Eric M. Nelsen

Distribution of Body Fat and its Influence on Esophageal Inflammation and Dysplasia in Patients with Barrett's Esophagus

BACKGROUND & AIMS Increased waist circumference and visceral fat are associated with increased risk of Barretts esophagus (BE) and esophageal adenocarcinoma. This association might be mediated by mechanical and endocrine mechanisms. We investigated the distribution of fat in subjects with BE and its association with esophageal inflammation and dysplasia. METHODS We collected data from 50 BE cases and 50 controls (matched for age and sex, identified from a radiology trauma database) seen at the Mayo Clinic in 2009. Abdominal (subcutaneous and visceral) and gastroesophageal junction (GEJ) fat area was measured using computed tomography with standard techniques. Esophageal inflammation (based on a histologic score) and dysplasia grade were assessed from esophageal biopsies of BE cases by a gastrointestinal pathologist. Conditional logistic regression was used to assess the association of body fat depot area with BE status, esophageal inflammation, and dysplasia. RESULTS All BE subjects had controlled reflux symptoms without esophagitis, based on endoscopy. The GEJ fat area (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.3-27.7; P = .02), visceral fat area (OR, 4.9; 95% CI, 1.0-22.8; P = .04), and abdominal circumference (OR, 9.1; 95% CI, 1.4-57.2; P = 0.02) were associated with BE, independent of body mass index (BMI). The subcutaneous fat area was not associated with BE. Visceral and GEJ fat were significantly greater in BE subjects with esophageal inflammation (compared with those without, P = .02) and high-grade dysplasia (compared with those without, P = .01), independent of BMI. CONCLUSIONS GEJ and visceral fat are associated with BE, and with increased esophageal inflammation and high-grade dysplasia in BE subjects, independent of BMI. Visceral fat therefore might promote esophageal metaplasia and dysplasia.

Metabolic Syndrome as a Risk Factor for Barrett Esophagus: A Population-Based Case-Control Study

OBJECTIVES To assess the association between Barrett esophagus (BE) and the metabolic syndrome in patients with and without reflux symptoms and to determine whether this association is reflux independent and metabolically driven. PATIENTS AND METHODS Case patients with BE and controls were residents of Olmsted County, Minnesota (1999-2006). Two control groups (one with and one without symptoms of gastroesophageal reflux) were identified from a cohort of patients who had responded to a validated gastrointestinal symptom questionnaire. Cases and controls were individually matched by age, sex, and duration of follow-up. Controls did not have a known diagnosis of BE. The association of the metabolic syndrome and its individual components with BE was assessed using univariate and multivariate conditional logistic regression separately for each control group. RESULTS A total of 309 patients were included (103 BE cases, 103 controls with reflux symptoms, and 103 controls without reflux symptoms). A total of 64% of cases, 47% of controls with reflux symptoms, and 50% of controls without reflux symptoms had the metabolic syndrome. The metabolic syndrome was associated with a 2-fold increased risk of BE relative to those with (odds ratio, 2.00; 95% CI, 1.10-3.65; P=.02) and without (odds ratio, 1.90; 95% CI, 1.03-3.60; P=.04) reflux symptoms. This association was independent of smoking, alcohol consumption, and body mass index and remained robust with sensitivity analysis. CONCLUSION The metabolic syndrome is associated with BE independent of reflux symptoms, which may reflect a reflux-independent pathway of BE pathogenesis.

Diagnosis and Management of Barrett's Esophagus

Barrett esophagus is characterized by the replacement of squamous mucosa in the esophagus by specialized intestinal metaplasia. Its clinical significance lies in it being the strongest risk factor for and known precursor for esophageal adenocarcinoma. Diagnosis requires endoscopic confirmation of columnar metaplasia in the distal esophagus and histologic confirmation of specialized intestinal metaplasia. Recommendations for the management of subjects diagnosed with Barrett esophagus include periodic endoscopic surveillance to detect the development of high-grade dysplasia or adenocarcinoma. Careful endoscopic evaluation with high-resolution endoscopy and endoscopic resection is recommended in the evaluation of subjects with high-grade dysplasia and early adenocarcinoma.

