Hypertensive Gastropathy Research Articles

Prophylactic cyanoacrylate injection for gastric extension of esophageal varices: a randomized controlled trial

Aim of the studyGastric variceal bleeding is more severe and fatal than esophageal bleeding. Injection of cyanoacrylate into bleeding gastric varices is recommended, but prophylactic injection is debatable. Aim of this study is to evaluate prophylactic cyanoacrylate injection into gastric extension of esophageal varices type 2 (GOV2).Material and methodsThis randomized controlled trial included 75 patients (3 groups) with risky or bleeding esophageal varices and non-bleeding GOV2. Group A received a cyanoacrylate GOV2 injection, esophageal variceal band ligation (EBL), and β-blocker (BB); group B received EBL and BB; and group C received EBL. Follow-up for ≥ 24 weeks to check for bleeding or death was performed.ResultsBaseline variables were comparable among the 3 groups. During follow-up (median, 37.5 weeks), increasing gastric extension and or bleeding risk signs were significantly lower in group A (0%) than B (12%) and C (32%) (p < 0.001). Bleeding occurred more in groups B (24%) and C (24%) than in A (8%) (p = 0.2). Gastric extension size was an independent predictor of bleeding (p = 0.03). Portal hypertensive gastropathy (PHG) decreased in groups A (24%) and B (24%) more than in C (8%) (p = 0.5). Mortality rates were 0.0% in group A, 8% in B, and 4% in C (p = 0.2).ConclusionsProphylactic cyanoacrylate injection into GOV2 before EBL significantly decreased the varix size and risk signs for bleeding with a statistically insignificant tendency to decrease the bleeding rate. A large gastric extension was an independent predictor of bleeding. Adding β-blockers can potentially decrease PHG and bleeding risk. An independent study with a larger sample size is recommended to confirm the rate of bleeding and test the mortality difference.

Comparison of portal hypertensive gastropathy and gastric antral vascular ectasia: an update.

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two distinct entities that are frequently mistaken with each other, because they present with similar manifestations. This issue may cause catastrophic outcomes, as each one of them has a unique pathophysiology, thereby making their management approaches completely different. There are clinical clues that help physicians distinguish these two. Direct vision via upper endoscopy is often mandatory to establish the diagnosis, and sometimes biopsy is required. In this review, we sought to discuss different aspects of both conditions and highlight clinical evidence that may help in identifying and managing the disease appropriately.

Case report on Horseshoe kidney with hypothyroidism with cryptogenic cirrhosis of the liver with portal hypertension

Horseshoe kidney is rare non-fatal congenital abnormality of renal development. This conditions usually asymptomatic and in various cases it discovered incidentally. The incidence of horseshoe kidney is approximately 1 in 500 in the average population and this anamoly is found in men than in female. Horseshoe kidney means two kidneys joined together and form the U shape like a horseshoe. It is also known as Renal Fusion. The most problem of horseshoe kidneys is nephrolithiasis. There is no cure for horseshoe kidneys, but supportive treatments can treat symptoms. Patient medical history : The Patient has come with the chief complaints of breathing difficulty, swelling, facial puffiness for 15 days, abdominal distension, repeated episode of vomiting blood (hematemesis), and melena. The Patient had a history of hypothyroidism for two years and cryptogenic cirrhosis of the liver with portal hypertension for one year. Diagnostic evaluation : Endoscopy procedure done to screen esophageal varices, there are large esophageal varices and severe portal hypertensive gastropathy USG: cirrhosis of liver, mild splenomegaly. Echo: Severe portal hypertension, mild Tricuspid Regurgitation with Right Ventricular Systolic Pressure, Mildly dilated Right Atrium and Right Ventricle. Therapeutic intervention : Provide beta-blockers, antibiotics, antiemetics, vitamin supplements, biliary agents, and antidiuretic used to treat the client, but the Patient’s overall health was deteriorating. Conclusion : Treatment and care for horseshoe kidney disease on time will help to prevent further life-threatening consequences.

