HYPERSENSITIVITY PNEUMONITIS Clinical features Diagnosis and Treatment of Hypersensitivity

HYPERSENSITIVITY PNEUMONITIS (HP)

• It is also called extrinsic allergic alveolitisis an inflammatory disease of alveolar walls, and terminal airways caused by repeated exposure to organic agents in a susceptible person.
• It’s also called farmer’s lung, commonly due to the HP caused by moldy hay.
• Usually the organisms responsible for the hypersen­sitivity reactions are Actinomyces, Micropolyspora faeni and Aspergillus.

HYPERSENSITIVITY PNEUMONITIS History —

• Acute form: Develops 2–9 hours following exposure
• Cough, dyspnea, fever, chills, diaphoresis, headache, nausea
• Symptoms last hours to days

Chronic form: Develops after several months of exposure:

• Progressively worsening cough and dyspnea
• Also develop fatigue, weight loss, anorexia

Subacute form: Develops after several days to weeks:

• Marked by worsening respiratory symptoms

Other important points in history include:

• History of pulmonary disease or recurrent infections
• Recent change in work or home
• Known exposure to pets, hot tubs, areas with water damage
• Symptomatic improvement when away from work or home

Etiology of Hypersensitivity

• · Different names are given to the different dis­eases depending on the occupation of host, the antigen’ exposed to, and the habit of the person.
• E.g. Farme(s lung due to moldy hay.
• · Chemical wo kers lung
• · Mushroom worker’s disease
• Bagassosis in sugarcane workers
• Wood workers’ lung.
• Humidity, temperature, concentration of antigen, du­ration of exposure and habits like smoking all increase the incidence of HP.

Clinical features of Hypersensitivity

• There is Lnterstitial pneumonitis.
• · Presentation may be acute, subacute or chronic.
• · Symptoms are cough, fever, dyspnoea, chills, malaise, from 6-8 hrs after exposure, to months from onset. Symptoms may persist for years.
• · In chronic form, there is pulmonary fibrosis, cy­anosis, clubbing, pulmonary hypertension, res­piratory failure and death.
• · On physical examination, there are bilateral basal crackles, reduced carbon monoxide diffusion capacity, and hypoxemia.

Diagnosis of Hypersensitivity 

Lab Tests —

• •May have increased inflammatory markers (erythrocyte sedimentation rate, C-reactive protein)
• •Leukocytosis and increased gammaglobulins typically seen
• •Specific IgG antibody to offending agent can be detected and checked serially to detect response to treatment :
• Not always present (likely because many unknown antigens)
• Low specificity (10% of people exposed to farmer’s lung antigen develop antibodies; only 0.3% show symptoms)
• •Rheumatoid factor often positive (unknown cause)
• •Negative blood, sputum, throat cultures
• •Bronchoalveolar lavage (BAL)
  • Acute form with neutrophils and CD4 T lymphocytes
  • Chronic form with high number of CD8 T lymphocytes
  • BAL may help to differentiate chronic hypersensitvity pneumonitis from sarcoid, which has high CD8 T lymphocytes
• -There is neutrophilia, lymphopenia, increased ESR, increased C reactive protein, rheumatoid factor, raised serum immunoglobulins.

Chest x-ray

• Acute: Diffuse ground-glass infiltrates, nodular or striated patchy opacities. Up to 20% have normal CXR.
• Subacute: Same as acute, may have sparing of lung bases
• Chronic: Upper lobe fibrosis, reticular opacities, volume loss, honeycombing
• may be normal or show patchy or dif­fuse infiltrates or discrete nodular infiltrates. There may be honey-combing.

CT scanning

• is diagnostic showing the details of fi­brosis, and nodules.

Pulmonary function test (PFT)

• shows a restrictive or obstructive pattern, decreased lung volume, im­paired diffusion capacity, bronchial hyper reactivity and reversibility.
• BAL (Broncho alveolar lavage)
  • shows lymphocytic alveolitis.
• Lung biopsy through bronchoscopy, may be diagnostic.
• Inhalation challenge i.e. a positive response to in­haled antigen may be done for transient airflow ob­struction.

Treatment of Hypersensitivity

• The condition should be diagnosed by occupa­tional history, lifestyle, livelihood, Hlo exposure to antigens .
• The exposure should be checked by wearing of appropriate masks, pollen masks, personal dust respirators, air helmets, ventilated helmets with fresh air.
•   Glucocorticoids – Prednisone 1 mglkglday for 1-2 weeks tapered in 6 wks. Maintenance dose may be continued at the lowest possible dosage if symptoms recur.
• •Avoidance of offending antigen is primary therapy.

Corticosteroids

• Prednisone: 1–2 mg/kg/day, to max of 50–60 mg p.o. daily
• Initial course of 1–2 weeks with progressive taper
• Low-dose therapy (20 mg p.o. daily) may be as effective as avoidance.

Contraindications  : Refer to the manufacturer’s literature.

• •Precautions: Observation for side effects:
  • Acne
  • Hirsutism
  • Behavioral changes
  • Immunosuppression
  • Salt and water retention
  • OsteoporosisWeight gain/appetite increase