Systemic vasculitis is generally believed to be an immune complex deposition in blood vessels. Gastrointestinal com­plications of vasculitis have been described as pain, diarrhea, rectal bleeding and abnormal liver enzymes. Taken in isolation, the symptoms are difficult to distinguish from in­flammatory bowel disease, infectious colitis or ischemic coli­tis, although gastrointestinal vasculitis rarely presents without other clinical evidence of systemic vasculitis. Histo- logical proof is difficult to obtain because biopsies from the gastrointestinal tract usually show only nonspecific inflam­mation and ulceration. Camilleri and Pusey suggested that this may be because endoscopic biopsies are too superfi­cial and proposed that endoscopic examination was the best method to determine extent of disease. Diagnosis is often made clinically from the involvement of other organ systems because biopsies frequently show no evidence of a specific vasculitis. Therapy is aimed at treating the systemic vasculi- tis with immunosuppressive medications and with surgical intervention in the event of gastrointestinal complications such as hemorrhage or perforation.

Vasculitic involvement of the gastrointestinal tract is more common in polyarteritis nodosa and microscopic polyarteritis (50% to 70%) and Chrug-Strauss syndrome (20%) than in Wegener’s granulomatosis. Walton published autopsy studies of patients with Wegener’s granu- lomatosis and found gastrointestinal involvement in 24%, although none of these patients had symptoms referable to the gastrointestinal tract. Two large groups of patients with We- gener’s granulomatosis have been followed for over 20 years, and neither study describes gastrointestinal complica­tions throughout the course of the disease. Case reports of gastrointestinal involvement in Wegener’s granulomatosis have described cases of enterocolitis, gastrointestinal hemor­rhage, intestinal perforation and recurrent pancreatitis.

Enterocolitis has presented as bloody diarrhea and ab­dominal pain, with endoscopic evaluation revealing superfi­cial ulcerations in both the small and large intestines. The differentiation between inflammatory bowel disease rested on biopsy evidence as well as extraintestinal sympto­matology. Several reports have been made of gastrointestinal hemorrhage due to ulcers in the ileum, jejunum and colon, as well as perforations of the small and large bowel. Questions have been raised as to whether immuno­suppressive medications may exacerbate ulcerations, although further improvement despite continuation of immunosuppressive therapy argues against this theory.

Esophageal involvement in Wegener’s granulomatosis has rarely been reported. In an autopsy series of 29 cases, Fa- hey et al found one patient with asymptomatic esophag- eal arteritis. Symptomatic vasculitic ulcerations of the esophagus associated with Wegener’s granulomatosis have been reported in one case of upper gastrointestinal hemor­rhage and in a second case resulting in severe odynophagia. These two cases of esophageal involve­ment of Wegener’s granulomatosis, in addition to our case, are noteworthy to gastroenterologists and rheumatologists. Esophageal symptoms in patients with Wegener’s granulo- matosis are frequently attributed to reflux esophagitis or in­fections due to immunosuppressive medications. The presence of esophageal symptoms in the context of a sys­temic vasculitis should alert the clinician to the possibility of active disease as an etiology and prompt further evaluation before initiation of antireflux or antifungal agents.
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