Systemic and pulmonary hemodynamics in patients with extrahepatic portal vein obstruction is similar to compensated cirrhotic patients

Background  Patients with cirrhosis and portal hypertension exhibit a hyperdynamic circulation manifesting as increased cardiac output, heart rate and plasma volume; and decreased arterial blood pressure, systemic vascular resistance, and pulmonary vascular resistance. It is believed that these changes are related to both hepatocellular dysfunction and portal hypertension. However, the role of portal hypertension per se in producing these changes in circulation has not been clear. Extrahepatic portal vein obstruction (EHPVO), a vascular disorder of the liver characterized by cavernomatous transformation of the main portal vein, is an excellent model to study the role of portal hypertension per se in producing these changes because there is no hepatic dysfunction in EHPVO. The main aim of our study was, therefore, to evaluate alterations of systemic and pulmonary vascular systems in patients with EHPVO and compare them with patients with compensated cirrhosis. Patients and methods  Consecutive patients of EHPVO, 15 years or older, and past variceal bleeders were studied. For comparison, consecutive patients with compensated cirrhosis and history of variceal bleed, matched for variceal status, and body surface area were included. The hemodynamic studies included the measurements of cardiac index (by Fick’s oxygen method), and systemic and pulmonary vascular resistance indices. Results  Fifteen patients of EHPVO and same number of controls (compensated cirrhotics) were included in the study. The baseline parameters in the two groups were comparable. Both EHPVO patients and cirrhotics had similar values in all the measured systemic and pulmonary hemodynamic parameters. The median (range) cardiac index in EHPVO was 3.8 (2.3–7.7) l min⁻¹ m⁻², whereas it was 4.4 (2.8–8.9) l min⁻¹ m⁻² in cirrhosis (P = 0.468). The median (range) systemic vascular resistance index in EHPVO was 1,835 (806–3400) dyne s cm⁻⁵ m⁻², which was similar to that in cirrhotic patients (1,800 [668–3022], P = 0.520). Similarly, the values of median (range) pulmonary vascular resistance index were comparable in the two groups (71 [42–332] vs. 79 [18–428], P = 0.885). A subgroup analysis was done for 8 patients of EHPVO and 8 age-matched compensated cirrhotic patients, which also revealed similar values of cardiac index, cardiac output, systemic vascular resistance index, systemic vascular resistance, pulmonary vascular resistance index, and pulmonary vascular resistance in the two groups. Conclusions  EHPVO patients have hyperdynamic circulation manifested by high cardiac index and low systemic and pulmonary vascular resistance indices. These hemodynamic changes are comparable with compensated cirrhotic patients who have similar grade of portal hypertension. This suggests a predominant role of portal hypertension per se in the genesis of systemic and pulmonary hemodynamic alterations.     

Prevalence of autonomic dysfunction in cirrhotic and noncirrhotic portal hypertension

OBJECTIVE: Autonomic dysfunction is common in patients with cirrhosis of the liver, but more so in patients with decompensated state, and is associated with increased mortality. We evaluated the presence and extent of autonomic dysfunction in patients with extrahepatic portal venous obstruction (EHPVO) and noncirrhotic portal fibrosis (NCPF), diseases with relatively preserved liver functions. METHODS: Heart rate variability in response to standing, deep breathing, and Valsalva maneuver and blood pressure response to sustained handgrip and standing were studied in 18 patients with EHPVO (13 mol/L, 5 F, mean age 15.2 +/- 6 yr), 12 patients with NCPF (5 mol/L, 7 F, mean age 26.4 +/- 8 yr), 15 patients with cirrhosis (7 mol/L, 8 F, mean age 12.6 +/- 6 yr), and 17 healthy controls (11 mol/L, 6 F, mean age 18.6 +/- 3 yr). Time-domain parameters of heart rate variability on 24-h ambulatory monitoring were assessed in all the patients. RESULTS: Autonomic dysfunction was observed in 67% of EHPVO, 25% of NCPF, and 80% of cirrhotic subjects but none of the healthy controls (p < 0.05). Four of five time-domain heart rate variability indices showed significant abnormalities in patients with EHPVO (p < 0.05) and cirrhosis (p < 0.05), when compared with patients with NCPF and healthy controls. CONCLUSIONS: Autonomic dysfunction is frequently encountered in patients with EHPVO and cirrhosis, and the presence of autonomic dysfunction in patients with noncirrhotic portal hypertension suggests a primary role of portal hypertension per se in the dysfunction.     

