Difference between revisions of "Medical lung diseases"

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Notes:
Notes:
*''Leyden'' in ''Charcot-Leyden'' is also seen written as ''Leiden''.
*''Leyden'' in ''Charcot-Leyden'' is also seen written as ''Leiden''.
**Finding associated with hypereosinophilia<ref name=pmid6162378>{{Cite journal  | last1 = Dincsoy | first1 = HP. | last2 = Burton | first2 = TJ. | last3 = van der Bel-Kahn | first3 = JM. | title = Circulating Charcot-Leyden crystals in the hypereosinophilic syndrome. | journal = Am J Clin Pathol | volume = 75 | issue = 2 | pages = 236-43 | month = Feb | year = 1981 | doi =  | PMID = 6162378 }}</ref> - ''not'' pathognomonic for asthma.
*[[Pulmonary cytopathology]]:  
*[[Pulmonary cytopathology]]:  
**''Curschmann's spirals'' =  spiral-shaped mucous plugs.<ref name=pmid9812228>{{cite journal |author=Cenci M, Giovagnoli MR, Alderisio M, Vecchione A |title=Curschmann's spirals in sputum of subjects exposed daily to urban environmental pollution |journal=Diagn. Cytopathol. |volume=19 |issue=5 |pages=349–51 |year=1998 |month=November |pmid=9812228 |doi= |url=}}</ref>
**''Curschmann's spirals'' =  spiral-shaped mucous plugs.<ref name=pmid9812228>{{cite journal |author=Cenci M, Giovagnoli MR, Alderisio M, Vecchione A |title=Curschmann's spirals in sputum of subjects exposed daily to urban environmental pollution |journal=Diagn. Cytopathol. |volume=19 |issue=5 |pages=349–51 |year=1998 |month=November |pmid=9812228 |doi= |url=}}</ref>

Revision as of 13:24, 1 April 2013

The medical lung diseases are a huge topic. Most pathologists have little to do with 'em. They are the domain of respirology. An introduction to lung pathology is in the lung article, along with a general approach. Interstitial lung disease is dealt with in the diffuse lung diseases article.

Infectious pneumonia

Main article: Pneumonia

Includes:

Asthma

Cytopathology: Asthma in pulmonary cytopathology

General

  • The bread and butter of respirology.
  • May be associated with atopy (allergies), medications (e.g. NSAIDs), occupational exposures.[1]

Pathogenesis

  • T-cell response TH2 dominant.

Sequence:[2]

  • Antigen TH2 lymphocyte -> IgE B-cell -> mast cell IgE Fc -> leukotrienes + other mediators -> bronchospasm, edema, leukocyte recruitment -> airway remodeling.

Gross

  • Lung over-inflation.
  • Mucous plugs.
  • Focal resorption atelectasis,[3] i.e. collapse.

Microscopic

Features:[4]

  • Edema.
  • Mucous (plugs).
  • +/-Smooth muscle hypertrophy.
  • +/-Inflammation - especially with eosinophils.
  • +/-Charcot-Leyden crystals (formed from eosinophil granules -- breakdown product).
    • Sharp edge, diamond shaped, intense pink.

Images:

Notes:

  • Leyden in Charcot-Leyden is also seen written as Leiden.
    • Finding associated with hypereosinophilia[5] - not pathognomonic for asthma.
  • Pulmonary cytopathology:
    • Curschmann's spirals = spiral-shaped mucous plugs.[6]
    • Creola bodies = clusters of (ciliated) bronchial epithelial cells.[7]

Emphysema

Chronic obstructive pulmonary disease, abbreviated COPD, redirects here.

General

  • Usually due to smoking.
  • Often lumped together with chronic bronchitis and called chronic obstructive pulmonary disease (COPD).[8]

Causes of emphysema other than smoking:[9]

Pathologic classification

Based on morphology:[10]

  1. Centriacinar (centrilobular) emphysema - associated with heavy smoking.
  2. Panacinar (panlobular) emphysema - associated with alpha-1 antitrypsin deficiency.
  3. Distal (paraseptal) acinar emphysema - associated with spontaneous pneumothorax.
  4. Irregular emphysema - usu. insignificant.
  • Q. Why does smoking lead to centriacinar emphysema?
  • A. The bad stuff from smoking gets enters the acinus at the centre; ergo, this is the location of the most damage.

Gross

  • Holes (blebs, bullae), usually upper lung field predominant.
  • Lungs may overlap the heart.[11]

Notes:

Microscopic

Features:[11]

  • Large alveoli.
  • Thin septa (no interstitial thickening).