AUTO IMMUNE HEPATITIS AS A LIVER MANIFESTATION OF COMMON VARIABLE IMMUNODEFICIENCY: A CASE REPORT

Common variable immunodeficiency (CVID) is a primary immunodeficiency disorder characterized by impaired differentiation of B cells with defective immunoglobulin production and paradoxically the development of autoimmune disorders. It is estimated that the prevalence of the liver disease is less than 10%. The most reported is focal nodular hyperplasia and, to a lesser extent, primary biliary cholangitis, primary sclerosing cholangitis and autoimmune hepatitis (AIH). present the case of a 22-year-old male who was admitted for hematemesis. He was diagnosed with immune thrombocytopenia 12 years ago without treatment and common variable immunodeficiency six years ago, currently three years without treatment. No family history of autoimmune or liver diseases. After extraction of the 4th molars, he presented swelling, redness, heat in the left submandibular region, unquantified fever, for which he received antibiotic treatment and non-steroidal anti-inflammatory drugs; 12 hours before admission, he began with hematemesis and hematochezia with data of hemodynamic instability, for which crystalloids are administered, the physical examination presents scleras with jaundice, an edematous, erythematous area with local heat in the left submandibular region, flat, symmetrical abdomen, absence of collateral circulation, Non-painful hepatomegaly, without shifting dullness. Laboratory admission with anemia, thrombocytopenia, cholestatic pattern in liver biochemistry tests, chronic viral infectious processes are ruled out and antibodies are made for autoimmune diseases, ANA 1:1200 is documented, other antibodies negative. Esophagogastroduodenoscopy where large esophageal varices of Baveno and severe portal hypertensive gastropathy (image 1 panel A). Doppler ultrasound reports diffuse liver disease, 14mm portal vein, with the presence of free fluid perihepatic and perisplenic, without biliary obstruction data (image 1 panel B). Percutaneous liver biopsy: fibrosis F2-3 on the scale of Metavir, interface hepatitis, associated with infiltrate lymphoplasmacytic integrating diagnosis of AIH (image 1 panel C). The prevalence of this condition is estimated at 1 in every 50,000 people worldwide. Up to 25% of patients with CVID will have an association with autoimmune diseases, representing the heterogeneous nature of the disease. The presentation of liver disease commonly reported in case series is anicteric cholestasis, and biopsies show evidence of non-cirrhotic portal hypertension. However, the association of CVID and AIH is rare; its diagnosis requires biopsies due to the lack of expression of antibodies in most cases. In CVID patients with altered liver function tests, the association with autoimmune liver diseases should be ruled out to initiate timely treatment and avoid late complications. The authors declare that there is no conflict of interest.

Accuracy of virtual chromoendoscopy in differentiating gastric antral vascular ectasia from portal hypertensive gastropathy: A proof of concept study

BACKGROUNDAccurate detection of gastric antral vascular ectasia (GAVE) is critical for proper management of cirrhosis-related gastrointestinal bleeding. However, endoscopic diagnosis of GAVE can be challenging when GAVE overlaps with severe portal hypertensive gastropathy (PHG).AIMTo determine the added diagnostic value of virtual chromoendoscopy to high definition white light for real-time endoscopic diagnosis of GAVE and PHG.METHODSWe developed an I-scan virtual chromoendoscopy criteria for diagnosis of GAVE and PHG. We tested our criteria in a cross-sectional cohort of cirrhotic adults with GAVE and PHG when high-definition white light endoscopy (HDWLE) diagnosis was in doubt. We then compared the accuracy of I-scan vs HDWLE alone to histology.RESULTSTwenty-three patients were included in this study (65.2% Caucasians and 60.9% males). Chronic hepatitis C was the predominant cause of cirrhosis (43.5%) and seven adults (30.4%) had confirmed GAVE on histology. I-scan had higher sensitivity (100% vs 85.7%) and specificity (75% vs 62.5%) in diagnosing GAVE compared to HDWLE. This translates into a higher, albeit not statistically significant, accuracy of I-scan in detecting GAVE compared to HDWLE alone (82% vs 70%). I-scan was less likely to lead to an accurate diagnosis of GAVE in patients on dialysis (P < 0.05) and in patients with elevated creatinine (P < 0.05). I-scan had similar accuracy to HDWLE in detecting PHG.CONCLUSIONThis pilot work supports that virtual chromoendoscopy may obviate the need for biopsies when the presence of GAVE is in doubt. Larger studies are needed to assess the impact of virtual chromoendoscopy on success of endoscopic therapy for GAVE.