Nitric oxide levels in chronic liver disease patients with and without oesophageal varices

Introduction Patients with chronic liver disease ultimately progress to develop cirrhosis and portal hypertension. Recently it seems well established that nitric oxide disturbances play a key role in the pathogenesis of chronic liver disease and portal hypertension. The aim of this work was to clarify the correlation between chronic liver disease stages, liver function status, esophageal varices presence and nitric oxide disturbances. Subjects and methods All subjects (n = 120) in the present study were classified into; group I which included 15 age and sex matched healthy volunteers (taken as control), group II which included 20 patients with chronic active hepatitis, and group III which included 85 patients with hepatic cirrhosis. All subjects included were subjected to full clinical assessment, routine laboratory investigations, serum nitrate level determination using colorimetric method, abdominal ultrasonography and upper endoscopy. Results Increased serum nitrate level could not be detected in patients with chronic active hepatitis as well as those with early cirrhosis (Child’s class A). Progressive and significant increase of serum nitrate levels were detected in more advanced stages of cirrhosis (Child’s class B & C). The best non-invasive predictor for the presence of oesophageal varices was a combination of platelet count <150.000/mm³, splenomegaly >18 cm, Child’s class B or C and serum nitrate ≥38 μmol/l, with 93.3% sensitivity and 100% specificity. Conclusion Serum nitrate level can be used as a non-invasive predictor for progression of chronic liver disease as well as for the presence of oesophageal varices. An erratum to this article can be found at     

Small-Intestinal Bacterial Overgrowth in Patients with Liver Cirrhosis,Diagnosed with Glucose H2 or CH4 Breath Tests

Background: Small-intestinal bacterial overgrowth (SIBO) has been considered a predisposing factor of spontaneous bacterial peritonitis in cirrhotic patients by bacterial translocation or hematogenous spread during spontaneous bacteremia. We investigated 45 cirrhotic patients and 28 healthy subjects to assess the prevalence of SIBO and its relationship with the severity of liver dysfunction and the presence of ascites. Methods: Bacterial overgrowth was measured by the glucose hydrogen and methane breath test. Results: SIBO was documented in 16 (35.6%) of the 45 cirrhotic patients and in 1 (3.6%) of the 28 healthy controls. The prevalence of SIBO was significantly higher in patients with Child-Pugh class B or C (50%) than in those with class A (19%) and had no relationship with the presence or absence of ascites. Conclusions: We conclude that the prevalence of SIBO in cirrhotic patients is approximately 35.6% and that it is related to the severity of liver disease. There was no difference among various causes of cirrhosis, such as viral, alcoholic, or idiopathic.     

Small intestinal bacterial overgrowth is common both among patients with alcoholic and idiopathic chronic pancreatitis

