Hypersensitivity pneumonitis classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

Overview

The clinical presentations of hypersensitivity pneumonitis depend on the frequency, length, exposure, and duration of illness. Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes. Hypersensitivity pneumonitis may be classified into several subtypes based on various classifications methods such as classical classification, boyd classification, cormier classification, and selman classification.

Classification

  • The clinical presentations of hypersensitivity pneumonitis depend on:
    • Frequency
    • Length
    • Exposure
    • Duration of illness
  • Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes.
  • Hypersensitivity pneumonitis may be classified into several subtypes based on:
    • Classical classification:
      • Acute
        • Abrupt in onset.
        • Occurs after heavy exposure to antigen.
        • Symptoms can be confused with bacterial or viral infection.
        • On auscultation diffuse crackles and tachypnea are notable.
        • Histopathology reveals non-caseating interstitial granulomas with giant cells. 
      • Subacute
        • Gradual in onset.
        • Symptom like cough, fatigue, weightloss, and dyspnea may be seen.
        • Removal of exposure leads to complete resolution.
        • On auscultation diffuse crackles and tachypnea may be seen.
        • Histopathology reveals more well formed non-caseating interstitial granulomas and interstitial fibrosis.
      • Chronic
        • Insidious in onset with history of acute episodes.
        • Digital clubbing may be seen. [1]
        • Pulmonary fibrosis leads to disabling and irreversible respiratory symptoms.[2]
    • Boyd classification:[3]
      • Acute progressive
        • Severe symptoms occur after exposure to antigen.
        • Recurrent exposure leads to symptom progression.
        • Clinically patients are pyrexial with bilateral crackles on chest auscultation.
        • Patients may require hospitalization due to respiratory compromise.
      • Acute intermittent nonprogressive
        • Similar to acute progressive disease but less intense.
        • Patients feel well in between episodes.
        • Subsequent exposure leads to less severe symptoms.
        • Patients are clinically stable in the long run.
        • Pulmonary inflammatory response deteriorates with recurrent exposure to the antigen.[4]
      • Chronic progressive disease
        • Occurs after recurrent acute episodes or insidiously.[5]
        • Patients are diagnosed in the late stages.
        • Only clue for diagnosis is antigen exposure.
        • Patients often present with permanent disability in the form of pulmonary fibrosis or respiratory failure.
        • Disease is not reversed even after antigen exposure is avoided. [6]
      • Subclinical disease
        • Patients are immunological sensitized but are asymptomatic.
        • Patients with recurrent exposure to antigens may convert to chronic form.
    • Cormier classification:
      • Active
      • Residual
    • Selman classification:
      • Active non-progressive and intermittent
      • Acute progressive and intermittent
      • Chronic
        • Nonprogressive
        • Progressive

References

  1. Sansores R, Salas J, Chapela R, Barquin N, Selman M (1990). "Clubbing in hypersensitivity pneumonitis. Its prevalence and possible prognostic role". Arch. Intern. Med. 150 (9): 1849–51. PMID 2393316.
  2. Vourlekis JS, Schwarz MI, Cherniack RM, Curran-Everett D, Cool CD, Tuder RM, King TE, Brown KK (2004). "The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis". Am. J. Med. 116 (10): 662–8. doi:10.1016/j.amjmed.2003.12.030. PMID 15121492.
  3. Walls AF, Bennett AR, Godfrey RC, Holgate ST, Church MK (1991). "Mast cell tryptase and histamine concentrations in bronchoalveolar lavage fluid from patients with interstitial lung disease". Clin. Sci. 81 (2): 183–8. PMID 1653661.
  4. Bourke SJ, Banham SW, Carter R, Lynch P, Boyd G (1989). "Longitudinal course of extrinsic allergic alveolitis in pigeon breeders". Thorax. 44 (5): 415–8. PMC 461848. PMID 2763241.
  5. Fink JN, Sosman AJ, Barboriak JJ, Schlueter DP, Holmes RA, Ohtani Y, Saiki S, Sumi Y, Inase N, Miyake S, Costabel U, Yoshizawa Y (1968). "Pigeon breeders' disease. A clinical study of a hypersensitivity pneumonitis". Ann. Intern. Med. 68 (6): 1205–19. doi:10.1016/S1081-1206(10)61863-7. PMID 4231667.
  6. Fink JN, Sosman AJ, Barboriak JJ, Schlueter DP, Holmes RA (1968). "Pigeon breeders' disease. A clinical study of a hypersensitivity pneumonitis". Ann. Intern. Med. 68 (6): 1205–19. PMID 4231667.