The relationship between portal hypertension and portal hypertensive gastropathy

Background and aim Portal hypertensive gastropathy (PHG) most commonly occurs in the setting of increased portal pressure in patients with cirrhosis. Here, we aimed to understand the correlation between hepatic venous pressure gradient (HVPG) and the presence and severity of PHG in patients with cirrhosis. Methods We examined patients with cirrhosis who underwent HVPG measurement at the Medical University of South Carolina between 2014 and 2020. Extensive demographic, clinical, laboratory, procedural (including precise grading of PHG severity using standard definitions), and outcome data were abstracted at the time of HVPG measurement. Results Three hundred and ten patients with HVPG measurements and cirrhosis were identified. Seventy-three patients having endoscopy within 6 months of HVPG measurement were included (mean age 54 ± 11, 44% female). The most common causes of cirrhosis were alcohol (41%) and non-alcoholic steatohepatitis (32%). The average HVPG was 15 mmHg (±6) and 62 patients had clinically significant portal hypertension (CSPH) (HVPG ≥ 10 mmHg). Of the 73 patients with HVPG measured, 45 (62%) had PHG, including 40 (89%) of whom had CSPH. Out of the 45 patients with PHG, 41 and four had mild or severe PHG, respectively. MELD scores were similar in patients with and without PHG [15 ± 9 (SD) and 17 ± 9, respectively; p = .37]. HVPG was higher in patients with PHG (17 ± 7 mmHg) than those without PHG (13 ± 4 mmHg) (p = .01) but did not differ between mild and severe PHG. Conclusion A weak correlation exists between HVPG level and the presence of PHG.

Peptic Ulcer Diseases in Patients with Liver Cirrhosis and Portal Hypertension: Experience in a Tertiary Level Hospital in Bangladesh

Introduction: Cirrhosis of liver and peptic ulcer disease (PUD) are very common in Bangladesh. PUD may coexist with cirrhosis and portal hypertension. Haematemesis and melaena in cirrhosis of liver are not always from ruptured oesophageal varices; rather it may be due to bleeding peptic ulcer disease. Objective: To find the prevalence of PUD among patients with liver cirrhosis and portal hypertension. Materials and Methods: This cross sectional, descriptive study was conducted on 96 patients of cirrhosis of liver diagnosed with oesophageal varices at endoscopy unit of Kurmitola general hospital, during endoscopic evaluations in 4 months period from september 2017 to december 2017. Results: Total cirrhotic patients enrolled were 96 (M=61, F=35), mean age was 51.8 ± 14.2 yrs (18-86years). Hepatitis B virus (HBV) was the leading cause of cirrhosis in 54.1%, Hepatitis C virus (HCV) 5.2 %, proven non-alcoholic steatohepatitis (NASH) were 11.5% and rest were from unknown aetiology. Their average Child-Turcotte-Pugh (CTP) score were 8.6 (12-5), 37.6% associated with portal hypertensive gastropathy. Grade-III oesophageal varices found in 52 patients, whereas grade-II in 25 patients. Among this 96 patients 39 (40.6%) revealed peptic ulcer disease more in the form of gastric ulcer (n=23) than duodenal ulcer (n=10) and both (n=6). Most of the ulcers belonged to Forrest class III (76.9%). Conclusions: Variceal bleeding and portal hypertensive gastropathy are the common causes of bleeding and anaemia in patients with cirrhosis of liver. Peptic ulcer disease has been found to be one of the potential causes of haematemesis, melaena, and anaemia among these patients in Bangladesh. Large multicenter controlled studies are needed to confirm the reports. JAFMC Bangladesh. Vol 16, No 2 (December) 2020: 68-71

Safety and Efficacy of JAK Inhibitor Therapy in BCR-ABL Negative MPN Patients with Underlying Portal Hypertension

