Protein-losing enteropathies

Gastrointestinal (GI) protein loss can result from a heterogeneous group of diseases, including lymphangiectasia, inflammatory bowel disease, neoplasia, ulceration, intussusception, and histoplasmosis. Protein-losing enteropathy (PLE) should be suspected in any hypoalbuminemic patient with no evidence of exudative protein loss, proteinuria, or hepatic insufficiency. A minimum laboratory database for the suspected PLE patient should include a complete blood cell count, a biochemical and electrolyte profile, urinalysis ( urine protein: creatinine ratio), and pre- and postprandial bile acid determinations. Fecal alpha(1)-proteinase inhibitor concentrations may be used to confirm the presence of GI protein loss in cases with concurrent renal or hepatic disease. Because PLE is a syndrome and not a specific disease, the most effective therapy must be directed at the underlying cause. Multiple high-quality endoscopic biopsies are sufficient to diagnose most patients with PLE, although full-thickness biopsies are required in some cases. Patients with PLE are often clinically fragile, and careful symptomatic therapy must be integrated with dietary and medical management strategies in most cases.