Gastrointestinal and Hepatic Manifestations of Systemic Lupus Erythematosus

Abstract

In this review of the gastrointestinal (GI) and hepatic manifestations of systemic lupus erythematosus (SLE), 180 articles from the English literature, found using a medline search from January 1965 to December 2010, were examined. Vasculitis may cause ulcerations, bleeding, stricture formation, and perforation from ischemia and infarction. Otherwise, GI symptoms, occurring in about 50% of patients, are usually mild. Esophageal dysmotility may result in heartburn, regurgitation, and dysphagia. Occasionally, pneumatosis cystoides intestinalis may develop, sometimes associated with benign pneumoperitoneum. Patients are prone to salmonella bacteremia, presenting more commonly with fever and abdominal pain than with diarrhea. Intestinal pseudoobstruction usually is found with active lupus serology, preferentially involving small rather than the large bowel. Protein-losing enteropathy, characterized by diarrhea, edema, and hypoalbuminemia, can be the initial presentation of SLE. Malabsorption with a prevalence of 9.5% is occasionally associated with celiac disease. Pancreatitis, with an annual incidence of 0.4 to 1/1000, has an overall mortality of 27% that is decreased with corticosteroid therapy. Acute and chronic ascites may be due to lupus peritonitis or to associated diseases, such as pancreatitis, nephrotic syndrome, heart failure, or infections. Abnormal liver function tests may be due to steatosis from lupus or from corticosteroid therapy. Only about 10% of patients with autoimmune hepatitis have lupus. Up to 4.7% of patients with SLE have chronic active hepatitis correlating strongly with the presence of antibody to ribosomal P protein. SLE can involve the entire GI tract and the liver. Treatment with corticosteroids, cytotoxic agents, and/or immunosuppressants is often successful.

Chronic Diarrhea as the Presenting Complaint of Systemic Lupus Erythematosus in a Man

“…Patients with PLE present with severe pitting edema, diarrhea, hypoalbuminemia and hypocomplementemia. Patients with PLE have increased stool antitrypsin levels and high stool losses of radiolabeled albumin (10). Tc-99 albumin scintigraphy, the gold standard for diagnosing PLE was not performed in this case due to unavailability.…”

Gastrointestinal manifestations associated with systemic lupus erythematosus

“…Choroba wątroby w TRU może przebiegać w postaci nieznacznego podwyższenia aktywności enzymów wątrobowych, ciężkiego zapalenia lub niewydolności narządowej. Jest to wynik zapalenia narządu w przebiegu choroby podstawowej, stłuszczenia wątroby, skutek toksyczności stosowanych leków, wystąpienia epizodów choroby zakrzepowo-zatorowej, infekcji, a także innych współtowarzyszących autoimmunologicznych chorób wątroby [37]. Autorzy podają różną częstość występowania chorób wątroby -w przedziałach 21-55% lub 10-32% [38,39].…”

Professor Witold Nowicki – a greatly spirited pathologist

“…Pneumatosis cystoides can develop on the basis of various disorders of the gut, such as enteritis, inflammatory bowel disease, neonatal necrotizing enterocolitis, infectious colitis, disorders of connective tissue, diverticulosis as well endoscopic interventions, autoimmune diseases, pulmonary diseases such as cystic fibrosis, chronic obstructive lung disease, etc. [10,11,12,13].…”