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INTRODUCTION: Phlegmonous gastritis (PG) is a rare cause of abdominal infection with a mortality rate up to 42%. PG presents a diagnostic and therapeutic challenge given the low incidence and non-standardized treatment options. We present a case of PG successfully treated with early antibiotic therapy. CASE DESCRIPTION/METHODS: A 47-year-old man with uncontrolled type 2 diabetes mellitus presented with four days of subjective fevers, abdominal pain, and vomiting. The patient was tachycardic (122 beats/min) and had epigastric tenderness without guarding or rebound. Initial studies revealed leukocytosis (30,000/mm³) and Gram-positive bacteremia, later identified as ß-hemolytic group A Streptococcus. The stomach was diffusely thickened to 16 mm on contrast-enhanced computed abdominal tomography (Figure 1). Endoscopy revealed diffuse gastric thickening with erythema and a nonbleeding 6 mm ulcer on the lesser curvature of the gastric body. Deep biopsy of the ulcer by cold forceps produced a purulent drainage (Figure 2). Subsequent endoscopic ultrasonography (EUS) found a 12 mm thickened gastric wall involving the deep mucosa, thus further biopsy was obtained. The biopsies from both endoscopy and EUS showed acute neutrophilic inflammation with micro-abscesses; Helicobacter pylori was not identified. The patient received three days of piperacillin/tazobactam followed by seven days of ampicillin/sulbactam, with resolution of symptoms. DISCUSSION: PG is a rapidly progressive and frequently fatal bacterial infection of the gastric wall. The etiology of PG remains unclear, but can be caused by local or hematogenous spread of infection. Streptococcusspp. accounts for 70% of cases, and up to one-third of infections are polymicrobial. Risk factors include gastric mucosal injury, diabetes mellitus, and alcoholism. Diagnosis is commonly delayed as clinical manifestations are nonspecific. High clinical suspicion and early radiographic testing are important to identify gastric wall thickening, which is supportive of the diagnosis. PG primarily affects the gastric submucosa but may extend to deeper layers. Histopathology is of limited benefit, as standard forceps biopsy collects insufficient submucosal tissue. Optimal treatment is not known. When diagnosis is delayed, surgical intervention is often required. Medical therapy alone has been associated with increased mortality rates; however, in cases of early diagnosis and empiric antibiotic treatment, medical therapy alone may be sufficient.

INTRODUCTION: Celiac disease is an immune-mediated disorder triggered by a reaction to gluten with elevated levels of IgA antibodies. Symptoms typically resolve with a gluten free diet. However, refractory cases have been reported despite dietary adherence. Our discussion involves an elderly woman with severe, refractory celiac disease with concomitant IgA deficiency. CASE DESCRIPTION/METHODS: An 80-year-old woman presented our clinic with exacerbation of chronic, non-bloody diarrhea. She has a history of celiac disease diagnosed 20 years ago after an episode of acute pancreatitis. She also has IgA deficiency and her total IgA level remains low at 37, despite infusions 3 times per week. She is strictly adherent to a gluten free diet, but continues to have multiple episodes of diarrhea and has lost over 100 pounds since her diagnosis. Patient had bidirectional endoscopy notable for antral gastropathy as well as fissures and flattening of the duodenal mucosa. Biopsies were consistent with celiac sprue. Capsule endoscopy showed diffuse flattening of the small bowel villi with erythema and cracked, scalloped mucosa as well as multiple, small, aphthous ulcers throughout the bowel (Figures 1, 2, and 3). Patient has had an extensive workup, but everything else have been unrevealing. Steroids have been initiated as a last-ditch effort, but she continues to have “more bad days than good days” despite being on a high dose prednisone. DISCUSSION: The diagnosis and treatment of celiac disease can be complicated by coexisting immunodeficiencies. Usually, titers of tissue transglutaminase IgA will be elevated and are involved in the immune reaction that causes damage to the lining of the small bowel with characteristic flattening of the villi as well as chronic diarrhea and malabsorption. A connection between IgA deficiency and celiac disease has been well established and likely contributes to the refractory nature of our patient’s disease. In patients with IgA deficiency it is important to utilize other forms of serologic testing, typically with IgG tissue transglutaminase, in addition to duodenal biopsies. Symptoms typically resolve with a gluten free diet. However, refractory cases have been reported with persistent diarrhea and villous atrophy for over 1–2 years. Symptom management can be difficult for these patients and may require the use of steroids as the last resource.

