Atypical adult-onset Still's disease with an initial and sole manifestation of liver injury: A case report and review of literature.

BACKGROUND: Adult-onset Still's disease (AOSD) typically presents with a high spiking fever, polyarthritis, transient maculopapular rash, neutrophilic leukocytosis, and hepatosplenomegaly. It has a wide spectrum of clinical symptoms ranging from mild to severe, with extensive involvement of almost every organ. Although liver involvement in the form of increased hepatic enzymes and bilirubin is common, no AOSD case with liver involvement as the initial manifestation of AOSD has been reported. CASE SUMMARY: A 35-year-old woman presented to the hepatology department with progressively worsening jaundice for one week. Liver chemistry tests revealed a significantly increased liver enzymes and bilirubin level. Given that the clinical examination was unremarkable, liver biopsy was considered because the patient had a history of AOSD 6 years ago. Liver histopathology revealed that most hepatic lobules were still recognizable. Fusional necrosis was observed around most central veins. A few bridging necrotic zones were also found. Infiltration of multiple plasma cells were observed in the necrotic zone, and the reticular scaffold was still expanded. Additionally, no obvious fibrosis was observed in the portal area. Mild mixed inflammatory cell infiltration was noted in the interstitium of the portal area. Further examination was unremarkable except for a remarkably high level of ferritin. Collectively, a presumptive diagnosis of liver injury secondary to AOSD was made. The hepatic involvement responded well to glucocorticoid treatment. CONCLUSION: This case highlights that hepatic involvement as an initial and sole manifestation could be a pattern of relapsed AOSD. The diagnosis of AOSD should be considered in the case of nonresolving liver injury after the exclusion of common etiologies for liver diseases. A liver biopsy can be useful for the differential diagnosis of liver injury associated with AOSD.

lncRNA BCAR4 sponges miR­370­3p to promote bladder cancer progression via Wnt signaling.

Accumulating evidence suggests that the aberrant expression of long non­coding RNAs (lncRNAs) is involved in the initiation, development and metastasis of bladder cancer (BC). Although several differentially expressed lncRNAs have been identified via lncRNA expression profiling of BC tissues, their functions and the molecular mechanisms underlying these functions remain to be fully elucidated. In the present study, elevated levels of lncRNA breast cancer anti­estrogen receptor 4 (BCAR4) were identified in BC tissues compared with matched healthy tissues. Silencing of BCAR4 inhibited cell proliferation and induced apoptosis in BC cell lines 5637 and T24. Downregulation of BCAR4 led to the inactivation of Wnt signaling. Mechanistically, BCAR4 directly sponged microRNA (miR)­370­3p and elevated Wnt7a expression. Endogenous expression of Wnt7a reversed BCAR4 silencing­mediated cell growth arrest and induction of apoptosis in BC cells accompanied with a re­activation of Wnt signaling. Reverse transcription­quantitative PCR indicated that there was a strong association between BCAR4, miR­370­3p and Wnt7a expression in tumors from patients with BC compared with healthy control tissues. In conclusion, results of the present study suggest that lncRNA BCAR4 promoted proliferation and survival of BC cells via downregulation of miR­370­3p. Therefore, lncRNA BCAR4 may be a lncRNA of oncogenic potential in BC.