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The aims of this study were to phenotype pain in patients with interstitial lung disease (ILD) by investigating the association between sensitization-associated symptoms with quality of life, anxiety/depression, pain catastrophizing, and kinesiophobia levels and identifying those risk factors explaining the variance of quality of life in individuals with ILD and pain. One hundred and thirty-two (38.6% women, mean age: 70, standard deviation: 10.5 years) patients with ILD completed clinical (age, sex, height, weight), psychological (Hospital Anxiety and Depression Scale [HADS] and the Pittsburgh Sleep Quality Index), and health-related quality of life (EQ-5D-5L) variables, as well as the Central Sensitization Inventory (CSI), the Self-Report Leeds Assessment of Neuropathic Symptoms (S-LANSS), Pain Catastrophizing Scale, and Tampa Scale for Kinesiophobia (TSK-11) questionnaires. The prevalence of sensitization-associated symptomatology (CSI), neuropathic-like features (S-LANSS), anxiety symptoms, depressive symptoms, or poor sleep was 20.5%, 23.5%, 23.6%, 22.9%, or 51.6%. Significant associations between CSI, S-LANSS, HADS-A, HADS-D, Pain Catastrophizing Scale, TSK-11, and EQ-5D-5L (.220 < r < .716) were found. The regression analysis revealed that CSI, TSK-11, and HADS-D explained 44.8% of the variance of EQ-5D-5L (r 2 adjusted: .448). This study found the presence of sensitization-associated and neuropathic-like symptoms as well as other central nervous system-derived symptoms, such as anxiety, depression, poor sleep, pain catastrophizing, and kinesiophobia in 25% of ILD patients with pain. Sensitization-associated symptoms, depression, and kinesiophobia were associated with a worse quality of life. These findings would support that individuals with ILD can exhibit different pain phenotypes, including nociplastic-like pain phenotype based on self-reported measurements. PERSPECTIVE: Pain in patients with ILD can fulfill features of different phenotypes, including nociplastic pain, when sensory, emotional, and cognitive mechanisms are involved at the same time., (Copyright © 2024 United States Association for the Study of Pain, Inc. Published by Elsevier Inc. All rights reserved.)

Patients with interstitial lung disease (ILD) represent a vulnerable population against an acute SARS-CoV-2 infection. It has been observed that up to 80% of patients with ILD can develop post-COVID-19 symptomatology one year after. This secondary analysis aimed to, 1, compare serological biomarkers before and after surpassing a SARS-CoV-2 infection in individuals with interstitial lung disease (ILD) and, 2, to compare serological biomarkers between ILD patients who develop and those who do not develop post-COVID-19 symptoms. Seventy-six patients with ILD (40.4% women, age: 69, SD: 10.5 years) who survived a SARS-CoV-2 infection participated. High-resolution computerized tomography (CT) of the lungs, two pulmonary function tests (forced vital capacity (FVC) and diffusion value of carbon monoxide (DLCO)) and fourteen serological biomarkers were collected before and after SARS-CoV-2 infection. Participants were asked for the presence of post-COVID-19 symptomatology a mean of twelve (SD: eight) months after infection. Sixty patients (79%) showed post-COVID-19 symptoms (mean: 3.5, SD 1.1), with fatigue (68.4%), dyspnea (31.5%), and concentration loss (27.6%) being the most prevalent. Creatine phosphokinase (CPK) was the only biomarker showing differences in our study. In fact, CPK levels were higher after the acute SARS-CoV-2 infection (mean difference: 41.0, 95%CI 10.1 to 71.8, p = 0.03) when compared to before the infection. Thus, CPK levels were also higher in ILD patients with post-COVID-19 fatigue (mean difference: 69.7, 95%CI 12.7 to 126.7, p = 0.015) or with post-COVID-19 dyspnea (mean difference: 34.8, 95%CI 5.2 to 64.4, p = 0.025) than those patients without these post-COVID-19 symptoms. No significant changes in CT or functional pulmonary tests were observed after COVID-19 in patients with ILD. In conclusion, patients with ILD exhibited an increase in CPK levels after SARS-CoV-2 infection, albeit no changes in other serological biomarkers were identified. Similarly, the presence of post-COVID-19 fatigue or dyspnea was also associated with higher CPK levels in ILD patients. Studies investigating long COVID mechanisms in vulnerable populations such as ILD are needed.