Fatal Gastrointestinal Bleeding Research Articles

Disseminated Talaromyces marneffei infection initially presenting as cutaneous and subcutaneous lesion in an HIV-Negative renal transplant recipient: a case report and literature review

BackgroundThe incidence of Talaromyces marneffei (T. marneffei) infection has increased in recent years with the development of organ transplantation and the widespread use of immunosuppressive agents. However, the lack of clinical suspicion leading to delay or misdiagnosis is an important reason for the high mortality rate in non-human immunodeficiency virus (HIV) and non-endemic population. Herein, we report a case of disseminated T. marneffei infection in a non-HIV and non-endemic recipient after renal transplant, who initially presented with skin rashes and subcutaneous nodules and developed gastrointestinal bleeding.Case presentationWe describe a 54-year-old renal transplantation recipient presented with scattered rashes, subcutaneous nodules and ulcerations on the head, face, abdomen, and right upper limb. The HIV antibody test was negative. The patient had no obvious symptoms such as fever, cough, etc. Histopathological result of the skin lesion sites showed chronic suppurative inflammation with a large number of fungal spores. Subsequent fungal culture suggested T. marneffei infection. Amphotericin B deoxycholate was given for antifungal treatment, and there was no deterioration in the parameters of liver and kidney function. Unfortunately, the patient was soon diagnosed with gastrointestinal bleeding, gastrointestinal perforation and acute peritonitis. Then he rapidly developed multiple organ dysfunction syndrome and abandoned treatment.ConclusionsThe risk of fatal gastrointestinal bleeding can be significantly increased in kidney transplant patients with T. marneffei infection because of the long-term side effects of post-transplant medications. Strengthening clinical awareness and using mNGS or mass spectrometry technologies to improve the detection rate and early diagnosis of T. marneffei are crucial for clinical treatment in non-HIV and non-endemic population.

Secondary aortoenteric fistula: a narrative review of the view of the surgeon

Aortoenteric fistula (AEF) is defined as the abnormal communication between the aorta and the gastrointestinal tract. AEFs are divided into primary and secondary usually after abdominal aortic aneurysm (AAA) recovery and are a rare but quite dangerous cause of gastrointestinal bleeding that the general surgeon may face during his/her career. Secondary AEF was first described in 1953 to a 44-year-old woman 3 months after an AAA operation. This review presents the role of the surgeon in the management of secondary aortoenteric fistulas. AEFs are a rare but fatal gastrointestinal bleeding cause that the general surgeon may be asked to manage. Diagnosis requires the combination of strong clinical suspicion and the presence of a history of AAA surgery. Although a vascular surgery case, general surgeons play a role in choosing the technique of restoring the intestinal tract, which seems to be significantly related to subsequent morbidity and mortality.

PAZEC: a Dutch Gynaecological Oncology Group open-label, multicenter, phase II study of pazopanib in metastatic and locally advanced hormone-resistant endometrial cancer

ObjectiveThere is a continued need for improvement of second-line systemic treatment for metastatic and/or recurrent endometrial cancer.MethodsIn this phase II, open-label study, eligible patients had histologically or cytologically confirmed endometrial...

Not Your Everyday Duodenal Ulcer: Massive Gastrointestinal Bleed Secondary to Extramedullary Plasma Cell Myeloma

The differential for gastrointestinal (GI) bleeding is broad, ranging from peptic ulcers and Helicobacter pylori infection to variceal hemorrhage and neoplasms. The rarer causes of GI bleeds are frequently overlooked and as such can ultimately be more dangerous. Extramedullary multiple myeloma, an atypical plasma cell dyscrasia arising outside of the bone marrow, involves the GI tract in <5% of cases and often presents with nonspecific symptoms. We describe a rare case of such GI involvement of a plasma cell tumor, with subsequent transmural duodenal ulceration involving the gastroduodenal artery, ultimately resulting in a fatal GI bleed.

The Use of Avapritinib in Advanced Systemic Mastocytosis: Report of an Open-Label Compassionate Use Program in the United Kingdom

