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:: Penetrating gastric ulcer (into pancreas) Helicobacter pylori gastritis

This is a 13 y.o. boy with recurrent iron deficiency anemia since age four, managed with chronic iron supplementation. Recent recurrence of anemia in the last 6 weeks accompanied by epigastric pain, and several episodes of emesis. Two episodes of vomiting contained blood (hematemesis).

Generally well developed, thin, pale male. Abdomen is soft, non-tender, non-distended without masses or organomegaly.

Labs: Hgb 9.8, Hct 32.7, MCV 71.1, Reticulocyte count 2.6, WBC 6.6, platelets 570, stool guaiac positive, CRP 3.86, ESR 23, iron 11.

Amylase and lipase are within normal limits.

Abdominal ultrasound: Hypoechoic heterogeneous mass in the head of the pancreas extending along the body of the pancreas with reactive lymph nodes anterior to the pancreas head.

Abdominal CT with contrast: Enlarged pancreatic head with edema at the junction of the head and body and disruption anteriorly. Marked gastric wall thickening and distention with a collection of fluid along the posterior stomach wall.

• Gastric Ulcer disease (H. pylori vs hyperacidity)
• Trauma with pancreatic laceration
• Walled-off perforation
• Pancreatic pseudocyst
• Pancreatitis

Dx: Penetrating gastric ulcer (into pancreas) Helicobacter pylori gastritis

Dx Confirmed by: EGD (Endoscopy) with biopsy

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Started on medical triple therapy and doing well. 6 week follow-up EGD showed healing of ulcer.

EGD:
Large 5 cm ulcer at the antrum of the stomach with penetration into the pancreas.

Pathology:
Inflammatory infiltrate with curvilinear bacilli seen in the crypt lumens and on the surface of the superficial epithelium consistent with Helicobacter pylori gastritis. Positive rapid urease test.

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Gastric ulcers are due to a disruption in the integrity of the stomach lining often a result from an imbalance between acid secretion and stomach wall defenses against the noxious environment. They can be classified into four groups based on location and association with duodenal ulcers. Type I (60%) ulcers occur on the lesser curvature near the incisure, are most common and may have low to normal acid output. They are generally not associated with duodenal pyloric or prepyloric mucosal abnormalities. However, Type I gastric ulcers are almost universally associated with antral gastritis due to Helicobacter pylori infection beneath the mucosal surface and on the luminal epithelium and this is the likely cause of ulcer disease. Type II and III gastric ulcers account for 15% and 20% of lesions, respectively, and are both associated with acid hypersecretion and possible duodenal lesions. However, Type II ulcers occur in the body of the stomach, whereas Type III ulcers are prepyloric. Finally Type IV ulcers are the least common at 10% occurring high on the lesser curvature near the gastroesophageal junction. They may not be associated with excess acid secretion. Gastric ulcers can occur on the greater curvature of the stomach, but their incidence is less than 5%. Generally the closer the ulcer is to the pylorus, the more likely it is associated with increased acid secretion, thus suggesting that Types I and IV are possibly due to decreased defenses.

H. pylori infection is the most common cause of ulcer disease. It is a gram negative curvilinear rod. Infection impairs normal parietal cell inhibition, thus resulting in increased acid secretion. NSAID use is the second most common cause of ulcer disease. By decreasing prostaglandin production, mucus and bicarbonate production are also reduced, thereby impairing the stomach’s ability to protect itself from the caustic environment. Other risk factors and causes of ulcer disease include smoking, alcohol, stress, cocaine, Zollinger-Ellison syndrome, long-term corticosteroid therapy, and delayed gastric emptying resulting in gastric stasis. For gastric ulcers in particular acid secretion is essential, even normal amounts can be ulcerogenic. Therapy targeted at decreasing gastric acid allows for significant healing of the ulcer.

Typically, gastric ulcers do not occur before the age of 40 years, with peak incidence between 55 and 65 years of age. They are more common in lower socioeconomic classes and slightly more common in the non-white population. There has been a recent decline in ulcer disease over the last few decades due to improved visualization methods and treatment.

Gastric ulcers may present with intermittent epigastric pain, nausea, vomiting, appetite loss, weight loss, bleeding, gastric outlet obstruction, or even perforation. Epigastric pain is classically said to occur shortly into the post-prandial period versus the pain of a duodenal ulcer which presents several hours later. However, these relationships are often poor indicators for disease type. Epigastric tenderness is the most common physical exam finding, but is relatively non-specific. Hematemesis or melena indicate bleeding and a rigid abdomen could be associated with perforation, the most common complication of gastric ulcers.

Gastric ulcers are frequently identified via fiberoptic endoscopy, which allows for tissue biopsy. While contrast radiography can visualize the majority of gastric ulcers, they are difficult to differentiate from malignancy, thus EGD with biopsy is necessary to rule out malignancy. Early endoscopic evaluation is indicated with significant weight loss, vomiting suggestive of gastric outlet obstruction, palpable mass, guaiac positive stool, or blood loss anemia. An upright abdominal radiograph my evaluate for free air due to perforation. Standard laboratory tests include complete blood count and a complete metabolic panel. A serum gastrin level can be measured in those with refractory disease. Several tests, both invasive and non-invasive, exist to diagnose H. pylori infection including rapid urease assay, histology, culture, urea breath test, and serology.

Today, therapy is primarily medical focused on eradication of H. pylori with antibiotics and decreasing acid secretion with proton pump inhibitors(PPI) or H2 receptor antagonists. Triple therapy, which includes two antibiotics and a PPI, has a greater than 85% cure rate. Quadruple therapy includes a PPI, bismuth subsalicylate, tetracycline, and metronidazole and is used if triple therapy fails or in areas where resistance to metronidazole is high. Typical treatment regimens last for 10-14 days. While surgical techniques to decrease acid secretion exist, they are rarely used at this time and may result in significant morbidity. Surgery is generally reserved for the complications of ulcer disease, such as perforation.