BackgroundSmall intestinal bacterial overgrowth (SIBO) is known to occur in patients with chronic pancreatitis, particularly of alcoholic etiology. There are, however, scanty data on frequency of SIBO in patients with chronic idiopathic pancreatitis and factors associated with its occurrence.Methods68 patients with chronic pancreatitis and 74 age and gender-matched healthy subjects (HS) were evaluated for SIBO using glucose hydrogen breath test (GHBT). Persistent rise in breath hydrogen 12 ppm above basal (at least two recordings) was diagnostic of SIBO.ResultSIBO was diagnosed more often among patients with chronic pancreatitis than controls (10/68 [14.7%] vs. 1/74 controls [1.3%]; p = 0.003). Of 68 patients, 22 (32.3%) had alcoholic and 46 (67.6%) had idiopathic chronic pancreatitis. SIBO was as commonly detected among patients with alcoholic as idiopathic pancreatitis (3/22 [13.6%] vs. 7/46 [15.2%]; p = 0.86). Age, gender, body mass index (BMI), steatorrhoea, pain, analgesic use, pancreatic calcifications and use of pancreatic enzyme supplements had no relationship with the presence of SIBO. Diabetes mellitus tended to be commoner among patients with chronic pancreatitis with than without SIBO (6/10 [60%] vs. 18/58 [31%]; p = 0.07).ConclusionSIBO was commoner among patients with chronic pancreatitis, both alcoholic and idiopathic, than HS. Though presence of SIBO among patients with chronic pancreatitis tended to be commoner among those with diabetes mellitus, there was no relationship with age, gender, BMI, steatorrhoea, pain, analgesic use, pancreatic calcifications and use of pancreatic enzyme supplements.     

Portal Venous Flow Pattern as a Useful Tool for Predicting Esophageal Varix Bleeding in Cirrhotic Patients

This study aimed to evaluate whether (1) the portal venous flow pattern determined by color Doppler sonography could be related to the clinical severity of liver cirrhosis and (2) whether the flow patterns differ between patients with bleeding and nonbleeding esophageal varices. One hundred twenty-nine cirrhotic patients and 60 noncirrhotic healthy controls were enrolled after endoscopic survey for the presence of esophageal varices. Each patient received color Doppler echography to define the pattern of blood flow direction as hepatopetal or nonhepatopetal (hepatofugal, turbulence, and bidirection) in type. The patients with esophageal varices were further categorized into two groups: with recent bleeding (BEV; n = 99) and without recent bleeding (NBEV; n = 30). More patients in the BEV group (72.7%) had a nonhepatopetal Doppler flow pattern than in the control group (1.7%) and NBEV group (13.3%) (P < 0.001). Among the 129 cirrhotic patients, the nonhepatopetal flow pattern of the portal vein was higher in 96% of Child–Pugh grade C patients than in 41.8% of grade A patients and 57.6% of grade B patients (P < 0.05). Moreover, for those cirrhotic patients with Child–Pugh grades A and B, the nonhepatopetal Doppler flow pattern was more commonly found in the BEV group than in the NBEV group (63.0 vs. 13.8%; odds ratio, 10.64; 95% CI, 0.03–0.299; P < 0.001). Portal venous blood flow pattern is related to severity of cirrhosis. The presence of a nonhepatopetal flow pattern implicates an increased risk of esophageal varices bleeding, especially for those cirrhotic patients with Child–Pugh grades A and B.     

Coagulation profile and platelet function in patients with extrahepatic portal vein obstruction and non-cirrhotic portal fibrosis

BACKGROUND AND AIMS: Coagulation disorders commonly develop in patients with cirrhosis of the liver. They have also been reported in patients with non-cirrhotic portal fibrosis (NCPF) and extra-hepatic portal venous obstruction (EHPVO); the two conditions with portal hypertension and near-normal liver functions. The spectrum and prevalence of coagulation abnormalities and their association with the pathogenesis of these diseases and with hypersplenism was prospectively studied. METHODS: Eighteen EHPVO patients that included an equal number of NCPF patients and 20 healthy controls were prospectively studied. The coagulation parameters assessed included: international normalized ratio, partial thromboplastin time, and fibrinogen and fibrinogen degradation products. Platelet aggregation and malondialdehyde levels were measured. RESULTS: Both EHPVO (83%) and NCPF (78%) patients had a significantly prolonged international normalized ratio and a decrease in fibrinogen and platelet aggregation. The EHPVO patients had a significant prolongation in partial thromboplastin time (67% patients), with increased levels of fibrinogen degradation product levels occurring in all patients; these were normal in NCPF patients. Platelet malondialdehyde levels were normal in both groups. Hypersplenism was present in four EHPVO and seven NCPF patients. It did not significantly influence the coagulation profile in either NCPF or EHPVO patients. CONCLUSIONS: Coagulation anomalies are common and significant in both NCPF and EHPVO patients, suggestive of a mild disseminated intravascular coagulation disorder. These imbalances could be caused by chronic subclinical endotoxemia and cytokine activation after the initial portal thromboembolic event. The persistence of these abnormalities in adolescent patients indicates an ongoing coagulation derangement.     

Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Background: Extrahepatic portal venous obstruction (EHPVO) developing due to thrombotic occlusion of the portal vein in children is generally considered a benign disease. Whether hepatic dysfunction develops in these patients in the absence of a gastrointestinal bleed has not been well studied. Materials and methods: Forty‐three patients with EHPVO who had not bled in the last 3 months were studied. Patients were divided into those with (group I) or without ascites (group II). Matched cirrhotic patients with ascites (group III) served as controls. Clinical, biochemical, ultrasonographic, and histopathological evaluation was carried out. Portal biliopathy was assessed in five patients in group I and in 12 patients in group II by cholangiography. Results: Of 43 EHPVO patients, ascites was seen in nine (21%) patients (group I). Thirty‐four patients had no ascites (group II). Serum ALT (54±24 vs. 34±10 IU/l, P<0.01), albumin (3.2±0.3 vs. 3.7±0.4 g/dl, P<0.01), and prothrombin time difference (9.0±4.5 vs. 2.4±1.9 s, P<0.05) were deranged in patients in group I compared with group II. Patients in group I were 4 years older, and the duration of portal hypertension was longer than in group II (11.5 vs. 5.6 year, P<0.05). Portal biliopathy changes were significantly more severe in group I than in group II patients. Ascites was high gradient in all the patients in group I and the serum‐ascitic albumin gradient was comparable between groups I and III. None of the EHPVO patients, but four cirrhotic patients, developed spontaneous bacterial peritonitis during a follow‐up of 11±4 months. Conclusions: Hepatic dysfunction in the form of ascites and deranged liver functions is not uncommon in patients with EHPVO, more so in patients with prolonged portal hypertension. Based on our data it would be worthwhile to study whether prolonged portal vein thrombosis in EHPVO patients could lead to progressive liver disease.     

Lower frequency of MMC is found in IBS subjects with abnormal lactulose breath test,suggesting bacterial overgrowth

We have recently described an association between irritable bowel syndrome (IBS) and abnormal lactulose breath test, suggesting small intestinal bacterial overgrowth (SIBO). However, the mechanism by which SIBO develops in IBS is unknown. In this case–control study we evaluate the role of small intestinal motility in subjects with IBS and SIBO. Small intestinal motility was studied in consecutive IBS subjects with SIBO on lactulose breath test. After fluoroscopic placement of an eight-channel water-perfused manometry catheter, 4-hr fasting recordings were obtained. Based on this, the number and duration of phase III was compared to 30 control subjects. To test whether there was a relationship between the motility abnormalities seen and the SIBO status of the patient at the time of the motility, subjects with a breath test within 5 days of the antroduodenal manometry were also compared. Sixty-eight subjects with IBS and SIBO were compared to controls. The number of phase III events was 0.7 ± 0.8 in IBS subjects and 2.2 ± 1.0 in controls (P < 0.000001). The duration of phase III was 305 ± 123 sec in IBS subjects and 428 ± 173 in controls (P < 0.001). Subjects whose SIBO was still present at the time of manometry had less frequent phase III events than subjects with eradicated overgrowth (P < 0.05). In conclusion, phase III is reduced in subjects with IBS and SIBO. Eradication of bacterial overgrowth seems to result in some normalization of motility.     