Image:

Chronic bronchitis

General

  • Often seen together with emphysema with which it is lumped together with in the term COPD.
  • It's a clinical diagnosis - criteria:[1]
    • Cough with sputum for thee months in at least two consecutive years.
    • No other cause identified.

Clinical:[1]

Microscopic

Features:[1]

  • Mucous gland hypertrophy + mucinous secretions in airway.
  • Goblet cell metaplasia.
  • Bronchiolar inflammation and fibrosis.

Pulmonary edema

General

  • Seen in a number of conditions, e.g. congestive heart failure.

Gross

Features - autopsy:

  • Bubbles - when squeezed (due to surfactant).
  • Heavy.

Microscopic

Features:[14]

  • Dilated capillaries.
  • Blood in airspace, focal.
  • Plasma proteins in airspace - light pink acellular junk.
  • +/-Hemosiderin-laden macrophages (known as heart failure cells in this context).

DDx:

Images:

Bronchiectasis

General

Gross

  • Large airways at the periphery of the lung.
  • Central airways larger than the adjacent arteries.
  • Typically focal.

Images:

Radiologic:

  • Central airways larger than the adjacent arteries.
  • Airway wall-thickening.[17]
  • "Tree-in-bud" abnormalities.

Microscopic

Features:

  • Dilated airways.
    • Airways larger than arteries.

Image:

Pulmonary hemorrhage

General

  • Many causes.

A few causes:

Pulmonary hemorrhage syndromes:[18]

Radiology

  • Airspace opacity.

Microscopic

Features:

DDx:

  • Decomposition.

Constrictive bronchiolitis

  • AKA bronchiolitis obliterans, AKA obliterative broncholitis,[19] AKA bronchiolitis obliterans syndrome (BOS).[20]

General

  • Not the same as (idiopathic) bronchiolitis obliterans organizing pneumonia (BOOP) - in short:
    • BOOP: clogs the airway, has Masson bodies, treated with steroids - good prognosis.
    • Constrictive bronchiolitis: fibrosis around airways, crappy prognosis.
  • No good treatment.
  • Progressive.

Etiology/associations:[19]

Microscopic

Features:[19]

  1. Bronchiolitis - mononuclear and neutrophilic.
    • May be minimal late in the disease.
  2. Fibrosis - submucosal and peribronchiolar.
    • Can be patchy.

Notes:

  • Bronchioles = noncartilagenous airways usu. < 2 mm in diameter.[19]

Images:

Stains

  • Elastic trichrome - useful for delineation of obliterated bronchioles.

Diffuse lung diseases

Main article: Diffuse lung diseases

These are also known as idiopathic interstitial pneumonias.

Fibrosis

Histomorphological classification

  1. Hyaline membranes - glassy pink material lining airways & alveoli.
  2. Microscopic honeycombing - "holes" in the lung.
  3. Bronchiolization - ciliated (respiratory) epithelium in distal airway.
  4. Uniform alveolar septal thickening - septae look similar at low power.
  5. Peripheral lobular fibrosis - septae thickening peripheral, HRCT shows: irregular peripheral reticular opacities.[22]
    • Reticular = net-like.[23]
  6. Siderophages in alveoli - macrophages with hemosiderin the alveoli.
  7. Fibrinous pleuritis - peripheral only (based on imaging).
  8. Granulomata, non-necrotizing.
  9. Abundance of vacuolated cells.
  10. Chronic inflammation.
  11. Bronchiolocentric scarring - fibrosis concentrated around airway/assoc. with airway.

Radiologic/gross pathologic DDx by location

Causes of lower lung fibrosis BAD RASH:[24]

Note:

Causes of upper lung fibrosis FASSTEN:[24]

Prognosis

  • The pattern and severity of fibrosis seems to be the most important factors prognostically - more important than the underlying cause (ILD, CVD, drug reaction etc.).[26][27]

Patterns of fibrosis:

  • "Linear" - follows alveolar walls, no architectural distortion.
  • UIP-like (honeycombing).

Disease with fibrosis

There are many of 'em.

Fibrosing pleuritis

General

  • Benign.

Microscopic

Features:[28]

  • Fibrosis.
    • Spindle cells.
    • Moderate cellularity.
  • No necrosis.