Background: Advanced systemic mastocytosis (AdvSM) is a rare haematological neoplasm occurring due to clonal proliferation of mast cells in extracutaneous organs. In up to 95% of cases, the driver mutation is KIT D816V. AdvSM encompasses aggressive SM (ASM), mast cell leukaemia and SM with an associated haematological neoplasm (SM-AHN). In this latter, the AHN component often dictates the clinical course, being most frequently associated with chronic myelomonocytic leukaemia (CMML). Treatment for AdvSM has evolved recently with the introduction of targetted tyrosine kinase inhibitors (TKI). Avapritinib, a highly selective inhibitor for KIT and PDGFRA, produced robust responses in measures of mast cell/disease burden in the PATHFINDER trial, leading to approval in USA and Europe. We report the clinical experience of AdvSM patients who have received avapritinib at 11 centers in the United Kingdom via an open-label compassionate use program. Methods: Avapritinib was commenced in AdvSM patients with progressive disease-related symptoms and end-organ damage. The initial dose was adjusted according to tolerability and kept continuously until disease progression or unmanageable toxicity. Results: In a cohort of 13 patients, with an age average of 68.8 years (range 57-76), 11 patients (84.6%) were diagnosed with SM-AHN; 81.8% with a concomitant diagnosis of CMML. 2 patients (15.4%) were diagnosed with ASM. All patients harbored the D816V mutation and 8 patients (61.5%) presented with additional mutations; 5 with SRSF2 and 1 with ASXL1. On application of prognostic scores; International Prognostic Scoring system for Mastocytosis (IPSM) 10 patients (76.9%) were classified as AdvSM-3/4 and Mutation-Adjusted Risk Score for Advanced Systemic Mastocytosis (MARS) 7 patients (53.8%) were stratified as high risk. Treatment: 10 patients (76.9%) received avapritinib as a first-line regime, and 9 patients (69.2%) started at a dose of 200 mg od. Three patients were previously treated with other regimes - one patient with midostaurin, one with cladribine and one with azacytidine. Response: Median duration of treatment was 503.7 days (range 75 - 1168 days). Baseline median blood parameters for this cohort were tryptase level of 168 ng/mL (range 91-811), alkaline phosphatase (ALP) of 437 IU/L (range 127-1235), albumin of 34.5 g/L (range 24-48) and a spleen size of 16.4 cm (range 12-26), measured by radiologically. At response evaluation, 9 patients (69.2%) had a tryptase level <20 ng/mL and 11 patients (84.6%) had normalised their ALP and albumin levels. None of the patients had a clinically enlarged spleen, with 9 patients (69.2%) having a normal spleen size on abdominal ultrasound. 8 patients had a complete pathological remission. The overall response rate (using the modified IWG-ECNM-MRT criteria) was 76.9% with a complete response (CR) or CR with partial haematologic recovery in 53.8% of patients. At the last follow-up, 3 patients (23.1%) died; 1 from SM progression, 1 from haematemesis and 1 due to progression of the AHN component but had a partial response of the SM with avapritinib. Toxicities:10 patients (76.9%) had haematological toxicities. Bleeding was reported in 4 patients (30.8%); 3 patients with grade 1/2 (1 mucocutaneous and 2 mild gastrointestinal bleeds), and 1 fatal gastrointestinal bleed. No intracranial bleeds were reported. Fluid retention was noted in 3 patients (23.1%). Less frequent side effects noted were nausea/vomiting (2 patients) and skin/hair discoloration (1 patient). 11 patients (84.6%) needed dose reduction of avapritinib due to haematological toxicity with 8 patients (72.7%) remaining at 100 mg od. 4 patients (36.4%) had to intermittently stop treatment until haematological recovery. Avapritinib was stopped in 2 patients (15.4%) due to disease progression or unmanageable toxicity. Conclusion: This small cohort of patients reflects the clinical heterogeneity of AdvSM and mirrors the PATHFINDER trial outcomes in 'real world 'experience in the UK. Avapritinib as 1st line was tolerated, producing sustained clinical and pathological responses in the majority of this group of non-selected patients with AdvSM with high risk disease. Dose adjustments due to anticipated myelosuppression were made, with 72.2% of patients maintained on 100mg Avapritinib od. 2 patients with SM-AHN are referred for HSCT as a curative treatment as a result of achieving a CR with Avapritinib.

OR29-3 High-specific-activity Iodine 131 Metaiodobenzylguanidine for the Treatment of Advanced Pheochromocytoma and Paraganglioma: A Real-world Study

