subretinal neovascularizations and macular atrophy. Other manifestations include premature gastrointestinal angina and/or bleeding, intermittent claudication of arm and leg muscles, stroke, renovascular hypertension, and cardiovascular complications (angina/myocardial infarction). Most affected individuals live a normal life span.
Surfactant metabolism dysfunction, pulmonary, 2
MedGen UID:
410078
Concept ID:
C1970470
Disease or Syndrome
Pulmonary surfactant metabolism dysfunction-2 (SMDP2) is a rare autosomal dominant disease associated with progressive respiratory insufficiency and lung disease with a variable clinical course. The pathophysiology of the disorder is postulated to involve intracellular accumulation of a structurally defective SPC protein (Thomas et al., 2002). For a general phenotypic description and a discussion of genetic heterogeneity of pulmonary surfactant metabolism dysfunction, see SMDP1 (265120).
Autoimmune pulmonary alveolar proteinosis
MedGen UID:
410079
Concept ID:
C1970472
Disease or Syndrome
Pulmonary alveolar proteinosis is a pathologic entity characterized by intraalveolar surfactant accumulation. There are 3 clinically distinct forms: hereditary (usually congenital), secondary, and acquired. The acquired form of pulmonary alveolar proteinosis is the most common form, accounting for approximately 90% of cases. The mean age at diagnosis is 39 years and it is associated with smoking in 72% of cases. The estimated incidence and prevalence are 0.36 and 3.70 cases per million, respectively (Trapnell et al., 2003; Seymour and Presneill, 2002). Secondary pulmonary alveolar proteinosis develops in association with conditions involving functional impairment or reduced numbers of alveolar macrophages. Such conditions include some hematologic cancers, pharmacologic immunosuppression, inhalation of inorganic dust or toxic fumes, and certain infections. Congenital pulmonary alveolar proteinosis is a rare, severe, often fatal disorder of newborns associated with pulmonary surfactant metabolism dysfunction caused by mutations in genes involved in surfactant metabolism (see, e.g., SMDP1, 265120) (Trapnell et al., 2003). See 300770 for information on congenital PAP due to CSF2RA (306250) deficiency.
Surfactant metabolism dysfunction, pulmonary, 4
MedGen UID:
393858
Concept ID:
C2677877
Disease or Syndrome
Pulmonary alveolar proteinosis (PAP) is a rare lung disorder in which surfactant-derived lipoproteins accumulate excessively within pulmonary alveoli, causing severe respiratory distress. Three forms of PAP have been described: hereditary (usually congenital), secondary, and acquired. Hereditary PAP is associated with mutations in the CSF2RA gene or in genes encoding surfactant proteins. Secondary PAP develops in conditions in which there are reduced numbers or functional impairment of alveolar macrophages and is associated with inhalation of inorganic dust (silica) or toxic fumes, hematologic malignancies, pharmacologic immunosuppression, infections, and impaired CSF2RB (138960) expression. Acquired PAP (610910), the most common form, usually occurs in adults and is caused by neutralizing autoantibodies to CSF2 (138960) (Martinez-Moczygemba et al., 2008). For a general phenotypic description and a discussion of genetic heterogeneity of congenital pulmonary surfactant metabolism dysfunction, see SMDP1 (265120).
Dyskeratosis congenita, autosomal dominant 3
MedGen UID:
462795
Concept ID:
C3151445
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 1
MedGen UID:
766531
Concept ID:
C3553617
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 3
MedGen UID:
901644
Concept ID:
C4225346
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 4
MedGen UID:
903928
Concept ID:
C4225347
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Autoimmune interstitial lung disease-arthritis syndrome
MedGen UID:
1800821
Concept ID:
C5243948
Disease or Syndrome
Systemic autoinflammation and autoimmunity with immune dysregulation (AIAISD) is an autosomal dominant systemic autoinflammatory disorder with autoimmunity and immune dysregulation. Affected individuals present in the first decade of life with variable features that may include interstitial lung disease, alveolar hemorrhage, inflammatory arthritis, neuromyelitis optica, livedo reticularis, dysautonomia, recurrent infections, and renal disease. Laboratory studies usually show high-titer autoantibodies and features of inflammation, including a type I interferon (e.g., 147660) signature and elevation of inflammatory cytokines. The disorder shows significant incomplete penetrance; most carrier parents are unaffected (summary by Watkin et al., 2015; Delafontaine et al., 2024).