小肠细菌过度生长与肝硬化并发自发性腹膜炎

目的探讨小肠细菌过度生长(SIBO)与肝硬化并发自发性腹膜炎(SBP)之间的关系,方法对80例肝硬化患者的SIDO和并发SBP情况进行分析,并与健康对照组进行比较。结果 80例肝硬化患者中27例SIBO阳性,阳性率33.75%(27/80),按Child-Pugh分级分组,分为A级、B级、C级三组,其SIBO阳性率分别为14.8%(4/27)、29.6%(8/27)、57.7%(15/26),各组间比较差异有显著性(P<0.01)。健康对照组25例SIBO全为阴性,与肝硬化组比较差异有显著性(P<0.01)。58例肝硬化并发SBP患者中有25例SIBO阳性,阳性率为43.1%;22例未并发SBP患者2例存在SIBO阳性,阳性率为9.1%,两组比较有统计学差异(P<0.01)。肝硬化并发SBP且SIBO阳性的25例患者,经2周治疗后有20例SIBO转阴,其中并发SBP的有2例,而在治疗后SIBO仍然阳性的5例患者中,并发SBP者有4例。结论肝硬化患者SIBO发生率高,并且随着肝功能损害程度的加重,SIBO发生率也随之增加,肝硬化伴SBP者SIBO发生率增加尤为显著。治疗SIBO能显著减少SBP的发生率。     

肝硬化患者小肠细菌过度生长及其外周血单个核细胞TLR4表达的变化

目的探讨肝硬化患者小肠细菌过度生长（SIBO）和外周血单个核细胞表面TLR4表达的变化。方法采用乳果糖-氢呼气试验（LHBT）检测40例肝硬化患者和16例正常人小肠细菌生长情况,使用流式细胞仪检测外周血单个核细胞表面TLR4表达。结果肝硬化患者SIBO检出率为42.5%（17/40）,显著高于正常人的6.3%（1/16,P<0.01）;肝硬化患者外周血单个核细胞表面TLR4相对表达量为（23.4±11.4）,显著高于正常人的【（14.4±5.2）,P<0.05】;17例肝硬化SIBO阳性患者外周血单个核细胞表面TLR4表达为（30.2±12.3）,显著高于23例肝硬化SIBO阴性患者【（19±8.6）,P<0.05】。结论肝硬化患者存在较高的SIBO发生率,外周血单个核细胞表面TLR4表达上调,SIBO可能通过与TLR4的作用在肝硬化病情进展中发挥作用。     

Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension.

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; Budd-Chiari syndrome, 2] were prospectively studied. Eighty-three patients had Child's A, 17 had Child's B, and 7 had Child's C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 +/- 3.4 months (range, 1-52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P less than 0.05) or EHPVO (8.7%; P less than 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of follow-up was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P less than 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child's C than Child's A patients (87% vs. 13%; P less than 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P less than 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension, coexisting gastric varices and is not directly correlated with intravariceal pressure.     

Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension

OBJECTIVE: Altered small bowel motility and a high prevalence of small intestinal bacterial overgrowth (SIBO) has been observed in patients with liver cirrhosis. Our aim was to explore the relationship between motility abnormalities, portal hypertension, and SIBO. METHODS: Twenty-four patients with liver cirrhosis were included. Twelve had portal hypertension (PH) and 12 had liver cirrhosis (LC) alone. Child-Pugh score was the same in the groups. Antroduodenojejunal pressure recordings were performed, and noninvasive variceal pressure measurements were undertaken. Thirty-two healthy volunteers served as a reference group. Bacterial cultures were obtained from jejunal aspirates. RESULTS: The PH group had a higher proportion of individual pressure waves that were retrograde in the proximal duodenum during phase II (52% vs 13% vs 8% of propagated contractions; p < 0.001) as well as postprandially (49% vs 18% vs 13%; p < 0.01) compared with LC and controls, respectively. Long clusters were more common in PH than in controls (9.1 +/- 2.1 vs 4.9 +/- 0.8; p < 0.05), and a higher motility index in phase III in the proximal and distal duodenum was seen in the PH as compared with the other groups. The mean variceal pressure was 21 +/- 1 mm Hg. Motor abnormalities were not correlated to the level of variceal pressure. Thirty-three percent of the patients in the PH group but none in the LC group had SIBO. CONCLUSIONS: Abnormal small bowel motility and SIBO is common in patients with liver cirrhosis with concomitant portal hypertension. Portal hypertension per se might be significantly related to small bowel abnormalities observed in patients with liver cirrhosis.     