Abstract Introduction Metastatic pheochromocytomas/paragangliomas (mPPGLs) are rare tumors with limited treatment options. High-specific-activity 131I-meta-iodobenzylguanidine (HSA 131I-MIBG) is the only approved therapy for mPPGLs. We summarized the efficacy and safety profile of HSA 131I-MIBG in patients with mPPGL. Methods This is a retrospective cohort study in patients with mPPGL treated with HSA 131I-MIBG on label at a tertiary cancer center. The primary endpoint was radiographic treatment response determined with CT/MRI according to RECIST v1.1 and 123 I-MIBG scan. Secondary endpoints were blood pressure changes and HSA 131I-MIBG related adverse events. We correlated responses with the genetic background as an exploratory endpoint. Results Twenty-four patients were treated including 15 men (62%). Median age at the time of treatment was 44 years (range 18–82). Twenty-three patients had distant metastases and one patient had an unresectable primary tumor. Seventeen patients (70%) had hormonally active tumors and 17 patients (70%) were on antihypertensive medications before HSA 131I-MIBG therapy [7 patients on alpha-blockers only and 10 on combination antihypertensive therapy]. Thirteen patients (54%) previously received antineoplastic treatment. Eleven patients (46%) received one dose of HSA 131−I-MIBG, the remaining received two doses. Median duration of follow-up was 15 months (range 2–52). In 23 evaluable patients, radiographic responses included: 2 complete responses (CR), 10 partial responses (PR), 8 stable diseases (SD), 2 mixed responses (MR), and 1 progressive disease (PD) yielding disease control rate (DCR) of 87%. Median time to response was 12.5 months (95% CI, 4.6 to 25.1). Radiographic responses in patients with sporadic disease were [6/11 SD, 3/11 PR, 1/11 MR, 1/11 PR], while the response in patients with a genetic mutation (SDHB, VHL, RET) was [2/12 CR, 7/12 PR, 2/12 SD, 1/12 MR]. In 17 hormonally active tumors, plasma metanephrines normalized in 3(18%), improved by 50% in 5(29%), increased in 4(24%), 4 patients (24%) had no repeat levels and one had stable levels. Blood pressure was evaluable in 22 (92%) patients. Blood pressure normalized in 9 patients (41%) leading to discontinuation of antihypertensive therapy. One patient had an improvement in the blood pressure leading to a reduction of antihypertensive medications. The most common adverse events were grade I/II nausea/vomiting and transient bone marrow suppression. One patient developed premature ovarian failure. Grade III/IV myelosuppression was seen in 3/24 (12%) patients. One patient had fatal pneumonitis, and one patient developed fatal gastrointestinal bleeding a month after treatment with unclear attribution to HSA 131 −I-MIBG. Conclusions In mPPGL, HSA 131I-MIBG is associated with high DCR regardless of underlying genetic mutation. Severe adverse events are infrequent but can be fatal. Presentation: Tuesday, June 14, 2022 10:15 a.m. - 10:30 a.m.

S1795 Portobiliary Fistula on Single Operator Cholangioscopy

Introduction: Portobiliary fistula formation is an exceedingly rare complication following endoscopic retrograde cholangiopancreatography (ERCP), with a scarcity of cases reported in scientific literature. Patients may present with ensuing—often fatal—gastrointestinal hemorrhage with challenges in diagnosis and management as a result. Case Description/Methods: We present a case of 78-year-old male who was found to have opacification of vascular structures on intraoperative cholangiography during laparoscopic cholecystectomy. This was concerning for the development of a biliary-vascular fistula. The patient had recently undergone ERCP with biliary stent placement at an outside facility for choledocholithiasis. Gastroenterology was consulted for endoscopic evaluation. An ERCP was performed. Selective biliary cannulation was achieved, and contrast was injected to identify an irregularity in the distal common bile duct with upstream dilatation up to 13 mm. No clear contrast extravasation was noted in the biliary tree. The biliary tree was then swept using a 15 mm extraction balloon with successful removal of gallstones and sludge. Despite multiple contrast injections, extravasation was not seen, as previously noted on intraoperative cholangiography. Therefore, single operator cholangioscopy was introduced and advanced to the hilum of the common hepatic duct. Examination revealed a small defect in the common bile duct communicating with a thrombosed vascular structure, likely a branch of the portal vein (Figure). After a multidisciplinary discussion with surgery service, a fully covered 10 mm by 8 cm metallic stent was placed across the defect, anchored by a second 7 French by 10 cm double-pigtail plastic stent, with trans-papillary drainage. Discussion: We present a novel approach for the identification and management of portobiliary fistulas. Our case demonstrates the utility of biliary stents in the management of this disease. Our patient tolerated the procedure well with no post-operative complications.Figure 1.: Portobiliary Fistula on Single Operator Cholangioscopy.

