Spontaneous rupture of splenic hamartoma in a patient with hepatitis C virus-related cirrhosis and portal hypertension:A case report and review of the literature

Spontaneous rupture is a rare complication of splenic hamartoma. A review of the literature revealed only four such cases. To the best of our knowledge, this is the first report of spontaneous rupture of splenic hamartoma associated with liver cirrhosis and portal hypertension. A 53-year-old woman, who was followed up for aortic dissection and hepatitis C virus （HCV）-related liver cirrhosis, was referred with sudden left chest and shoulder pain. An abdominal ultrasound showed intraabdominal bleeding, and computed tomography indicated rupture of a splenic tumor. Emergent splenectomy was carried out. The postoperative course was uneventful, and the patient was discharged on the 13th postoperative day. Pathology revealed the tumor to be a ruptured splenic hamartoma. The non-tumorous splenic parenchyma revealed congestive changes. We consider that the presence of liver cirrhosis and portal hypertension are risk factors for spontaneous rupture of the splenic hamartoma.

Effect of endotoxin on portal hemodynamic in rats

AIM: To study the effects of endotoxin on portal hemodynamic of normal and noncirrhotic portal hypertensive rats. METHODS: Normal rats were intraperitoneally injected with 0.1, 0.25, 0.5, 1.0, 2.0, 4.0mg.kg(-1) of lipopolysaccharide(LPS) respectively, portal vein ligation(PVL) and intrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of 1.0mg.kg(-1) of LPS, the portal vein pressure(PVP), portal venous flow(PVF), inferior vena cava pressure(IVCP) and portal vein resistance(PVR) were detected 4 hours after injection. RESULTS: PVF of the 5 groups of rats accepting intraperitoneal injection of LPS were increased from 14.0 to 18.0, 22.2, 26.2, 34.8, 39.6, 38.8 mL.min(-1) 4 hours after injection of LPS(P【0.01). PVP of the 4 groups of rats accepting more than 0.1mg/kg.b.w of LPS was increased from 1.04 to 1.25, 1.50, 1.80, 1.95, 2.05 kPa(P【0.01). The increments of PVF and PVP were in a dose-dependent manner of LPS. PVR of the 5 groups of rats was decreased from 51 to 42,44,48,45,44,47 kPa.min.L(-1) (P【0.05) and no dose-dependent manner was observed. PVF of PVL, IPO and sham-operated rats increased from 22.6 to 32.8, 22.0 to 28.0, 14.0 to 34.8 mL.min(-1) (P【0.01), and PVP increased from 1.86 to 2.24, 1.74 to 1.95, 1.04 to 1.80 kPa(P【0.01), PVR decreased from 71 to 61, 67 to 61, 52 to 44 kPa.min.L(-1) after intraperitoneal injection of 1mg.kg(-1) of LPS. The increments of PVF and PVP of PVL and IPO rats were significantly less than the sham-operated rats(P【0.01), There was no significant difference between the amounts of PVR decreased in the two groups of PHT model rats and sham-operated rats(P】0.05) after intraperitoneal injection 1mg.kg(-1) of LPS. CONCLUSION: Endotoxin could prompt portal hypertension of the normal and noncirrhotic portal hypertensive rats by increasing portal blood flow mainly.

Impact of hepatitis C oral therapy in portal hypertension

Chronic hepatitis C is a leading cause of morbidity and mortality, mainly related to fibrosis/cirrhosis and portal hypertension. Direct antiviral agents are highly effective and safe and can now cure > 90% of the patients. Sustained viral response (SVR) after interferon-based regimens has been associated with improvement in liver function, fibrosis and portal hypertension in a significant proportion of patients, although a point of no return seems to exist from which viral elimination is no longer capable of preventing portal hypertension progression and liver decompensation. Indeed, although SVR is associated with improvement of hepatic venous pressure gradients and therefore a decreased risk of de novo esophageal varices, several studies show that viral clearance does not eliminate the risk of variceal progression, liver decompensation and death in patients with pre-established portal hypertension. Although evidence about the effects of direct antiviral agents (DAAs) on clinically significant outcomes is still scarce and with short follow-up, DAAs can decrease the burden of the disease if patients are timely treated before significant fibrosis and portal hypertension develops. Studies with longer follow-up are waited to establish the real magnitude of hepatitis C treatment on portal hypertension. Future studies should also focus on predictors of portal hypertension resolution since it can influence management and avoid unnecessary monitoring

