Upper Gastrointestinal Endoscopy in Children’s Abdominal Pains in Ivory Coast

Since a longtime considered as functional and psychological, children’s abdominal pains (CAP) is a public health problem. Advances in digestive endoscopy and Helicobacter pylori (H. pylori) discovery have reignited the debate of the organicity of CAP. The aim of this study is to determine the diagnosis rentability of upper gastrointestinal endoscopy (UGIE) in CAP in Ivory Coast. Patients and Methods: This a retrospective analytical study based on reports of UGIE performed in 2 university hospital and 3 private clinics of Abidjan from march 2007 to march 2016. The children (from 1 day to 15 years) in which UGIE were performed for abdominal pains were included in the study. Results: 116 UGIE were performed in children for abdominal pains during the study period. Epigastric pain was the main indication of UGIE (88%). The diagnosis rentability of UGIE was more than 70% in this study. The main anomalies observed in UGIE were gastropathies. Ulcers were rarely found. Conclusion: UGIE play an important diagnosis role in CAP in Ivory Coast. However gastric biopsies for Helicobacter pylori research are not common practice in our country.

Portal hypertension and gastrointestinal bleeding:Diagnosis,prevention and management

Bleeding from esophageal varices is a life threatening complication of portal hypertension.Primary prevention of bleeding in patients at risk for a first bleeding episode is therefore a major goal.Medical prophylaxis consists of non-selective beta-blockers like propranolol or carvedilol.Variceal endoscopic band ligation is equally effective but procedure related morbidity is a drawback of the method.Therapy of acute bleeding is based on three strategies:vasopressor drugs like terlipressin,antibiotics and endoscopic therapy.In refractory bleeding,self-expandable stents offer an option for bridging to definite treatments like transjugular intrahepatic portosystemic shunt(TIPS).Treatment of bleeding from gastric varices depends on vasopressor drugs and on injection of varices with cyanoacrylate.Strategies for primary or secondary prevention are based on non-selective beta-blockers but data from large clinical trials is lacking.Therapy of refractory bleeding relies on shuntprocedures like TIPS.Bleeding from ectopic varices,portal hypertensive gastropathy and gastric antral vascular ectasia-syndrome is less common.Possible medical and endoscopic treatment options are discussed.

Portal hypertensive gastropathy:A systematic review of thepathophysiology,clinical presentation,natural history andtherapy

AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.

Reliability in endoscopic diagnosis of portal hypertensive gastropathy

AIM: To analyze reliability among endoscopists in diagnosing portal hypertensive gastropathy (PHG) and to determine which criteria from the most utilized classifications are the most suitable. METHODS: From January to July 2009, in an academic quaternary referral center at Santa Casa of S o Paulo Endoscopy Service, Brazil, we performed this singlecenter prospective study. In this period, we included 100 patients, including 50 sequential patients who had portal hypertension of various etiologies; who were previously diagnosed based on clinical, laboratory and imaging exams; and who presented with esophageal varices. In addition, our study included 50 sequentialpatients who had dyspeptic symptoms and were referred for upper digestive endoscopy without portal hypertension. All subjects underwent upper digestive endoscopy, and the images of the exam were digitally recorded. Five endoscopists with more than 15 years of experience answered an electronic questionnaire, which included endoscopic criteria from the 3 most commonly used Portal Hypertensive Gastropathy classifications (McCormack, NIEC and Baveno) and the presence of elevated or flat antral erosive gastritis. All five endosco- pists were blinded to the patients' clinical information, and all images of varices were deliberately excluded for the analysis. RESULTS: The three most common etiologies of portal hypertension were schistosomiasis (36%), alcoholic cirrhosis (20%) and viral cirrhosis (14%). Of the 50 patients with portal hypertension, 84% were Child A, 12% were Child B, 4% were Child C, 64% exhibited previous variceal bleeding and 66% were previously endoscopic treated. The endoscopic parameters, presence or absence of mosaic-like pattern, red point lesions and cherry-red spots were associated with high inter-observer reliability and high specificity for diagnosing Portal Hypertensive Gastropathy. Sensitivity, specificity and reliability for the diagnosis of PHG (%) were as follows: mosaic-like pattern (100; 92.21; High); fine pink speckling (56; 76.62; Unsatisfactory); superficial reddening (69.57; 66.23; Unsatisfactory); red-point lesions (47.83; 90.91; High); cherry-red spots (39.13; 96.10; High); isolated red marks (43.48; 88.31; High); and confluent red marks (21.74; 100; Unsatisfactory). Antral elevated erosive gastritis exhibited high reliability and high specificity with respect to the presence of portal hypertension (92%) and the diagnosis of portal hypertensive gastropathy (88.31%). CONCLUSION: The most suitable endoscopic criteria for the diagnosis of PHG were mosaic-like pattern, redpoint lesions and cherry-red spots with no subdivisions,which were associated with a high rate of inter-observer reliability.