S1889 A Case of Ruptured Gastroduodenal Artery Pseudoaneurysms in a Patient With Chronic Pancreatitis

Introduction: Pancreatic pseudoaneurysm is a rare vascular complication of pancreatitis, with an estimated prevalence of 10%. Pseudoaneurysm can result from trauma, inflammation, infection, and iatrogenic causes. Due to its weak structural support, the risk of rupture is higher for pseudoaneurysm than that of a true aneurysm of similar size. Pancreatic pseudoaneurysms can lead to life-threatening complications such as rupture and bleeding, with increased morbidity and mortality up to 90% in untreated patients and 12.5% despite treatment. Due to its high mortality rate with rupture, pseudoaneurysms should be treated immediately once it is identified, regardless of their size or whether it is symptomatic or not Case Description/Methods: We present a case of a 68-year-old male patient with a past medical history significant for chronic pancreatitis who presented with altered mental status and hypovolemic shock secondary to unexplained gastrointestinal and retroperitoneal hemorrhage (Table). Computed tomography (CT) Angiography was done which showed an enlarging retroperitoneal and right-sided intraperitoneal hematoma with suspicion for active arterial extravasation or punctate pseudoaneurysms in the pancreatic head (Figure). Celiac angiogram was done under fluoroscopic guidance, which showed gastroduodenal and superior pancreaticoduodenal artery pseudoaneurysms. He underwent successful endovascular coil embolization of the gastroduodenal artery. Post procedure he was monitored in intensive care unit. His clinical condition continued to improve and was discharged to a skilled nursing facility in stable condition. Discussion: Physicians should be aware of pancreatic pseudoaneurysms as rare vascular complication associated with chronic pancreatitis that may lead to fatal gastrointestinal or retroperitoneal bleeding with a high mortality rate. Our case highlights the importance of early diagnosis and prompt treatment in these patients.Figure 1.: A: CT abdomen and pelvis without intravenous contrast showing peripancreatic inflammation surrounding the pancreatic body and head along with retroperitoneal bleed (red arrow). Pancreatic calcifications present (yellow arrow) signifying radiologic evidence of chronic pancreatitis B: CT Angiography showing retroperitoneal and right-sided intraperitoneal hematoma with active arterial extravasation or punctate pseudoaneurysms in the pancreatic head. Table 1. - Laboratory Investigation Investigation Day 1 of Hospitalization Day 5 At Time of Discharge Reference Range White Blood Cell count 24.3 14.3 k/uL 7 k/uL 4.8-10.8 k/uL Red Blood Cell Count 4.77 2.69 MIL/uL 3.19 MIL/uL 4.50-5.90 MIL/uL Hemoglobin 15.8 8.5 mg/dl 10.2 mg/dl 12.0-16.0 g/dL Hematocrit 47.6 25.7 % 30.5% 42-51 % Platelet count 171 155 k/uL 215 k/uL 150-400 k/uL Sodium, Serum 132 139 mEq/L 140 mEq/L 135-145 mEq/L Potassium, Serum 3.0 3.2 mEq/L 3.9 mEq/L 3.5-5.0 mEq/L Blood Urea Nitrogen, Serum 41 17 mg/ml 10 mg/ml 8-26 mg/dL Creatinine, Serum 1.2 0.5 mg/dl 0.6 mg/dl 0.5-1.5 mg/dL Bilirubin, Serum total 0.5 0.7 mg/dl 0.3 mg/dl 0.2-1.1 mg/dL Serum Direct Bilirubin 0.3 0.3 mg/dl < 0.2 mg/dl 0.0-0.3 mg/dL Alkaline Phosphatase 51 48 units/L 73 units/L 56-155 unit/L Aspartate Transaminase 125 21 units/L 18 units/L 9-48 unit/L Alanine Aminotransferase 81 30 units /L 12 units /L 5-40 unit/L Lactic acid Level 8.2 0.8 mmoles/L 1.1 mmoles/L 0.5-1.6 mmoles/L Prothrombin Time 15.2 13.9 sec 10.5 sec 9.9-13.3 seconds International Normalized Ratio 1.31 1.20 0.92 0.85-1.14 Serum Calcium 6.6mg/dl 7.6 mg/dl 9.2 3 mg/dl 8.5-10.5 mg/dl Serum Lipase 24 U/L < =61U/L Serum Triglyceride 163mg/gl 55-150 mg/dl Serum Ethanol < 10 < = 10mg/dl Urine Toxicology Cocaine and methadone Negative