▪BackgroundThe BCR-ABL-negative Myeloproliferative neoplasms (MPNs) are clonal stem cell disorders characterized by constitutive activation of the JAK-STAT pathway that include Polycythemia Vera, Essential Thrombocytosis, Primary (PMF) and Secondary Myelofibrosis (SMF). Splenomegaly is a characteristic feature of MPNs that can be ameliorated by JAK inhibitors (JAKi). Up-to one-third of MPN patients also experience portal hypertension (PH). Thrombosis of the splanchnic circulation is the most widely recognized etiology of PH in MPNs, however PH also occurs in the absence of intra-abdominal thrombosis. The influence of PH on outcomes of JAKi therapy in MPN patients has not been characterized. To this end, we aimed to determine the safety and efficacy of JAKi therapy in MPN patients complicated by PH with and without underlying splanchnic circulation thrombosis (ST).MethodsAll patients with MPNs assessed at Princess Margaret Hospital between 01/1998 and 01/2021 were identified from the MPN program's database. Patients who had undergone esophagogastroduodenoscopy (EGD) and had endoscopic evidence of PH, namely esophageal or gastric varices or portal hypertensive gastropathy were included. The study population was further limited to patients who started JAKi therapy following diagnosis of PH. Outcomes were compared between patients with and without underlying ST. The primary endpoint was palpable spleen reduction at 24 weeks. Secondary endpoints included best palpable spleen reduction within one year of starting JAKi, improvement in PH severity as determined by serial EGD assessments during JAKi therapy, overall survival, and ≥grade 3treatment emergent adverse events. Statistical differences in the frequencies of baseline characteristics were assessed using the Wilcoxon rank sum and Chi-Square tests. Overall-survival (OS) estimates were calculated by the Kaplan-Meier method using STATA/IC 16.1 software.ResultsAll MPN patients with evidence of PH on endoscopy who started JAKi therapy after diagnosis of PH were included (n=33). Thirteen patients experienced ST prior to the start of JAKi. The proportion of younger patients and those with PH-related complications (i.e., variceal bleeding and/or ascites) was higher in patients with underlying ST (5/20 [25%] vs 9/13 [69%], p=0.01). The median palpable spleen change at approximately 24 weeks of therapy and the best palpable spleen reduction within the first year of therapy was -40.5% ([-100%[ -[+100%]) and-50% ([-100%]-0%) in the entire cohort, respectively. Better spleen responses with JAKi therapy were observed in PH patients without prior ST compared to those with underlying ST (median palpable spleen change at approximately 24 weeks was -58% (-24%-(-100%)] (n=13) vs -26.5% ([-100%]-[+100%]) (n=9), p=0.062; median best palpable spleen change at any time within 1 year of JAKi therapy start was -71% ([-14%]) -[-100%]) (n=17) vs -35% ([0%-[-100%]) (n=9), p=0.045). Of 21 patients with serial EGDs during JAKi treatment, improvement in PH severity as observed in 8 (38%). There were no differences in survival between patients with and without prior ST. Grade 3 treatment-emergent adverse events included anemia (5/33 [15%]), thrombocytopenia (5/33 [15%]), neutropenia (1/33 [3%]), and suspected Wernicke encephalopathy associated with Momelotinib (1/33 [3%]).Conclusion:In this observational study, JAK inhibitor therapy appears to be safe and effective in MPN patients complicated by PH, with a trend towards improved spleen responses among portal hypertensive patients without splanchnic circulation thrombosis. DisclosuresMaze: Novartis: Honoraria, Membership on an entity's Board of Directors or advisory committees; Celgene-BMS: Honoraria; Takeda: Research Funding; PharmaEssentia: Research Funding; Kronos Bio: Research Funding. Gupta: AbbVie: Consultancy, Honoraria; Incyte: Honoraria, Research Funding; Sierra Oncology: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Constellation Pharma: Consultancy, Honoraria; Novartis: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Roche: Consultancy; Pfizer: Consultancy; BMS-Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees.

Differences between sporadic hyperplastic gastric polyps and portal hypertensive gastric polyps: a review.

Portal hypertension (PH) is one of the most severe complications of chronic liver diseases. It is defined as an increase in pressure in the portal venous system which results in a portosystemic gradient >5 mmHg. In the western world, cirrhosis is the most frequent cause of PH, mainly due to nonalcoholic fatty liver disease and alcoholic liver disease. Patients with PH have esophageal varices in 68-73% of cases, portal hypertensive gastropathy in 51-73% and hyperplastic polyps (HPs) in 0.9-2%. Recent studies have shown that HPs found in PH patients are different from classical HPs. They constitute a new entity called portal hypertensive polyps (PHPs). The main difference between sporadic HPs and PHP is the presence of larger and more numerous vascular capillaries in the lamina propria. The clinical course of PHPs is unknown. Their physiopathology seems different from HPs: the increased congestion caused by higher portal pressure in the stomach may induce capillaries proliferation and neoangiogenesis. PHPs may be responsible for symptoms, such as pyloric obstruction, iron deficiency and anemia. Their prevalence in portal hypertensive and cirrhotic patients is from 1% to 8%. PHPs can be single or numerous, in the antrum or the gastric corpus. Their size ranges from 2 to 3 cm. PHPs seem to disappear or shrink with the treatment of PH. They should be resected in case of symptom and if >10 mm, after Helicobacter pylori eradication if present. However, their recurrence is frequent (40-79%), thus surveillance endoscopy is mandatory, at the same time as esophageal varices.

