eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Protein-Losing Enteropathy: Differential Diagnoses & Workup

Author: Simon S Rabinowitz, MD, PhD, Professor of Clinical Pediatrics, New York Medical College; Chairman, Chief and Medical Administrator, Department of Pediatrics, Chief, Pediatric Gastroenterology and Nutrition, Richmond University Medical Center
Contributor Information and Disclosures

Updated: Aug 17, 2009

Differential Diagnoses

Atopic Dermatitis
Kwashiorkor
Burns, Chemical
Liver diseases that compromise synthetic function
Burns, Electrical
Nephrotic Syndrome
Burns, Thermal
Noonan Syndrome
Burns: Surgical Perspective

Other Problems to Be Considered

See Causes.

Workup

Laboratory Studies

Patients with edema and documented hypoalbuminemia but without clinical or biochemical evidence of liver or renal disease should have a thorough evaluation for protein-losing enteropathy (PLE). In the past, protein-losing enteropathy was often considered a diagnosis of exclusion; however, several approaches for determining abnormal protein loss in the GI tract are currently noted. The ideal test for protein-losing enteropathy is able to detect a serum protein in the stool that is not secreted, digested, or reabsorbed in the GI tract. However, no ideal test is available.

Three established types of tests have been used to evaluate for protein-losing enteropathy. The first involves the intravenous administration of a radiolabeled substrate followed by the determination of radioactivity in the feces. The second type of test directly measures endogenous proteins in the feces. A third approach is the use of nuclear scintigraphy, not only for diagnosis, but also to identify potential regional or localized areas of protein loss. A recent publication described the use of MRI as an alternative method to diagnose and localize this condition.6

  • History of radiolabeled proteins
    • Use of radiolabeled proteins to measure albumin turnover dates back to 1950 with Kinsell.7
    • In the late 1950s, Swartz, and later Citrin, administered iodine 131–albumin to patients in an attempt to measure albumin turnover. In a patient with hypertrophic gastritis and protein-losing enteropathy, Citrin reported that the131 I-albumin lost in the stomach was degraded and the free131 I was then absorbed and excreted in the urine, making the measurement of131 I in the stools unreliable.
    • Gordon reported the use of polyvinylpyrrolidone iodine I 125 (131 I-PVP) as a marker for protein metabolism.8 PVP is a macromolecule that is not digested by intestinal enzymes and is poorly absorbed when taken by mouth. In patients with protein-losing enteropathy, intravenously administered131 I-PVP results in detectable levels of radioactivity in the stool. The problem with this substance is that it is not a normal metabolite, has a wide range of molecular weights, and can be partially absorbed and secreted. More importantly, the131 I is easily released from the carrier, which then can be absorbed and excreted in the urine. This is problematic if urine contamination of the stool occurs as in pediatric patients.
    • In 1961, the next radioactive substrate used was chromium 51–albumin. This method had several advantages. The51 Cr bound tightly to albumin and was poorly absorbed from the GI tract. Thus, little or no radioactivity was detectable in the urine.
    • In practice, approaches using radiolabeled compounds are now rarely used because 48-72 hours of stool collection is required in the hospital, care must be taken to avoid contamination of stool collection with urine, and the tests involve radiation exposure.
  • Measurement of endogenous proteins
    • In 1977, Crossley and Elliot demonstrated that the stools of patients with protein-losing enteropathy as determined by51 Cr-albumin excretion also had high levels of A1-AT.
    • A1-AT is an endogenous protein not present in the diet; the molecular weight is similar to albumin. It is not actively secreted, absorbed, or digested.
    • A1-AT is stable in feces at 37°C, allowing collection over several days.
    • Because A1-AT is not excreted in urine, urine contamination of the stool sample does not alter the spot determination of fecal A1-AT.
    • Stool samples are simply lyophilized, and A1-AT is extracted by solubilization.
    • Fecal A1-AT can then be detected by immunoassay. Measurement of fecal A1-AT can be used as a spot determination or to calculate the clearance of A1-AT using the following formula:

        A1-AT clearance = [(fecal A1-AT concentration) (stool volume/24 h]/(A1-AT serum concentration)
    • Many studies have demonstrated the efficacy of using fecal A1-AT levels and A1-AT clearance for diagnosis and follow-up care in patients with protein-losing enteropathy.
  • Nuclear scintigraphy (described below)