Ultrasonography in differentiation between chronic viral hepatitis and compensated early stage cirrhosis

AIM: To assess the value of gray scale (GS) and colour Doppler ultrasonography (CDU) in differentiating the progression of chronic viral hepatitis (CVH) and compensated liver cirrhosis (CIR). METHODS: Seventy-two patients and 32 normal individuals who were used as controls were studied. Forty-four patients suffered from CVH and 28 from CIR. All patients were underwent to liver biopsy. Multiple qualitative and quantitative variables were studied in liver, portal vein (PV), hepatic artery (HA) and spleen with GS and CDU. On the basis of the obtained CDU data, several known indexes were calculated. In addition, alternative indices [PV diameter (D)/time average mean velocity (VTAM), HA/PV VTAM ratio] were calculated and studied. RESULTS: ROC analysis showed that PV congestion index, PV D/VTAM and HA/PV VTAM indices had the best sensitivity and specificity in discriminating CVH from CIR. Stepwise discriminant analysis showed that 88.9% of the originally grouped cases could be correctly classified by the three qualitative and four quantitative variables selected as statistically significant predictors. Among the CVH patients who underwent to biopsy, statistically significant changes were found in those at fibrosis stage 5 compared to fibrosis stages 1-4. CONCLUSION: Simple GS and CDU parameters discri-minate CVH from CIR. The alternative Doppler indexes can accurately differentiate chronic virus hepatitis from cirrhosis. These indexes can be used in monitoring chronic virus hepatitis and avoiding unnecessary biopsies.

Effect of Huanglian Jiedu Decoction on cardiac endoplasmic reticulum stress in spontaneously hypertensive rats

Huanglian Jiedu Decoction(HLJDD)is a quintessential prescription renowned for its heat-clearing and detoxifying properties.It is primarily prescribed to counteract the syndrome characterized by the excessive heat of the Sanjiao fire.Notably,the hyperactivity of liver fire is frequently linked with hypertension,where wind fire and wind toxicity emerge as pivotal pathogenic factors.This study aimed to investigate the impact of HLJDD on the endoplasmic reticulum in spontaneously hypertensive rats(SHR),further delving into the interplay between endoplasmic reticulum stress(ERS)and myocardial remodeling and damage.Fifty SHR rats were stratified randomly into five cohorts:model,low-dose HLJDD,medium-dose HLJDD,high-dose HLJDD,and captopril groups.For comparison,a set of Wistar-Kyoto(WKY)rats served as the baseline control group,with each group comprising 10 rats.While the model and control groups received equivalent volumes of normal saline via gavage,the other groups were administered the respective drug dosages through the same route daily for a span of 6 weeks.Upon the experiment’s conclusion,metrics such as the heart mass index(HWI)and left ventricular mass index(LVWI)were assessed.Cardiac tissue anomalies were identified using H&E staining,while ERS-related protein and mRNA expression levels were ascertained via Western blotting analysis and qPCR.Moreover,TUNEL staining was employed to detect cardiomyocyte apoptosis.The findings indicated that increasing HLJDD concentrations corresponded with escalated HWI and LVWI in rat hearts(P<0.05).There was a marked enhancement in myocardial structural integrity,accompanied by a notable reduction in collagen fibers.The mRNA and protein expressions of myocardial inositol-dependent enzyme 1α(IRE1α),X-box binding protein 1(XBP1),glycoregulatory protein 78(GRP78),and CCAAT enhancer binding protein homologous protein(CHOP)in the medium and high-dose groups saw significant declines(P<0.05).These effects mirrored those observed in the captopril group.The study underscored HLJDD’s efficacy in mitigating myocardial tissue damage in SHR.This therapeutic effect was potentially attributed to the downregulation of IRE1α,XBP1,GRP78,and CHOP,curbing excessive ERS,diminishing cardiomyocyte apoptosis,and thereby conferring cardioprotection.

