Gastrointestinal involvement is the most common clinical overlap feature with SSc, occurring in approximately 60 to 80 percent of patients. Disordered motility in the upper gastrointestinal tract is the most common problem, and this may be associated with development of SSc. Esophageal biopsies may show severe atrophy and loss of smooth muscle cells in the muscular layer of the lower esophagus, followed by fibrosis. The atrophied tissues show deposition of immunoglobulin (Ig) G and C3 on immunofluorescence microscopy. There have been case reports of hemoperitoneum, hematobilia, duodenal bleeding, megacolon, pancreatitis, ascites, protein-losing enteropathy, primary biliary cholangitis (previously referred to as primary biliary cirrhosis), portal hypertension, pneumatosis intestinalis, and autoimmune hepatitis. [1] Malabsorption syndrome can occur secondarily to small bowel dilation with bacterial overgrowth.
Liver involvement in the form of chronic active hepatitis and Budd-Chiari syndrome has been described. Pseudodiverticulae, identical to those seen in SSc, may be seen along the antimesenteric border of the colon. Abdominal pain in MCTD may result from bowel hypomotility, serositis, mesenteric vasculitis, colonic perforation, and pancreatitis.[2]
