Very late-onset of inflammatory bowel disease. A case report

Introduction Inflammatory bowel disease (IBD) in most cases is classified into Crohn’s disease (CD) or ulcerative colitis (UC). It appears in 25-35 years of age and the second peak is after fifties. It is very rare to recognize it in the elderly. Case presentation We present a case of a 79-year-old female patient who was admitted to the Chair and Department of Gastroenterology with Endoscopic Unit at the Medical University of Lublin in December 2018 with an acute lower gastrointestinal hemorrhage and dyselectrolytemia. Additionally, she suffered from atrial fibrillation. She has been treated with an anticoagulant therapy and has been receiving dabigatran for many years. After 16 days of diagnostic research and intensive treatment the patient was discharged home with no previous symptoms. After the next 12 days at home our patient returned to the hospital with recurrent gastrointestinal bleeding, abdominal pain and after fainting episode. Digital rectal exam was positive and laboratory test showed anemia again. Colonoscopic findings on admission showed proximally to the splenic flexure blood signs, on Bauhin’s valve a flat ulcer. The histopathological report confirmed the inflammatory bowel disease. After diagnosis of IBD, an effective treatment with mesalazine and prednisone was started. Conclusions Despite the newest clinical trials are more and more common in Crohn’s disease or ulcerative colitis, the elderly patients are mostly excluded from them because of the other accompanying diseases and their burdensome side effects. Choosing the right therapy becomes the main problem in these patients after setting a proper diagnosis which can take years and many unnecessary hospitalizations

Netosis as a bridge between inflammation and liver cell injury

One of programmed cell death types, netosis, discovered in ’96, was first described by Zychlinsky et al. and has gained elevating popularity among many researchers. It is a process occurring in order to catch pathogens into a trap and kill them. This trap is a scaffold somewhat consisting of chromatin and particles with antimicrobial properties such as histones. Extracellular histones are capable of proinflammatory cytokines production and platelets aggregation what accounts for inflammatory response. Unfortunately, these proteins have also a toxic potential which leads to cell injury through Toll like receptors presented by neutrophils. Mentioned neutrophils participate in an oxidative burst which yields to production reactive oxygen species performing a crucial role in the development of hepatocytes injury. Thus, alcohol abuse appears to result in a rapid development of liver cell injury through progression of inflammation induced by netosis. However, controlled NETs forming can be a future therapeutic option

The Helicobacter pylori Genome Project : insights into H. pylori population structure from analysis of a worldwide collection of complete genomes

Helicobacter pylori, a dominant member of the gastric microbiota, shares co-evolutionary history with humans. This has led to the development of genetically distinct H. pylori subpopulations associated with the geographic origin of the host and with differential gastric disease risk. Here, we provide insights into H. pylori population structure as a part of the Helicobacter pylori Genome Project (HpGP), a multi-disciplinary initiative aimed at elucidating H. pylori pathogenesis and identifying new therapeutic targets. We collected 1011 well-characterized clinical strains from 50 countries and generated high-quality genome sequences. We analysed core genome diversity and population structure of the HpGP dataset and 255 worldwide reference genomes to outline the ancestral contribution to Eurasian, African, and American populations. We found evidence of substantial contribution of population hpNorthAsia and subpopulation hspUral in Northern European H. pylori. The genomes of H. pylori isolated from northern and southern Indigenous Americans differed in that bacteria isolated in northern Indigenous communities were more similar to North Asian H. pylori while the southern had higher relatedness to hpEastAsia. Notably, we also found a highly clonal yet geographically dispersed North American subpopulation, which is negative for the cag pathogenicity island, and present in 7% of sequenced US genomes. We expect the HpGP dataset and the corresponding strains to become a major asset for H. pylori genomics

Wilson’s Disease: An Update on the Diagnostic Workup and Management

Wilson’s disease (WD) is a rare autosomal recessive disorder of hepatocellular copper deposition. The diagnostic approach to patients with WD may be challenging and is based on a complex set of clinical findings that derive from patient history, physical examination, as well as laboratory and imaging testing. No single examination can unequivocally confirm or exclude the disease. Timely identification of signs and symptoms using novel biomarkers and modern diagnostic tools may help to reduce treatment delays and improve patient prognosis. The proper way of approaching WD management includes, firstly, early diagnosis and prompt treatment introduction; secondly, careful and lifelong monitoring of patient compliance and strict adherence to the treatment; and, last but not least, screening for adverse effects and evaluation of treatment efficacy. Liver transplantation is performed in about 5% of WD patients who present with acute liver failure at first disease presentation or with signs of decompensation in the course of liver cirrhosis. Increasing awareness of this rare inherited disease among health professionals, emphasizing their training to consider early signs and symptoms of the illness, and strict monitoring are vital strategies for the patient safety and efficacy of WD therapy

