The Unveiled Triad: Clinical, Radiological and Pathological Insights into Hypersensitivity Pneumonitis

Abstract

Hypersensitivity pneumonitis (HP) is a diffuse parenchymal lung disease (DLPD) characterized by complex interstitial lung damage with polymorphic and protean inflammatory aspects affecting lung tissue targets including small airways, the interstitium, alveolar compartments and vascular structures. HP shares clinical and often radiological features with other lung diseases in acute or chronic forms. In its natural temporal evolution, if specific therapy is not initiated promptly, HP leads to progressive fibrotic damage with reduced lung volumes and impaired gas exchange. The prevalence of HP varies considerably worldwide, influenced by factors like imprecise disease classification, diagnostic method limitations for obtaining a confident diagnosis, diagnostic limitations in the correct processing of high-resolution computed tomography (HRCT) radiological parameters, unreliable medical history, diverse geographical conditions, heterogeneous agricultural and industrial practices and occasionally ineffective individual protections regarding occupational exposures and host risk factors. The aim of this review is to present an accurate and detailed 360-degree analysis of HP considering HRCT patterns and the role of the broncho-alveolar lavage (BAL), without neglecting biopsy and anatomopathological aspects and future technological developments that could make the diagnosis of this disease less challenging.

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“…For this reason, in addition to the exclusion of atypical pneumonia, accurate exposure history is essential for the correct evaluation of the patient. Typical HRCT features of acute HP are multiple bilateral small centrilobular nodules with upper lung zone predominance, lobular areas of decreased attenuation and vascularity suggestive of "air trapping" and patchy and/or diffuse GGO areas [9,12,17]. Chronic HP shows a typical "three density pattern" characterized by bilateral and diffuse lobular areas of decreased attenuation (air-trapping areas), patchy areas of real GGO in a predominant peribronchovascular distribution with traction bronchiectasis and bronchiolectasis inside (fibrosis signs), and also areas of a relative increase in density related to the normal CT appearance of the lung (GGO-like areas).…”

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“…The distinguishing feature of HP, also called extrinsic allergic alveolitis, is that it is triggered by repeated inhalation of specific organic antigens to which a person is sensitized [1]. The incidence of HP in the UK is estimated at 1 case per 100,000, while in the US that value is between 1.67-2.71 per 100,000 [2]. In Poland, its incidence is estimated at 1.7/100,000 cases [3].…”

“…More than 300 antigens responsible for HP have been described, among them are distinguished those of bacterial, fungal, animal and plant origin. Exposure can result from work, hobbies, or the home environment [1,2]. The current state of knowledge does not allow a clear determination of the cause of the occurrence of the aforementioned immune response in only part of the exposed individuals, but one of the most common hypotheses is the so-called 'two-hit' theory, in which multiple exposures to an antigen act as an inducing factor, and genetic factors act as conducive to the onset of the disease [2].…”

“…Physical examination in HP may reveal the presence of tachypnoea, focal or diffuse crackles, or inspiratory wheezes. At a later stage of the disease, finger clubbing may be present [2].…”

“…Pulmonary function tests usually show restrictive abnormalities with reduced diffusing capacity (DLCO). It is not possible to distinguish between HP with and without fibrosis by using pulmonary function tests, but they are used to monitor disease progression or response to treatment [2].…”