S2807 Portal Hypertensive Polyps as a Unique Cause of Bleeding in Cirrhosis

Introduction: Portal hypertension is due to resistance to portal blood flow commonly due to a fibrotic, cirrhotic liver. This leads to a multitude of complications including esophageal varices, portal hypertensive gastropathy, and ascites. Portal hypertensive polyps (PHP) is a recently described entity with prevalence estimated to be 1-3% of all gastric polyps found in cirrhotics especially since gastric polyps in the general population is already a relatively uncommon finding. We present a patient with complications due to PHP. Case Description/Methods: A 60-year-old male with a history of alcoholic liver cirrhosis (MELD 8) and esophageal varices that were previously banded, presented to the ED with melena and a hemoglobin of 5.9 gm/dl. The first EGD showed gastric antral-pyloric polyps, likely thought to be portal hypertensive polyps, with active minor oozing. There was one large polyp 2.5 cm in size and multiple smaller polyps in the surrounding area. The decision was made to intervene on these polyps during a repeat EGD. Argon plasma coagulation (APC) was used to coat the polyps with successful hemostasis. A subsequent outpatient EGD showed stable polyps without bleeding. The patient was referred for transjugular intrahepatic portosystemic shunt (TIPS) placement in hopes to reduce portal hypertension to limit future episodes of GI bleeding. Discussion: Being a relatively new phenomenon, the diagnostic criteria/clinical relevance for PHP is not yet clear. The histological characteristics of PHP are similar to hyperplastic polyps with foveolar hyperplasia and proliferating ectatic capillaries in the lamina propria. Furthermore, most cases of PHP involve multiple lesions. However, studies have shown that they do not degenerate to malignancy. Independent predictors of PHP include Child-Pugh > 6, MELD > 16, and rubber band ligation of varices. Variceal ligation is thought to be due to increased formation of portosystemic shunts leading to increase portal pressure in the gastric wall inducing proliferation/angiogenesis; our patient did have a history of banded varices. Studies have also shown no active bleeding from the PHP in any of the endoscopies, but our instance of PHP did have active bleeding. Recurrence after polypectomy is common and it is not recommended to routinely remove the polyps, but APC can be used for bleeding polyps. Ultimately TIPS has shown to reverse portal hypertensive gastropathy but there is no studies on its utility in treating PHP; as this area of focus demands further study.Figure 1.: Portal Hypertensive Polyp in Gastric Antrum.

S1852 Colonic Varices Due to Alcoholic Cirrhosis

Introduction: Ectopic varices (all varices outside the gastroesophageal region) account for 1-5% of all variceal bleeding episodes. Specifically, colon varices are rare, as incidence of colonic varices, irrespective of etiology, is around 0.07%. If colonic varices bleed, treatment is urgent, as delay in treatment can potentially be fatal. Case description/methods: A 55 year old male with a past medical history of complicated diverticulitis status post open sigmoidectomy and heavy alcohol abuse with history of deliriums tremens who was admitted due to having hematochezia with bowel movements for two days. He denied any hematemesis, abdominal pain, melena or NSAID use. Patient was hypotensive on arrival to the ED with MAPs in the 40s. On physical exam, scleral icterus along asterixis and tremors in his hands were noted. CTA Abdomen and Pelvis showed no signs of active gastrointestinal bleeding with signs of hepatic cirrhosis with extensive esophageal, gastric varices, and descending colon varices. Patient had two more episodes of hematochezia in the ED. Patient was given 2 units of emergent blood in the ED to help stabilize his blood pressure. Patient did not have a diagnosis of cirrhosis prior to presentation. He admitted to drinking a six pack of beer daily for the past thirty years. Last colonoscopy was five years ago which showed tubular adenomatous polyps in the rectum and ascending colon. Diverticulosis was also present in the ascending colon. Patient had EGD performed which showed some mild esophagitis and some portal hypertensive gastropathy (PHG) located in the antrum, body and fundus. Flexible sigmoidoscopy was then performed which showed a large amount of fresh and old blood coming from a sigmoid varix at 25 cm located in the sigmoid colon. Hemostasis was achieved with using a Bear claw clip (Figure 1). Discussion: Colonic varices can develop secondary to portal hypertension, congenital anomalies in venous outflow, mesenteric or splenic vein thrombosis, congestive heart failure, or formation of collateral vessels from previous abdominal surgeries. Patients with suspected bleeding colonic varices need immediate assessment, resuscitation, and hemodynamic stabilization. There are no evidence based guidelines for treatment for bleeding colonic varices, but options include medical, endoscopic, interventional radiological and surgical modalities.Figure 1.: Bear claw clip was used to achieve hemostasis.