Fanconi renotubular syndrome 5
MedGen UID:
1711127
Concept ID:
C5394473
Disease or Syndrome
Fanconi renotubular syndrome-5 (FRTS5) is a mitochondrial disorder characterized by proximal renotubular dysfunction from birth, followed by progressive kidney disease and pulmonary fibrosis. It occurs only in individuals of Acadian descent (Crocker et al., 1997 and Hartmannova et al., 2016). For a discussion of genetic heterogeneity of Fanconi renotubular syndrome, see FRTS1 (134600).
Interstitial lung disease 2
MedGen UID:
1794136
Concept ID:
C5561926
Disease or Syndrome
Interstitial lung disease (ILD) comprises a heterogeneous group of rare diseases affecting the distal part of the lung and characterized by a progressive remodeling of the alveolar interstitium. The manifestations form a spectrum ranging from idiopathic interstitial pneumonia (IIP) or pneumonitis to the more severe idiopathic pulmonary fibrosis (IPF). IPF is associated with an increased risk of developing lung cancer, which occurs in a subset of patients with ILD. Clinical features of ILD include dyspnea, clubbing of the fingers, and restrictive lung capacity. Imaging typically shows ground glass opacities and inter- and intraseptal thickening, while histologic studies usually show a pattern consistent with 'usual interstitial pneumonia' (UIP) (review by Gross and Hunninghake, 2001; summary by Legendre et al., 2020). Idiopathic pulmonary fibrosis is one of a family of idiopathic pneumonias sharing clinical features of shortness of breath, radiographically evident diffuse pulmonary infiltrates, and varying degrees in inflammation, fibrosis, or both on lung biopsy. In some cases, the disorder can be rapidly progressive and characterized by sequential acute lung injury with subsequent scarring and end-stage lung disease. Although older studies included several forms of interstitial pneumonia under the term 'idiopathic pulmonary fibrosis,' the clinical label of 'idiopathic pulmonary fibrosis' should be reserved for patients with a specific form of fibrosing interstitial pneumonia referred to as usual interstitial pneumonia (Gross and Hunninghake, 2001). It is estimated that 0.5 to 2.2% of cases of idiopathic pulmonary fibrosis are familial (Marshall et al., 2000). Gross and Hunninghake (2001) reviewed idiopathic pulmonary fibrosis, emphasizing definition, pathogenesis, diagnosis, natural history, and therapy. Antoniou et al. (2004) provided a 'top ten list' of references pertaining to etiopathogenesis, prognosis, diagnosis, therapy, and other aspects of idiopathic pulmonary fibrosis. For a discussion of genetic heterogeneity of ILD, see ILD1 (619611). Pulmonary fibrosis can also be a feature in patients with mutations in the TERT (187270) or the TERC (602322) gene; see PFBMFT1 (614742) and PFBMFT2 (614743). Some patients with surfactant protein C deficiency (610913) who survive to adulthood manifest features of pulmonary fibrosis.
Interstitial lung disease 1
MedGen UID:
1794231
Concept ID:
C5562021
Disease or Syndrome
Interstitial lung disease (ILD) comprises a heterogeneous group of rare diseases affecting the distal part of the lung and characterized by a progressive remodeling of the alveolar interstitium. The manifestations form a spectrum ranging from idiopathic interstitial pneumonia (IIP) or pneumonitis to the more severe idiopathic pulmonary fibrosis (IPF). IPF is associated with an increased risk of developing lung cancer, which occurs in a subset of patients with ILD. Clinical features of ILD include dyspnea, clubbing of the fingers, and restrictive lung capacity. Imaging typically shows ground glass opacities and inter- and intraseptal thickening, while histologic studies usually show a pattern consistent with 'usual interstitial pneumonia' (UIP) (summary by Nathan et al., 2016, Doubkova et al., 2019). Genetic Heterogeneity of Interstitial Lung Disease See also ILD2 (178500), caused by mutation in the SFTPA2 gene (178642) on chromosome 10q22.
Pulmonary fibrosis and/or bone marrow failure syndrome, telomere-related, 8
MedGen UID:
1841132
Concept ID:
C5830496
Disease or Syndrome
Telomere-related pulmonary fibrosis and/or bone marrow failure syndrome-8 (PFBMFT8) is an autosomal dominant disorder characterized by the onset of progressive pulmonary fibrosis in adulthood. Some affected individuals have signs of bone marrow failure, such as thrombocytopenia, or liver dysfunction, including hepatopulmonary syndrome. Other features of dyskeratosis congenita, including premature graying of the hair, may be observed. Telomeres are shortened compared to controls (Kelich et al., 2022). For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742).

