Chronic Gastrointestinal Bleeding Research Articles

Recurrent gastric antral vascular ectasia: a single center experience.

Gastric antral vascular ectasia (GAVE) is a rare cause of chronic or acute gastrointestinal bleeding. This condition accounts for ∼4% of upper gastrointestinal bleeding cases. This disease is often associated with systemic diseases, such as liver cirrhosis, chronic kidney failure, autoimmune conditions, diabetes mellitus, hypothyroidism, and cardiovascular diseases. However, its etiopathogenesis remains controversial. We retrospectively reviewed the cases of GAVE treated at our digestive surgery unit. A total of nine patients were identified with a male/female ratio of 1.25:1 and an average age of 75.51 years (SD ± 9.85). All patients underwent endoscopic argon plasma coagulation (APC) treatment. At the time of the review, data on eight patients were available after 36 months of follow-up. APC appears to be safe and effective for hemostasis of bleeding vascular ectasia. Only one (11.1%) patient required surgical intervention due to hemodynamic instability after multiple unsuccessful endoscopic treatments. No intraoperative and postoperative complication or bleeding relapse was experienced. Based on our findings, we concluded that endoscopic APC is technically simple, but requires multiple re-interventions due to the incidence of relapses. Furthermore, larger randomized studies should be conducted to assess the role of elective surgery as the first intervention in stable patients with severe pathology and the timing of surgery after failed endoscopic treatment.

Impact of left atrial appendage closure in patients on anticoagulation for atrial fibrillation and recurrent or chronic gastrointestinal bleeding

Impact of left atrial appendage closure in patients on anticoagulation for atrial fibrillation and recurrent or chronic gastrointestinal bleeding

Chronic gastrointestinal bleeding and anemia in a pancreas transplant recipient: A creative solution to a previously uncharacterized complication

Chronic gastrointestinal bleeding and anemia in a pancreas transplant recipient: A creative solution to a previously uncharacterized complication

An Exceptional Presentation of “Watermelon Stomach” in a 30- Year-Old Cirrhotic Male

Gastric antral vascular ectasia (GAVE) is an unusual cause of chronic upper gastrointestinal bleeding commonly described in elderly females, with associated autoimmune diseases, and in cirrhotic males. The entity is characterized by angioectasia in the pyloric antrum, giving its classic streaky “watermelon stripe” appearance. This report highlights the rare presentation of a 30-year-old male with liver cirrhosis, who presented with anemia and fatigability. Diagnosis of GAVE was made using endoscopy, and trials of argon plasma coagulation were administered. Following this, an antrectomy was performed since there was a further drop in hemoglobin. The patient made a full recovery with no subsequent dependence on blood transfusions. GAVE can be mistakenly underdiagnosed as a treatable cause of occult gastrointestinal bleeding. This report mandates caution on endoscopy for younger patients with an upper gastrointestinal bleed while taking other more common causes of gastrointestinal bleeding (peptic ulcers, esophageal varices, and non-steroidal anti-inflammatory drugs [NSAID]-induced gastritis) into account.

Evaluation of Endoscopic Mucosal Band Ligation for Treatment of Portal Hypertensive Gastropathy in Cirrhotic Patients

Background: Portal hypertensive gastropathy (PHG) is a clinical condition that can lead to chronic gastrointestinal (GIT) hemorrhage in cirrhotic patients, presented by chronic anemia. The diagnosis is based on the endoscopic features. The aim of the study was to evaluate the safety and efficacy of the use of endoscopic mucosal band ligation for treatment of portal hypertensive gastropathy in cirrhotic patients.
 Patients and methods: This prospective study included 80 cirrhotic anemic patients. They divided into four equal groups: Group (A) included patients who were treated with drugs as beta-blockers. Group (B) included patients treated with argon plasma coagulation (APC). Group (C) included patients treated with endoscopic mucosal band ligation and Group (D) included patients treated with combined endoscopic mucosal band ligation and APC in subsequent sessions.
 Results: There was statistical significant decrease in TIBC throughout follow up in the four studied groups. And there was statistical significant increase in Hb, and serum ferritin throughout follow up in the four studied groups.
 Conclusion: after 2nd follow-up in managing PHG, we have found that there is significant increase in Hb, serum ferritin and significant decrease in recurrent GI bleeding among all groups.

An Unusual Cause of GI Blood Loss

Chronic gastrointestinal bleeding is the leading cause of iron deficiency anemia in developed countries, and most occult bleeds are attributed to upper gastrointestinal tract lesions, which are broadly categorized into mass lesions, vascular, infectious, and inflammatory abnormalities. Gastric polyps account for an exceedingly small portion of these lesions but are of clinical importance because of the risk for progression to malignancy. We describe a patient found to have a gastric foveolar-type adenoma as a rare cause of iron deficiency anemia, with an incidentally found gastric neuroendocrine tumor.