S3715 A Leather Bottle Stomach: Rare Case of Gastric Adenocarcinoma With Signet Cell Features

Introduction: Gastric cancer is one of the most common cancers worldwide - and was previously the leader of cancer related mortality until the 1980’s. With advancements in discovery of etiologies, namely the detection of H. Pylori - incidence of gastric cancer has declined over the past decades. A common finding on imaging is the diffuse gastric wall thickening - the “leather water bottle” or Linitis Plastica. A representation of diffuse infiltration of the cancer into the wall of a hollow organ, in this case - the stomach, giving it’s rugged and preserved structural shape. We present a case of poorly differentiated gastric adenocarcinoma with signet ring cell features in setting of portal hypertensive gastropathy. Case Description/Methods: 70-year-old female with PMH of HCV (treated with SVR) and 20 pack year tobacco history presented with complaints of weight loss, decreased appetite and early satiety with no other complaints for one month. Physical exam significant for bi-temporal wasting otherwise unremarkable. Initial chemistries within normal limits. CT abdomen and pelvis revealing a prominent thickening of the wall of the stomach as well as inhomogeneous soft tissue attenuation in the omentum concerning for neoplastic disease. EGD showed evidence of portal hypertensive gastropathy with distal gastric body thickening in addition to the examined duodenum revealing duodenitis. Biopsies of the stomach revealed poorly differentiated adenocarcinoma with signet ring cell features while the duodenal mucosa was negative for significant histopathologic abnormality. H. pylori immunostain was negative. Insufficient tissue for HER2 and PDL-1 assessment. Oncology evaluation included PET CT with significant circumferential thickening and hypermetabolic activity of the stomach with additional focus of modular hypermetabolic activity at pyloric and duodenal 2nd portion suggestive of multi centric disease. Diffuse omental modularity and ascites at low level metabolic activity consistent with omental metastasis and malignant ascites. Discussion: While our patient presented late in the disease course, there are still available palliative chemotherapy opportunities. Advances have been made in molecular identification and subtypes within the gastric cancer umbrella for more targeted therapy. Recent FDA approval (April 2021) of the addition of Opdivo (immunotherapy) to FOLFOX (chemotherapy) for treatment of metastatic gastric cancer has allowed our patient to receive the most up to date treatment option.Figure 1.: Figures 1-A through C are endoscopic images of the gastric body (evidence of portal hypertensive gastropathy), the duodenal bulb (suggesting duodenitis) and the 2nd portion of the duodenum. Figure 1-D is a CT Abdomen-Pelvis with Contrast depicting the classic radiographic finding of gastric cancer - 'linitis plastica' with surrounding peri-gastric lymphadenopathy. Figures 1-E and F are NM PET scan's with evidence of diffuse hypermetabolic activity in the stomach wall with uptake of SUV max 10.1 in addition to the 2nd portion of the duodenum with uptake of SUV max 5.7 - suggestive of multi-centric disease.

S2906 Medical Management of Variceal Bleeding Associated With Portal Hypertension Secondary to Significant Metastatic Burden in the Liver: Strategies for Reducing Rebleeding Events

Introduction: Portal hypertension (pHTN) is a cirrhosis complication that can uncommonly develop in patients with high liver metastatic tumor burden, especially those undergoing oxaliplatin chemotherapy. Symptomatic pHTN, such as gastrointestinal variceal bleeding, can complicate oncological management. Transjugular intrahepatic portosystemic shunt (TIPS) may not be a safe option, but medical therapy strategies are lacking. Case Description/Methods: A 70-year-old male with a history of colorectal carcinoma metastatic to the liver, status-post ileocolectomy and end-ileostomy with mucus fistula, and treated with oxaliplatin-bevacizumab based therapy, presented twice in one week to the emergency department with acute anemia and bleeding from his mucus fistula and then his ostomy. Abdominal CT at presentation was notable for progressed metastatic tumor burden in the liver and splenomegaly, raising concern for developing pHTN. Vascular abdominal ultrasound showed umbilical vein recanalization. EGD revealed small esophageal varices and moderate portal hypertensive gastropathy, but ileoscopy did not show a bleeding source. Venography studies showed peri-fistular and stomal varices, which were successfully treated with transcutaneous sclerotherapy, and subsequent direct portal pressure of 16mmHg. Given high rebleeding risk, the patient required long-term therapies for pHTN management. His malignancy burden and hypercoagulable risk precluded him from TIPS. Medical management was recommended, patient started on carvedilol 12.5 mg twice daily and atorvastatin was increased to 80mg daily; he was discharged without further bleeding to date. Discussion: This case illustrates a difficult case of pHTN that can be can be associated with both metastatic liver burden but also fibrosis associated with oxaliplatin therapy. Bevacizumab is an additional cause for increased bleeding risk and poor wound healing. Oncologic regimens may also need to be altered given the new pHTN occurrence. While data support the use of beta blockers and statins in pHTN and variceal bleeding management, much of this evidence comes from cirrhosis literature. Further investigation into pharmacologic management of portal hypertension in patients with significant metastatic burden in the liver. Interestingly, the downregulation of VEGF synthesis by high-dose statins may assist with anti-angiogenesis effect of bevacizumab and may be of interest for future clinical research.Figure 1.: Figure 1a - CT imaging showing metastatic burden to the liver; figure 1b -- venography showing peristomal varices.Table 1.: Pertinent lab values at various points of disease course from diagnosis of metastatic cancer onward.

