Helicobacter pylori versus Platelet-to-Spleen Ratio as a Risk Factor for Variceal Bleeding in Patients with Liver-Cirrhosis-Related Portal Hypertension

Khaled Metwally ◽  
Tarek Essam ◽  
Ahmed Atwa ◽  
Samah Awad ◽  
Eman Abdelsameea
2013 ◽  
Vol 28 (9) ◽  
pp. 1444-1449 ◽  
Yoshihiro Sakamoto ◽  
Kazuhiko Oho ◽  
Atsushi Toyonaga ◽  
Masafumi Kumamoto ◽  
Tsuyoshi Haruta ◽  

2020 ◽  
Vol 3 (31) ◽  
pp. 53-61
T. Bentsa ◽  

Introduction. Liver cirrhosis (LC) is an important medical and socio-economic problem not only in Ukraine, but throughout the world. The urgency of this disease is due to its significant spread, increase of the number of etiological factors, as well as the occurrence of severe complications, which often leads to death. The prognosis depends on several factors, such as etiology, the severity of liver damage, the presence of complications and concomitant diseases. The aim of the study. To review the scientific literature and summarize the published studies devoted to the study of the etiology, classification, clinical picture and diagnosis of liver cirrhosis. Materials and methods. The content analysis, the method of systemic and comparative analysis, the bibliosemantic method of studying the current scientific research on the etiology, classification, clinical picture and diagnosis of LC were used. The search for sources was carried out in scientometric databases: PubMed-NCBI, Medline, Research Gate, Cochrane Database of Systematic Reviews for the keywords: liver cirrhosis, diagnosis, treatment. 37 literary sources were selected and analyzed. Results. LC is currently ranked 11th among the most common causes of death. The common causes of LC are chronic alcohol intoxication and viral hepatitis B, C, and D. LC is represented by an increase in severity, which is characterized by the lesions of the liver parenchyma with necrosis, dystrophy of hepatocytes, their nodular regeneration, as well as its interstitium with diffuse proliferation of connective tissue, leading to liver failure and portal hypertension. Most patients with cirrhosis remain asymptomatic until they develop decompensated LC. Despite the existence of a number of LC classifications – by morphology, etiology, severity, course, hepatocellular insufficiency stage, the severity of the disease is usually assessed by evaluation of the hepatic functional reserve (according to the C. G. Child – R. N. Pugh classification). Patients with LC often have life-threatening conditions such as variceal hemorrhages, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome. Variceal bleeding is a major complication of portal hypertension, which is associated with significant mortality. Ascites represents the most common decompensating event in patients with LC. The appearance of ascites is strongly related to portal hypertension, which leads to splanchnic arterial vasodilation, reduction of the effective circulating volume, activation of endogenous vasoconstrictor systems, and avid sodium and water retention in the kidneys. Bacterial translocation further worsens hemodynamic alterations of patients with cirrhosis and ascites. Ascites is also associated with a high risk of developing the further complications of cirrhosis such as dilutional hyponatremia, spontaneous bacterial peritonitis and/or other bacterial infections and acute kidney injury. Pharmacotherapy for LC should be implemented in accordance with up-to-date guidelines and in conjunction with etiology management, nutritional optimization and patients’ education. The main treatment of uncomplicated ascites is diuretics such as spironolactone in combination with a loop one. Vasoconstrictors and albumin are recommended for the treatment of refractory ascites. In its turn antibiotics play a well-established role in the treatment and prevention of spontaneous bacterial peritonitis. The administration of vasopressor terlipressin and albumin is recommended for the treatment of hepatorenal syndrome. Pharmacological therapy of variceal bleeding aims to decrease the portal pressure by acting on its pathophysiological mechanisms such as increased hepatic vascular tone and splanchnic vasodilatation. Propranolol blocks the β-1 in the heart and the peripheral β-2 adrenergic receptors. β-1 blockade of cardiac receptors reduces heart rate, cardiac output and subsequently decreases flow into splanchnic circulation. β-2 blockade leads to unopposed α-1 adrenergic activity that causes splanchnic vasoconstriction and reduction of portal inflow. Both effects contribute to reduction in portal pressure. Carvedilol is more powerful in reducing hepatic venous pressure gradient than traditional nonselective β-blockers. Endoscopic treatment in many cases is used for the variceal bleeding (eg., ligation of the esophageal varices and tissue glue usage for the gastric varices). A shunt (transjugular intrahepatic portosystemic shunting – TIPS) is used to treat severe and often repeat variceal hemorrhage or refractory ascites. Non-selective β-blockers effectively reduce variceal re-bleeding risk in LC patients with moderate/large varices. Conclusions. Liver cirrhosis is one of the most dangerous multi-organ diseases of a human with multiple pathogenetic links, the causes of which invariably remain hepatitis viruses, alcohol, toxic substances, drugs, ultraviolet radiation, genetic factors, some chronic diseases of the internal organs. There are a number of classifications of liver cirrhosis – by morphology, etiology, severity, course, severity of hepatocellular insufficiency etc. Examination of this category of patients requires timeliness, scrupulousness, compliance with a comprehensive approach using modern clinical, laboratory and instrumental methods. During the objective examination of a patient a doctor traditionally draws attention to the presence of telangiectasia, palmar erythema, jaundice, “raspberry” tongue, scratching marks, gynecomastia in men, ascites and “caput medusae”, during the palpation the liver is enlarged, dense, with a sharp lower edge, spleen is enlarged. Among the laboratory methods, in addition to routine ones, the immunological tests are used, among the main instrumental examination – ultrasound, computed tomography, indirect elastometry of the liver or Fibroscan, esophagogastrofibroscopy, puncture biopsy of the liver, in particular modern ones – vibrational transient elastography and magnetic resonance elastography. Although liver cirrhosis is the final stage of liver disease, this diagnosis cannot be considered a verdict for a patient, because today there are quite effective treatments using the principles of differentiation – the impact on the etiological factor, liver state and comorbid lesions and their complications often allows if not to cure the patient, then to prevent the negative disease course. Among them, there are diet, the use of etiotropic drugs, intestinal sanitation, correction of clinical and laboratory syndromes, portal hypertension syndrome, endothelial and autonomic dysfunction as causes of comorbid lesions and their complications.

