The impact of hiatus hernia in hypersensitivity pneumonitis

has demonstrated that 60% of HP patients have a HH, over half of which are moderate-to-large. There was no association with poorer outcomes, yet their prevalence and association with CT signs of aspiration may further elucidate HP aetiopathogenesis.


S C I E N T I F I C L E T T E R The impact of hiatus hernia in hypersensitivity pneumonitis
2][3] HH has been reported in approximately one-third of patients with hypersensitivity pneumonitis (HP), but data are sparse. 3There are parallels between fibrotic HP and IPF suggesting HH may have a similar impact in both conditions. 4A causal relationship between HH and lung fibrosis has not been established.HH and chronic microaspiration (CMA) might promote or potentiate lung fibrosis, 1 and it is hypothesised that increased negative intrathoracic pressure caused by lung fibrosis can lead to retraction of the gastro-oesophageal junction into the thoracic cavity. 5n this study, we explored the prevalence and impact of HH in patients with HP.
One hundred and forty-one consecutive patients with a multidisciplinary diagnosis of HP, 6,7 referred to the Royal Brompton Hospital between January 2010 and December 2014, were retrospectively evaluated (Table 1).The presence and size of HH (graded 0-4) was determined on computed tomography (CT) scans by two consultants. 3,5The extent (nearest 5%) and pattern of fibrosis, were recorded as were CT features potentially indicative of CMA (consolidation, oesophageal dilatation and tree-in-bud pattern).In a control population of 175 patients without interstitial lung disease (ILD) undergoing CT coronary angiography, the presence and size of HH was also assessed.
Presence and size of HH were not associated with BMI.There was no relationship between the presence of HH and visual extent of fibrosis on CT (with HH, mean fibrosis extent (±SD) on CT 53.0% (±24.7%)versus without HH, 43.9% (±29.5%);p > 0.05).
2][3] The prevalence of HH in our control group (25%) was similar to the 23% prevalence in a study of nearly 5000 non-ILD patients. 5here was no association between HH and lung function decline or mortality.This contrasts with data in IPF where there is an established association between HH, disease progression and survival. 1,3In the subgroup of HP patients with a UIP pattern, there was a trend to an association between HH and mortality and a similar direction of lung function decline.Numbers in this group were small and so this observation needs further exploration, but is plausible given similar previous findings in patients with IPF.
We attempted to establish the directionality to the relationship between HH and HP.There was no association between increased fibrosis (on CT or lung function) and larger HH, suggesting that negative intrathoracic pressure does not promote the development of HH.However, consolidation, a non-specific CT marker of aspiration, was increasingly more apparent in HP patients with HH of increasing size.This suggests that HH and subsequent CMA, could potentiate ILD in HP. 8 With up to 60% of HP cases having an unidentified causative antigen, and only 5%-15% of those exposed to causative antigens developing HP, we speculate that CMA could drive the development of HP in genetically predisposed individuals. 9,10This theory is supported by a recent Mendelian randomization study that showed GORD increased the risk of IPF, yet not vice versa. 11With this potential multi-hit hypothesis involving CMA, further research in HP patients could involve objective measures of aspiration with gastrointestinal physiology studies to unlock novel pathomechanistic understandings of HP. 12 There were several study limitations.Firstly, our data was acquired retrospectively from a single centre.Our HP-UIP sub-group was small and so future studies could expand this.While most HP patients had 12-month FVC and DLco data, future studies could assess longer-term lung function trajectory.HRCT is not the gold-standard investigation for detecting HH; high-resolution manometry, barium swallow radiography or endoscopy are more routinely used. 3However, HRCT is accurate in detecting HH and all scans were reviewed by two experienced consultants. 3Other strengths include complete survival data and the inclusion of a relevant control group. 2 Our study has demonstrated that 60% of HP patients have a HH, over half of which are moderate-to-large.There was no association with poorer outcomes, yet their prevalence and association with CT signs of aspiration may further elucidate HP aetiopathogenesis.

T A B L E 1
Comparison of the baseline, demographic and clinical characteristics of the hypersensitivity pneumonitis study subjects (N = 141) between those with and without a hiatus hernia.

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I G U R E 1 Kaplan-Meier survival curves for assessing the survival in fibrotic hypersensitivity pneumonitis patients with hiatus hernia and the presence of consolidation in different grades of HH.HH presence was assessed against survival in (A) the entire HP cohort (n = 141), (B) those with a UIP pattern of fibrosis on CT scan (n = 23) or (C) those without a UIP pattern of fibrosis on CT scan (n = 118).(D) The presence of consolidation was assessed as grade 0 (n = 57), grade 1 (n = 39) and grade 2 (n = 32) shown separately.Grades 3 and 4 (n = 13) combined due to smaller size of group.A Fisher's exact test was performed across all the grades individually.*: p < 0.05; **: p < 0.005.HH, hiatus hernia; UIP, usual interstitial pneumonia.