Hypersensitivity pneumonitis: antigen diversity and disease implications

Article in PressHypersensitivity pneumonitis (HP) is an immune-mediated syndrome triggered by inhalation of a wide variety of allergens, to which an individual has previously been sensitized. More than 200 agents responsible for the disease have already been identified; however, HP occurs only in a small number of individuals exposed to causal antigens. The present report provides an overview of the role of antigen role in HP, highlighting its diversity, research methods, and prevention strategies, as well as the impact on disease prognosis following elimination of antigen. HP is an underdiagnosed disease and, therefore, it is difficult to accurately estimate its incidence. Triggering antigens can be divided into six broad categories: bacteria, fungi, mycobacteria, animal and plant proteins, chemicals, and metals, represented by disease prototypes. The identification of causal antigen is a major challenge; it is impossible to obtain in about 30-60% of cases. The acute form of HP, with early detection and immediate eviction of causal antigen, tends to have an excellent prognosis. In the chronic form, partial recovery of disease is still possible; however, some cases tend to progress to fibrosis, even after removal from exposure. In conclusion, HP diagnosis should be based on a proactive search for potential antigen sources, although their identification is hampered by the lack of standardized methods of demonstrating the specific antigen sensitization. Antigen avoidance is a critical determinant in disease prognosis.(undefined)info:eu-repo/semantics/acceptedVersio

"Equine Asthma” – integrative biologic relevance of a recently proposed nomenclature

International audienc

Ongoing risk of bladder cancer among former workers at the last benzidine manufacturing facility in the USA

ObjectiveTo determine whether there is an ongoing risk of developing bladder cancer in a previously studied cohort of workers exposed to both benzidine and dichlorobenzidine or dichlorobenzidine only in the last benzidine manufacturing plant in the USA.MethodsWorkers (n=488) were identified from the quarterly 941 forms the employer was required to submit to the Social Security Administration from 1960 to 1977. Exposures were assigned based on dates worked and known benzidine/dichlorobenzidine production schedules. Incidence, vital status and cause of death were determined through 2014. Analyses were restricted to white men.ResultsBladder cancer incidence and mortality were significantly increased (25 incident cases, standardised incidence ratio (SIR) 2.19, 95% CI 1.42 to 3.23, and 5 deaths, standardised mortality ratio (SMR) 3.79, 95% CI 1.23 to 8.84). There were significant increases in incidence and mortality in those exposed to both benzidine and dichlorobenzidine (SIR 3.11, 95% CI 1.97 to 4.67, SMR 4.10, 95% CI 1.12 to 10.50), but not among workers exposed to dichlorobenzidine only (two incident cases, SIR 0.89, 95% CI 0.11 to 3.23 and one death, SMR 2.90, 95% CI 0.07 to 16.15). Bladder cancer incidence and mortality were increased in individuals with &gt;20 years since last exposure with &gt;5 years worked (six observed, SIR 5.94, 95% CI 2.18 to 12.92 and two deaths, SMR 7.93, 95% CI 0.96 to 28.65).ConclusionsIncidence and mortality due to bladder cancer increased among workers exposed to benzidine but not among workers exposed only to dichlorobenzidine. The risk of incidence and death from bladder cancer remain elevated more than 20 years after last exposure to benzidine in those who worked &gt;5 years.</jats:sec