Effect of early propranolol administration on portal hypertensive gastropathy in cirrhotic rats

AIM:To investigate any protective effect of early propranolol administration in the development of portal hypertensive gastropathy in cirrhotic rats. METHODS:For the development of liver cirrhosis and portal hypertensive gastropathy,60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein,followed by phenobarbital and carbon tetrachloride(CCl4) administration.After two weeks of CCl4 administration, the rats were randomly separated into two groups.In group A,propranolol was continuously administered intragastrically throughout the study,whereas in group B normal saline(placebo)was administered instead. Hemodynamic studies and vascular morphometric analysis of gastric sections were performed after complete induction of cirrhosis. RESULTS:Vascular morphometric studies showed higher numbers of vessels in all mucosal layers in the control group.Statistical analysis revealed a significantly higher total vascular surface in the control group compared to the propranolol group,but with no statistically significant difference between the mean vascular surfaces between the groups.Our study clearly shows that the increased mucosal blood flow is manifested by a marked increase of vessel count. CONCLUSION:Early propranolol's administration in portal hypertensive cirrhotic rats seems to prevent intense gastric vascular congestion that characterizes portal hypertensive gastropathy.

N-acetylcysteine modulates angiogenesis and vasodilation in stomach such as DNA damage in blood of portal hypertensive rats

AIM: To evaluate the antioxidant effect of N-acetylcysteine(NAC) on the stomach of rats with portal hypertension.METHODS: Twenty-four male Wistar rats weighing ± 250 g were divided into four experimental groups(n =6 each): Sham-operated(SO),SO + NAC,partial portal vein ligation(PPVL),and PPVL + NAC. Treatment with NAC in a dose of 10 mg/kg(i.p.) diluted in 0.6 m L of saline solution was administered daily for 7 d starting 8 d after the surgery. Animals from the PPVL and SO group received saline solution(0.6 m L) for the same period of time as the PPVL + NAC and SO + NAC group. On the 15 th day the animals were anesthetized and we evaluated portal pressure by cannulating mesenteric artery. After,we removed the stomach for further analysis. We performed immunohistochemical analysis for endothelial nitric oxide synthase(e NOS),vascular endothelial growth factor(VEGF),and nitrotirosine(NTT) proteins in stomach. We also evaluated e NOS and VEGF by Western blot analysis and assessed DNA damage in blood samples by the comet assay.RESULTS: The portal hypertension group exhibited increases in portal pressure when compared to SO group(29.8 ± 1.8 vs 12.0 ± 0.3 mm Hg)(P < 0.001). The same was observed when we compared the e NOS(56.8 ± 3.7 vs 13.46 ± 2.8 pixels)(P < 0.001),VEGF(34.9 ± 4.7 vs 17.46 ± 2.6 pixels)(P < 0.05),and NTT(39.01 ± 4.0 vs 12.77 ± 2.3 pixels)(P < 0.05) expression by immunohistochemistry of the PPVL animals with the SO group. The expression of e NOS(0.39 ± 0.03 vs 0.25 ± 0.03 a.μ)(P < 0.01) and VEGF(0.38 ± 0.04 vs 0.26 ± 0.04 a.μ)(P < 0.01) were also evaluated by Western blot analysis,and we observed an increase of both proteins on PPVL animals. We also evaluated the DNA damage by comet assay,and observed an increase on damage index and damage frequency on those animals. NAC decreased portal pressure values in PPVL + NAC animals(16.46 ± 2 vs 29.8 ± 1.8 mm Hg)(P < 0.001) when compared to PPVL. The expression of e NOS(14.60 ± 4.1 vs 56.8 ± 3.7 pixels)(P < 0.001),VEGF(19.53 ± 3.2 vs 34.9 ± 4.7 pixels)(P < 0.05) and NTT(21.84 ± 0.7 vs 39.01 ± 4.0 pixels)(P < 0.05) evaluated by immunohistochemistry were also reduced in PPVL + NAC animals. Also,when evaluated by Western blot e NOS expression(0.32 ± 0.03 vs 0.39 ± 0.03 a.μ)(P < 0.05) and VEGF expression(0.31 ± 0.09 vs 0.38 ± 0.04 a.μ)(P < 0.01). Furthermore,NAC modulated DNA damage in PPVL + NAC animals.CONCLUSION: In view of these results,we believe NAC is able to protect the stomach from the alterations induced by the PPVL procedure.