2014 ◽  
Vol 2014 ◽  
pp. 1-2
Murat Biyik ◽  
Ramazan Ucar ◽  
Sami Cifci ◽  
Orhan Ozbek ◽  
Gokhan Gungor ◽  

Variceal bleeding is the major complication of portal hypertension in patients with liver cirrhosis. Hemorrhage mainly occurs in gastrointestinal lumen. Extraluminal hemorrhages are quite rare, such as intraperitoneal hemorrhages. We aimed to present a variceal bleeding case from the anastomosis on the anterior abdominal wall, as an extraordinary bleeding location, in a patient with portal hypertension in whom there were no esophageal and gastric varices.

2020 ◽  
Vol 11 (SPL2) ◽  
pp. 228-234
Karthick M ◽  
Prabakaran P T ◽  
Rajendran K ◽  
Gowrishankar A ◽  
Halleys Kumar E ◽  

Portal hypertension is associated with liver cirrhosis and esophageal varices is a common complication. Cirrhotic liver increases resistance to the passage of blood and thereby increased splanchnic blood flow secondary to vasodilation. Prevalence of portal hypertension varies from 50-60% in patients with liver cirrhosis. The first episode of variceal bleeding causes mortality, which ranges from 40-70%. All cirrhotic patients should be screened for the oesophageal varices according to  Baveno III consensus conference on portal hypertension and recommendation for endoscopy is at 2-3 years intervals in patients without varices and at 1-2 years interval in patients with small varices in order to evaluate the development or variceal progression. But this is questionable as endoscopy is an invasive procedure and also cost-effective. Only 9-36% of patients with cirrhosis were found to have varices on screening endoscopy. Non-invasive assessment of variceal bleeding with good predictivity includes biochemical, clinical and ultrasonographic parameters. Thus unnecessary intervention is avoided and at the same time, the patients at risk of bleeding are also not missed. This study emphasizes the need for an annual ultrasonogram examination as a part of a surveillance program for screening of oesophageal varices in patients of chronic liver disease.

2016 ◽  
Vol 38 (6) ◽  
pp. 408-413 ◽  
Raffaele Licinio ◽  
Giuseppe Losurdo ◽  
Sonia Carparelli ◽  
Andrea Iannone ◽  
Floriana Giorgio ◽  

2008 ◽  
Vol 49 (8) ◽  
pp. 951-954 ◽  
A. Park ◽  
W. Cwikiel

Two infants with portal hypertension were treated on an emergency basis for life-threatening uncontrollable variceal bleeding. One 9-month-old girl had portal vein thrombosis, and the other 28-months-old girl had liver cirrhosis secondary to biliary atresia. Following percutaneous transhepatic embolization of the varices, successful bleeding control was achieved in both patients.