Professional guidelines

PubMed

Severo CR, Chomiski C, Valle MBD, Escuissato DL, Paiva EDS, Storrer KM
J Bras Pneumol 2022;48(6):e20220145. Epub 2022 Dec 2 doi: 10.36416/1806-3756/e20220145. PMID: 36477171Free PMC Article

Recent clinical studies

Etiology

Loddé B, Giroux-Metges MA, Galinat H, Kerspern H, Pougnet R, Saliou P, Guerrero F, Lafère P
Int J Environ Res Public Health 2023 Aug 3;20(15) doi: 10.3390/ijerph20156516. PMID: 37569056Free PMC Article
Izadi S, Esmaili S, Emami S, Izadi S, Eskandari M, Yadollahzadeh M, Saleh M, Khavandegar A, Bakhtiyari M
Acta Cardiol 2023 Apr;78(2):250-255. Epub 2022 Sep 9 doi: 10.1080/00015385.2022.2066776. PMID: 36082926
Liang J, Cao H, Liu Y, Ye B, Sun Y, Ke Y, He Y, Xu B, Lin J
Arthritis Res Ther 2021 Jul 23;23(1):198. doi: 10.1186/s13075-021-02578-9. PMID: 34301306Free PMC Article
Shi S, Chen L, Qiu X, Zhao Q, Xiao Y, Yan X
Dis Markers 2019;2019:9709531. Epub 2019 Nov 11 doi: 10.1155/2019/9709531. PMID: 31827650Free PMC Article
Martinez FJ, Flaherty K
Proc Am Thorac Soc 2006 Jun;3(4):315-21. doi: 10.1513/pats.200602-022TK. PMID: 16738195Free PMC Article

Diagnosis

Azour L, Segal LN, Condos R, Moore WH, Landini N, Collazo D, Sterman DH, Young I, Ko J, Brosnahan S, Babb J, Chandarana H
Clin Imaging 2024 Nov;115:110307. Epub 2024 Oct 4 doi: 10.1016/j.clinimag.2024.110307. PMID: 39383681
He H, Tong X, Ning Z, Zhou J, Du C, Wang Y, Wang Q, Xu D, Zeng X, He ZX, Zhao X
RMD Open 2023 Dec 7;9(4) doi: 10.1136/rmdopen-2023-003391. PMID: 38088247Free PMC Article
Izadi S, Esmaili S, Emami S, Izadi S, Eskandari M, Yadollahzadeh M, Saleh M, Khavandegar A, Bakhtiyari M
Acta Cardiol 2023 Apr;78(2):250-255. Epub 2022 Sep 9 doi: 10.1080/00015385.2022.2066776. PMID: 36082926
Grosicka A, Manasar A, Kucharz EJ, Kotyla PJ
Best Pract Res Clin Rheumatol 2018 Aug;32(4):541-549. Epub 2019 Feb 14 doi: 10.1016/j.berh.2019.01.005. PMID: 31174823
Martinez FJ, Flaherty K
Proc Am Thorac Soc 2006 Jun;3(4):315-21. doi: 10.1513/pats.200602-022TK. PMID: 16738195Free PMC Article