Out of sight for the endoscopist? Gastrointestinal bleeding after aortic repair

Background and study aim Secondary Aortoenteric Fistulas (sAEF) are difficult to diagnose and usually result in fatal gastrointestinal (GI) bleeding following aortic repair. Outcomes are largely dependent on a timely diagnosis, but AEFs remain challenging to identify endoscopically and are usually diagnosed on computed tomography (CT) scans. The aim of our study was optimize diagnosis of AEF by identifying patients developing GI bleeding after aortic repair, investigate their clinical course and identify factors specific to different bleeding sources. Methods A retrospective, single-center study capturing all patients developing upper or lower GI bleeding after aortic surgery between January 2009 and March 2020 was performed. Electronic health records were screened for diagnostic codes of the relevant procedures. Bleeding was classified into three groups: AEF with demonstrable fistula, ischemic – macroscopic ulceration plus histological confirmation or imaging and “other” due to other recognized conventional cause, such as peptic ulcer disease. Results 47 GI bleeding episodes in 39 patients were identified. Of these, 10 episodes (21%) were caused by AEF, 16 (34%) by ischemic ulceration and 21 (45%) due to other causes. Patients with AEF exhibited more frequent hemodynamic instability requiring vasopressors and had higher mortality, while ischemic ulcerations were associated with more recent operation or hypotensive episode. Conclusions GI bleeding complications are uncommon following aortic surgery. AEF and ischemic ulceration are however frequent bleeding causes in this cohort. In patients presenting with fulminant bleeding, primary CT-scanning should be considered.

Central adverse drug reactions of NSAIDs

Non-steroidal anti-inflammatory drugs (NSAIDs) is a group of drugs used for analgesia, antinflammatory, antipyretical properties, and antiplatelet effects. NSAIDs are widely used in the treatment of osteoarthritis, musculoskeletal pain, gout and other pathological conditions, however, their use is associated with the risk of developing adverse drug reactions, including serious and fatal ones, for example, gastrointestinal bleeding, or myocardial infarction and stroke. Many NSAIDs can also cross the blood-brain barrier and cause central adverse drug reactions that can be mistaken by practical health care professionals for the manifestation of a new pathologies or insufficient effectiveness of treatment of an existing disease, but not with the use of NSAIDs, that may lead to errors in treatment tactics, additional prescription of drugs and an increased risk of complications. The purpose of this article is to inform practical health care professionals about the potential risks of central adverse drug reactions (including psychiatric ones) of NSAIDs, and thus, to increase the effectiveness and safety of therapy.

Severe Liver Disorder Following Liver Transplantation in STING-Associated Vasculopathy with Onset in Infancy

STING-associated vasculopathy with onset in infancy (SAVI) is a type-I interferonopathy, characterized by systemic inflammation, peripheral vascular inflammation, and pulmonary manifestations. There are three reports of SAVI patients developing liver disease, but no report of a SAVI patient requiring liver transplantation. Therefore, the relevance of liver inflammation is unclear in SAVI. We report a SAVI patient who developed severe liver disorder following liver transplantation. SAVI was diagnosed in a 4-year-old girl based on genetic analysis by whole-exome sequencing. We demonstrated clinical features, laboratory findings, and pathological examination of her original and transplanted livers. At 2months of age, she developed bronchitis showing resistance to bronchodilators and antibiotics. At 10months of age, she developed liver dysfunction with atypical cholangitis, which required liver transplantation at 1year of age. At 2years of age, multiple biliary cysts developed in the transplanted liver. At 3.9years of age, SAVI was diagnosed by whole-exome sequencing. Inflammatory cells from the liver invaded the stomach wall directly, leading to fatal gastrointestinal bleeding unexpectedly at 4.6years of age. In pathological findings, there were no typical findings of liver abscess, vasculitis, or graft rejection, but biliary cysts and infiltration of inflammatory cells, including plasmacytes around the bile duct area, in the transplanted liver were noted, which were findings similar to those of her original liver. Although further studies to clarify the mechanisms of the various liver disorders described in SAVI patients are needed, inflammatory liver manifestations may be amplified in the context of SAVI.

Risk of Severe Bleeding With Extended Rivaroxaban to Prevent Venous Thromboembolism in Acute Medically Ill Patients With Bronchiectasis.

