The relationship between portal hypertension and portal hypertensive gastropathy

Author(s):  
Mohamad Kareem Marrache ◽  
Halim Bou Daher ◽  
Don C. Rockey
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Zhu ◽  
Wen Xu ◽  
Wei Hu ◽  
Fang Wang ◽  
Yan Zhou ◽  
...  

Abstract Background Portal hypertension induced esophageal and gastric variceal bleeding is the main cause of death among patients of decompensated liver cirrhosis. Therefore, a standardized, biomarker-based test, to make an early-stage non-invasive risk assessment of portal hypertension, is highly desirable. However, no fit-for-purpose biomarkers have yet been identified. Methods We conducted a pilot study consisting of 5 portal hypertensive gastropathy (PHG) patients and 5 normal controls, sampling the gastric mucosa of normal controls and PHG patients before and after endoscopic cyanoacrylate injection, using label-free quantitative (LFQ) mass spectrometry, to identify potential biomarker candidates in gastric mucosa from PHG patients and normal controls. Then we further used parallel reaction monitoring (PRM) to verify the abundance of the targeted protein. Results LFQ analyses identified 423 significantly differentially expressed proteins. 17 proteins that significantly elevated in the gastric mucosa of PHG patients were further validated using PRM. Conclusions This is the first application of an LFQ-PRM workflow to identify and validate PHG–specific biomarkers in patient gastric mucosa samples. Our findings lay the foundation for comprehending the molecular mechanisms of PHG pathogenesis, and provide potential applications for useful biomarkers in early diagnosis and treatment. Trial registration and ethics approval: Trial registration was completed (ChiCTR2000029840) on February 25, 2020. Ethics Approvals were completed on July 17, 2017 (NYSZYYEC20180003) and February 15, 2020 (NYSZYYEC20200005).


2008 ◽  
Vol 22 (5) ◽  
pp. 469-474 ◽  
Author(s):  
Spyros Goulas ◽  
Konstantina Triantafyllidou ◽  
Stephanos Karagiannis ◽  
Panayiota Nicolaou ◽  
Petros Galanis ◽  
...  

INTRODUCTION: Data on small bowel abnormalities in patients with portal hypertension (PHT) are limited. Bleeding from the gastrointestinal tract and anemia are common complications in these patients. Capsule endoscopy (CE) was used to evaluate small bowel (SB) pathology in patients with PHT and anemia, and possible associations with various parameters were examined.METHODS: Thirty-five patients with PHT referred for CE investigation of the SB for anemia were prospectively enrolled in the study, as well as 70 age- and sex-matched control patients with anemia, normal liver function and no evidence of PHT who underwent CE.RESULTS: Findings compatible with portal hypertensive enteropathy (PHE) were detected in 65.7% of the patients and in 15.7% of the controls (χ2=26.641, P=0.000). Abnormalities in PHT patients included varices in 25.7%, diffuse changes of mucosa with inflammatory-like appearance in 42.9%, and angiodysplasias and/or spider angiomas in 22.9% of cases. The presence of PHE was significantly associated only with the presence of severe portal hypertensive gastropathy, while the presence of SB varices alone was significantly associated with the presence of severe portal hypertensive gastropathy, larger esophageal varices and the presence of colonic varices.CONCLUSIONS: Varices, diffuse changes of mucosa with inflammatory-like appearance, and angiodysplasias and/or spider angiomas are detected more often in patients with PHT than in controls, and probably constitute the endoscopic characteristics of PHE. CE of the SB added a significant number of likely important findings to those detected by conventional endoscopic techniques for the clinical management of patients with PHT and anemia.


2014 ◽  
Vol 70 (1) ◽  
pp. 355-360 ◽  
Author(s):  
Yunfu Lv ◽  
Xiaoguang Gong ◽  
Xianhe Xie ◽  
Baochun Wang ◽  
Yijun Yang ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ferial El-Kalla ◽  
Loai Mansour ◽  
Abdelrahman Kobtan ◽  
Asmaa Elzeftawy ◽  
Lobna Abo Ali ◽  
...  