Helicobacter pylori and portal hypertensive gastropathy

To the Editor:H. pylori lives in the gastric epithelial cells, sometimes in gastric glands.Whetherornottheproliferationandbiologicalbehavior of H. pylori can be influenced by the status of the gastric mucosa is still unknown. Portal hypertensive gastropathy (PHG) is a blood drainage obstructive disease. In this pathologic environment, gastric mucosa may be further impaired when patients are infected with H. pylori. The role of H. pylori in the pathogenesis of PHG and

Lymphomatoidgastropathy mimicking extranodal NK/T cell lymphoma,nasal type:A case report

Extranodal natural killer(NK)/T-cell lymphoma,nasal type,exhibits aggressive tumor behavior and carries a poor prognosis.Recently,lymphomatoid gastropathy with NK/T cell infiltration into gastric mucosa has been recognized as a pseudo-malignant disease which regresses without treatment.Because the conventional immunohistochemical criteria of lymphomatoid gastropathy is similar to that of extranodal NK/T-cell lymphoma nasal type,it is difficult to distinguish between the two conditions by histopathological evaluation only.Here,we report a rare case of lymphomatoid gastropathy in a 57-year-old female.Gastroendoscopy on routine check-up revealed elevated reddish lesions < 1 cm in diameter in the gastric fornix and body.Although repeat endoscopies at 1 and 6 mo later revealed no gastric lesions at any locations without any treatments,at 12 mo later gastric lymphomatoid lesions recurred at gastric fornix and body.Histological examination of endoscopic biopsy specimens at 12 mo showed atypical NK cell infiltration with CD3+,CD4-,CD5-,CD7+,CD8-,CD20-,CD30-,CD56+,CD79a-and T-cell-restricted intracellular antigen-1+ into gastric mucosa.After treatment for Helicobacter pylori(H.pylori) eradication,the lesions disappeared in all locations of the gastric fornix and body over the subsequent 12 mo.Here,we report a case of H.pylori-positive lymphomatoid gastropathy with massive NK-cell proliferation,and also review the literature concerning newly identified lymphomatoid gastropathy based on comparison of extra nodal NK/T-cell lymphoma nasal type.In any case,these lesions are evaluated with biopsy specimens,the possibility of this benign entity should be considered,and excessive treatment should be carefully avoided.Close follow-up for this case of lymphomatoid gastropathy is necessary to exclude any underlying malignancy.

