Coexistence of liver abscess, hepatic cystic echinococcosis and hepatocellular carcinoma: A case report

BACKGROUND Human cystic echinococcosis(CE)is a life-threatening zoonosis caused by the Echinococcus granulosus(sensu lato).Hepatocellular carcinoma(HCC)is a leading cause of cancer-related mortality in the world.The coexistence of CE and HCC is exceedingly rare,and only several well-documented cases have been reported.In addition to this coexistence,there is no report of the coexistence of CE,HCC,and liver abscess to date.Herein,we aimed to report a case of coexistence of liver abscess,hepatic CE,and HCC.CASE SUMMARY A 65-year-old herdsman presented to the department of interventional therapy with jaundice,right upper abdominal distension and pain for 10 d.Laboratory test showed that he had positive results for HBsAg,HBeAb,HBcAb,and echino-coccosis IgG antibody.The test also showed an increased level of alpha fetopro-tein of 3400 ng/mL.An abdominal computed tomography(CT)scan revealed an uneven enhanced lesion of the liver at the arterial phase with enhancement and was located S4/8 segment of the liver.In addition,CT scan also revealed a mass in the S6 segment of the liver with a thick calcified wall and according to current guideline and medical images,the diagnoses of hepatic CE(CE4 subtype)and HCC were established.Initially,transarterial chemoembolization was performed for HCC.In the follow-up,liver abscess occurred in addition to CE and HCC;thus,percutaneous liver puncture drainage was performed.In the next follow-up,CE and HCC were stable.The liver abscess was completely resolved,and the patient was discharged with no evidence of recurrence.CONCLUSION This is the first reported case on the coexistence of liver abscess,hepatic CE,and HCC.Individualized treatment and multidisciplinary discussions should be performed in this setting.Therefore,treatment and diagnosis should be based on the characteristics of liver abscess,hepatic CE,and HCC,and in future clinical work,it is necessary to be aware of the possibility of this complex composition of liver diseases.

Interleukin-37 promotes colitis-associated carcinogenesis via SIGIRR-mediated cytotoxic T cells dysfunction

Interleukin-37b(hereafter called IL-37)was identified as fundamental inhibitor of natural and acquired immunity.The molecular mechanism and function of IL-37 in colorectal cancer(CRC)has been elusive.Here,we found that IL-37 transgenic(IL-37tg)mice were highly susceptible to colitis-associated colorectal cancer(CAC)and suffered from dramatically increased tumor burdens in colon.Nevertheless,IL-37 is dispensable for intestinal mutagenesis,and CRC cell proliferation,apoptosis,and migration.Notably,IL-37 dampened protective cytotoxic T cell-mediated immunity in CAC and B16-OVA models.CD8^(+)T cell dysfunction is defined by reduced retention and activation as well as failure to proliferate and produce cytotoxic cytokines in IL-37tg mice,enabling tumor evasion of immune surveillance.The dysfunction led by IL-37 antagonizes IL-18–induced proliferation and effector function of CD8+T cells,which was dependent on SIGIRR(single immunoglobulin interleukin-1 receptor-related protein).Finally,we observed that IL-37 levels were significantly increased in CRC patients,and positively correlated with serum CRC biomarker CEA levels,but negatively correlated with the CD8+T cell infiltration in CRC patients.Our findings highlight the role of IL-37 in harnessing antitumor immunity by inactivation of cytotoxic T cells and establish a new defined inhibitory factor IL-37/SIGIRR in cancerimmunity cycle as therapeutic targets in CRC.