Background: Bronchiectasis is a chronic inflammation of the bronchi with recurrent infections and hemoptysis. The MAGELLAN study compared oral rivaroxaban, 10 mg once daily (QD), for 35 ± 4 days with subcutaneous enoxaparin 40 mg QD for 10 ± 4 days followed by placebo for 25 ± 4 days to prevent venous thromboembolism in patients hospitalized with an acute medical illness. MAGELLAN included a subset of patients with bronchiectasis. In a post hoc analysis, we evaluated the incidence and severity of pulmonary bleeding in patients with bronchiectasis who were hospitalized for an acute medical illness. This analysis included MAGELLAN patients diagnosed with bronchiectasis at baseline. Patients were evaluated by treatment group for International Society on Thrombosis and Haemostasis major bleeding, non-major clinically relevant (NMCR) bleeding, and the composite of the 2 (ie, clinically relevant bleeding). Results: Medically ill patients with bronchiectasis were randomized to rivaroxaban (n = 60) or enoxaparin/placebo (n = 61). There were 2 fatal pulmonary bleeds and 1 fatal gastrointestinal bleed in the rivaroxaban arm and no fatal or major bleeding in the enoxaparin/placebo arm. The incidence of major bleeding was 5% in the rivaroxaban arm. One NMCR bleed occurred in the rivaroxaban arm and 2 NMCR bleeds occurred in the enoxaparin/placebo arm. The incidence of clinically relevant bleeding was 6.7% versus 3.3% in the rivaroxaban and enoxaparin/placebo groups, respectively (relative risk = 2.06 [95% confidence interval: 0.351-12.046]). Conclusion: In-patients hospitalized with bronchiectasis and an acute medical illness, clinically relevant bleeding, including fatal pulmonary hemorrhage, occurs more frequently with extended rivaroxaban thromboprophylaxis than with enoxaparin followed by placebo.

Colonic varices treated with embolization after pancreatoduodenectomy with portal vein resection: a case report

BackgroundPancreatoduodenectomy with resection of the portal vein or superior mesenteric vein confluence has been safely performed in patients with pancreatic head cancer associated with infiltration of the portal vein or superior mesenteric vein. In recent years, left-sided portal hypertension, a late postoperative complication, has received focus owing to increased long-term survival with advances in chemotherapy. Left-sided hypertension may sometimes cause fatal gastrointestinal bleeding because of the rupture of gastrointestinal varices. Here, we present a case of colonic varices caused by left-sided portal hypertension after pancreatoduodenectomy with portal vein resection.Case presentationA 69-year-old man diagnosed with pancreatic head cancer was referred to our department for surgery after undergoing chemotherapy with nine courses of gemcitabine and nab-paclitaxel. Computed tomography showed a mass 25 mm in diameter and in contact with the portal vein. He had undergone subtotal stomach-preserving pancreatoduodenectomy with portal vein resection. Four centimeters of the portal vein had been resected, and end-to-end anastomosis was performed without splenic vein reconstruction. We had to completely resect the right colic vein, accessary right colic vein, and middle colic vein due to tumor invasion. The pathological diagnosis was ypT3, ypN1a, ypM0, and ypStageIIB, and he was administered TS-1 as postoperative adjuvant chemotherapy. Seven months after therapeutic radical surgery, he presented with melena with progressive anemia. Computed tomography revealed transverse colonic varices. He was offered interventional radiology. Trans-splenic arterial splenic venography showed that transverse colonic varices had developed as collateral circulation of the splenic vein and inferior mesenteric vein system. An embolic substance was injected into the transverse colonic varices, which halted the progression of the anemia caused by melena. Fifteen months after therapeutic radical surgery, local recurrence of the tumor occurred; he died 28 months after the surgery.ConclusionsWhen subtotal stomach-preserving pancreatoduodenectomy with portal vein resection is performed without splenic vein reconstruction, colonic varices may result from left-sided portal hypertension. Interventional radiology is an effective treatment for gastrointestinal bleeding due to colonic varices, but it is important to be observant for colonic necrosis and new varices.

The compounding effects of hepatitis c infection with liver cirrhosis, hepatocellular carcinoma, and budd-chiari syndrome in fatal gastrointestinal haemorrhage

This case study reports a patient with hepatitis C infection with advanced liver cirrhosis, and undiagnosed hepatocellular carcinoma, who presented with acute Budd-Chiari syndrome and fatal gastrointestinal haemorrhage. Budd-Chiari syndrome is defined as hepatic venous outflow tract obstruction, and can present with signs of acute liver failure, including nausea and vomiting, abdominal distension, jaundice, coagulopathy, and abnormal liver function tests, and may progress to multiorgan failure and death. Budd-Chiari syndrome can arise in the setting of malignancy, via direct compression or invasion of vascular structures, with hepatocellular carcinoma most commonly described. The majority of hepatocellular carcinomas arise in the setting of liver cirrhosis, with chronic viral hepatitis (hepatitis B and C) a leading cause. Liver cirrhosis may result in portal hypertension, which promotes the development of oesophageal and gastric varices. Liver disease can also affect the production of clotting factors, which may increase the risk of potential haemorrhage. This case highlights the combined effects of potentially reduced clotting factors, oesophageal varices, and disseminated intravascular coagulation, and how their overlapping aetiologies may increase the risk of developing potentially fatal spontaneous gastrointestinal haemorrhage.

