The serum level of diamine oxidase (DAO) reflects the integrity and maturation of the small intestinal mucosa. This measure is important in diagnosing various diseases, including chronic urticaria tachyphylaxis, multiple organ dysfunction syndrome, preterm abortion, and migraine. This review aimed to summarize the findings of previous studies on the changes in DAO levels in diverse diseases and the application of this enzyme in the clinical setting, as well as the roles of this enzyme under physiological and pathological conditions. The advances in the mechanism and clinical application of DAO presented in this review will contribute to a better understanding of this enzyme and open up new and broader perspectives for future basic research and clinical applications.

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Background Pulmonary ischemia/reperfusion (I/R) injury derived from hemorrhagic shock-resuscitation is a significant cause of death in trauma patients. However, effective preventive interventions in early trauma resuscitation are lacking. Aims To investigate the critical role of the HMGB1-TLR4 pathway in the early inflammatory response after ischemia-reperfusion lung injury, and its specific regulatory mechanisms and the types of downstream cytokines regulated by this pathway. Methods In this study, to determine the molecular mechanism underlying pulmonary I/R injury and identify effective therapeutic targets to reduce the incidence and mortality, the expression of the HMGB1-TLR4 pathway in a pulmonary I/R injury model, its correlation with downstream inflammatory factors, and the effects of HMGB1-neutralizing antibodies on inflammation were evaluated. Results IL-6 and TNF-α levels in the three mouse models showed a rapid increase， IL-1β, IL-6, and TNF-α were upregulated in alveolar macrophages after LPS stimulation，TNF-α and HMGB1 were upregulated in TLR4+/+ cells and peaked at 48 h but was not upregulated in TLR4-/- cells. Western blot assays revealed that in TLR4+/+ cells, TLR4 was upregulated after stimulation by LPS and was rapidly downregulated after treatment with the HMGB1-neutralizing antibody. In contrast, TLR4-/- cells did not respond to LPS stimulation, and the HMGB1-neutralizing antibody did not significantly alter the TLR4 concentration. Conclusions HMGB1-TLR4 pathway plays an important role in the regulation of inflammation in pulmonary I/R injury. Furthermore, HMGB1 upregulated downstream inflammatory factors via TLR4. HMGB1-neutralizing antibodies had a protective effect against lung injury by downregulating the inflammatory response.

With its low morbidity and high mortality rates, thrombotic thrombocytopenic purpura (TTP) has imposed a critical physical and economic burden on both society and individuals. Thrombocytopenia commonly occurs in severe liver failure, and a variety of hepatitis viruses are known to induce immune thrombocytopenic purpura. However, TTP is extremely rare in hepatitis E virus infection. We hereby report a case of a 53-year-old male who present with TTP caused by severe hepatitis E, and the patients achieved successful recovery after treatment. Therefore, we propose considering AMAMTS13 testing as an essential and beneficial approach for accurately diagnosing and treating patients with severe hepatitis or infection with notable platelet decline.

With low morbidity and high mortality, Thrombotic Thrombocytopenic Purpura (TTP) has brought critical physical and economic burden to society and individual. Thrombocytopenia is very common in severe liver failure, and a variety of hepatitis viruses can induce immune thrombocytopenic purpura. However, it is extremely rare in HEV infection. We hereby report the case of a 53-year-old man who present with TTP caused by severe hepatitis E, and the patients recovered well after treatment. Thus, we propose considering that for patients with severe hepatitis or infection with notable platelet decline, AMAMTS13 testing is very necessary and beneficial for the accurate diagnosis and treatment.