Impact of left atrial appendage closure in patients on anticoagulation for atrial fibrillation and recurrent or chronic gastrointestinal bleeding

BackgroundOral anticoagulation in non-valvular atrial fibrillation is associated with an increased risk of bleeding, particularly gastrointestinal bleeding, leading to treatment withdrawal in up to 50% of patients and putting them at risk of embolic events. Left atrial appendage closure (LAAC) can be an alternative to chronic anticoagulation. We aim to describe the impact of LAAC in patients with gastrointestinal bleeding (GIB) or chronic iron deficiency anaemia (CIDA) on healthcare resources consumption. MethodsObservational retrospective study of patients who underwent LAAC for GIB or CIDA at a single centre. ResultsNineteen patients with a median age of 74 years and a median Charlson score of six points were included in the study. Angiodysplasias were the most frequent cause of GIB or CIDA. The procedural success rate of LAAC was 100% with a median anticoagulant and antiplatelet treatment duration of 92 days. One year after the LAAC, we found a significant improvement in the lowest haemoglobin concentration and a reduction in the number of red blood cells transfusion, hospital admissions due to GIB and CIDA and the number of endoscopic examinations. One patient died due to a pulmonary thromboembolism. No deaths related to GIB were observed. ConclusionsLAAC seems to be a safe and effective alternative to anticoagulation in patients with GIB or CIDA.

Comparison of hospitalization cause and risk factors between patients undergoing hemodialysis and peritoneal dialysis

This retrospective study was designed to compare the cause of hospitalization and influencing factors between patients undergoing hemodialysis (HD) and peritoneal dialysis (PD). Baseline data and laboratory parameters of 192 dialysis patients (92 HD patients and 100 PD patients) were compared. Quantitative parameters with normal distribution were assessed using independent t-test or analysis of variance (ANOVA). Quantitative parameters with non-normal distribution were assessed by non-parametric test. Qualitative data were statistically compared using χ2 test. The number of patients with urban employee medical insurance (88 HD patients and 60 PD patients) and rural cooperative medical care (12 HD patients and 40 PD patients) significantly differed (P < .01). The hospitalization rate of PD patients was significantly higher than that of HD counterparts. The average length of hospital stay of PD patients was 10 days, remarkably longer than 8 days of HD patients (P < .01). The primary cause of hospitalization for HD patients was infection-related complications, followed by cardiovascular, cerebrovascular complications and dialysis access disorders. The primary cause of hospitalization for PD patients was infection-related complications, followed by dialysis access disorders, cardiovascular, and gastrointestinal complications. Compared with the HD group, the levels of hemoglobin, serum albumin, alkaline phosphatase, intact parathyroid hormone were significantly decreased, whereas serum urea nitrogen, serum creatinine, phosphorus levels and cardiothoracic ratio were remarkably increased in the PD group (all P < .01). The hospitalization rate of PD patients is relatively higher, and the length of hospital stay is longer. Extensive attention and efforts should be delivered to enhance the understanding of disease and lower the risk of complications for patients.

Evaluation of Frequency and Type of Severe Anemia in Patients Referred to the Baqiyatallah Hospital in Tehran in Six Months; A Descriptive Cross-Sectional Study

Purpose: To investigate the frequency and types of severe unknown anemia in patients referred to the Baqiyatallah Hospital (Tehran) for six months.&#x0D; Methods: In this descriptive cross-sectional study, the patients with severe unknown anemia referred to the Baqiyatallah Hospital (Tehran, Iran) were selected over six months. Following consideration of inclusion and exclusion criteria, 230 patients with severe anemia (hemoglobin (Hb) &gt; 8gr/dl) were included. Complete medical history was obtained from the patients and additional biochemical blood analyses were applied to determine the frequency and type of anemia. SPSS (v.19) software was used to analyze the findings and the significance level was defined as a p-value &lt;0.05.&#x0D; Results: In chronic disease anemia (47.5%), gastrointestinal bleeding-associated anemia (29%), bleeding malignancies anemia (21.5%), and aplastic anemia (2%). There were significant differences (p&lt;0.05) in the frequency of different types of normocytic anemia. The highest frequency was detected in folate deficiency anemia (46%), hypothyroidism anemia (34%), and B12 deficiency anemia (20%), respectively. The hemolytic anemia represented a significant difference (p&lt;0.05) in comparison with sickle cell anemia (95%). Also, sickle cell anemia showed a significant difference (p&lt;0.05) between thalacemia-associated anemia (95%) and malignancy-related anemia (95%)&#x0D; Conclusion: Respectively, the highest frequency of anemia in patients was found in chronic diseases and gastrointestinal bleeding. It is suggested that more attention should be paid to the type of anemia of patients referred to the urgency of hospitals.

