Abstract

Introduction: SLE is a multisystem autoimmune disorder. Lupus enteritis is potentially rare complication of SLE presenting as abdominal pain. Case report: A 32 year old woman with the history of SLE came for evaluation of 1 week history of subjective fever, cough, and pleuritic chest pain after failing outpatient treatment for community acquired pneumonia with levofloxacin. She had stable vitals on admission. Laboratory investigations showed leukopenia, anemia, raised C-reactive protein, and positive anti-dsDNA antibodies with higher titers from baseline and low complement levels. Her CXR and echocardiogram showed moderate bilateral pleural effusion and mild pericardial effusion. The patient was started on IV steroid to treat SLE flare. On day four of hospitalization, she complained of nausea, vomiting, and severe abdominal pain. Abdominal CT scan showed dilated and thickened small bowel loops, mild abdominal ascites without any evidence of arterial and venous thrombosis. She was given bowel rest and empirically started on IV antibiotics, and steroids were continued. Stool studies including C diff, bacterial cultures and ova and parasites were negative. She had clinical improvement in 2-3 days and was able to tolerate diet. Antibiotics were discontinued, and she was discharged home on tapering doses of steroid. Discussion: Lupus enteritis is an uncommon condition in SLE patients with the prevalence of about 0.9 %. About 8%-40% of SLE patients have acute abdominal pain during the stage of an active disease. Inflammatory vasculitis secondary to immune complex deposition and thrombosis of the intestinal vessels are the proposed pathogenic mechanisms. It can cause very severe abdominal symptoms and signs and sometimes is diagnosed as the acute surgical abdomen. Early diagnosis is critical to allow prompt treatment to avoid unnecessary surgical intervention. Characteristic CT abdomen findings include dilated bowel, focal or diffuse bowel wall thickening, abnormal bowel wall enhancement which is also called “target sign,” mesenteric edema, stenosis or engorgement of mesenteric vessels which is also called “the comb sign” and ascites. Treatment is symptomatic management and high dose intravenous methylprednisolone. Those who do not have an adequate response to steroids should be considered for immunosuppressive agents like intravenous cyclophosphamide. When a rapid response to immunosuppressive therapy is not achieved, surgical intervention should be considered.Figure: Thickened loops of small bowel on CT abdomen and pelvis.

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