Selective EGLN Inhibition Enables Ablative Radiotherapy and Improves Survival in Unresectable Pancreatic Cancer.

When pancreatic cancer cannot be removed surgically, patients frequently experience morbidity and death from progression of their primary tumor. Radiation therapy (RT) cannot yet substitute for an operation because radiation causes fatal bleeding and ulceration of the nearby stomach and intestines before achieving tumor control. There are no FDA-approved medications that prevent or reduce radiation-induced gastrointestinal injury. Here, we overcome this fundamental problem of anatomy and biology with the use of the oral EGLN inhibitor FG-4592, which selectively protects the intestinal tract from radiation toxicity without protecting tumors. A total of 70 KPC mice with autochthonous pancreatic tumors received oral FG-4592 or vehicle control ± ablative RT to a cumulative 75 Gy administered in 15 daily fractions to a limited tumor field. Although ablative RT reduced complications from local tumor progression, fatal gastrointestinal bleeding was observed in 56% of mice that received high-dose RT with vehicle control. However, radiation-induced bleeding was completely ameliorated in mice that received high-dose RT with FG-4592 (0% bleeding, P < 0.0001 compared with vehicle). Furthermore, FG-4592 reduced epithelial apoptosis by half (P = 0.002) and increased intestinal microvessel density by 80% compared with vehicle controls. EGLN inhibition did not stimulate cancer growth, as treatment with FG-4592 alone, or overexpression of HIF2 within KPC tumors independently improved survival. Thus, we provide a proof of concept for the selective protection of the intestinal tract by the EGLN inhibition to enable ablative doses of cytotoxic therapy in unresectable pancreatic cancer by reducing untoward morbidity and death from radiation-induced gastrointestinal bleeding. SIGNIFICANCE: Selective protection of the intestinal tract by EGLN inhibition enables potentially definitive doses of radiation therapy. This might allow radiation to be a surgical surrogate for unresectable pancreatic cancer.Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/79/9/2327/F1.large.jpg.

Strongyloides stercoralis Hyperinfection Syndrome as a Cause of Fatal Gastrointestinal Hemorrhage.

ABSTRACTStrongyloides stercoralis is a small intestinal nematode that is widespread in regions with poor sanitation. We present a 57-year-old man from Colombia who was undergoing corticosteroid therapy for a meningioma who presented after neurosurgery with abdominal pain and a profound gastrointestinal (GI) bleed. The patient underwent an esophagogastroduodenoscopy (EGD), an attempted embolization, and an exploratory laparotomy to remove the necrosed duodenum. His pathology examination revealed Strongyloides infection of the duodenum, and he died of profound blood loss. This rare diagnosis displays the importance of screening patients at a high risk of Strongyloides infection before starting glucocorticoid therapy.

Prediction and feature selection for fatal gastrointestinal bleeding recurrence in hospital via machine learning

To propose a method of prediction for fatal gastrointestinal bleeding recurrence in hospital and a method of feature selection via machine learning models. 728 digestive tract hemorrhage samples were extracted from the first aid database of PLA General Hospital, and 343 patients among them were diagnosed as fatal gastrointestinal bleeding recurrence in hospital. A total of 64 physiological or laboratory indicators were extracted and screened. Based on the ten-fold cross-validation, Logistic regression, AdaBoost and XGBoost were used for classification prediction and comparison. XGBoost was used to search sequence features, and the key indicators for predicting fatal gastrointestinal bleeding recurrence in hospital were screened out according to the importance of the indicators during training. Logistic regression, AdaBoost and XGBoost all get better F1.5 score under each feature input dimension, among which XGBoost had the best effect and the highest score, which was able to identify as many patients as possible who might have fatal gastrointestinal bleeding recurrence in hospital. Through XGBoost iteration results, the Top 30 indicators with high importance for predicting fatal gastrointestinal bleeding recurrence in hospital were ranked. The F1.5 scores of the first 12 key indicators peaked at iteration (0.893), including hemoglobin (Hb), calcium (CA), red blood cell count (RBC), mean platelet volume (MPV), mean erythrocyte hemoglobin concentration (MCH), systolic blood pressure (SBP), platelet count (PLT), magnesium (MG), lymphocyte (LYM), glucose (GLU, blood gas analysis), glucose (GLU, blood biochemistry) and diastolic blood pressure (DBP). Logistic regression, AdaBoost and XGBoost could achieve the purpose of early warning for predicting fatal gastrointestinal bleeding recurrence in hospital, and XGBoost is the most suitable. The 12 most important indicators were screened out by sequential forward selection.

Risk Factors for Acute Hemorrhagic Rectal Ulcer Syndrome and Its Prognosis: A Density Case-Control Study.