Indications and hemoglobin thresholds for red blood cell transfusion and iron replacement in adults with gastrointestinal bleeding: An algorithm proposed by gastroenterologists and patient blood management experts.

Gastrointestinal (GI) bleeding is associated with considerable morbidity and mortality. Red blood cell (RBC) transfusion has long been the cornerstone of treatment for anemia due to GI bleeding. However, blood is not devoid of potential adverse effects, and it is also a precious resource, with limited supplies in blood banks. Nowadays, all patients should benefit from a patient blood management (PBM) program that aims to minimize blood loss, optimize hematopoiesis (mainly by using iron replacement therapy), maximize tolerance of anemia, and avoid unnecessary transfusions. Integration of PBM into healthcare management reduces patient mortality and morbidity and supports a restrictive RBC transfusion approach by reducing transfusion rates. The European Commission has outlined strategies to support hospitals with the implementation of PBM, but it is vital that these initiatives are translated into clinical practice. To help optimize management of anemia and iron deficiency in adults with acute or chronic GI bleeding, we developed a protocol under the auspices of the Spanish Association of Gastroenterology, in collaboration with healthcare professionals from 16 hospitals across Spain, including expert advice from different specialties involved in PBM strategies, such as internal medicine physicians, intensive care specialists, and hematologists. Recommendations include how to identify patients who have anemia (or iron deficiency) requiring oral/intravenous iron replacement therapy and/or RBC transfusion (using a restrictive approach to transfusion), and transfusing RBC units 1 unit at a time, with assessment of patients after each given unit (i.e., “don’t give two without review”). The advantages and limitations of oral versus intravenous iron and guidance on the safe and effective use of intravenous iron are also described. Implementation of a PBM strategy and clinical decision-making support, including early treatment of anemia with iron supplementation in patients with GI bleeding, may improve patient outcomes and lower hospital costs.

Loss of NKCC1 function increases epithelial tight junction permeability by upregulating claudin-2 expression.

Conditions that cause the loss of epithelial barrier integrity are often accompanied by dysregulation of tight junction protein expression and/or localization. Recently, we have reported that patients with mutations in SLC12A2, the gene encoding the basolateral Na+-K+-2Cl- cotransporter (NKCC1), suffer from severe gastrointestinal deficits, including chronic gastrointestinal inflammation, gastrointestinal hemorrhage, intestinal obstruction, and constipation. Although the intestinal inflammation observed in patients with loss of NKCC1 function may or may not be due to tight junction dysfunction, we investigated whether the loss of NKCC1 function affects paracellular ion transport and epithelial barrier function. Wild-type HT29-MTX-E12 and CRISPR/Cas9-mediated NKCC1 knockout (KO) HT29 clones were tested for tight junction protein expression and localization. Tightness of epithelial cell monolayer was assessed by measurement of transepithelial electrical resistance and permeability of molecular tracers in transwell filters. Tight junction protein localization was assessed by immunofluorescence. Loss of NKCC1 expression strongly increases the expression of claudin-2 and occludin in epithelial cell monolayers. Loss of NKCC1 significantly reduces the transepithelial electrical resistance (TER) indicating an increase in paracellular ions flux, consistent with upregulation of the cation-selective and channel-forming claudin-2. In addition, NKCC1-KO monolayers showed a significant increase in the paracellular flux of small molecules like fluorescein (0.33 kDa), whereas the permeability of higher molecular weight TRITC-Dextran (4 kDa and 70 kDa) remained unchanged. Thus, NKCC1 regulates tight junction protein expression and loss of NKCC1 function affects epithelial barrier integrity.

Metabolomics: The Key to Unraveling the Role of the Microbiome in Visceral Pain Neurotransmission.

