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Acid Peptic Diseases in the Pediatric

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Acid Peptic Diseases in the Pediatric In The Name of God Peptic Ulcer Diseases in the Pediatric Age Hosseini M.D. Pediatric Gastroenterologist Mofid pediatric Medical Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran The terms acid peptic diseases, peptic diseases, acid-related disorders are used synonymously to describe conditions that involve gastric acid and pepsin in their pathogenesis Spectrum of disease Gastritis; presence of inflammatory cells, Thus the diagnosis is purely histologic Gastropathy; gastric mucosal damage and abnormalities in the absence of inflammatory cells. Gastropathies often have a typical endoscopic appearance (e.g., portal hypertensive gastropathy, prolapse gastropathy) peptic ulcer disease; is on the severe end of the spectrum of gastritis and gastropathy, leading to mucosal barrier injury penetrating into gastric submucosa and muscularis propria Gastric Ulcers Ulcers Primitive ulcers are caused by alterations of the gastric function (i.e., increased HCl production and pepsin function); Most often associated with Helicobacter pylori infection Mainly single lesions and are usually found at the small gastric curve and at the antrum. Secondary ulcers stress caused by sepsis, shock, or an intracranial lesion (Cushing ulcer), severe burn injury (Curling ulcer). using aspirin or NSAIDs; hypersecretory states like Zollinger-Ellison syndrome They can be multiple and can have a spread localization within the stomach. PUD in children is reported worldwide with an estimated frequency of 8.1% in Europe and of 17.4% in the US PUD mainly occurs in the second decade of life and the most common identified causes in the pediatric age are HP infection and the use of NSAIDs The mortality rate for PUD is approximately 1 death per 100.000 cases Associations of PUD celiac disease, portal hypertension, intestinal transplantation, neurofibromatosis Pathogenesis of peptic ulcer disease imbalance: AGGRESSIVE FACTORS DEFENSIVE FACTORS Prostaglandins Acid Mucosal blood flow Mucous gel layer Pepsin HCO3 H. pylori Epithelial junctions NSAIDS Regeneration of the epithelial layer Epidermal growth factor Etiology Etiologic Classification of Peptic Ulcers Symptoms Symptoms In the neonatal period, gastric perforation can be the initial presentation. Younger children feeding difficulty, vomiting, crying episodes, hematemesis, or melena. Older children, aged 10 years and above, may present with more adult-typical symptoms such as dyspepsia, epigastric abdominal pain or fullness, anemia, and weight loss. Hematemesis or melena is reported in up to half of the patients with peptic ulcer disease. Symptoms of frank gastric outlet obstruction are uncommon in children. epigastric pain alleviated by the ingestion of food, is present only in a minority of children The pain is often described as dull or aching, rather than sharp or burning, as in adults. It can last from minutes to hours; patients have frequent exacerbations and remissions lasting from weeks to months. Nocturnal pain waking the child is common in older children Alarm signs Diagnosis The definitive diagnosis of gastritis and peptic ulcer disease is by upper GI endoscopy and biopsies All suggestive gastric ulcers should be examined by repeat upper gastrointestinal endoscopy 8–12 weeks after initiating appropriate therapy. Although gastric ulcers that clearly develop in association with NSAID use do not always need biopsy, they should be observed until healed Helicobacter pylori testing Invasive tests Biopsy specimens obtained by endoscopy H. pylori-associated urease activity ((e.g. CLO test, Hpfast, PyloriTek, Pronto Dry) Urease tests have 90% sensitivity with specificity of 95– 100%. Biopsy tests may give false-negative results in patients who are bleeding acutely or who have been given short courses of antibiotics. Noninvasive tests ELISA (IgG) antibodies to H. pylori; not recommended for documenting eradication after therapy. Breath tests may be performed using either 13C-urea or 14C-urea false-negative results can be produced by intake of PPIs, bismuth compounds, H2RA, and antibiotics. these drugs should be held for 2–4 weeks prior to examination Fecal antigen tests use an enzymatic immunoassay (HpSA) to detect H. pylori antigen in stool specimens with high levels of sensitivity and specificity. Visceral penetration may be diagnosed or confirmed by CT or MRI. In patients who present with significant vomiting, an upper GI contrast study is necessary to rule out malrotation Thank You Any Question?.
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