CORRELATION BETWEEN HELICOBACTER PYLORI INFECTION AND RISK OF ESOPHAGOGASTRIC VARICEAL BLEEDING IN LIVER CIRRHOSIS

Background: Bleeding from esophageal and gastric varices is a fatal event in patients with liver cirrhosis and portal hypertension. Objective: Evaluation the correlation between Helicobacter Pylori infection and risk of esophagogastric variceal bleeding in liver cirrhosis. Patients and Methods: This study was carried out on one hundred (100) patients, suffering from post hepatitic cirrhosis and portal hypertension: fifty (50) of them presented with esophageogastric varices without bleeding selected from patients coming for screening of esophagogastric varices for anti-hepatitis c virus treatment, and the other fifty (50) presented with acute variceal bleeding. All patients attending to Internal Medicine outpatient’s clinic and Internal Medicine Department of Al-Azhar University Hospital at new Damietta during the period from September 2018, to April 2020. All patients were subjected to complete history, clinical assessment, abdominal ultrasonography, upper GIT endoscope and laboratory investigations. Results: There was a significant relation between H.Pylori infection and the presence of esophagogastric variceal hemorrhage and H. Pylori infection was positive in 92% of the patients in group II, and 24% patients was grade II oseophageal varices, 70% grade III oseophagogastric varices, and 6% grade IV oseophagogastric varices, There was a statistically significant correlation of increased esophageal varices (grade three) in positive H pylori in group II, while in group I detection of H.pylori showed 24% patients were positive, and 76% patients were negative. Endoscopic examination showed 40 patients without esophagogastric varices (80%), 8% patients grade I, 4% patients grade II, 6% patients grade III, 2% patients grade IV, and there was a statistically significant increase on esophageal varices (grade zero) in negative H pylori in group I. Conclusion: Helicobacter Pylori infection helped in the development of portal hypertensive gastropathy as well as its severity, and increased risk of esophagogastric variceal bleeding in patients with liver cirrhosis. So, eradication and treatment of Helicobacter Pylori in all patients with liver cirrhosis helped to decrease risk of esophagogastric variceal bleeding in these patients.

Портальная гипертензивная гастропатия (Обзор литературы)

Статья посвящена портальной гипертензивной гастропатии (ПГГ) — вторичному изменению слизистой оболочки и подслизистого слоя желудка на фоне цирроза печени (ЦП) любой этиологии и сопутствующей ему портальной гипертензии. В обзоре представлены данные, касающиеся истории изучения данной патологии, эпидемиологии, патогенеза, клинических проявлений, методов диагностики и лечения. Показано, что в основе заболевания лежит портальная гипертензия, приводящая к нарушению микроциркуляции в слизистой желудка, и как следствие — к полнокровию и венозному застою. Клиническое течение ПГГ в большинстве случаев бессимптомное. Основным методом диагностики является эндоскопический, базирующийся на определенных макроскопических признаках. В обзоре рассмотрены основные эндоскопические классификации ПГГ. Основные гистологические изменения при ПГГ включают расширение капилляров и венул в слизистом и подслизистом слое без существенного воспаления. Течение ПГГ динамичное. К осложнениям ПГГ относятся хронические и, реже, острые кровотечения. Лечение медикаментозное, с использованием неселективных бета-блокаторов

Gastric mucosal function in portal hypertensive gastropathy secondary to schistosomal hepatic fibrosis: effect of sclerotherapy

Gastric mucosal function in portal hypertensive gastropathy secondary to schistosomal hepatic fibrosis [SHF] was evaluated. Group I comprised 20 patients with no bleeding;10 had portal hypertensive gastropathy [PHG]. Group II comprised 20 patients with bleeding. Free acidity, total acidity, basal acid output, serum pepsinogen I, gastric mucosal blood flow [GMBF] and gastrin were significantly lower in group II, whereas serum gastrin and somatostatin staining were significantly higher. No histopathological changes were noted between both groups, In conclusion, bleeding caused by SHF results in hypoacidity, hypergastrinaemia and hypopepsinogenaemia. Estimated GMBF distinguishes patients with PHG and those who are bleeders

ENDOSCOPIC PROFILE OF UPPER GASTROINTESTINAL BLEEDING IN A TERTIARY CARE CENTRE.