INTRODUCTION: Herpes simplex virus (HSV 1&2) is an uncommon cause of asymptomatic hepatitis and acute liver failure. Fatal disease often occurs in immunocompromised adults but is a rare event in immunocompetent patients. Early suspicion of infection is imperative as late diagnosis and treatment carries poor prognosis and high mortality. We describe a case of acute hepatic failure from HSV-1 virus in an immunocompetent adult successfully treated with medical therapy without need for liver transplantation. CASE DESCRIPTION/METHODS: A 55-year-old diabetic male with recent hospitalization for necrotizing fasciitis of the groin (discharged on amoxicillin/clavulanate 5 days ago) presented to the hospital with fever, vomiting, abdominal pain and was found to have severe elevation in liver enzymes. Patient denied prior history of liver disease. Physical exam was notable for fever: 102 degree F, tachycardia, multiple small circular lesions on the oral mucosa and tender hepatomegaly. Liver tests at baseline were normal and on admission showed: AST 1317 U/L (normal:< 32 U/L), ALT 966 U/L (normal:< 36 U/L), total bilirubin 0.4mg/dL (normal:0.2-1.2 mg/dL), alkaline phosphatase 86 U/L (normal:45-117 U/L) and INR 1.7 (normal:0.8-1.2). Urine drug screen was negative of acetaminophen. Imaging excluded hepatic venous thrombosis. Laboratory tests for viral and autoimmune hepatitis, wilson’s disease were negative. Patient was empirically started on IV acyclovir given concern for herpes hepatitis based on oral exam. Diagnosis was confirmed with a positive blood and oral swab HSV DNA PCR and a liver biopsy (Figures 1 and 2) showing herpes simplex viral inclusions. Due to progressive worsening of liver tests and patient’s condition while on treatment, intravenous immunoglobulin (IVIG) therapy was added eventually leading to clinical and laboratory signs of improvement (Table 1). He was discharged on an oral course of valganciclovir and continues to do well on follow up visit. DISCUSSION: Fulminant liver failure from herpes virus has been infrequently reported in immunocompetent adults and usually represents disseminated infection. It is a potentially treatable condition that requires high degree of diagnostic suspicion as presenting symptoms can be non-specific. Early empiric treatment with acyclovir while awaiting HSV PCR or liver biopsy has been shown to improve outcomes and decrease need for liver transplantation. We herein describe a novel approach to treat HSV hepatic failure with combination therapy of acyclovir and IVIG.

INTRODUCTION: Intussusception is telescoping of a proximal segment of bowel into the lumen of the adjacent distal segment of bowel. This condition is usually seen in the pediatric population and is most often due to a benign pathologic lead point. Intussusception remains a rare condition in adults, representing approximately 1–5% of mechanical bowel obstructions typically due to malignancy. We present a rare case of Colo-colic intussusception secondary to a sub-mucosal benign lipoma. CASE DESCRIPTION/METHODS: A 33-year-old Caucasian woman with no past medical or surgical history, presented with one month of intermittent left-sided and mid-abdominal cramping, which intensified the week prior to presentation. She reported increasing post-prandial pain with associated nausea and bloating. Physical exam revealed stable hemodynamics, and diffuse abdominal tenderness to palpation. Laboratory testing was unremarkable, including a serum pregnancy test. Contrasted CT Abdomen/Pelvis revealed intussusception of the mesenteric tissues and transverse colon into the descending colon with a discrete mass lesion as the lead point (Figure 1). A colonoscopy revealed a large, non-obstructing, hard, negative pillow sign, subepithelial mass, with a short stalk at the hepatic flexure was encountered (Figure 2). The patient underwent laparotomy by colorectal surgeon. A proximal transverse colon intussusception was identified and a right hemicolectomy with ileocolonic anastomosis was completed. Surgical pathology results revealed a 6.5 cm submucosal lipoma without evidence of dysplasia or malignancy (Figure 3). The patient recovered well post-operatively and was discharged. DISCUSSION: In adults, the diagnosis of intussusception can be difficult to make based on clinical presentation alone due to the rarity and non-specific complaints. The condition is commonly related to malignancy. Generally, colo-colic intussusceptions are the least common. Cross sectional imaging, such as CT scans with IV contrast are the most sensitive diagnostic tests. Our case identifies an uncommon cause of abdominal pain in an adult patient with the CT scan and diagnostic laparotomy revealing a colo-colic intussusception. In this fortunate case, pathology revealed a benign lesion as the lead point. Although colonic lipomas are common this patient has low risk factors such as age and no metabolic syndrome, they are often asymptomatic and have been rarely reported to cause similar presentations as they increase in size ( >4 cm).