Hypersensitivity pneumonitis “HP” Testing
and Other Blood Tests for Mold Exposure
Hypersensitivity pneumonitis (also called extrinsic allergic alveolitis, EAA) is an inflammation of the air sacs of the lungs or alveoli within the lungs caused by hypersensitivity to inhaled organic dusts such as, mold spores or Beta Glucans. Hypersensitivity pneumonitis can cause a permanent scaring of the lungs.
In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise (a general feeling of being unwell), cough, chest tightness, dyspena (shortness of breath) and headaches. Symptoms resolve within 12 hours to several days upon cessation of exposure.
Acute HP is characterized by poorly formed noncaseating interstitial granulomas (when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate) and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.
On chest radiographs, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients.” In high-resolution CT scan, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO)). Many patients have hypoxemia at rest, and all patients desaturate with exercise.
Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones. Findings may be present in patients who have experienced repeated acute attacks. The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneunonis, and interstitial fibrosis
In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. Avoiding any further exposure is recommended. Clubbing (deformity of fingers and finger nails) is observed in 50% of patients. Tachypnea (rapid breathing), respiratory distress, and inspiratory crackles over lower lung fields often are present.
On chest radiographs, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans.
Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.