Severe Anion Gap Metabolic Acidosis From Acetaminophen Use Secondary to 5-Oxoproline (Pyroglutamic Acid) Accumulation

Abstract:Anion gap metabolic acidosis (AGMA) is commonly encountered in medical practice. Acetaminophen-induced AGMA is, however, not widely recognized. We report 2 cases of high anion gap metabolic acidosis secondary to 5-oxoproline accumulation resulting from acetaminophen consumption: the first case caused by acute one-time ingestion of large quantities of acetaminophen and the second case caused by chronic repeated ingestion in a patient with chronic liver disease. Recognition of this entity facilitated timely diagnosis and effective treatment. Given acetaminophen is commonly used over the counter medication, increased recognition of this adverse effect is of important clinical significance.

Anti-synthetase syndrome presenting as cryptogenic organizing pneumonia

Interstitial lung disease (ILD) is a unique group of lung diseases that can be associated with inflammatory conditions, such as polymyositis-dermatomyositis (PM-DM). Presentation of PM-DM with ILD is not uncommon but clinical and radiological features can be similar to other conditions (e.g. atypical pneumonia) and can be challenging to diagnose. Delayed diagnosis of PM-DM can be associated with progression of pulmonary involvement and potentially increase morbidity. We report a patient presenting with pulmonary symptoms who had positive anti-Jo-1 antibodies and cryptogenic organizing pneumonia features on biopsy, which is a rare reported finding.

52-Year-Old Man With Liver Enzyme Abnormalities and Elevated Ferritin Level

94 Mayo Clin P A 52-year-old man presented for a general medical examination. His medical history included hypertriglyceridemia, obesity (body mass index of 32 kg/m), and impaired fasting blood glucose levels. Laboratory studies 4 years previously had shown persistent elevation of aminotransferase levels (reference ranges shown parenthetically)—aspartate aminotransferase (AST), 51 U/L (8-48 U/L) and alanine aminotransferase (ALT), 64 U/L (7-55 U/L)— and an elevated serum ferritin level of 675 g/L (24-336 g/L). At that time, he consumed alcohol regularly (2 drinks nightly). Additional laboratory abnormalities included hypertriglyceridemia (triglyceride level of 186 mg/dL). Testing for chronic hepatitis B and C virus infections yielded negative results. The patient failed to return for appointments over the next 4 years. At the current appointment, he stated that he had no symptoms and had come to the clinic only at his wife’s suggestion. Vital signs included an elevated blood pressure of 170/90 mm Hg. Physical examination revealed hepatomegaly characterized by a 17-cm liver span in the midclavicular line with a firm, nontender liver edge palpable 2 fingerbreadths below the right costal margin. There was notable absence of cutaneous stigmata of chronic liver disease and splenomegaly. Further review of the medical record showed an elevated blood pressure over the past several years consistent with hypertension. His liver enzyme and ferritin values remained elevated despite cessation of alcohol intake, with AST of 55 U/L, ALT of 88 U/L, and ferritin of 885 g/L. Hydrochlorothiazide treatment was initiated and follow-up scheduled with repeated laboratory testing.

EMR of large periampullary neuroendocrine tumor

A 74-year-old man with a history of hypertension, chronic kidney disease, and diabetes mellitus type 2 presented with a 2-day history of melena. His hemoglobin level remained unchanged during hospitalization. He underwent an upper endoscopy that showed a 2to 3-cm periampullary mass (Fig. 1A) concerning for malignancy just distal to the ampulla (Figs. 1B and C). Examination of initial pinch biopsy specimens showed negative results. Subsequent EUS showed a 21by 11-mm mass that was mucosal in origin without invasion through the muscularis propria. Examination of core biopsy specimens revealed a neuroendocrine (carcinoid) tumor. The patient was referred to surgery; however, he declined surgical intervention and requested attempts for endoscopic removal. He underwent upper endoscopy under general anesthesia with a plan for EMR (Video 1, available online at www.VideoGIE.org). Injection of 5 mL of epinephrine (1:20,000) was performed in and around the tumor, and a large hexagonal snare was used to remove the tumor in 1 piece with the use of 30 W set to