Imaging Studies

  • Nuclear scintigraphy
    • Several radiopharmaceuticals tagged to proteins have been used to examine protein-losing enteropathy, including indium-111 (111In)–transferrin, technetium-99m (99mTc)–human serum albumin, and 99mTc-dextran. The latter compound is reported to be superior for numerous technical reasons.
    • This technique has been reported to be useful in the diagnosis of protein-losing enteropathy, but no studies have compared the sensitivity of scintigraphy with fecal A1-AT determination. However, it may be extremely useful in identifying sites of involvement in protein-losing enteropathy (ie, stomach vs small intestine or even regional differences in the small bowel).
  • MRI: MRI was able to reveal abnormalities in both the intestine and mesentery and documented dilated thoracic duct and mesenteric lymphatic as well as prominent subcutaneous lymphatics in the extremity.6

Procedures

  • In addition to the investigations listed above to document and localize the protein-losing enteropathy, a thorough orderly evaluation is required in the patient with protein-losing enteropathy to determine the underlying etiology of the protein loss. This usually begins with cultures for the infectious causes listed above, serologic evaluation for the immune conditions listed above, and radiographic studies (contrast studies, CT scans, MRI) to localize the area of involvement and identify characteristic patterns.
  • Often, endoscopy is also performed to assess for specific features such as the hypertrophic gastric folds of Menetrier disease, the pseudomembranes of C difficile colitis, the scalloping of the duodenum in sprue, and the stigmata of inflammatory bowel disease. At the time of endoscopy, biopsies are obtained to confirm the histological findings listed below.

Histologic Findings

  • Intestinal and more rarely gastric biopsies are at times required to definitively diagnose the underlying diseases that are the cause of the protein-losing enteropathy. Examples include Crohn disease, ulcerative colitis, celiac disease, graft versus host disease, Whipple disease, lymphoma, Hirschsprung disease, pseudomembranous colitis, eosinophilic gastroenteritis, allergic enteropathy, and some infectious diseases.
  • Lymphangiectasia is also a histologic diagnosis, revealing dilated lacteals in the mucosa.

More on Protein-Losing Enteropathy

Overview: Protein-Losing Enteropathy
Differential Diagnoses & Workup: Protein-Losing Enteropathy
Treatment & Medication: Protein-Losing Enteropathy
Follow-up: Protein-Losing Enteropathy
References
Further Reading
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References

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Further Reading

  • Proujanksy R. Protein-Losing Enteropathy. In Walker, Durie, Hamilton, et al eds: Pediatric Gastrointestinal Disease. BC Decker Inc. 2002.
  • Levin MS. Miscellaneous diseases of the small intestine: Protein-losing gastroenteropathy. In Tadataka Y, ed: Textbook of Gastroenterology. KB Lippincott. 1996.

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Keywords

protein-losing enteropathy, PLE, chronic diarrhea, hypoproteinemia, hypoalbuminemia, protein-losing gastroenteropathy, idiopathic hypoproteinemia, edema disease, nephrosis without nephrosis, nephrotic syndrome, liver disease, jaundice, splenomegaly, ascites, malrotation, tuberculosis, lymphoma, sarcoidosis, arsenic poisoning, Gaucher disease, Langerhans cell histiocytosis, constrictive pericarditis, congestive heart failure, cardiomyopathy, Clostridium difficile, Clostridium perfringens, Giardia lamblia, Helicobacter pylori, colonic malakoplakia, cytomegalovirus, malaria, measles, rotavirus, salmonella, schistosomiasis, graft versus host disease, Henoch-Schönlein purpura, Hirschsprung disease, inflammatory bowel disease, necrotizing enterocolitis, juvenile rheumatoid arthritis, malnutrition, systemic lupus erythematosus, tropical sprue, treatment, diagnosis

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Contributor Information and Disclosures

Author

Simon S Rabinowitz, MD, PhD, Professor of Clinical Pediatrics, New York Medical College; Chairman, Chief and Medical Administrator, Department of Pediatrics, Chief, Pediatric Gastroenterology and Nutrition, Richmond University Medical Center
Simon S Rabinowitz, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Gastroenterology, American Gastroenterological Association, American Medical Association, New York Academy of Sciences, North American Society for Pediatric Gastroenterology and Nutrition, Phi Beta Kappa, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Associate Professor, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania
Robert Baldassano, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

David A Piccoli, MD, Chief of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine
David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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