Protein-losing enteropathy caused by systemic lupus erythematosus.

Correspondence Protein-losing enteropathy caused by systemic lupus erythematosus SIR,-We have read with great interest the recent paper by Wood et al in the September 1984 issue of Gut' referring to a case of protein losing entero-pathy (PLE) complicating the clinical course of a patient with systemic lupus erythematosus (SLE). In our opinion, the work contains some errors and omissions which question the originality of this paper. The authors quote only three other cases prior to their description, submitted in October 1983. We disagree with respect to this point. In a recent review by us,2 dealing with a patient similar to that described by Wood, we have found at least eight other cases in the literature, " seven of them before 1983. Protein losing enteropathy as initial manifestation of SLE, however, occurred only in three, including our patient. Moreover, it is not clear whether the authors have ruled out pericarditis, gastrointestinal malignancies, ulcerations, or other primary enteropathies, known causes of PLE. On the other hand, we think that the patient described by Wood and his colleagues does not fulfil all the criteria for diagnosis of SLE and other collagen diseases have not been clearly excluded: more specifically mixed connective tissue disease (speckled pattern of staining by indirect immunofluorescence; antibodies to RNP and absence of antibodies to DNA). Against these findings , antibodies to DNA (Crithidia luciliae) were present in our patient. Abnormalities in serum cholesterol are also of great interest. Increased concentrations of serum cholesterol and triglycerides were present in some patients. 1(No one to date has emphasised this finding which is very interesting, because it goes against traditional opinion that cholesterol is usually low in PLE.l In respect to pathogenesis, the authors postulate increased capillary permeability, presumably because of products of plasma C3 conversion. In our opinion, this is very speculative. Deposits of immune complexes in many extrarenal tissues (including gastrointestinal tract) have been found by several authors in some experimental animal models ,'2 13 as well as in studies of patients with SLE.14 15 Finally, the authors do not comment on the racial origin of their patient. It is very interesting that, in our review, five of nine patients5 7 8 10 (including ours2) had non-Anglo-Saxon origin: three Japanese, one Lebanese and one Spanish. This has led us to consider the possibility that external antigenic factors absorbed through the alimentary tract could explain the occurrence of this complication in …