Gastrointestinal manifestations of systemic lupus erythematosus
- Elena M Massarotti, MD
Elena M Massarotti, MD
- Associate Professor of Medicine
- Harvard Medical School
- Section Editor
- David S Pisetsky, MD, PhD
David S Pisetsky, MD, PhD
- Section Editor — Lupus
- Professor of Medicine and Immunology
- Duke University Medical Center
- Deputy Editors
- Monica Ramirez Curtis, MD, MPH
Monica Ramirez Curtis, MD, MPH
- Deputy Editor — Rheumatology
- Instructor of Medicine, Part-time
- Harvard Medical School
- Shilpa Grover, MD, MPH, AGAF
Shilpa Grover, MD, MPH, AGAF
- Deputy Editor — Gastroenterology/Hepatology
- Assistant Professor of Medicine, Part-time
- Harvard Medical School
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease of unknown cause that can affect the skin, joints, kidneys, lungs, nervous system, serous membranes, and/or other organs of the body.
The gastrointestinal manifestations of SLE in adults will be reviewed here. An overview of other clinical manifestations as well as the treatment of SLE in adults are presented separately. (See "Overview of the clinical manifestations of systemic lupus erythematosus in adults" and "Overview of the management and prognosis of systemic lupus erythematosus in adults".)
Gastrointestinal involvement is common in patients with systemic lupus erythematosus (SLE), and up to 40 percent of patients have gastrointestinal manifestations during their lifetime [1-5]. These manifestations may be due to vasculitis, side-effects of the medications used to treat SLE, infection, or other intercurrent processes (eg, uremia).
Dysphagia is the most frequent gastrointestinal complaint in patients with systemic lupus erythematosus (SLE) and may occur in association with retrosternal chest pain, heartburn, regurgitation, or odynophagia. These symptoms may be due to an underlying esophageal motility disorder, concomitant gastroesophageal reflux disease, or other causes of esophagitis such as medication-induced esophagitis or Candida esophagitis.
Approximately 20 to 70 percent of patients with SLE have an underlying esophageal motility disorder [6-8]. Esophageal motility disorders do not appear to be associated with disease activity, duration, and treatment of SLE . Although esophageal motility disorders have been associated with the Raynaud phenomenon and the presence of antiribonucleoprotein antibodies, it is unclear if this association is due to the presence of other connective tissue disorders . The mechanism by which SLE leads to an esophageal motility disorder is not known. It may result from an inflammatory reaction in the esophageal muscles, or by ischemic or vasculitic changes to Auerbach's plexus [10,11]. (See "Esophageal motility disorders: Clinical manifestations, diagnosis, and management".)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- ESOPHAGEAL INVOLVEMENT
- GASTRIC INVOLVEMENT
- Peptic ulcer disease
- SMALL BOWEL AND COLON INVOLVEMENT
- Intestinal pseudo-obstruction
- Protein-losing enteropathy
- HEPATIC INVOLVEMENT
- Autoimmune hepatitis
- Lupus hepatitis
- PANCREATIC INVOLVEMENT
- Acute pancreatitis
- Mesenteric vasculitis/ischemia
- Peritonitis and ascites
- SUMMARY AND RECOMMENDATIONS