Therapy

Loddé B, Giroux-Metges MA, Galinat H, Kerspern H, Pougnet R, Saliou P, Guerrero F, Lafère P
Int J Environ Res Public Health 2023 Aug 3;20(15) doi: 10.3390/ijerph20156516. PMID: 37569056Free PMC Article
Cheng H, Zou Y, Shah CD, Fan N, Bhagat TD, Gucalp R, Kim M, Verma A, Piperdi B, Spivack SD, Halmos B, Perez-Soler R
Lung Cancer 2021 Apr;154:99-104. Epub 2021 Feb 17 doi: 10.1016/j.lungcan.2021.02.015. PMID: 33636454Free PMC Article
Shi S, Chen L, Qiu X, Zhao Q, Xiao Y, Yan X
Dis Markers 2019;2019:9709531. Epub 2019 Nov 11 doi: 10.1155/2019/9709531. PMID: 31827650Free PMC Article
Foster GR, Zeuzem S, Pianko S, Sarin SK, Piratvisuth T, Shah S, Andreone P, Sood A, Chuang WL, Lee CM, George J, Gould M, Flisiak R, Jacobson IM, Komolmit P, Thongsawat S, Tanwandee T, Rasenack J, Sola R, Messina I, Yin Y, Cammarata S, Feutren G, Brown KK
J Viral Hepat 2013 Apr;20(4):e115-23. Epub 2013 Feb 14 doi: 10.1111/jvh.12020. PMID: 23490379
Erckens RJ, Mostard RL, Wijnen PA, Schouten JS, Drent M
Graefes Arch Clin Exp Ophthalmol 2012 May;250(5):713-20. Epub 2011 Nov 27 doi: 10.1007/s00417-011-1844-0. PMID: 22119879Free PMC Article

Prognosis

de Roos MP, Heijnen RM, Dijkstra NG, Brinkman K, Jonkman NH, Bresser P
Chron Respir Dis 2024 Jan-Dec;21:14799731231222284. doi: 10.1177/14799731231222284. PMID: 38333995Free PMC Article
Izadi S, Esmaili S, Emami S, Izadi S, Eskandari M, Yadollahzadeh M, Saleh M, Khavandegar A, Bakhtiyari M
Acta Cardiol 2023 Apr;78(2):250-255. Epub 2022 Sep 9 doi: 10.1080/00015385.2022.2066776. PMID: 36082926
Liang J, Cao H, Liu Y, Ye B, Sun Y, Ke Y, He Y, Xu B, Lin J
Arthritis Res Ther 2021 Jul 23;23(1):198. doi: 10.1186/s13075-021-02578-9. PMID: 34301306Free PMC Article
Shi S, Chen L, Qiu X, Zhao Q, Xiao Y, Yan X
Dis Markers 2019;2019:9709531. Epub 2019 Nov 11 doi: 10.1155/2019/9709531. PMID: 31827650Free PMC Article
Martinez FJ, Flaherty K
Proc Am Thorac Soc 2006 Jun;3(4):315-21. doi: 10.1513/pats.200602-022TK. PMID: 16738195Free PMC Article

Clinical prediction guides

Izadi S, Esmaili S, Emami S, Izadi S, Eskandari M, Yadollahzadeh M, Saleh M, Khavandegar A, Bakhtiyari M
Acta Cardiol 2023 Apr;78(2):250-255. Epub 2022 Sep 9 doi: 10.1080/00015385.2022.2066776. PMID: 36082926
Gülhan PY, Arbak PM, Annakkaya AN, Balbay EG, Balbay ÖA
Am J Infect Control 2022 Oct;50(10):1125-1132. Epub 2022 Jul 20 doi: 10.1016/j.ajic.2022.07.003. PMID: 35870662Free PMC Article
Shi S, Chen L, Qiu X, Zhao Q, Xiao Y, Yan X
Dis Markers 2019;2019:9709531. Epub 2019 Nov 11 doi: 10.1155/2019/9709531. PMID: 31827650Free PMC Article
Grosicka A, Manasar A, Kucharz EJ, Kotyla PJ
Best Pract Res Clin Rheumatol 2018 Aug;32(4):541-549. Epub 2019 Feb 14 doi: 10.1016/j.berh.2019.01.005. PMID: 31174823
Martinez FJ, Flaherty K
Proc Am Thorac Soc 2006 Jun;3(4):315-21. doi: 10.1513/pats.200602-022TK. PMID: 16738195Free PMC Article

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