DDx:[29]

  • Mesothelioma, desmoplastic.
    • Mesothelioma should not be diagnosed on core biopsy.[28]

Lymphocytic lesions of the lung

Diagnosis Key histologic feature Radiology Other diagnostic
Lymphocytic interstitial pneumonia interstitial lymphoid cells, usu. no nodules interstitial pattern
Follicular bronchiolitis/bronchitis lymphoid cell around bronchioles / bronchus, normal parenchyma interstitial pattern
Nodular lymphoid hyperplasia abundant lymphoid cells in nodules nodules /interstitial pattern stains to exclude lymphoma; germinal centres do not exclude lymphoma
Lymphoma (BALToma) abundant lymphoid cells usu. in nodules nodules / interstitial pattern may require stains to prove, germinal centres may be present

Lymphocytic interstitial pneumonia

Main article: Lymphocytic interstitial pneumonia

Follicular bronchitis/bronchiolitis

General

Gross/radiology

  • No distinct nodule or mass.
  • Classically: increased reticular marking, i.e. interstitial pattern.

Images: Intersitial pattern - radiographs (ucsf.edu).

Microscopic

Features:[33]

  • Peribronchiolar/peribronchial lymphoid nodules with:
    • Reactive germinal centres.
      • Lack of these should raise suspicion for lymphoma.
    • Plasma cells.
  • +/-Lymphoid nodules in the interlobular septa.

Notes:

  • Lung parenchyma distant from nodule = normal; no lymphocytic infiltrate.

DDx:

Pulmonary nodular lymphoid hyperplasia

  • AKA pseudolymphoma - a term some dislike.[33]

General

  • Definition - reactive lymphoid cells.

Gross/radiology

  • Has nodules radiographically.

Microscopic

Features:[33]

  • Reactive lymphoid nodules.

Notes:[34]

  • Presence of germinal centres do not exclude lymphoma - may still be a BALToma.
    • BALT = bronchial/bronchus associated lymphoid tissue.

DDx:

Smoking associated disease

Main article: Smoking
  • RB = respiratory bronchiolitis.
  • RBILD = respiratory bronchiolitis interstitial lung disease.
  • DIP = desquamative interstitial pneumonia.
  • Eosinophilic granuloma (of lung) - AKA pulmonary langerhans cell histiocytosis.

All of the above are assoc. with smoking. RBILD & DIP are considered by many to be on a continuum, i.e. RBILD is early DIP.

Respiratory bronchiolitis

  • Diagnosis is based on clinical criteria.

Microscopic

Features:

  • Inflammation.
  • No interstitial lung disease, i.e. no fibrosis.

Respiratory bronchiolitis interstitial lung disease

Main article: Respiratory bronchiolitis interstitial lung disease

Desquamative interstitial pneumonia

Main article: Desquamative interstitial pneumonia

Pulmonary Langerhans cell histiocytosis

  • AKA eosinophilic granuloma of the lung.

General

Subtypes:[35]

  • Cellular form.
  • Fibrotic form.

One form usually predominates.

Radiology

  • Upper lung zones.

Microscopic

Features:[36]

  • Cellular peribronchiolar nodules with:
    • Langerhans cells - key feature:
      • Pale staining nucleus (H&E) with nuclear infolding - "crumpled tissue paper" appearance.
    • +/-Smoker's macrophages (brown pigmented airspace macrophages).
    • +/-Eosinophilia (may be rare) - significantly narrow DDx.
    • Chronic inflammatory cells (lymphocytes). (???)

Images:

IHC

  • Langerhans cells: S100+ and CD1a+.[36]

Granulomatous lung disease

See: Granulomas for an introduction to the general topic.

Most common:

  • Infectious - mycobacterial and fungal.[37]

Noninfectious causes:[37]

  • Aspiration pneumonia.
  • Hypersensitivity pneumonitis.
  • Hot tub lung.
  • Talc granulomatosis.
  • Sarcoidosis.
  • Wegener granulomatosis.

Sarcoidosis

Main article: Sarcoidosis

General

  • Diagnosis of exclusion - infection must be excluded.
  • Radiologic differential diagnosis includes carcinomatosis.[38]

Microscopic

Features:

  • Granulomata, well-formed, non-necrotizing.
    • Negative for microorganisms with special stains (PAS-D, GMS, AFB).
    • Granulomata - interstitial location.

Image(s):

Pulmonary talcosis

General

Microscopic

Features:

  • Granulomas with foreign material.
    • Foreign material often polarizes.

Images:

Miscellaneous diseases

Pneumoconioses

Main article: Pneumoconioses

Pneumocytoma

  • AKA benign sclerosing pneumocytoma.[41]
  • Previously known as sclerosing hemangioma.

