Postmenopausal women with hyperandrogenemia:Three case reports

BACKGROUND Diagnosing hyperandrogenemia in postmenopausal women is very difficult.It occasionally manifests as excessive hair growth or with no clinical manifestations,and is therefore often misdiagnosed or missed altogether.Ovarian steroid cell tumors that cause hyperandrogenemia in women account for approximately 0.1%of all ovarian tumors.Due to the low incidence,corresponding imaging reports are rare,so ovarian steroid cell tumors lacks typical imaging findings to differ-entiate it from other ovarian tumors.Therefore,we summarized its clinical and imaging characteristics through this case series,and elaborated on the differential diagnosis of steroid cell tumors.CASE SUMMARY We report three cases of postmenopausal women with hyperandrogenemia.Only 1 patient showed virilization symptoms,the other two patients were completely asymptomatic.All patients underwent total hysterectomy+bilateral adnexe-ctomy.Histological results showed one case of Leydig cell tumor and two cases of benign,non-specific steroid cell tumor.After the operation,the androgen levels of all patients returned to normal,and there was no clinical recurrence since follow-up.CONCLUSION Although virilization caused by increased serum testosterone levels is an important clinical feature of ovarian steroid cell tumors,it is often asymptomatic.A solid,slightly hypoechoic,round or oval mass with uniform internal echo,richer blood flow in the solid part,and low resistance index are typical imaging features of ovarian steroid cell tumors.Diagnosis of ovarian steroid cell tumors after menopause is challenging,but surgery can be used for both diagnosis and clear treatment.

Interleukin-18, matrix metalloproteinase-22 and -29 are independent risk factors of human coronary heart disease

Background： Coronary heart disease （CHD） is characterized by arterial wall inflammation and matrixdegradation. Matrix metalloproteinase （MMP）-22 and -29 and pro-inflammatory cytokine interleukin-18 （IL18） arepresent in human hearts. IL18 may regulate MMP-22 and -29 expression, which may correlate with CHD progression.Methods and results： Immunoblot analysis showed that ILl8 induced MMP-22 expression in human aortic smoothmuscle cells. The Mann Whitney test from a prospective study of 194 CHD patients and 68 non-CHD controlsdemonstrated higher plasma levels of IL18, MMP-22 and-29 in CHD patients than in the controls. A logistic regressiontest suggested that plasma IL18 （odds ratio （OR）=1.131, P=0.007）, MMP-22 （OR=1.213, P=0.040）, and MMP-29（OR=1.198, P=0.033） were independent risk factors of CHD. Pearson＇s correlation test showed that IL18 （coefficient（r）=0.214, P=0.045; r=0.246, P=0.031） and MMP-22 （t=0.273, P=0.006; r=0.286, P=0.012） were associated with theGensini score before and after adjusting for potential confounding factors. The multivariate Pearson＇s correlation testshowed that plasma MMP-22 levels correlated positively with high-sensitive-C-reactive protein （hs-CRP） （r=0.167,P=0.023）, and MMP-29 levels correlated negatively with triglyceride （t=-0.169, ,P=-0.018）. Spearman＇s correlation testindicated that plasma IL18 levels associated positively with plasma MMP-22 （t=0.845, P〈0.001） and MMP-29 （r=0.548P〈0.001）. Conclusions： Our observations suggest that IL18, MMP-22 and -29 serve as biomarkers and independentrisk factors of CHD. Increased systemic IL18 in CHD patients may contribute to elevated plasma MMP-22 and -29levels in these patients.

Inhibition of neddylation ameliorates DSS-induced colitis

Immune disorders are characterized by excessive immune cell activation and aberrant inflammatory responses.Cell signals have been noted to regulate immune cell functions and to contribute to immune diseases,for example,upon extracellular stimulation,cell receptormediated signals,including mammalian target of rapamycin/signal transducer and activator of transcription factor 31,2 and mitogen-activated protein kinase/nuclear factor-κB,3,4 induce the expression of proinflammatory cytokines and molecules,thereby resulting in immune cell activation and sustained inflammation,as seen in inflammatory bowel diseases and other immune disorders.