20 research outputs found

    A rare and often unrecognized cause of hematochezia and tenesmus in childhood: Solitary rectal ulcer syndrome

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    Solitary rectal ulcer syndrome (SRUS) is an unusual disorder of childhood, which usually presents with rectal bleeding, mucous discharge, prolonged straining, tenesmus, and localized pain in the perineal area. After the first description by Cruveilhier, Madigan and Morson further detailed the clinical and pathologic features of SRUS in 1969. The pathogenesis of the syndrome is not well-understood. The postulated mechanism responsible for rectal prolapse in most cases seems to be excessive straining efforts during which high intra-abdominal pressure forces the anterior rectal mucosa firmly into the contracting puborectalis muscle. The anterior rectal mucosa is frequently forced into the anal canal and as a consequence becomes strangulated, causing congestion, edema, and ulceration. Histologically, the presence of fibromuscular obliteration of the lamina propria with disorientation of muscle fibers is characteristic, which could be secondary to chronic mechanical and ischemic trauma and inflammation by hard stools, and intussusception of the rectal mucosa. Although the syndrome is well-recognized in adults, the pediatric experience with this condition is limited and often remains unrecognized or misdiagnosed. A misdiagnosis has been reported in one fourth of adult cases, and the correct diagnosis usually delayed approximately 5 to 7 years. There are few pediatric case reports in English literature. Here, we describe 2 children with SRUS, aged 11 and 14 years, whose SRUS was diagnosed 2 and 6 years, respectively, after the onset of the first signs and symptoms

    Autoimmune complications associated with hepatitis A virus infection in children

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    Hepatitis A virus infection is usually a self-limited disease during childhood. Autoimmune manifestations are rarely reported among patients. We describe two children with acute hepatitis A infection who developed immune thrombocytopenia and hepatic venous thrombosis during the course of acute infection. Antiphospholipid antibodies were increased in both of them during the thrombocytopenic and thrombotic complications and decreased during the resolution of these events

    Thromboembolic complications in children with Crohn's disease

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    Clinical Practice: Helicobacter pylori infection in childhood

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    Helicobacter pylori infection is recognised as a cause of gastritis and peptic ulcer disease (PUD) and usually acquired during the first years of life. While there is a decline in the prevalence of H. pylori infection in northern and western European countries, the infection is still common in southern and eastern parts of Europe and Asia. Symptoms of H. pylori-related PUD are nonspecific in children and may include epigastric pain, nausea and/or vomiting, anorexia, iron deficiency anaemia and hematemesis. Besides, only a small proportion of children develop symptoms and clinically relevant gastrointestinal disease. H. pylori infection can be diagnosed either by invasive tests requiring endoscopy and biopsy or non-invasive tests including the C-13-urea breath test, detection of H. pylori antigen in stool and detection of antibodies in serum, urine and saliva. The aim of treatment is at least 90 % eradication rate of the bacteria, and a combination of two antibiotics plus a proton pump inhibitor has been recommended as first-line treatment. However, frequent use of antibiotics during childhood is associated with a decline in eradication rates and the search for new treatment strategies as well. This is an overview of the latest knowledge and evidence-based guidelines regarding clinical presentation, diagnosis and treatment of H. pylori infection in childhood

    Endoscopic and Histopathologic Findings Associated with H-pylori Infection in Very Young Children

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    Most of the individuals infected with H. pylori acquire the infection early in life. However, there is limited data regarding endoscopic and histopathologic findings of H. pylori infection when it is acquired during infancy. The aim of this study was to investigate the H. pylori-related endoscopic and histopathological findings in children younger than 2 years of age. One hundred and fifty-two infants who underwent upper gastrointestinal endoscopy were included in the study. The diagnosis of H. pylori infection was based on histopathology and a positive rapid urease test. Forty of 152 (26.3%) infants were infected with H. pylori, and 65% of the infected infants had histopathologic gastritis. There were no clinical or endoscopic findings suggestive of H. pylori infection. No correlation could be found between the density of H. pylori and the severity of gastritis. H. pylori infection is associated with various degrees of gastritis in more than half of the infected infants. Since the likelihood of normal histopathology is rare in H. pylori-infected infants, its long-term complications should be cautiously followed up in endemic areas
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