General

  • Derived from type 2 pneumocyte.[42]
  • Progesterone-receptor positive stromal cells.[43]

Epidemiology

  • Female in 40s.[44]
  • Considered benign; excision is curative.

Gross

  • Peripheral, solitary.
  • Well-circumscribed.

Microscopic

Features:[44]

  • Mixed cell population.
  • Variable architecture:
    • Papillary.
    • Sclerotic.
    • Solid.
    • Hemorrhagic.
  • +/-Granulomas.

DDx:[45]

Image:

IHC

Features:[47]

  • EMA +ve.
  • PR +ve.[43]

Negative stains:[47]

  • SMA -ve.
  • CEA -ve.
  • CD34 -ve.
  • S100 -ve.
  • Chromogranin A -ve.

Others:[42]

  • TTF-1 +ve.
  • HNF-3 alpha +ve.
  • HNF-3 beta +ve.

Lymphangioleiomyomatosis

  • Abbreviated LAM.
  • AKA lymphangiomyomatosis.

General

  • Clinical: dyspnea, recurrent pneumothorax.
  • May be an indication for lung transplantation.
  • Non-neoplastic muscle proliferation vs. tumour that can metastasize.[48]

Notes:

Epidemiology

Radiology

  • Bullae/thin walled cysts - distributed in all lung fields.
  • Lymphadenopathy.

Radiologic DDx (of cysts):

  • Eosinophilic granuloma (assoc. with smoking).
  • Interstitial pulmonary fibrosis (UIP).
  • Emphysema.

Microscopic

Features:[51]

  • Spindle cells with small nuclei + larger epithelioid cells with clear cytoplasm and round nuclei.
  • Cyst formation.
  • Thick arterial walls.

Images:

IHC

  • HMB-45 +ve.
  • ER +ve.
  • PR +ve.
  • SMA +ve.

Pulmonary alveolar proteinosis

  • Abbreviated PAP.

General

  • Associated with smoking - particularily in men.[52]

Pathophysiology:

  • GM-CSF (granulocyte-macrophage colony stimulating factor) signaling in macrophages/lack of GM-CSF.
    • GM-CSF is required by alveolar macrophages to clear surfactant.

Classification:[52]

  1. Congenital:
      • Abnormal surfactant.
      • GM-CSF receptor defect.
  2. Secondary:
    • Infections.
    • Haematologic malignancy.
  3. Acquired:
    • Dusts - interfere with macrophage function.

Clinical:

  • Dyspnea & cough - gradual onset.

Radiology

Microscopic

Features:

  • Crap in the alveoli:
  • "Dense bodies" - dead macrophages ("Chatter" in the alveoli).
    • Edema - has pink stuff in the alveoli like PAP but no dense bodies.

DDx - may mimic:[53]

Images:

Images of DDx:

Diffuse panbronchiolitis

  • Abbreviated DPB.

General

  • Rare lung disease predominantly found among asians.[55]
  • Has been likened to cystic fibrosis - but doesn't really share any features with it.

Gross

Features:[55]

  • Bronchiectasis.
  • Hyperinflation.
  • Small nodules (~2-3 mm) around the small airways.
  • Diffuse involvement of both lungs.

Microscopic

Features:[55]

  • Transmural inflammation of bronchioles - esp. respiratory bronchioles.
    • Lymphocytes, plasma cells, histiocytes.
  • Neutrophils within the airway.

Images:

Pulmonary amyloidosis

Main article: Amyloidosis

General

Microscopic

Features:

  • Interstitial cotton candy-like material - see amyloidosis.

DDx:

Images:

Drug reactions

  • Effects are often non-specific.

Website: http://www.pneumotox.com

Pulmonary hypertension

Main article: Pulmonary hypertension

General classification:

  • Primary, i.e. primary pulmonary hypertension, or
  • Secondary, e.g. due to congenital heart disease (like ventricular septal defect), interstitial pulmonary fibrosis.

Non-secondary pulmonary hypertension

Main article: Pulmonary hypertension

Causes:[57]

Severity

Eosinophilic pneumonia

Specific entities:[58]

  • Churg-Strauss syndrome.
  • Acute eosinophilic pneumonia.
  • Chronic eosinophilic pneumonia.
  • Eosinophilic granuloma (pulmonary histiocytosis X, Langerhans cell granulomatosis).