Prevalence of hepatopulmonary syndrome in cirrhosis and extrahepatic portal venous obstruction

OBJECTIVE: Hepatopulmonary syndrome (HPS) is characterized by arterial hypoxemia in patients with chronic liver disease caused by abnormal intrapulmonary vasodilations. Data on its frequency vary from 5% to 29%. Most of these studies are from the West and in patients with cirrhosis. We, therefore, studied the prevalence of HPS in patients with liver cirrhosis and extrahepatic portal venous obstruction (EHPVO). METHODS: We studied 54 consecutive patients with liver cirrhosis (42 men and 12 women; mean age = 44.2 +/- 13 yr; Child grade A: 13, B: 22, and C: 19) and 50 patients with EHPVO (31 men and 19 women; mean age = 23.3 +/- 7.8 yr) Diagnosis of cirrhosis was made by history, liver function abnormalities, endoscopy, and sonography, whereas EHPVO was diagnosed by demonstration of a block in the splenoportovenous axis on sonography. Each of the patients underwent chest x-ray, arterial blood gas analysis, contrast-enhanced echocardiography (CEE), and pulmonary function tests. HPS was diagnosed in a patient with positive CEE, in the presence of hypoxia (PaO2 < 70 mm Hg) and/or elevated alveolar arterial oxygen gradient of > 20 mm Hg in the absence of any underlying cardiopulmonary disease. RESULTS: Ten of 54 patients (18.5%) with cirrhosis were positive on CEE compared with two of 50 patients (4%) with EHPVO. Six of the 10 patients positive with cirrhosis for CEE had associated hypoxia, whereas only one EHPVO patient with positive CEE had an elevated pulmonary alveolar arterial oxygen gradient of > 20 mm Hg. Thus, the incidence of HPS was 11.1% in patients with cirrhosis, compared with 2% in patients with EHPVO. One patient with HPS and cirrhosis had clinical cyanosis. CONCLUSION: HPS occurs more commonly in patients with cirrhosis but can also be seen in patients with EHPVO.     

小肠细菌过度生长相关性轻微肝性脑病患者的血浆内毒素水平

目的观察肝硬化患者小肠细菌过度生长相关性轻微肝性脑病患者的内毒素水平,探讨内毒素与轻微肝性脑病的关系。方法对90例肝硬化患者及20例健康志愿者进行内毒素水平、葡萄糖氢呼气试验（GHBT）、数字连接试验（NCT—A和NCT—BC）和数字符号试验（DST）检测,观察小肠细菌过度乍长相关性轻微肝性脑病患者的内毒素水平变化。结果肝硬化组小肠细菌过度生长（36．7％,33／90）明显高于健康对照组（5％,1／20）。20名健康志愿者未检出轻微肝性脑病（MHE）;90例肝硬化患者轻微肝性脑病37例（41．1％）,其中伴小肠细菌过度生长肝硬化患者轻微肝性脑病发生率高于不伴小肠细菌过度生长患者。肝硬化组内毒素水平（69．6±21．3）pg／mL高于健康对照组（18．7±8．6）pg／mL;肝硬化小肠细菌过度生长组内毒素水平（89．5±17．6）pg／mL高于无小肠细菌过度生长组（57．3±15．8）pg／mL（P〈0．05）。应用抗生素抑制小肠细菌过度生长及乳果糖治疗1周后GHBT、内毒素水平、NCT—A、NCT-BC及DST检查结果改善。结论内毒素与伴小肠细菌过度生长的轻微肝性脑病的发生及进展可能有一定的关系。     

