bubble_chart Overview

Connective tissue diseases involving the gastrointestinal tract include scleroderma, systemic lupus erythematosus, polyarteritis nodosa, dermatomyositis, rheumatoid arthritis, etc., with scleroderma being the most prominent.

bubble_chart Pathological Changes

1. In 57% of patients with scleroderma, the small intestine is involved. Pathological changes in the small intestine include atrophy of smooth muscle, patchy collagen fiber deposition in the submucosal layer, muscular layer, and serosal layer, and chronic inflammatory cell infiltration in the lamina propria.

2. In dermatomyositis, the small intestine exhibits varying degrees of dilation and segmentation, accompanied by hypomotility and prolonged transit time. Macroscopically, the intestinal wall shows edema and thickening. Microscopic examination reveals multiple mucosal erosions, submucosal edema, atrophy and fibrosis of the muscular layer with lymphocytic and plasma cell infiltration. Small arteries from the submucosal to the serosal layer, as well as small veins, show intimal thickening, predisposing to thrombosis and luminal occlusion.

3. Intestinal damage in systemic lupus erythematosus is primarily the result of vasculitis, manifesting as fibrinoid degeneration, thrombosis, hemorrhage, and ischemia. It mainly affects the submucosal layer, muscular layer, and small arteries and veins of the mesentery.

4. Polyarteritis nodosa can involve any part of the intestine but primarily affects small and medium-sized arteries of the mesentery, as well as small arteries in the submucosal and muscular layers, followed by small veins. The lesions are segmentally distributed, involving all layers of the vessel wall. Histological features include fibrinoid degeneration, necrosis, thrombosis, and inflammatory cell infiltration.

5. Rheumatoid arthritis can also complicate small intestinal malabsorption, steatorrhea, and selective lactose intolerance. Malabsorption is caused by concomitant small intestinal amyloidosis and may also be accompanied by gastrointestinal protein loss.

bubble_chart Clinical Manifestations

1. Patients with scleroderma may clinically present with intestinal dysfunction such as abdominal discomfort, abdominal distension and fullness, postprandial borborygmi, decreased appetite, nausea, vomiting, and intermittent alternation between diarrhea and constipation.

2. In dermatomyositis, the small intestine exhibits varying degrees of dilation and segmentation, accompanied by hypomotility and prolonged transit time. Macroscopically, the intestinal wall shows edema and thickening.

3. Intestinal damage in systemic lupus erythematosus is primarily a result of vasculitis. Common gastrointestinal symptoms include abdominal pain, loss of appetite, nausea, and vomiting. Less frequent manifestations include diarrhea, melena, and occasionally intestinal obstruction. A minority of patients may exhibit villous atrophy, accompanied by small intestine malabsorption, protein-losing enteropathy, regional enteritis, nonspecific ulcerative colitis, or acute appendicitis.

4. In polyarteritis nodosa, intestinal symptoms are very common. When local ischemia occurs in the intestines, symptoms such as abdominal pain, nausea, vomiting, or diarrhea may arise. Occlusion of the affected blood vessels can lead to intestinal ulcers, infarction, or perforation. Sometimes, the clinical symptoms closely resemble those of regional enteritis or nonspecific ulcerative colitis.

bubble_chart Auxiliary Examination

1. Scleroderma: X-ray examination reveals characteristic dilatation of the duodenum and proximal jejunum, sometimes involving the entire small intestine, with often thickened circular folds. The barium-filled intestinal lumen shows a spiculated margin.

2. Dermatomyositis: Microscopic examination shows multiple mucosal erosions, submucosal edema, muscular layer atrophy, and fibrosis accompanied by lymphocyte and plasma cell infiltration. Small arteries and veins from the submucosal to the serosal layer exhibit intimal thickening, prone to thrombosis and luminal occlusion.

3. Polyarteritis nodosa: X-ray examination demonstrates small intestinal mucosal irregularities, ulcers, polypoid hyperplasia, segmental stenosis, etc., closely resembling the radiographic manifestations of regional enteritis or nonspecific ulcerative colitis.

bubble_chart Treatment Measures

1. In 57% of patients with scleroderma, the small intestine is affected. Among those with small intestine involvement, 50% experience malabsorption syndrome and steatorrhea. This occurs due to intestinal dilation and stasis, leading to excessive bacterial proliferation, which decomposes bile salts and reduces conjugated bile salts, thereby affecting micelle formation and fat absorption. Bacteria also hinder the absorption of vitamin B₁₂ by binding to its intrinsic factor complex. The use of antibiotics to suppress intra-abdominal bacterial overgrowth can restore characteristic fecal fat and vitamin B₁₂ malabsorption to normal within a few days.

2. Systemic lupus erythematosus: Drug therapy primarily involves adrenal corticosteroids and azathioprine. Surgical intervention is required as early as possible for complications such as intestinal perforation.

3. Polyarteritis nodosa: Prednisone can alleviate gastrointestinal symptoms. If there is no significant intestinal bleeding, anticoagulants may be added. For cases of massive intestinal bleeding or perforation, surgical treatment should be performed as soon as possible.