Protein losing enteropathy in systemic lupus erythematosus: role of diet and octreotide

Ossandon, A; Bombardieri, Michèle; Coari, Giulio; Graziani, Grazia; Valesini, Guido

doi:10.1191/0961203302lu233xx

Cited by 15 publications

(5 citation statements)

References 8 publications

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“…Supplemental therapies including serum albumin infusion and diuretics should be given at the same time. In addition, octreotide could reduce intestinal microvascular blood flow, decrease local lymph formation, and ameliorate lymphatic dilation [33,41].…”

Section: Discussionmentioning

confidence: 99%

Lupus protein-losing enteropathy (LUPLE): A systematic review

Al-Mogairen

2011

Rheumatol Int

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Lupus protein-losing enteropathy (LUPLE) is a well reported but a rare manifestation of systemic lupus erythematosus (SLE). The main objectives of this study are to raise awareness of LUPLE that can be easily missed by internist, rheumatologist, gastroenterologist and nephrologist, and then to be considered in any patient with unexplained edema, ascites, and hypoalbuminemia. A systematic review was performed with 112 patients who met the eligibility criteria and were critically appraised. The LUPLE was ultimately diagnosed by either Tc-(99m) albumin scintography ((99m)Tc-HAS) or fecal alpha-1-antitrypsin clearance test. Clinical features of patients, at the time of LUPLE diagnosis, were as follows: age was 34 ± 14.2 years; the female to male ratio was 5.8:1; the mean time to development of LUPLE after diagnosis of SLE was 4.19 ± 4.7 years. There was a predominance of Asian (64.7%) while 29.5% were white or Hispanic patients. Eighty percent had peripheral edema, 48% had ascites, 38% had pleural effusion, and 21% had pericardial effusion. Forty-six percent had diarrhea, 27% had abdominal pain, 22% had nausea, and 19% had vomiting. Hypoalbuminemia was the most common characteristic laboratory finding (96%). A 24-h urine protein was less than 0.5 gm in (71%). Almost all patients (96%) had positive ANA with predominant speckled patterns (55%) and hypocomplementemia (79%). Colonoscopy showed mucosal thickening in 44% of patients, and the majority of patients (52%) revealed no abnormalities; on the other hand, intestinal histology either revealed mucosal edema, inflammatory cell infiltrate, lymphangiectasia, mucosal atrophy or vasculitis in 80% of patients. All patients were started on steroids. Thirty-four percent responded to steroids alone. Sixty-six percent were started with other immunosuppressive therapies, which include cyclophosphamide (46%), azathioprine (33%), and a combination of cyclophosphamide and azathioprine (7%). A few reported cases responded to either cyclosporine or etanercept. Prognosis was very good with steroids combined with immunosuppressive therapy. This is the first systematic review of LUPLE and should be considered as an etiology of unidentified edema, ascites, and hypoalbuminemia.

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Section: Discussionmentioning

confidence: 99%

Lupus protein-losing enteropathy (LUPLE): A systematic review

Al-Mogairen

2011

Rheumatol Int

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“…52 Octreotide reduces intestinal blood flow, thus decreasing local lymph formation and lymphatic flow, and has immunomodulatory effects.…”

Section: Malabsorption and Protein-losing Enteropathymentioning

confidence: 99%

Gastrointestinal and Hepatic Manifestations of Systemic Lupus Erythematosus

Ebert

Hagspiel

2011

Journal of Clinical Gastroenterology

136

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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.

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“…Some success has recently been reported with octreotide, a synthetic longacting preparation of somatostatin. 26,27 This agent decreases intestinal blood flow and thus local lymph production. As a result, lower intraluminal lymphatic pressure reduces lymphatic dilatation.…”

Section: Absent Naive T Cells Is Intestinal Lymphangiectasia (Inl)mentioning

confidence: 99%