枯草杆菌二联活菌肠溶胶囊联合枸橼酸莫沙必利治疗乙肝肝硬化合并小肠细菌过度生长疗效探究

目的:探究枯草杆菌二联活菌肠溶胶囊联合枸橼酸莫沙必利治疗乙肝肝硬化合并小肠细菌过度生长(SIBO)疗效。方法:选取潍坊市人民医院感染科2020年10月-2021年4月收治的68例失代偿期乙肝肝硬化患者,行葡萄糖甲烷氢呼气试验诊断乙肝肝硬化合并SIBO 48例,随机分为试验组(24例)和对照组(24例),对照组给予保肝、低蛋白饮食、抗病毒等常规治疗,试验组在常规治疗的基础上加用枯草杆菌二联活菌肠溶胶囊(500 mg/次,3次/饭后)联合枸橼酸莫沙必利(5 mg/次,3次/饭前)治疗,观察2组治疗前后葡萄糖甲烷氢呼气试验、血清谷草转氨酶(AST)、谷丙转氨酶(ALT)、内毒素、白细胞介素-6(IL-6)、肿瘤坏死因子(TNF-α)、肝功能Child-Pugh及腹部不适变化。结果:48例患者中有44例完成试验,有4例退组,其中试验组有1例出现消化道出血,1例未规律服药,对照组有2例出现肝性脑病(HE)。治疗后,试验组呼气试验转阴率为63.6%,明显高于对照组的9.1%(P<0.01);腹部不适减轻总有效率为100.0%,显著高于对照组68.5%(P<0.01);内毒素、TNF-α...     

Portal vein thrombosis： Etiology and clinical outcome of cirrhosis and malignancy-related non-cirrhotic, non-tumoral extrahepatic portal venous obstruction

The etiology and pathogenesis of portal vein thrombosis are unclear. Portal venous thrombosis presentation differs in cirrhotic and tumor-related versus non-cirrhotic and non-tumoral extrahepatic portal venous obstruction (EHPVO). Non-cirrhotic and non-tumoral EHPVO patients are young and present with well tolerated bleeding.Cirrhosis and tumor-related portal vein thrombosis patients are older and have a grim prognosis. Among the 118 patients with portal vein thrombosis, 15.3% had cirrhosis, 42.4% had liver malignancy (primary or metastatic), 6% had pancreatitis (acute or chronic), 5% had hypercoagulable state and 31.3% had idiopathy,12% had hypercoagulable state in the EHPVO group.     

Fasting and postprandial plasma ghrelin levels are decreased in patients with liver failure previous to liver transplantation

Anorexia is a problem of paramount importance in patients with advanced liver failure. Ghrelin has important actions on feeding and weight homeostasis. Concentrations of ghrelin are controversial in liver cirrhosis. Our aim was to study fasting ghrelin and their response to an oral glucose tolerance test (OGTT) in liver failure patients and normal subjects. Methods We included 16 patients with severe liver failure prior to liver transplantation. As a control group we included 10 age- and BMI-matched healthy subjects. After an overnight fast, 75 g of oral glucose were administered; glucose, insulin, and ghrelin were obtained at baseline and at times 30, 60, 90, and 120 min, respectively. Results Fasting ghrelin (median and range) were statistically significantly lower for patients compared to the controls, 527 (377–971) pg/ml vs. 643 (523–2163) pg/ml, P = 0.045, for patients and controls, respectively. The area under the curve for total ghrelin post-OGTT were lower in end-stage liver failure patients than in the control group, 58815 (44730–87420) pg/ml min vs. 76560 (56160–206385) pg/ml min, for patients and controls, respectively, P = 0.027. Conclusions Ghrelin levels are significantly decreased both fasting and post-OGTT in patients with liver failure candidates for transplantation. Decreased ghrelin levels could contribute to anorexia in patients with cirrhosis.     