Inflammatory bowel disease (IBD), comprising Crohn’s disease and Ulcerative colitis, is a relapsing and remitting disease of the gastrointestinal tract, presenting with chronic inflammation, ulceration, gastrointestinal bleeding, and abdominal pain. Up to 80% of patients suffering from IBD experience acute pain, which dissipates when the underlying inflammation and tissue damage resolves. However, despite achieving endoscopic remission with no signs of ongoing intestinal inflammation or damage, 30–50% of IBD patients in remission experience chronic abdominal pain, suggesting altered sensory neuronal processing in this disorder. Furthermore, effective treatment for chronic pain is limited such that 5–25% of IBD outpatients are treated with narcotics, with associated morbidity and mortality. IBD patients commonly present with substantial alterations to the microbial community structure within the gastrointestinal tract, known as dysbiosis. The same is also true in irritable bowel syndrome (IBS), a chronic disorder characterized by altered bowel habits and abdominal pain, in the absence of inflammation. An emerging body of literature suggests that the gut microbiome plays an important role in visceral hypersensitivity. Specific microbial metabolites have an intimate relationship with host receptors that are highly expressed on host cell and neurons, suggesting that microbial metabolites play a key role in visceral hypersensitivity. In this review, we will discuss the techniques used to analysis the metabolome, current potential metabolite targets for visceral hypersensitivity, and discuss the current literature that evaluates the role of the post-inflammatory microbiota and metabolites in visceral hypersensitivity.

Gastric Antral Vascular Ectasia (GAVE) Disorder

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon cause of chronic gastrointestinal bleeding as well as iron deficiency anaemia. We present two cases of GAVE, one with pernicious anaemia associated and the other is portal hypertension related. In both cases, progressive mucosal changes, which results in formation of GAVE, were documented. The changes were progression of multiple antral erythematous spots into linear configuration and finally to watermelon stomach.

Chronic gastrointestinal bleeding caused by a Dieulafoy\u2019s lesion in the\xa0small intestine: a case report

IntroductionDieulafoy’s lesion, first found by Paul Georges Dieulafoy, is an infrequent but important cause of recurrent upper gastrointestinal bleeding. The bleeding is usually severe, but patients rarely present with chronic, occult gastrointestinal bleeding.Case presentationIn this article, we discuss the case of a 68-year-old caucasian man with a history of recurrent hematemesis and chronic anemia with evidence of extravasation of contrast in the lumen of the bowel loop on computed tomography angiography. The patient was taken to the operating room, and a laparotomy procedure was performed.ConclusionDue to the infrequency of Dieulafoy’s lesion compared with other causes of gastrointestinal bleeding, it is often missed in the process of differential diagnosis. In this article, we have demonstrated the importance of this disease and different approaches to the treatment of this lesion, considering the location of the lesion among other factors.

Blue rubber bleb nevus syndrome: a single-center case series in 12 years.

BackgroundBlue rubber bleb nevus syndrome is a rare congenital disease characterized by multiple venous malformations in skin and gastrointestinal tract, not all patients have typical cutaneous lesions, refractory anemia may be the only clinical symptom, it is easy to miss diagnosis.MethodsA retrospective single center study was conducted on 8 patients with blue rubber bleb nevus syndrome from 2009 to 2021. Data were analyzed including clinical feature, diagnostic workup and results, gene detection, treatment and follow-up.ResultsFive children (62.5%) developed the disease in infancy, which initial symptoms were all cutaneous venous malformations. All children had chronic refractory anemia and gastrointestinal bleeding. Cutaneous lesions were observed in 87.5%, 1 child had multiorgan involvement. Gastrointestinal venous malformations were observed in 100%, lesions were more common in small intestine than in stomach or colon. No somatic mutation in TEK was found in our children. Diagnostic interval was on average 4.7 years. Eighty-seven-point-five percent children received at least one endoscopic or surgical intervention, however, those methods could not eradicate all the lesions and prevent relapse. Two children treated with sirolimus for more than 8 years, only 1 have satisfactory therapeutic effect. Besides, I child has growth retardation and emotional problems during follow-up.ConclusionsBlue rubber bleb nevus syndrome needs to be considered when find bluish nodular cutaneous lesions, chronic anemia or gastrointestinal bleeding of unknown origin. Capsule endoscopy is the most sensitive in diagnosing of this disease. Oral sirolimus at a relatively low dosage is effective, further comprehensively studies are required to evaluation of its efficacy, safety and the optimal dosage about the children.

Cyanosis in a Previously Well Child.

Cyanosis in a Previously Well Child.

Gastrointestinal bleeding with Klippel\u2013Trenaunay syndrome: a case report

BackgroundGastrointestinal bleeding caused by gastrointestinal tract involvement in patients with Klippel–Trenaunay syndrome (KTS) is extremely rare and often overlooked.Case presentationA 9-year-old girl who presented with chronic gastrointestinal bleeding was admitted to our hospital. Laboratory examinations revealed microcytic hypochromic anemia and a positive fecal occult blood test. Computed tomography (CT) of the lower limbs combined with physical examination confirmed KTS. The pelvic CT showed concentric thickening of the sigmoid colon and rectum, with progressive enhancement after the administration of a contrast agent. Colonoscopy demonstrated vascular malformations of the sigmoid colon and rectum. The patient was finally diagnosed with KTS with gastrointestinal tract involvement. The patient improved after receiving conservative treatment.ConclusionsA suspicion of gastrointestinal tract involvement as an etiology for gastrointestinal bleeding should not be overlooked in patients with KTS. Endoscopy and imaging modalities can synergistically help diagnose this condition.

