For patients with cardiovascular disease, using the antidepressant escitalopram may lead to unexpected adverse events. Here, a rare repeated sinus bradycardia event due to escitalopram is first reported. In an 82-year-old female patient with cardiac dysfunction using digoxin, tachycardia (average heart rate of 93 beats/min) was demonstrated by electrocardiogram (ECG). She began to take escitalopram and lorazepam due to depression, but sinus bradycardia (93.7% heart rate was <60 beats/min) and sinus arrest were first detected after 3 months. Its proportion decreased to 0.1% after discontinuation of digoxin and escitalopram for 1 day, and the rhythm returned to normal 2 weeks later. After 2 months, escitalopram was prescribed again in combination with quetiapine; then, 17.1% heart rate was <60 beats/min. After escitalopram and quetiapine withdrawal, the ECG showed the heart rhythm had normalized again. No other drug changes were made during these periods. Escitalopram was deemed to be a highly possible cause of sinus bradycardia according to its Naranjo's Algorithm score. Furthermore, literature on escitalopram-mediated cardiovascular adverse events was reviewed and analyzed. Empirically, escitalopram should be discontinued immediately if iatrogenic causes cannot be ruled out. Furthermore, ECG monitoring in escitalopram-related cardiovascular adverse events is highlighted, especially in patients receiving certain drug classes simultaneously (i.e., sinoatrial node inhibitors, antipsychotics).

Drug‐ and herb‐induced liver injury (DILI and HILI) is an increasingly common and serious condition. Here, data for DILI and HILI patients from two large tertiary hospitals were retrospectively analyzed. Patient characteristics, causes and severity of DILI and HILI, the correlation between expression of p62 and the severity of DILI and HILI, treatment of DILI and HILI, and the prognostic factors of DILI and HILI were studied. A total of 82 patients with DILI and HILI were recruited for the study. Most patients presented with hepatocellular injury, followed by cholestatic injury and mixed injury. Our results indicate that traditional Chinese medicine or herbal and dietary supplements were the prevalent causal agents of HILI, which was characterized by higher frequencies of hepatocellular injury. Expression of p62 in the liver correlated with the severity of DILI and HILI. Improvements in the results of the liver enzymatic tests correlated with alanine transaminase (ALT) levels upon the first diagnosis of DILI and HILI and with the hepatocellular type of DILI and HILI. In conclusion, we provide an epidemiological assessment of DILI and HILI based on causality using the updated RUCAM on patients from two hospitals in China. ALT levels at first diagnosis and the hepatocellular type of injury may be prognostic factors of DILI and HILI.

Distal metastases result from metastatic microenvironment and tumour epithelial cell interactions, the cellular heterogeneity of primary colorectal cancer (CRC) and liver metastases (LM) was evaluated by integrating single‐cell sequencing data, and the collected gene expression data from metastatic epithelial cell subsets was used to construct a prognostic model and to identify intercellular receptor‐ligand interactions between epithelial and immune cells in CRC and LM. Multiplex immunofluorescence staining, and in vitro wound healing, cell migration and cell apoptosis assays were performed to further explore the biological relevance of identified potential regulatory molecules. In this study, approximately 17 epithelial cell subtypes were detected, with Epi‐11 cells being highly expressed in LM tissues compared with CRC samples. Furthermore, patients with high expression of the metastasis‐related genetic profile of Epi‐11 had a poorer prognosis. By predicting receptor–ligand interactions, Epi‐11 cells were found to interact more with myeloid and T/natural killer cells in LM tissues when compared to primary CRC samples, which was mediated by the PLXNB1/SEMA4D axis. In addition, high SEMA4D expression was correlated with decreased overall survival of patients with CRC, whereas PLXNB1 was not. SEMA4D knockdown prevented the migration and promoted the apoptosis of HCT116 cells in vitro. In summary, Epi‐11 cells, an important subset of epithelial cells, may drive the LM of CRC and act by crosstalk with immune cells through the PLXNB1/SEMA4D signalling axis.

Infective endocarditis (IE) is a rare disease but with high associated mortality. Currently, the mainstays of diagnosis are still echocardiography and blood cultures. Here, we reported a case of infective endocarditis with negative blood cultures, and blood and aortic valve tissue metagenomic next-generation sequencing (mNGS) results suggested Bartonella henselae. In addition, we obtained the whole genomic sequence of B. henselae ZJBH strain. To our knowledge, this is the first report of B. henselae genomic analysis isolated from clinic in China. Furthermore, we described the whole genome sequencing (WGS) data incorporating all B. henselae from diverse sources worldwide and shed light on underlying risk of B. henselae transmitted between cats and humans.

Fabry disease is characterized by an X sex chromosome gene mutation caused by α-galactosidase A deficiency, resulting in the accumulation of globotriaosylceramide and globotriaosylsphingosine in various organs, which induces end-organ lesions. In Fabry disease, enzymes with lost or decreased activity in the body are replaced by exogenous supplementation of normal-function α-galactosidase A. Currently, agalsidase α and agalsidase β are widely used for ERT therapy. However, this therapy has limitations such as high cost, short half-life, and production of neutralizing drug antibodies. The use of Migalastat as chaperone therapy has been approved in many countries, and it plays a therapeutic role by enhancing enzyme activity. However, companion therapy drugs are only suitable for patients with decreased enzyme activity, so the scope of their application is limited. In addition, there are several therapeutic drugs in development, including a new generation of ERT therapies, drugs resistant to neutralizing anti-drug antibody drugs, and substrate reduction therapy drugs. Due to the limitations of existing therapeutic drugs, researchers have begun to explore new therapeutic drugs for Fabry disease, so new pathogenic mechanisms and adjuvant therapeutic drugs have been continuously discovered, and the development of related drugs will contribute to disease control and treatment. This article summarizes the existing and potential drugs for treating Fabry disease to facilitate the selection of suitable and effective drugs for treatment.