Refractory ascites—the contemporary view on pathogenesis and therapy

Refractory ascites (RA) refers to ascites that cannot be mobilized or that has an early recurrence that cannot be prevented by medical therapy. Every year, 5–10% of patients with liver cirrhosis and with an accumulation of fluid in the peritoneal cavity develop RA while undergoing standard treatment (low sodium diet and diuretic dose up to 400 mg/day of spironolactone and 160 mg/day of furosemide). Liver cirrhosis accounts for marked alterations in the splanchnic and systemic hemodynamics, causing hypovolemia and arterial hypotension. The consequent activation of renin-angiotensin and sympathetic systems and increased renal sodium re-absorption occurs during the course of the disease. Cirrhotic patients with RA have poor prognoses and are at risk of developing serious complications. Different treatment options are available, but only liver transplantation may improve the survival of such patients

A rare case of a juvenile polyp of patient with Peutz-Jeghers syndrome, complicated with intussusception of the small intestine

We report a rare case of Peutz-Jeghers syndrome (PJS) in a 35-year-old female. The patient was diagnosed with PJS when she was 11 years old. She has remained under observation since then. We strongly believe that PJS is a very rare diagnosis. However, it can have serious complications such as the intussusception we observed in our patient. Her condition (recurrent abdominal pain and vomiting) in childhood required further diagnostic procedures. Although the diagnosis of PJS was made, among many resected polyps, one of them appeared to be a juvenile polyp. The diagnosis was confirmed in the histopathology report, which was incredibly unique. Genetic testing revealed LKB1/STK11 gene mutation. Clinicians should be aware of the malignant potential in the course of PJS. Hence, these patients require tailor-made management, long-term follow-up, and our particular attention

A Rare Case of Upper Gastrointestinal Bleeding: Osler-Weber-Rendu Syndrome

Osler-Weber-Rendu disease, also known as hereditary hemorrhagic telangiectasia (HHT), is a rare, autosomal dominant condition that affects approximately 1 in 5000 patients causing abnormal blood vessel formation. HHT patients have mucocutaneous telangiectasias and arteriovenous malformations in various organs. The most prominent symptom of HHT is epistaxis, which, together with gastrointestinal bleeding, may cause iron deficiency anemia. This study is a case report of a 62-year-old patient who was admitted to the Department of Gastroenterology due to acute upper gastrointestinal bleeding and a history of recurrent epistaxis and melena for 4 days, which was confirmed in digital rectal examination. Urgent upper gastrointestinal endoscopy revealed active bleeding from multiple angioectatic spots with bright-looking salmon-colored patches in the antrum and the body suggestive of HHT. The bleeding from two angioectatic spots was stopped by argon plasma coagulation, and four clips were placed to provide good hemostasis. The patient was treated with a proton pomp inhibitor infusion and iron infusion. She was discharged with no signs of GI bleeding, normalized iron levels and a diagnosis of HHT. She was referred to further genetic testing, including evaluation of first-degree relatives. She also had performed unenhanced thin-cut computed tomography (CT) with angiography to exclude the presence of pulmonary arteriovenous malformations (PAVMs). Due to the fact that the patient did not manifest any other HHT-related symptoms and that the instrumental screening discloses no silent AVMs in other organs, the “watch-and-wait strategy” was applied. Although, Osler-Weber-Rendu syndrome is widely described in the medical literature, effective treatment of gastrointestinal telangiectasias is not always available and still lacks standardization to date, which makes the management of gastroenterological involvement still a challenging issue

Selected Aspects of the Intricate Background of Immune-Related Cholangiopathies—A Critical Overview

Primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC) are rare immune-related cholangiopathies with still poorly explained pathogenesis. Although triggers of chronic inflammation with subsequent fibrosis that affect cholangiocytes leading to obliteration of bile ducts and conversion to liver cirrhosis are unclear, both disorders are regarded to be multifactorial. Different factors can contribute to the development of hepatocellular injury in the course of progressive cholestasis, including (1) body accumulation of bile acids and their toxicity, (2) decreased food intake and nutrient absorption, (3) gut microbiota transformation, and (4) reorganized host metabolism. Growing evidence suggests that intestinal microbiome composition not only can be altered by liver dysfunction, but in turn, it actively impacts hepatic conditions. In this review, we highlight the role of key factors such as the gut–liver axis, intestinal barrier integrity, bile acid synthesis and circulation, and microbiome composition, which seem to be strongly related to PBC and PSC outcome. Emerging treatments and future therapeutic strategies are also presented