Trans-cinnamaldehyde promotes nitric oxide release via the protein kinase-B/v-Akt murine thymoma viral oncogene-endothelial nitric oxide synthase pathway to alleviate hypertension in SHR.Cg-Lepr^(cp)/NDmcr rats

OBJECTIVE:To evaluate whether endothelial dysfunction and hypertension are prevented by trans-cinnamaldehyde(t CA) through the activation of endothelial nitric oxide synthase(e NOS).METHODS:Human umbilical vein endothelial cells(HUVECs) were cultured in vitro and stimulated with t CA to determine cell viability using the methyl thiazolyl tetrazolium assay.The effect of t CA on nitric oxide(NO) production was determined by diaminofluorescein-dyes in the absence or presence of inhibitors of e NOS,AMPK,PKA,and AKT.The effect of t CA on blood pressure was determined by the tail-cuff method in obesity spontaneous hypertension(SHR.Cg-Leprcp/NDmcr) rats.The phosphorylation of e NOS and protein expression of the insulin-signaling pathway(Ins R-IRS1-PI3 K-AKT)were measured by western blot.RESULTS:t CA at concentrations less than 100 μM did not affect cell viability in cultured HUVECs.Stimulation with t CA promoted NO release in a time-dependent manner compared with the control group.t CA-treated HUVECs also significantly increased AKT-Ser473 and e NOS-Ser1177 phosphorylation.In SHR-CP rats,treatment with t CA at a dose of 40 mg/kg/day for 6 weeks markedly reduced the systolic blood pressure and diastolic blood pressure,increased the phosphorylation of AKT and e NOS,and increased urinary nitric oxidation.CONCLUSION:t CA attenuated endothelial dysfunction and reduced blood pressure in SHR-CP rats.The underlying mechanisms may involve the increase in AKT and e NOS phosphorylation and the release of e NOS-derived NO.

Effect of Huanglian Jiedu Decoction on vascular endothelium factor and expression of RhoA protein factor in young spontaneously hypertensive rats

To investigate the mechanism of effect of Huanglian Jiedu Decoction(HLJD) on vascular endothelium, we assessed the protective effect of HLJD on vascular endothelium in spontaneously hypertensive rats(SHR) and the expression of RhoA in thoracic aorta. A total of 40 SHR rats were randomly and evenly divided into model group(SHR group), positive group(captopril group), HLJD high-dose group, and HLJD low-dose group. Simultaneously, 10 Wistar Kyoto rats were used in the blank group. All groups were treated by gavage for 6 weeks. The changes of nitric oxide synthase(NOS), von Willebrand factor(vWF), endothelin(ET-1) and calmodulin(CAM) in rat serum were tested by enzyme linked immunosorbent assay(ELISA) method. The expression of RhoA at the protein and mRNA levels in thoracic aorta was determined by Western blotting(WB) and quantitative real-time PCR, respectively. Compare with the blank group after 6 weeks, the levels of ET-l and VWF in serum of the model group were significantly increased(P<0.01), and the levels of NOS and CAM were significantly decreased(P<0.01). Conversely, the levels of ET-1 and vWF in the positive and HLJD groups were significantly decreased(P<0.01 or P<0.05), and the levels of NOS and CAM were significantly increased(P<0.01 or P<0.05) compared with the model group. The expression of Rho A at the mRNA and protein levels was decreased obviously(P<0.05) in HLJD high-dose group. The results shown that HLJD increased diastolic factor(CAM and NOS) in the vascular endothelial of rats, leading to reduced contraction factor(ET-1 and vWF). HLJD revealed the preventive function in the vascular endothelial dysfunction of the early stage hypertension through adjusting secretion of blood vessel endothelium(BVE) relaxing factor and improving vascular endothelial function. The mechanism might be associated with the inhibition of the activity of RhoA protein factor.