2015 ◽  
Vol 33 (4) ◽  
pp. 570-576 ◽  
Christian J. Steib ◽  
Julia Schewe ◽  
Alexander L. Gerbes

Background: Microbial infections are a relevant problem for patients with liver cirrhosis. Different types of bacteria are responsible for different kinds of infections: Escherichia coli and Klebsiella pneumoniae are frequently observed in spontaneous bacterial peritonitis or urinary tract infections, and Streptococcus pneumoniae and Mycoplasma pneumoniae in pulmonary infections. Mortality is up to 4-fold higher in infected patients with liver cirrhosis than in patients without infections. Key Messages: Infections in patients with liver cirrhosis are due to three major reasons: bacterial translocation, immune deficiency and an increased incidence of systemic infections. Nonparenchymal liver cells like Kupffer cells, sinusoidal endothelial cells and hepatic stellate cells are the first liver cells to come into contact with microbial products when systemic infection or bacterial translocation occurs. Kupffer cell (KC) activation by Toll-like receptor (TLR) agonists and endothelial sinusoidal dysfunction have been shown to be important mechanisms increasing portal pressure following intraperitoneal lipopolysaccharide pretreatment in cirrhotic rat livers. Reduced intrahepatic vasodilation and increased intrahepatic vasoconstriction are the relevant pathophysiological pathways. Thromboxane A2 and leukotriene (LT) C4/D4 have been identified as important vasoconstrictors. Accordingly, treatment with montelukast to inhibit the cysteinyl-LT1 receptor reduced portal pressure in cirrhotic rat livers. Clinical studies have demonstrated that activation of KCs, estimated by the amount of soluble CD163 in the blood, correlates with the risk for variceal bleeding. Additionally, intestinal decontamination with rifaximin in patients with alcohol-associated liver cirrhosis reduced the portal pressure and the risk for variceal bleeding. Conclusions: TLR activation of nonparenchymal liver cells by pathogens results in portal hypertension. This might explain the pathophysiologic correlation between microbial infections and portal hypertension in patients with liver cirrhosis. These findings are the basis for both better risk stratifying and new treatment options, such as specific inhibition of TLR for patients with liver cirrhosis and portal hypertension.

2021 ◽  
Vol 17 (3) ◽  
pp. 36-38
M.I. Tutchenko ◽  
S.L. Chub ◽  
T.S. Trofimova ◽  
H.H. Roshchin ◽  
V.V. Ridzhok

The paper deals with the results of the study of the effect of 2-ethyl-6-methyl-3-hydroxypyridine succinate (Elfunat) on erythroid lineage in patients with alcoholic liver cirrhosis and a history of gastroesophageal variceal bleeding. The study compared the impact on the central nervous system and blood values. The results of this study are important for the management of anemia and encephalopathy in this category of patients.

2011 ◽  
Vol 68 (11) ◽  
pp. 917-922 ◽  
Zeljka Savic ◽  
Vladimir Vracaric ◽  
Ljiljana Hadnadjev ◽  
Zora Petrovic ◽  
Dragomir Damjanov

Background/Aim. Portal hypertension (PH) is hemodynamical abnormality associated with the most serious complications of alcoholic liver cirrhosis (ALC): ascites, varices and variceal bleeding. The aim of this study was to determine characteristics of portal hypertension, especially of upper gastrointestinal bleedings in patients with alcoholic liver cirrhosis (ALC). Methods. A total of 237 patients with ALC were observed in a 3-year period. Results. A total of 161 patients (68%) were hospitalized because of PH elements: 86 (36.3%) had upper gastrointestinal bleeding, 75 (31.7%) were decompensated. Only 76 (32%) of the patients had icterus. General mortality was 85 (36%). According to the source of bleeding, 61 (71%) patients bled from varices, and 25 (29%) from other sources with existing varices but non-incriminated for bleeding in 16 (64%) of those patients. Active bleeding or stigmata of recent bleeding were found in 63 (73%) cases. Endoscopic treatment of variceal bleeding along with octreotide applied in 20 (32.78%) patients, just octreotide in 32 (52.46%), and octreotid plus balloon tamponade in 9 (14.75%). According to Child-Pugh classification, 25 (29%) of the bleeding patients were in class A, score 5.4; 43 (50%) in class B, score 7.8; and 18 (21%) in class C, score 10.9. Average hemoglobin level was 93 g/L, hematocrit 0.27, AST 71.52 U/L (normal to 37 U/L), ALT 37.74 U/L (normal to 40 U/L). Until this bleeding episode, 41 (47%) of the patients already bled. In the decompensated patients 3 (4%) were in Child Pugh class A, score 6; 42 (56%) in class B, score 8.3; and 30 (40%) in class C, score 10.6. Until this decompensation episode, 7 (9.3%) patients already bled. Conclusion. Patients with ALC need early detection of varices, primary and secondary profilaxis of variceal bleeding and adequate therapy of ascites. When bleeding occurs, patients need urgent upper endoscopy and intensive treatment.

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