Intravenous Drip of Somatostatin Followed by Restricted Fluid Resuscitation to Treat Upper Gastrointestinal Bleeding in Patients with Liver Cirrhosis.

OBJECTIVE: Liver cirrhosis is a common, often progressive, and usually fatal disorder. Upper gastrointestinal bleeding is a leading cause of death in patients with liver cirrhosis. The purpose of this study was to evaluate the effectiveness of somatostatin combined with restricted fluid resuscitation in the treatment of upper gastrointestinal bleeding in the patients with liver cirrhosis. METHODS: From January 2018 to December 2020, 84 patients with liver cirrhosis complicated by upper gastrointestinal bleeding admitted to the Department of Gastroenterology of Ningbo Yinzhou No. 2 Hospital were selected as study participants. They were randomly assigned into the study group (n = 42) and control group (n = 42). All patients were given intravenous drip of somatostatin. The study group was supplemented with restricted fluid resuscitation therapy. The hemoglobin (Hb), platelet, fibrinogen, hematocrit, transfusion volume of red blood cells, hemostatic time, hemostatic rates in 0 h-24 h, 24 h-48 h, and >48 h, rebleeding rates, resuscitation rate, and incidence rates of complications were compared between the two groups 48 h after treatment. RESULTS: It was found that the Hb, platelet, fibrinogen, and hematocrit were notably increased in the study group compared to the control group 48 h after treatment (P < 0.01). The proportion of patients with excellent response was notably higher in the study group than in the control group (P < 0.05). The overall response rate of the study group was 90.48%, which was significantly higher than 71.43% in the control group (P < 0.05). The study group had lower transfusion volume of red blood cells, shorter hemostatic time, and lower rebleeding rates than the control group (P < 0.01). The hemostatic rate of 0 h-24 h in the study group was remarkably higher than that in the control group (P < 0.05). The hemostatic rate of >48 h in the study group was lower than that in the control group (P < 0.05). The overall incidence rate of complications in the study group was 9.52%, which was significantly lower than 30.95% in the control group (P < 0.05). CONCLUSION: These data suggest that intravenous drip of somatostatin followed by restricted fluid resuscitation leads to a better clinical efficacy in treating upper gastrointestinal bleeding in patients with liver cirrhosis considering higher resuscitation rate and hemostatic rate and reduced incidence of complications, which is conducive to the recovery of patients and worthy of further clinical promotion.

Additional Benefits Conferred by Endoscopic Sclerotherapy to Liver Cirrhosis Patients Receiving Endoscopic Variceal Ligation.

OBJECTIVE: Gastroesophageal varices are a direct consequence of portal hypertension in cirrhosis. The management of gastroesophageal varices has evolved over the last decade resulting in reduced mortality and morbidity rates. The study was aimed to analyze the short-term and long-term efficacy of different endoscopic methods in the treatment of gastric varices in cirrhotic patients. METHODS: From January 2016 to December 2019, 135 patients with liver cirrhosis and gastric varices undergoing different endoscopic treatment protocols were retrospectively analyzed. The patients were divided into three groups according to endoscopic variceal ligation, endoscopic sclerotherapy, and a combination of both, respectively. Main outcomes including the overall response rate, hemostasis, short- and long-term rebleeding (3 months before and after treatment), complication, blood pressure, heart rate, portal venous pressure (PVP), portal vein diameter (PVD), portal vein velocity (PVV), portal vein blood flow (PVF) detected by ultrasound, recurrence rate, and mortality were analyzed after treatments. RESULTS: The overall response rate in the combined group was higher than that in the ligation group and the sclerotherapy group (P < 0.05). The incidence rate of complications in the combined group and the ligation group was lower than that in the sclerotherapy group (P < 0.05). After treatment, the PVP, PVD, and PVF were reduced in the combined group compared with the ligation group and the sclerotherapy group, while the PVV was not (P < 0.05). Lower rates of long-term rebleeding, recurrence, and mortality were noted in the combined group compared to the ligation group and the sclerotherapy group (P < 0.05). CONCLUSION: Endoscopic variceal ligation combined with endoscopic sclerotherapy is more effective than both alone in treating liver cirrhosis and gastric varices. The combined therapy contributed to reduced short-term and long-term rebleeding rate, decreased long-term recurrence rate, and mortality.

