A Study on Protein Losing Enteropathy In Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. Symptoms vary between people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. Often there are periods of illness, called flares, and periods of remission during which there are few symptoms Virtually every system and organ can be affected by SLE. Gastrointestinal symptoms are common in SLE patients, and more than half of them are caused by adverse reactions to medications and viral or bacterial infections. Though not as common as lupus nephritis, SLE-related gastrointestinal involvement is clinically important because most cases can be life-threatening if not treated promptly. Lupus mesenteric vasculitis is the most common cause, followed by protein-losing enteropathy, intestinal pseudo-obstruction, acute pancreatitis and other rare complications such as celiac disease, inflammatory bowel diseases, etc. Protein-losing gastroenteropathy (PLGE)is a condition characterized by profound edema and severe hypoalbuminemia secondary to excessive loss of serum protein from the gastrointestinal tract, clinically indistinguishable from nephrotic syndrome. Gastrointestinal loss of albumin is harder to investigate, as is its etiology. Consequently, in patients with hypoalbuminemia in which other possible etiologies have been excluded, protein-losing enteropathy must be considered and persistently investigated. The diagnosis of lupus-associated protein-losing enteropathy relies on characteristic clinical and laboratory features of SLE and on the exclusion of other possible causes of protein loss. Usually there are no findings suggestive of lymphatic leakage, such as steatorrhea, lymphocytopenia, and hypogammaglobulinemia; complement levels were low and serum cholesterol was high in about 70% of the reported cases . No antibodies were specifically associated with protein-losing enteropathy.Colonoscopy in (PLGE)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.Intestinal biopsy should be done to exclude other diseases but does not help in defining the etiopathogenesis of the protein loss. Intestinal biopsies were normal in many cases, and others showed nonspecific findings including mononuclear infiltration, lymphangiectasia, vasculitis, deposits of C3 in capillary walls, and shortened villi. Generally there are no lesions of the epithelial surface.calprotectin protein is found in large quantities in neutrophil granulocytes, where it represents 5% of total proteins and 60% of cytoplasmic proteins.In the presence of inflammatory processes, calprotectin is released following granulation of neutrophil granulocytes. In the case of an inflammation of the intestine, calprotectin can be detected in feces. Fecal dosing is the only one that can provide direct indications on the location of inflammation, while the dosage in serum or plasma shows a state of inflammation that can be present anywhere in the body of the analyzed patient.