Background. Portal hypertensive gastropathy (PHG) is a common anomaly with potential for bleeding found in portal hypertension. Blood ammonia levels correlate well with liver disease severity and existence of portosystemic shunts. Increased ammonia results in vasodilation and hepatic stellate cell activation causing and exacerbating portal hypertension.Objective. To assess the relation of blood ammonia to the presence and severity of portal hypertensive gastropathy in cirrhosis.Methods. This cross-sectional study included 381 cirrhotics undergoing screening for esophageal varices (EV) divided into a portal hypertensive gastropathy group (203 patients with EV and PHG), esophageal varix group (41 patients with EV but no PHG), and control group (137 patients with no EV or PHG). A full clinical examination, routine laboratory tests, abdominal ultrasonography, child score calculation, and blood ammonia measurement were performed for all patients.Results. Blood ammonia, portal vein, splenic vein, and splenic longitudinal diameters were significantly higher and platelet counts lower in patients with EV and EV with PHG than controls. Patients having EV with PHG had significantly higher bilirubin and ammonia than those with EV but no PHG. Severe PHG was associated with significantly higher ammonia, EV grades, and superior location and a lower splenic longitudinal diameter than mild PHG. The PHG score showed a positive correlation with blood ammonia and a negative correlation with splenic longitudinal diameter.Conclusions. Blood ammonia levels correlate with the presence, severity, and score of portal hypertensive gastropathy in cirrhosis suggesting a causal relationship and encouraging trials of ammonia-lowering treatments for the management of severe PHG with a tendency to bleed.


2012 ◽  
Vol 302 (12) ◽  
pp. G1458-G1465 ◽  
Author(s):  
Eva Erice ◽  
Elba Llop ◽  
Annalisa Berzigotti ◽  
Juan G. Abraldes ◽  
Ignacio Conget ◽  
...  

Insulin resistance (IR) is involved in the pathogenesis of endothelial dysfunction and is also present in patients with cirrhosis. Intrahepatic endothelial dysfunction plays a major role, increasing hepatic vascular resistance and promoting portal hypertension (PH). In addition, β-adrenergic agonists and insulin share several intracellular signaling pathways. Thus IR may influence the response to β-blockers. This study aimed at evaluating the relationship between IR and hepatic hemodynamics in patients with cirrhosis and with the portal pressure response to acute β-blockade. Forty-nine patients with cirrhosis and PH were included. Hepatic and systemic hemodynamics were measured, and IR was estimated by using the updated homeostasis model assessment (HOMA)-2 index. Patients with HOMA-2 > 2.4 were considered IR. In patients with hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) [clinically significant PH (CSPH)], hemodynamic measurements were performed again 20 min after intravenous propranolol. Mean HOMA-2 index was 3 ± 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had CSPH. HOMA-2 index was an independent predictor of CSPH. However, in patients with CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of esophageal varices. Response to propranolol was not different between patients with or without IR. In nondiabetic patients with cirrhosis, HOMA-2 index is directly associated with the presence of CSPH and indirectly with varices, but does not allow either grading HVPG or predicting its response to propranolol.


2017 ◽  
Vol 54 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Júlio Rocha PIMENTA ◽  
Alexandre Rodrigues FERREIRA ◽  
Eleonora Druve Tavares FAGUNDES ◽  
Paulo Fernando Souto BITTENCOURT ◽  
Alice Mendes MOURA ◽  
...  