Magnetic Resonance Imaging of Brain in Patients with Cirrhotic and Non-Cirrhotic Portal Hypertension

Background Hyperintense signals in the basal ganglia, namely the globus pallidus, have been reported on magnetic resonance imaging (MRI) in 70-100% of patients with cirrhosis of the liver. Deposition of paramagnetic substances, particularly manganese (Mn), has been reported to be responsible for these hyperintense signals. They are found in cirrhotics with or without overt/subclinical hepatic encephalopathy. Deposition of Mn has been attributed to hepatocellular failure and/or portosystemic shunting. Reports of MRI brain findings in patients with extra hepatic portal venous obstruction (EHPVO) and non-cirrhotic portal fibrosis (NCPF) are scanty in the literature. Aims The purpose was to determine the basal ganglia changes on MRI in patients with EHPVO and NCPF and to compare it with patients with cirrhosis of the liver. Patients and Methods A total of 27 patients (EHPVO = 10, mean age 28.4 +/- 19.0 years, NCPF = 7, mean age 37.1 +/- 10.4 years, cirrhosis = 10, mean age 47.0 +/- 19.6 years) was studied prospectively from January to December 2001. MRI of the brain was done with a standard spin echo axial T1- and fast spin echo T2-weighted scan obtained on a 1.5-T MRI unit. Two radiologists in a blinded fashion graded the signal intensity of basal ganglia on T1-weighted (T1 W) sequences by comparing it with the adjacent unaffected grey matter. Results None of the patients with EHPVO or NCPF had any past history of hepatic decompensation and/or overt encephalopathy. Seven (70%) of the cirrhotics had a past history of overt encephalopathy. None of the patients with EHPVO showed any hyperintensity of basal ganglia on T1-weighted MRI images. Hyperintense globus pallidus was seen in four (57%) and eight (80%) patients with NCPF and cirrhosis, respectively. Conclusion Hyperintense globus pallidus on MRI is common in patients liver cirrhosis and also occurs in patients with NCPF. Patients with EHPVO do not have hyperintense globus pallidus on T1-weighted MRI images.     

Relation of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 levels to growth retardation in extrahepatic portal vein obstruction

Background  Growth retardation has been described in patients with extrahepatic portal vein obstruction (EHPVO). An abnormal growth hormone (GH)–insulin-like growth factor (IGF) axis has been postulated as a possible etiology. We compared anthropometric parameters and IGF-1 and insulin-like growth factor binding protein-3 (IGFBP-3) levels in patients with EHPVO with their siblings as controls. Methods and patients  Consecutive patients diagnosed with EHPVO who presented to out-patient clinic in Department of Gastroenterology between February 2005 and February 2006 were enrolled along with their siblings whenever possible. After detailed history and clinical examination, anthropometric parameters such as age, height, weight, and mid-parental height were measured in patients and controls. IGF-1 and IGFBP-3 levels were also estimated. Results  Fifty-two patients (40 males, 32 adults) were enrolled. Sibling controls were available for 28 patients. Variceal bleeding was the presenting symptom in 41 of 52 (78.8%) patients. Target height was not achieved in 7 of 32 (22.6%) adults and 6 of 20 (30%) children, showing evidence of growth retardation. The mean IGF-1 levels in patients and controls were 124.71 ± 65.49 ng/ml and 233 ± 76.98 ng/ml (P < 0.01), respectively. The mean IGFBP-3 levels in patients and controls were 2.90 ± 1.07 μg/ml and 4.22 ± 0.77 μg/ml (P < 0.01), respectively. Hormonal levels between those with and without evidence of growth retardation did not differ significantly. Duration of symptoms, spleen size, platelet count, and age of presentation did not correlate with anthropometry and hormonal levels. Conclusions  Growth retardation by anthropometry was documented in a quarter of patients with EHPVO. All patients had significantly low IGF-1 and IGFBP-3 levels in comparison with controls despite normal anthropometry in majority of patients (75%).