Case Presentation: A 45-year-old male with a past medical history of ADHD presented to the emergency department with gradually progressive bilateral lower extremity pitting edema. Symptoms developed over the last three weeks and the edema now extended up to his waist. Review of systems was notable for bloating and mild abdominal discomfort that he attributed to constipation. Initial laboratory workup in the emergency department showed normal creatinine, aminotransferases, and TSH levels, but low albumin. CTA of the pulmonary arteries and CT abdomen/pelvis demonstrated moderately thickened stomach wall, mild hepatomegaly, and anasarca. An echocardiogram was unremarkable. To further evaluate the hypoalbuminemia, a urinalysis and urine protein to creatinine ratio were performed and found to be normal. He reported a well-balanced diet and was without concern for protein malnutrition. An MRI of the liver was obtained to further evaluate the hepatomegaly, revealing no evidence of cirrhosis but confirmed moderate diffuse thickening of the gastric folds. Given concern for protein-losing enteropathy, additional labs showed a low ceruloplasmin and transferrin levels. He was discharged with outpatient gastroenterology follow-up. Subsequent workup included a decreased alpha-1 antitrypsin clearance, an EGD showing foveolar hyperplasia, and negative tests for H. pylori and CMV. He was diagnosed with Menetrier’s Disease and started on a high protein diet and a three-month course of a proton pump inhibitor. Over the next several months, his albumin levels returned to normal, and his edema resolved.

Discussion: Menetrier’s Disease is a rare, acquired cause of protein losing enteropathy characterized by the triad of giant gastric mucosal folds, a protein losing state resulting in hypoalbuminemia, and diminished acid secretory capacity. Clinically, patients present with lower extremity edema and can have nausea, vomiting, abdominal pain, or diarrhea. Biopsy of the stomach shows foveolar hypoplasia with an atrophy of glands. The pathogenesis is not well understood but thought to be related to increased epithelial growth factor receptor signaling. It is most common in middle aged males and has been associated with infections such as H. pylori or CMV. Treatment is not well established but generally includes a high protein diet, a trial of acid suppression therapy, or cetuximab as a second line agent. Symptoms typically resolve but an increased risk of gastric cancer persists, and endoscopy is recommended for surveillance every two years.

Conclusions: Lower extremity edema is a common condition that can be caused by numerous diseases. It can result from either increased hydrostatic pressure from volume overload or decreased oncotic pressure with low albumin. While protein losing enteropathies are less common than other causes of lower extremity edema such as cardiac, renal, or liver disease, maintaining a high clinical suspicion is essential for accurate diagnosis.