Entities which may have eosinophilia as prominent feature:

Churg-Strauss syndrome

Main article: Churg-Strauss syndrome

Microscopic

Features:

Eosinophilic pleural effusions

  • Definition: 10%+ eosinophils.[59]
  • Uncommon 5-16% of effusions.[60]

Causes - mnemonic I'M PAID:[60]

  • Infection, e.g. tuberculosis.
  • Malignancy - uncommon.
  • Pulmonary emboli.
  • Asbestos exposure.
  • Inflammatory diseases.
  • Drug reactions.

Lung transplant pathology

Main article: Lung transplant pathology

This subspecialty is dealt with in its own article.

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 370. ISBN 978-1416054542.
  2. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 370-2. ISBN 978-1416054542.
  3. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 363. ISBN 978-1416054542.
  4. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 108. ISBN 978-1416002741.
  5. ↑ Dincsoy, HP.; Burton, TJ.; van der Bel-Kahn, JM. (Feb 1981). "Circulating Charcot-Leyden crystals in the hypereosinophilic syndrome.". Am J Clin Pathol 75 (2): 236-43. PMID 6162378.
  6. ↑ Cenci M, Giovagnoli MR, Alderisio M, Vecchione A (November 1998). "Curschmann's spirals in sputum of subjects exposed daily to urban environmental pollution". Diagn. Cytopathol. 19 (5): 349–51. PMID 9812228.
  7. ↑ Isohima, K.; Takahashi, K.; Soda, R.; Hukasaka, N.; Tanabe, K.; Ozaki, K.; Nakato, H.; Araki, M. et al. (Jul 1989). "[The clinical significance of Creola body in the sputum of asthmatic patients].". Arerugi 38 (7): 542-8. PMID 2818212.
  8. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 368. ISBN 978-1416054542.
  9. ↑ Lee, P.; Gildea, TR.; Stoller, JK. (Dec 2002). "Emphysema in nonsmokers: alpha 1-antitrypsin deficiency and other causes.". Cleve Clin J Med 69 (12): 928-9, 933, 936 passim. PMID 12546267.
  10. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 368. ISBN 978-1416054542.
  11. ↑ 11.0 11.1 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 369. ISBN 978-1416054542.
  12. ↑ URL: http://dictionary.reference.com/browse/bleb. Accessed on: 3 August 2011.
  13. ↑ URL: http://dictionary.reference.com/browse/bulla. Accessed on: 3 August 2011.
  14. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 102. ISBN 978-1416002741.
  15. ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 693. ISBN 978-1416031215.
  16. ↑ URL: http://library.med.utah.edu/WebPath/LUNGHTML/LUNG053.html. Accessed on: 21 February 2012.
  17. ↑ Stockley, RA. (Jun 1998). "Commentary: bronchiectasis and inflammatory bowel disease.". Thorax 53 (6): 526-7. PMID 9713456.
  18. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 745. ISBN 0-7216-0187-1.
  19. ↑ 19.0 19.1 19.2 19.3 Visscher, DW.; Myers, JL. (2006). "Bronchiolitis: the pathologist's perspective.". Proc Am Thorac Soc 3 (1): 41-7. doi:10.1513/pats.200512-124JH. PMID 16493150. http://pats.atsjournals.org/cgi/content/full/3/1/41.
  20. ↑ Sato, M.; Keshavjee, S. (2008). "Bronchiolitis obliterans syndrome: alloimmune-dependent and -independent injury with aberrant tissue remodeling.". Semin Thorac Cardiovasc Surg 20 (2): 173-82. doi:10.1053/j.semtcvs.2008.05.002. PMID 18707652.
  21. ↑ 21.0 21.1 Chien, JW.; Duncan, S.; Williams, KM.; Pavletic, SZ. (Jan 2010). "Bronchiolitis obliterans syndrome after allogeneic hematopoietic stem cell transplantation-an increasingly recognized manifestation of chronic graft-versus-host disease.". Biol Blood Marrow Transplant 16 (1 Suppl): S106-14. doi:10.1016/j.bbmt.2009.11.002. PMID 19896545.
  22. ↑ http://www.rsna.org/Publications/rsnanews/may06/jrnl_may06.cfm
  23. ↑ http://dictionary.reference.com/browse/reticular