Background:Astudy describing the endoscopic prole of upper gastrointestinal bleeding in a tertiary care centre. Aim:The aim was to study endoscopic prole in patients presenting with upper GI bleeding. Introduction: Upper gastrointestinal bleeding is a common medical emergency associated with signicant morbidity and mortality. The presentation of bleeding depends on the amount and location of bleed. The primary diagnostic test for evaluation of upper gastrointestinal bleeding is endoscopy. The aim was to study endoscopic prole in patients presenting with upper GI bleeding. Methods: This is a cross sectional study data conducted in Department of Gastroenterology DDHD Anna nagar Chennai from January 2019 to January 2020 . In this patients presenting with manifestations of upper gastrointestinal bleed were included and were subjected to upper GI endoscopy. Results: Atotal of 160 patients presenting with hematemesis and melena were studied. 124(77.5%) were males and 36(22.5%) were females. The mean age was 47.15 ± 17.12 . The most common ndings on endoscopy of upper gastrointestinal bleeding was portal hypertension related (esophageal and gastric varices, portal hypertensive gastropathy ) seen in 40% of patients, gastric erosions in 17.5% patients, peptic ulcer disease was seen in 13.75%, Esophagitis in 6.25% cases, Mallory-Weiss tear was seen in 6.25% patients, gastric malignancy in 5% patients, post EVL ulcers in 3.75% patients, Normal study in 3.75%, Duodenal erosions in 2.5% patients, Vascular ectasia of stomach in 1.25%. Conclusion: The present study reported portal hypertension as the most common cause of upper gastrointestinal bleeding, while most common endoscopic lesions reported were esophageal varices, followed by gastric erosions and peptic ulcer.

Portal hypertension after prolonged use of trastuzumab emtansine: nodular regenerative hyperplasia with autoimmune features

We report a rare complication associated with prolonged use of trastuzumab emtansine (T-DM1) – a composed therapy for HER2+ breast cancer – presenting with laboratorial autoimmune features that could have delayed the diagnosis or led to misdiagnosis. A 55-year-old female was referred to the hepatologist with a computed tomography suggestive of portal hypertension for etiological investigation. History of invasive ductal carcinoma in the right breast undergoing treatment for 5 years. She had already undergone neoadjuvant chemotherapy, mastectomy, radiotherapy and adjuvant chemotherapy. By the time of metastatic diagnosis, she was in monotherapy with T-DM1 for 2.5 years. Upper endoscopy showed esophageal varices and portal hypertension gastropathy. Laboratorial tests revealed increased transaminases, hypergammaglobulinemia and positive antinuclear antibody. Liver biopsy was performed for autoimmune hepatitis differential diagnosis but revealed nodular regenerative hyperplasia. T-DM1 was discontinued. After a 2-year follow-up, the patient did not present any complications of portal hypertension, although persisted with esophageal varices.

Relation between Helicobacter pylori infection and severity of portal hypertensive gastropathy in cirrhotic patients

ABSTRACT Background: Cirrhosis is a great health problem worldwide and is associated with many complications. Portal hypertensive gastropathy (PHG) is one of its most common complications and in some patients may lead to gastrointestinal bleeding. The relationship between Helicobacter pylori (H. pylori) infection and PHG is not clearly identified. Objective: This work aimed to study a possible association between H. pylori infection and PHG and to correlate the severity of PHG with H. pylori infection in cirrhotic patients. Methodology:A cross sectional comparative study included 90 cirrhotic patients, who were classified into 3 groups. G1: included 30 age and sex-matched cirrhotic patients with no PHG. G2: included 30 age and sex-matched cirrhotic patients with mild PHG. G3: included 30 age and sex-matched cirrhotic patients with severe PHG. Endoscopic examination was done to evaluate the presence and severity of portal hypertensive gastropathy and for diagnosis of H. pylori infection. Results: H. pylori infection by histopathology was detected in 61 studied patients (67.8%). H. pylori infection was more prevalent among cirrhotic patients with PHG (78.3%) than patients without PHG (46.7%) (P=0.0029). H. pylori infection was detected in 26(86.7%), 21(70.0%), 14(46.7%) in patients with severe, mild and no PHG respectively. H. pylori infection was more prevalent in patients with severe PHG relative to patients with no PHG (p-value = 0.001). Conclusion: The current study showed a significant relation between H. pylori infection and PHG in cirrhotic patients and it might have a role in the pathogenesis of severe PHG.

A Visual Engram Worth Remembering

Question: A 35-year-old man with known ulcerative colitis presented with severe proctitis. The patient’s history included orthotopic triple liver transplantation with colectomy and creation of a terminal ileostomy owing to primary sclerosing cholangitis, portal hypertensive gastropathy, thrombocytopenia and poor coagulation with substitution, hepatic encephalopathy, hepatorenal failure, and Jak2 inhibitor treatment.