[A new method for establishing a ventricular fibrillation model by TCEI in Tibetan miniature pig].

OBJECTIVE: To explore an economical, convenient, safe and efficient method for establishing a Tibetan miniature pig model of cardiac arrest (CA). METHODS: Cardiac puncture was performed in 12 Tibetan miniature pigs using two acupuncture needles. One needle was inserted into the fourth intercostal near the right side of the sternum about 3 cm in depth at an angle of 30° to 60° between the chest and the needle, and the depth was adjusted until the handle of the needle vibrated with the heartbeat without premature ventricular contraction on the electrocardiogram; the other was inserted into the subcutaneous tissue of the left armpit about 3 cm in depth without damaging important organs. The handles of the two needles were connected with 9V dry batteries to form a circuit and generate direct current stimulation. Ventricular fibrillation was produced in the pigs to induce CA by stimulation of transcutaneous electrical induction (TCEI) for 3 s, and the success rate of modeling was recorded. After an interval of 4 min without intervention, cardiopulmonary resuscitation (CPR) was performed using the standard Utstein style, and the survival of the pigs after recovery was observed. RESULTS: The success rate of ventricular fibrillation modeling was 91.67% (11/12) using this method, and CPR achieved a success rate of 45.45% (5/11) in these models. The subsequent survival of the pigs was 100% (5/5) at 24 h and 80% (4/5) at 72 h. After observation for 72 h, the resuscitated Tibetan miniature pigs were dissected, and no significant damage was found in the vital organs in the thoracic or abdominal cavities. CONCLUSIONS: We successfully established a model of CA using acupuncture needles and dry batteries in Tibetan miniature pigs, and this method is economical, convenient, safe and efficient.

Histological response to combination therapy with nucleos(t)ide analogs and peginterferon alpha in treatment-naïve chronic hepatitis B patients.

Although nucleos(t)ide analog (NA) monotherapy is effective in hepatitis B virus suppression and fibrosis regression, serological response rates are not satisfactory. Studies assessing the benefits of combination therapy with NAs and peginterferon alpha (PegIFNα) in patients with chronic hepatitis B (CHB) have produced conflicting results and mainly focused on serological outcomes. Histological changes in response to combination therapy have not been evaluated in real-world practice. This study aimed to evaluate the histological changes in response to NA-PegIFNα combination therapy in CHB patients and to comprehensively compare the efficacy of NA-PegIFNα combination therapy and NA monotherapy. We conducted a retrospective analysis of data from 40 CHB patients who underwent either NA-PegIFNα combination therapy or NA monotherapy. Changes in histology at 48 weeks after treatment initiation were evaluated. Serological characteristics were also analysed and compared between the NA-PegIFNα combination therapy and NA monotherapy groups and between histological responders and nonresponders. Compared to baseline biopsies, both fibrosis staging and necroinflammatory grading scores were significantly lower in the second biopsies examined post-treatment in both groups. Nearly all patients experienced a reduction in inflammation (87.5% in both groups), but there was a subgroup of patients who exhibited either no significant improvement or fibrosis progression (33.3% and 31.2% in the NA monotherapy and NA-PegIFNα combination therapy groups, respectively). Nearly, all patients achieved ALT normalization and sustained virological response (SVR) after 48 weeks of antiviral treatment. Approximately one-third of individuals (36.8% and 30% in the two groups, respectively) achieved HBeAg loss at 48 weeks after treatment initiation. Although there were no significant differences in overall rates of histological, biochemical, virological and serological responses between the two groups, an earlier virological response and a higher cumulative SVR rate over time were observed during long-term follow-up in patients treated with NA-PegIFNα combination therapy (P = 0.0129). Trends of more rapid HBeAg loss and a higher cumulative HBeAg loss rate throughout long-term follow-up were also observed but were not statistically significant. The ALT normalization rates at 24 and 48 weeks after treatment initiation were associated with the histological response. Significant regression of fibrosis and resolution of necroinflammation were induced with either NA-PegIFNα combination therapy or NA monotherapy. Significant biochemical, virological and serological responses were observed in both groups, and the response rates at 48 weeks were similar in the two groups. Over time during long-term follow-up, the virological and serological responses were faster and superior following the combination regimen.