Acute hemorrhagic rectal ulcer syndrome (AHRUS) can cause fatal gastrointestinal bleeding. However, there have been few epidemiological studies investigating risk factors of AHRUS. To determine the risk factors and predict one-year survival after onset of AHRUS, we conducted a retrospective density case-control study in a tertiary referral hospital. Patients with hematochezia, bloody stool, and rectal ulcer confirmed by colonoscopy between 2003 and 2011 were diagnosed as AHRUS (n = 38). Patients with malignancies, infectious colitis, ulcerative colitis, or solitary rectal ulcer syndrome were excluded. Control subjects (n = 123) without rectal ulcer were selected by risk set sampling for each AHRUS. Multivariate logistic regression analyses revealed that the significant adjusted odds ratio (95% confidence interval) of hospitalization, antithrombotic drug use, and one gram increase of serum albumin was 15.7 (2.25–108.9), 12.1 (1.53–94.4), and 0.11 (0.02–0.52), respectively. Endoscopic hemostasis for rectal bleeding was performed in 8 cases (21%). Seventeen percent of patients died within one year after the episode of AHRUS from non-AHRUS causes. This study revealed that hospitalization, antithrombotic drug use, and lower serum albumin value were significant risk factors for AHRUS, and that AHRUS was an unfavorable prognostic condition. This information could be helpful in recognizing high-risk patients of rectal bleeding and applying preventive measures.

Stereotactic body radiotherapy (SBRT) for patients with locally advanced pancreatic cancer: A single center experience

IntroductionDespite advances in treatment, notably in systemic therapy, the prognosis of pancreatic adenocarcinoma (PADC) remains dismal. Stereotactic body radiotherapy (SBRT) is an emerging tool in the complex management of PADC. We review outcomes of SBRT for PADC at our institution. MethodsWe reviewed patients treated with SBRT for either unresectable PADC or locally recurrent PADC after surgery. Treatment was delivered using a robotic radiosurgery system with respiratory tracking. The median prescribed dose was 30 Gy (30–35 Gy), delivered in 5–6 fractions. Toxicities were reported as per CTCAE v4.0. Survival was estimated using the Kaplan–Meier method. ResultsBetween October 2010 and March 2016, 21 patients were treated at our institution. The median follow-up was 7 months (range: 1–28). The 1-year local control rate was 57%. The 1-year overall survival was 25% for locally advanced patients and 67% for those with local recurrences (p = 0.27). Eighty percent of cancer related deaths were due to metastatic progression. Five patients (24%) had Grade I–II gastrointestinal acute toxicity; one patient had fatal gastrointestinal bleeding 6 months after SBRT. ConclusionIn PADC, fractionated SBRT dose schedules near 30 Gy may strike the best balance of local control and bowel toxicity. More work is required to integrate pancreatic SBRT with modern systemic therapy.

Lichenoid esophagitis presenting as fatal upper gastrointestinal bleeding in a 52\xa0year-old woman: a case diagnosed by autopsy

Background“Lichenoid esophagitis” is a descriptive term for a lichenoid pattern of inflammation in the esophagus for which a precise histologic diagnosis cannot be established. The differential diagnosis includes lichen planus, a drug-related reaction, and viral infection. Lichenoid esophagitis causing death has not been reported previously. We describe a case, diagnosed by autopsy, of lichenoid esophagitis in which massive bleeding from generalized epithelial sloughing and a large longitudinal ulcer proved fatal.Case presentationA 52 year-old diabetic woman collapsed at her home in front of an acquaintance. “Bloody vomit” was noted. Despite resuscitation efforts, the patient died. A complete autopsy was performed. The middle portion of the esophagus showed a 9 cm longitudinal ulcer situated 12 cm from the esophago-gastric junction. Microscopic examination showed complete sloughing of the esophageal epithelium with a striking subepithelial lichenoid lymphocytic infiltrate extending into the muscularis mucosae. The findings were considered compatible with lichenoid esophagitis. Laboratory studies also showed the presence of diabetic ketoacidosis.ConclusionsLichenoid esophagitis is an appropriate diagnostic term when clinical, histologic and laboratory findings do not allow for specific categorization of lichenoid inflammation in the esophagus. As illustrated here for the first time, lichenoid esophagitis may cause ulceration and mucosal sloughing severe enough to result in massive upper gastrointestinal bleeding and death. Translating these autopsy findings to the clinical setting, it is possible that the endoscopic finding of a longitudinal mid-esophageal ulcer in the presence of proximal stricture may be indicative of underlying lichenoid esophagitis.