Prolapse gastropathy syndrome may be a predictor of pathologic acid reflux

AIM： To assess the occurrence of gastric acid reflux into the esophagus in endoscopically confirmed prolapse gastropathy syndrome （PGS）. METHODS： Using ambulatory esophageal pH measurement （BRAVOTM wireless esophageal pH monitoring system）, twenty-six patients with PGS were compared with twenty-one patients with erosive esophagitis （EE） as controls. We assessed several reflux parameters, including the percentage of total time at pH 〈 4, and the DeMeester score. RESULTS： There were no statistical differences between the PGS group and the EE group as to mean age, sex ratio and pH recording time. The EE group showed more severe reflux than the PGS group, as evaluated in terms of the longest duration of reflux, the number of reflux episodes, the number of reflux episodes lasting 〉 5 min, the total time with pH 〈 4 during acid reflux episodes, and the DeMeester score, but none of these parameters showed statistically significant difference. Although 53.8% （14/26） of the PGS group and 76.2% （16/22） of the EE group demonstrated pathologic acid reflux （DeMeester score 〉 14.72）, there was no statistically significant difference between the two groups in the incidence of pathologic acid reflux （P = 0.11）. CONCLUSION： There was no statistically significant difference in pathologic acid reflux between the PGS and EE group. These data suggest that endoscopically diagnosed PGS might be a predictor of pathologic acid reflux.

Aloe vera attenuated gastric injury on indomethacin-induced gastropathy in rats

AIM: To evaluate the protective effects of Aloe vera on gastric injury in rats with indomethacin (IMN)-induced gastropathy.

Portal hypertensive gastropathy and its interrelated factors

OBJECTIVE: To investigate the influences of helicobacter pylori (Hp) infection, liver function, gastroesophageal varicosity, esophageal varicosity ligation (EVL), and esophageal varicosity sclerotherapy (EVS) on patients with portal hypertensive gastropathy (PHG). METHODS: Fourty-seven patients with liver cirrhosis included 34 patients with PHG and 13 patients without PHG. Liver function, Hp infection, and gastroesophageal varicosity were investigated clinically in all patients, and gastroscopy was made again in patients with EVL 1-2 months after operation to observe the changes of PHG. RESULTS: The rate of Hp infection was lower in patients with liver cirrhosis than in controls. There was no relationship between Hp infection and PHG. The patients with gastroesophageal varicosity had a high incidence of PHG. CONCLUSIONS: Despite no relationship between Hp infection and PHG, liver dysfunction can affect and promote PHG. Gastroesophageal varicosity may be closely related to PHG, but their degrees are not related. PHG can be caused or promoted by EVL.

Endothelin and neonatal capsaicin regulate gastric resistance to injury in BDL rats

AIM: To investigate the relationship between primary afferent neurons, endothelin (ET) and the role of its receptors on ethanol-induced gastric damage in cirrhotic rats. METHODS: Cirrhosis and portal hypertension were induced in rats by bile duct ligation (BDL) while controls had a sham operation. The association between ET and afferent neurons on the gastric mucosa was evaluated by capsaicin treatment in newborn rats, the use of ET agonists or antagonists, gastric ET-1 and -3 mRNA and synthetic capacity. Ethanol-induced damage was assessed using ex vivo gastric chamber experiments.Gastric blood flow was measured by laser-Doppler flow-metry. RESULTS: ET-3 and an ETB receptor antagonist sig- nificantly reduced the extent of ethanol-induced gastric damage in BDL rats. Gastric ET-1 and -3 levels were 30% higher in BDL rats compared to control rats. Cap-saicin treatment restored the gastric resistance and blood flow responses to topical application of ethanol in BDL rats and ET-1 and -3 production to levels observed in controls. CONCLUSION: Our results suggest that the reduced resistance of the gastric mucosa of cirrhotic rats to ethanol-induced injury is a phenomenon modulated by ET through the ET B receptor and by sensory afferent neurons.

The role of endotoxin in the pathogenesis of gastric mucosal damage in cirrhotic rats with portal hypertensive gastropathy

Objective:To study the role and the mechanism of endotoxin in the pathogenesis of gastric mucosa during portal vein hypertension gastrography(PHG) in the rats with cirrhosis.Methods: Rat model for PHG was established by injection of tetrachloride.The animals were injected with endotoxin i.p.at 3 mg/kg and endotoxin antagonist BPI21 i.v.at 2.0 mg/kg.The plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis factor alpha(TNF-α) was measured with azobenzene and ELISA respectively.Furthermore,the pathological changes of the gastric mucosa were studied with HE stainning.Results:In rats with PHG,increased endotoxin and TNF-αas well as the gastric pathological lesion were observed.Injection of endotoxin remarkably increased plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis TNF-αand induced more serious gastric lesion.Animals injected with endotoxin antagonist BPI21 showed improved gastric mucosal lesion,accompanied by the declining TNF-αlevel.Conclusions:Our results suggestes that endotoxin may play a pathogenetic role in PHG by inducing the expression of TNF-α.

