connective tissue enteritis



OVERVIEW

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

Etiology

The etiology of the disease is multifactorial and its onset is associated with immune dysregulation.

Symptoms

1. Scleroderma

Patients may have clinical manifestations of intestinal dysfunction such as abdominal discomfort, bloating, postprandial rumbling, loss of appetite, nausea, vomiting, and intermittent diarrhea and constipation alternately.

2. Dermatomyositis

The small intestine has different degrees of dilatation and segmentation changes, accompanied by low power and prolonged passage time, and edema and thickening of the intestinal wall can be seen by the naked eye.

3. Gastrointestinal symptoms

Intestinal damage in SLE is mainly the result of vasculitis. Common gastrointestinal symptoms include abdominal pain, loss of appetite, nausea, vomiting, rare diarrhea, black stools, and occasionally intestinal obstruction. A few patients have choriocapillaris atrophy, accompanied by small intestinal absorption without protein loss enteropathy, restrictive enterocolitis, non-specific ulcerative colitis, acute appendicitis and so on.

4. Nodular polyarteritis

Intestinal symptoms are very common, abdominal pain, nausea, vomiting or diarrhea when the intestines are locally ischemic. Occlusion of the lesion vessels may cause intestinal ulcer, infarction and perforation. Sometimes the clinical symptoms resemble limited enteritis or non-specific ulcerative colitis.

Examination

1. Scleroderma

X-ray examination of duodenum and proximal jejunum dilatation is characteristic, sometimes the whole small intestine dilatation, ring folds tend to thicken, barium-filled intestinal lumen edge is burr-like.

2. Dermatomyositis

Microscopic examination shows multiple mucosal erosion, submucosal edema, muscle layer atrophy and fibrosis with lymphocyte and plasma cell infiltration, intestinal submucosal layer to the plasma layer of small arteries, small veins, thickening of the intima-media is prone to thrombosis and lumen occlusion.

3.Nodular polyarteritis

X-ray examination shows small intestinal mucosal disorder, ulceration, polypoid hyperplasia, segmental stenosis, etc., which is also similar to the X-ray manifestation of restrictive enteritis or non-specific ulcerative colitis.

Diagnosis

The diagnosis can be confirmed on the basis of clinical manifestations and laboratory tests.

Differential diagnosis

Bacterial dysentery, viral enteritis, cholera, intestinal amebiasis, etc. are the main differentiators.

Treatment

1. Scleroderma patients

Most of them have small bowel involvement with malabsorption syndrome and steatorrhea. This is due to the dilatation and stagnation of the intestinal lumen, leading to the proliferation of bacterial flora, which breaks down the bile salts and reduces the binding of bile salts, thus affecting the formation of microglomerates and the absorption of fats, and the bacteria block the latter through the binding of the factor complexes within vitamin B12. Application of antibiotics to inhibit intra-abdominal bacterial colonization normalizes the characteristic impaired absorption of fecal fat and vitamin B12 within a few days.

2. Systemic lupus erythematosus

Pharmacologic treatment is based on adrenocorticotropic hormone and azathioprine. Complications such as intestinal perforation require early surgical treatment.

3.Nodular polyarteritis

Prednisone can reduce gastrointestinal symptoms. If there is no obvious intestinal bleeding, anticoagulant can be added, and those with intestinal hemorrhage or perforation should be operated as soon as possible.