  24. ↑ 24.0 24.1 Yeung, J.C.; Leonard, Blair J. N. (2005). The Toronto Notes 2005 - Review for the MCCQE and Comprehensive Medical Reference (2005 ed.). The Toronto Notes Inc. for Medical Students Inc.. pp. R13. ISBN 978-0968592854.
  25. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 90. ISBN 978-0781765275.
  26. ↑ Bjoraker JA, Ryu JH, Edwin MK, et al. (January 1998). "Prognostic significance of histopathologic subsets in idiopathic pulmonary fibrosis". Am. J. Respir. Crit. Care Med. 157 (1): 199-203. PMID 9445300. http://ajrccm.atsjournals.org/cgi/content/full/157/1/199.
  27. ↑ AC UBC S.425.
  28. ↑ 28.0 28.1 URL: http://www.ultrapath.org/oldsite/uscap/uscap05/meso1.html. Accessed on: 20 February 2012.
  29. ↑ Corson, JM. (Nov 2004). "Pathology of mesothelioma.". Thorac Surg Clin 14 (4): 447-60. doi:10.1016/j.thorsurg.2004.06.007. PMID 15559051.
  30. ↑ Nicholson AG (August 2001). "Lymphocytic interstitial pneumonia and other lymphoproliferative disorders in the lung". Semin Respir Crit Care Med 22 (4): 409–22. doi:10.1055/s-2001-17384. PMID 16088689.
  31. ↑ Aerni MR, Vassallo R, Myers JL, Lindell RM, Ryu JH (February 2008). "Follicular bronchiolitis in surgical lung biopsies: clinical implications in 12 patients". Respir Med 102 (2): 307–12. doi:10.1016/j.rmed.2007.07.032. PMID 17997299.
  32. ↑ Kinane BT, Mansell AL, Zwerdling RG, Lapey A, Shannon DC (October 1993). "Follicular bronchitis in the pediatric population". Chest 104 (4): 1183–6. PMID 8404188.
  33. ↑ 33.0 33.1 33.2 AFIP atlas of nontumour pathology. 2002. Vo. 2. P.277. ISBN 1-881041-79-4.
  34. ↑ AFIP atlas of nontumour pathology. 2002. Vo. 2. P.281. ISBN 1-881041-79-4.
  35. ↑ 35.0 35.1 Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 234. ISBN 978-0443066313.
  36. ↑ 36.0 36.1 Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 237. ISBN 978-0443066313.
  37. ↑ 37.0 37.1 Mukhopadhyay S, Gal AA (May 2010). "Granulomatous lung disease: an approach to the differential diagnosis". Arch. Pathol. Lab. Med. 134 (5): 667–90. PMID 20441499.
  38. ↑ URL: http://www.radiologyassistant.nl/en/46b480a6e4bdc. Accessed on: 23 May 2010.
  39. ↑ Davis, LL. (Dec 1983). "Pulmonary "mainline" granulomatosis: talcosis secondary to intravenous heroin abuse with characteristic x-ray findings of asbestosis.". J Natl Med Assoc 75 (12): 1225–8. PMC 2561715. PMID 6655726. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561715/.
  40. ↑ Marchiori, E.; Lourenço, S.; Gasparetto, TD.; Zanetti, G.; Mano, CM.; Nobre, LF. (Apr 2010). "Pulmonary talcosis: imaging findings.". Lung 188 (2): 165-71. doi:10.1007/s00408-010-9230-y. PMID 20155272.
  41. ↑ Chan, KW.; Gibbs, AR.; Lo, WS.; Newman, GR. (Jun 1982). "Benign sclerosing pneumocytoma of lung (sclerosing haemangioma).". Thorax 37 (6): 404-12. PMID 6291188.
  42. ↑ 42.0 42.1 Yamazaki, K. (Jul 2004). "Type-II pneumocyte differentiation in pulmonary sclerosing hemangioma: ultrastructural differentiation and immunohistochemical distribution of lineage-specific transcription factors (TTF-1, HNF-3 alpha, and HNF-3 beta) and surfactant proteins.". Virchows Arch 445 (1): 45-53. doi:10.1007/s00428-004-1023-3. PMID 15138814.
  43. ↑ 43.0 43.1 Einsfelder, BM.; Müller, KM. (Sep 2005). "["Pneumocytoma" or "sclerosing hemangioma": histogenetic aspects of a rare tumor of the lung]". Pathologe 26 (5): 367-77. doi:10.1007/s00292-005-0751-8. PMID 15731902. Cite error: Invalid <ref> tag; name "pmid15731902" defined multiple times with different content
  44. ↑ 44.0 44.1 Keylock, JB.; Galvin, JR.; Franks, TJ. (May 2009). "Sclerosing hemangioma of the lung.". Arch Pathol Lab Med 133 (5): 820-5. PMID 19415961.
  45. ↑ URL: http://www.med.muni.cz/biomedjournal/pdf/2004/01/37_42.pdf. Accessed on: 17 June 2010.
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