Pazopanib for severe bleeding and transfusion-dependent anemia in hereditary hemorrhagic telangiectasia

Hereditary hemorrhagic telangiectasia (HHT) is a rare angiogenic disorder causing chronic gastrointestinal bleeding, epistaxis, and severe anemia. Pazopanib is an oral multi-kinase angiogenesis inhibitor with promise to treat bleeding in HHT. We analyzed outcomes of HHT patients with the most severe bleeding causing RBC transfusion dependence treated on a predefined institutional pazopanib treatment pathway (with data collected retrospectively). The primary endpoint was achievement of transfusion independence. Secondary endpoints included hemoglobin, epistaxis severity score, RBC transfusion and iron infusion requirements, number of local hemostatic procedures, ferritin and transferrin saturation, compared using paired and repeated measures mean tests. Thirteen transfusion-dependent HHT patients received pazopanib [median (range) dose 150 (25–300) mg daily)] for a median of 22 months. All patients achieved transfusion independence. Compared with pretreatment, pazopanib increased mean hemoglobin by 4.8 (95% CI, 3.6–5.9) g/dL (7.8 vs. 12.7 g/dL, P < 0.0001) and decreased mean epistaxis severity score by 4.77 (3.11–6.44) points (7.20 vs. 2.43 points, P < 0.0001) after 12 months of treatment. Compared with 3 months of pretreatment, RBC transfusions decreased by 93% (median of 16.0 vs. 0.0 units, P < 0.0001) and elemental iron infusion decreased by 92% (median of 4500 vs. 0 mg, P = 0.005) during the first 3 months of treatment; improvements were maintained over time. Pazopanib was well-tolerated: hypertension, lymphocytopenia, and fatigue were the most common TEAEs. In conclusion, pazopanib was safe and effective to manage severe bleeding in HHT, liberating all patients from transfusion dependence and normalizing hematologic parameters at doses lower than used to treat malignancies. These findings require confirmation in a randomized trial.Supplementary InformationThe online version contains supplementary material available at 10.1007/s10456-021-09807-4.

Small Bowel Hemolymphangioma Treated by Polypectomy in a Pediatric Patient with Cystic Fibrosis

Small Bowel Hemolymphangioma Treated by Polypectomy in a Pediatric Patient with Cystic Fibrosis

Inactivation of the basolateral Na‐K‐2Cl cotransporter, NKCC1, increases intestinal barrier permeability

Background Epithelial tight junctions are defective in gastrointestinal diseases. Conditions that causes epithelial barrier loss are often accompanied by dysregulation of tight junction protein expression and/or localization. Recently we have reported that patients with mutations in SLC12A2; the gene encoding the basolateral Na+-K+-2Cl- cotransporter (NKCC1), suffer from severe gastrointestinal deficit; including chronic gastrointestinal inflammation, gastrointestinal hemorrhage, intestinal obstruction, and constipation. NKCC1-KO mice develop spontaneous gastrointestinal inflammation with bleeding in the intestine. We therefore ask whether loss of NKCC1 function affect intestinal epithelial barrier function. Methods Wild-type HT29-MTX-E12 and CRISPR/Cas9 NKCC1-deleted HT29 clones were tested for tight junction protein expression and localization. Epithelial cell monolayers permeability to molecular tracers was assessed in transwell filters. Tight junction protein localization was assessed by immunofluorescence. Results Loss of NKCC1 expression strongly increases the expression of claudin-2, occluding, and ZO-1 in epithelial cell monolayers. Loss of NKCC1 significantly reduces the trans-epithelial electrical resistance (TER) indicating an increase in paracellular ions flux, which is consistent with upregulation of the cation-selective and channel-forming claudin-2. In addition, NKCC1-KO monolayers showed a significant increase in paracellular flux of small molecules, as the 0.33 kDa fluorescein permeability increases in the NKCC1-KO monolayers compared to wild-type, while the high molecular weight 4 kDa TRITC-Dextran and 70 kDa TRITC-Dextran permeability remained unchanged. In addition, Loss of NKCC1 causes mis-localization of occludin from the tight junction complex. Conclusions NKCC1 regulate tight junction protein expression and localization. Loss of NKCC1 function is a previously unknown mechanism that causes intestinal epithelial barrier loss.