ABSTRACT BACKGROUND Bleeding of esophageal varices is the main cause of morbidity and mortality in children and adults with portal hypertension and there are few studies involving secondary prophylaxis in children and adolescents. OBJECTIVE To evaluate the efficacy of endoscopic secondary prophylaxis in prevention of upper gastrointestinal bleeding in children and adolescents with esophageal varices. METHODS This is a prospective analysis of 85 patients less than 18 years of age with or without cirrhosis, with portal hypertension. Participants underwent endoscopic secondary prophylaxis with sclerotherapy or band ligation. Eradication of varices, incidence of rebleeding, number of endoscopic sessions required for eradication, incidence of developing gastric fundus varices and portal hypertensive gastropathy were evaluated. RESULTS Band ligation was performed in 34 (40%) patients and sclerotherapy in 51 (60%) patients. Esophageal varices were eradicated in 81.2%, after a median of four endoscopic sessions. Varices relapsed in 38 (55.1%) patients. Thirty-six (42.3%) patients experienced rebleeding, and it was more prevalent in the group that received sclerotherapy. Gastric varices and portal hypertensive gastropathy developed in 38.7% and 57.9% of patients, respectively. Patients undergoing band ligation showed lower rebleeding rates (26.5% vs 52.9%) and fewer sessions required for eradication of esophageal varices (3.5 vs 5). CONCLUSION Secondary prophylaxis was effective in eradicating esophageal varices and controlling new upper gastrointestinal bleeding episodes due to the rupture of esophageal varices. Band ligation seems that resulted in lower rebleeding rates and fewer sessions required to eradicate varices than did sclerotherapy.


2009 ◽  
Vol 24 (9) ◽  
pp. 1554-1558 ◽  
Author(s):  
Go Anegawa ◽  
Hirofumi Kawanaka ◽  
Hideo Uehara ◽  
Tomohiko Akahoshi ◽  
Kozo Konishi ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
S. M. Mahmudul Hasan ◽  
Meghan Dmitriew ◽  
Jennifer Leonard

Portal hypertension caused by cirrhosis is the most common etiology of esophageal varices. However, abnormalities of the splenoportal axis in the absence of liver disease may also cause portal hypertension resulting in varices. We report a rare case of esophageal variceal bleed in a noncirrhotic patient with isolated splenomegaly secondary to chronic granulocyte colony stimulating factor (G-CSF) therapy. The patient is a 26-year-old male with Cohen syndrome who required long-term G-CSF treatment for chronic neutropenia. He presented with large volume hematemesis and pancytopenia in the setting of known splenomegaly with no evidence of cirrhosis. An urgent EGD revealed active variceal bleeding and portal hypertensive gastropathy. The patient was appropriately resuscitated and underwent a successful transjugular intrahepatic portosystemic shunt and CT-guided coil placement for the bleeding varices. We are the first to report variceal bleed as a complication of long-term G-CSF use, a life-threatening consequence that requires urgent intervention.


2019 ◽  
Vol 7 (2) ◽  
pp. 79-83 ◽  
Author(s):  
Herbert Djiambou-Nganjeu

Abstract Our aim was to explore the relationship between liver cirrhosis (LC), portal hypertension (PH), and diabetes mellitus (DM). LC displayed hemodynamic alterations reflected by signs and symptoms of hypertension and hyperdynamic circulation. Portal hypertension also caused splenomegaly because of the blood flow into the spleen from the portal vessels and portal flow. The alcoholic cirrhosis displayed abnormal values (AST, ALT, AST/ALT, albumin, ammonia, bilirubin, blood platelet, erythrocytes, glucose, Hb, international normalized ratio (INR), PT, prothrombin index (PI), thymol test, white blood cell (WBC) count), which demonstrated the presence of portal hypertension, ascites, DM, infection, and coagulopathy. The evaluation of liver enzymes and other laboratories data helped to determine the severity of the condition and prognosis. Diabetes appeared to be less affecting the prognosis of patients with cirrhosis than LC itself, showing that hepatocellular failure was largely responsible for patients’ mortality rather than diabetes and its complications. Patients displayed a BMI correlating obesity, although affected by concomitant diseases that commonly cause a severe weight loss. The elevated BMI in this case was accentuated by the presence of ascitic fluid, which is responsible for the increase in weight and the inaccurate BMI evaluation. Ascites affect patients’ recovery from liver diseases. Obese patients with cirrhosis can be related to have a large amount of ascites and that physicians should be expecting to notice changes in their BMI pre- and postoperatively, subsequently making a prior classification as obese inappropriate. Disease severity could be assessed through the evaluation of PH stage, which was characterized by a significant depletion of WBC and as well as platelet counts.


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