Tricuspid regurgitation: A newly recognized cause of protein-losing enteropathy, lymphocytopenia and immunologic deficiency

Abstract

Four patients with protein-losing enteropathy, hypoalbuminemia and lymphocytopenia secondary to tricuspid regurgitation and rheumatic heart disease are described. Gastrointestinal protein loss was detected by 125I-albumin and 51Cr-albumin turnover studies. Following medical treatment in two patients, right atrial pressure declined and both the protein loss and lymphocytopenia were ameliorated. The immunologic response in three of the patients with tricuspid regurgitation was tested with multiple skin tests to antigens which provoke a delayed type of reaction, and in all cases responses were diminished. One patient retained a skin allograft for fifty-seven days until death. The records of a total of thirty patients with tricuspid regurgitation and of eight patients with constrictive pericarditis were reviewed. The lymphocyte counts averaged 1,420 cells per cu. mm., compared to a normal value of 2,500 cells per cu. mm. Following operation, the lymphocyte count rose in eight of nine patients with tricuspid regurgitation and in all five patients with constrictive pericarditis. It is suggested that patients with rheumatic tricuspid regurgitation and other patients with cardiac disease associated with protein-losing enteropathy have a secondary intestinal lymphangiectasia resulting from systemic venous and lymphatic hypertension. The lymphangiectasia leads to loss of protein-rich and lymphocyte-rich lymph into the gastrointestinal tract. The protein loss leads to hypoproteinemia and the lymphocyte loss presumably explains the immunologic deficiency.