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

BACKGROUND Accurate 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).AIM To determine the added diagnostic value of virtual chromoendoscopy to high definition white light for real-time endoscopic diagnosis of GAVE and PHG.METHODS We 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.RESULTS Twenty-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).Iscan had similar accuracy to HDWLE in detecting PHG.CONCLUSION This 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.

Shared changes in angiogenic factors across gastrointestinal vascular conditions:A pilot study

BACKGROUND Neovascularisation is common to a variety of gastrointestinal(GI)disorders with differing aetiologies and presentations;usually affecting adults above 60 years.Shared angiogenic factors modulated by disease specific elements could be a common denominator and represent novel diagnostic and therapeutic targets.As yet,assessment of angiogenic factors across several GI vascular disorders associated with recurrent bleeding and anaemia has not been reported.AIM To assess serum levels of angiogenic factors in several intestinal vascular disorders.METHODS A case control study was performed in Tallaght University Hospital in patients with endoscopically proven small bowel angiodysplasia(SBA),portal hypertensive gastropathy(PHG),gastric antral vascular ectasia(GAVE)and nonbleeding,non-anaemic controls.Using enzyme-linked immunosorbent assay,concentrations of Angiopoietin 1(Ang-1),Ang-2 and vascular endothelial growth factor(VEGF)were measured from 2 serum tubes of blood following informed consent.The relative expression of Ang-1 and Ang-2 and Ang-1/2 ratio was calculated and compared between groups.Statistical analysis was applied using a t-test,and a P value of<0.05 was considered significant.RESULTS To date 44 samples were tested:10 SBA,11 PHG,8 GAVE and 15 controls.Mean age 60(range 20-85)years and 20(45%)were males.Controls were significantly younger(49 years vs 66 years,P=0.0005).There was no difference in VEGF levels between the groups(P=0.6).SBA,PHG and GAVE Ang-1 levels were similar and were significantly lower than controls,(P=0.0002,95%CI:241 to 701).Ang-2 levels were statistically higher in PHG and GAVE groups compared to controls(P= 0.01, 95%CI: 77.8 to 668) and as a result, also had a lower Ang-1/2 ratioscompared to controls. While SBA Ang-2 levels were higher than controls, this didnot reach statistical significance. Neither age nor haemoglobin level, which wassimilar between disease groups, could explain the difference. In addition, themedian Ang-1/Ang-2 ratio for all patients was found to be significantly lowercompared to controls, 8 vs 28 respectively, P = 0.001, 95%CI: -27.55 to -7.12.CONCLUSIONOur novel pilot study suggests common alterations in Ang-1 and Ang-2 levelsacross several GI vascular disorders. Differences in Ang-1/Ang-2 ratios amongvascular disorders compared to controls suggest disease-specific modulation.

Rebamipide and Pantoprazole Combination in NSAIDs-Gastropathy Treatment

The objective of this study was to investigate the pantoprazole and rebamipide efficiency on NSAIDs （nonsteroidal anti-inflammatory drugs）-gastropathy restoring and healing in patients with coronary heart disease, stable angina, who have been taking aspirin for a long time period. The study included three groups of patients according to the treatment they have got： ASA （acetylsalicylic acid） in the first group; ASA and pantoprazole in the second; ASA, pantoprazole and rebamipide in the third one. To obtain the results, endoscopic method and proinflammatory cytokines LTB4 and protective prostaglandin E2 determination in the blood were used. The research demonstrated no ulcer effects in the group of patients who were treated by rebamipide, and significantly fewer gastroduodenal erosions, in comparison to the group, where treatment contained ASA and pantoprazole. The LTB4 （leukotriene B4） level decreased in pantoprazole and rebamipide treatment groups, but the PGE2 （prostaglandin E2） level increased only after rebamipide therapy. Therefore, rebamipide should be included to the therapy for the better NSAIDs-gastropathy treatment, in reason of its good reparative and gastroprotective properties.