Histological responses of peginterferon alpha add-on therapy in patients with chronic hepatitis B with advanced liver fibrosis after long-term nucleos(t)ide analog treatment.

Although long-term antiviral treatment with nucleos(t)ide analogs (NAs) can lead to histological improvement in patients with chronic hepatitis B (CHB), a substantial proportion of patients still fail to achieve regression of fibrosis. Here, we investigated whether peginterferon alpha (Peg-IFNα） add-on therapy had benefits on fibrosis regression in patients with sustained severe fibrosis even after long-term NA treatment. We conducted a retrospective analysis of data from 50 patients with CHB receiving 48 weeks of Peg-IFNα add-on therapy. All enrolled patients had advanced fibrosis or cirrhosis (S score ≥ 3) at baseline and underwent NA treatment for at least 1 year before Peg-IFNα addition. Paired liver biopsies before and after Peg-IFNα add-on treatment and laboratory tests at baseline, 24 weeks of treatment, 48 weeks of treatment and long-term follow-up were analysed. Of the 50 patients enrolled in this study, 34 patients (68.0%) had significant regression of fibrosis, and 42 (84.0%) showed significant remission of inflammation after Peg-IFNα add-on treatment. Compared with nonresponders, patients with significant histological improvement showed faster hepatitis B surface antigen (HBsAg) decline and tended to have higher cumulative hepatitis B e antigen (HBeAg) and HBsAg loss rates during long-term follow-up. Peg-IFNα add-on therapy led to significant regression of fibrosis and resolution of inflammation in patients with advanced fibrosis after long-term NA treatment.

[Urotensin II induces hypertrophy of in vitro cultured neonatal rat cardiac myocytes].

OBJECTIVE: To examine whether urotensinII (UII) induces hypertrophy of neonatal rat cardiomyocytes cultured in vitro. METHODS: The primary cardiac myocytes cultured for 40 h followed by further culture in serum-free media for another 24 h were subjected to exposure to UII of varied concentrations for 24 h, after which the changes in the size of the cells were analyzed by flow cytometry with (3)H-leucine incorporation also measured. RESULTS: At the concentration of 1x10(-7) mol/L, UIIcould increase the size of the cultured cardiac myocardial cells (P=0.021) and 3H-Leucine incorporation (P=0.015). CONCLUSION: UII may induce hypertrophy of neonatal rat cardiac myocytes cultured in vitro.

[Effects of urotensin II on cultured cardiac fibroblast proliferation and collagen type I mRNA expression].

OBJECTIVE: To observe the effect of urotensin II on cultured cardiac fibroblast collagen type I mRNA expression and proliferation, thereby to explore the role of urotensin II in myocardial remodeling in the event of cardiac failure. METHODS: Cardiac fibroblasts of neonatal Sprague-Dawley rats isolated by trypsin digestion method were stimulated by urotensin II at varied concentrations when the cells reached growth arrest. MTT assay was employed to measure the proliferation and determine the number of the cells, and reverse transcriptional (RT)-PCR used to detect the collagen mRNA expression. RESULTS: With the increase of urotensin II concentration, the optical density at 570 nm of the fibroblasts as shown by MTT assay first increased but then decreased, and remained at a significantly higher level in the cells treated with 1x10(-8) or 1x10(-9) mol/L urotensin II as compared with the control (P<0.05). The collagen type I mRNA levels of the cells treated with 1x10(-7), 1x10(-8) or 1x10(-9) mol/L urotensin II were significantly higher than that of the control cells (P<0.01). CONCLUSION: Urotensin II can directly induce cardiac fibroblast proliferation and significantly increase collagen type I mRNA expression, suggesting the crucial role of urotensin II in myocardial remodeling.