Infarction of the sigmoid colon secondary to giant cell arteritis

M. A. Trimble and M. A. Weisz

The University of Oklahoma, College of Medicine, Tulsa, OK 74135, USA

SIR, Giant cell arteritis has long been known, its classic features usually including headache, temporal tenderness, jaw claudication and visual disturbances. Although rare, several extra-cranial manifestations have been reported. A Medline review revealed only nine cases of giant cell arteritis presenting as bowel ischaemia or infarction. All of these cases involved the small bowel. We describe what we believe to be the first reported case of giant cell arteritis presenting as infarction of the large bowel.

The patient was an 87-yr-old white male who presented to the hospital with complaints of severe abdominal pain. Examination revealed non-tender temporal arteries bilaterally and an acute surgical abdomen. Initial complete blood count and the chemistry profile were normal except for a haemoglobin level of 12.0 g/dl (normal range 13.0–16.7 g/dl) and an HCO3 concentration of 21 mmol/l (normal range 24–32 mmol/l). Liver profile, amylase, lipase and urinalysis were all normal. The patient was taken for emergent exploratory laparotomy.

At surgery, the colon was markedly distended, and an ischaemic segment of the sigmoid colon was resected. Microscopic examination showed early infarction of the colon. Giant cell arteritis was noted throughout the sections of the associated mesocolon. Figure 1Go shows a section of a mesenteric artery with several histopathological features characteristic of giant cell arteritis. Subsequent laboratory investigations revealed a markedly elevated erythrocyte sedimentation rate (ESR) of 90 mm/h (normal range 0–19 mm/h). An antineutrophil antibody screen and hepatitis A, B and C panels were all within normal limits. Prednisone therapy was initiated, and the ESR had dropped to 19 mm/h 5 days later. The postoperative period was uneventful.



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FIG. 1. Mesenteric artery showing multiple aspects charac teristic of giant cell arteritis. The first aspect to notice is the marked luminal narrowing, which is a result of intimal fibroplasia (A). There is infiltration of the entire vessel wall thick ness by numerous lymphocytes, resulting in panarteritis. A characteristic multinucleated giant cell is present in the media of the vessel (B). Of note, there is no evidence of a thrombotic plaque indicative of atheromatous causes of intestinal infarction.

 
Giant cell arteritis, or temporal arteritis, is an inflammation of large and medium-sized arteries and typically affects the branches of the aortic arch. Giant cell arteritis can have numerous presentations resulting from the local arterial involvement as well as constitutional symptoms related to the systemic nature of the disease. Signs and symptoms of classic cranial arterial involvement include headache, scalp tenderness, jaw or tongue claudication, temporal artery tenderness and visual disturbances. Constitutional signs and symptoms include fever, weight loss, anorexia, myalgias, arthralgias, malaise and fatigue. The most characteristic laboratory abnormality associated with giant cell arteritis is a markedly elevated ESR.

Giant cell arteritis should be included in the differential diagnosis when any of the preceding signs or symptoms are present. Prompt treatment can halt the disease process and prevent many long-term sequelae, including blindness. In addition to the classic manifestations of giant cell arteritis, several extracranial manifestations have been reported in the literature. Rare manifestations of giant cell arteritis reported previously include myocardial infarction, aortic dissection, limb claudication, pericarditis, myocarditis, interstitial lung disease, renal disease, peripheral neuropathy, breast mass, obstructive jaundice, scalp or tongue necrosis, hearing loss, thyroid disease and small bowel infarction.

The patient reported in this paper presented with colonic infarction. While hypotension, atheromatous disease and incarceration are more common causes of bowel infarction, the microscopic picture was consistent with giant cell arteritis as the cause of the colonic infarction. The giant cell arteritis had progressed to complete obliteration of the vessels supplying the area of overlying infarcted sigmoid colon. The elevated ESR, although non-specific in a patient with recent ischaemic bowel and laparotomy, is consistent with giant cell arteritis.

Giant cell arteritis has long been known clinically; however, atypical manifestations of giant cell arteritis have been increasing in incidence and necessitate a histopathological examination for diagnosis. Disease of the mesenteric vessels presenting with clinical signs and symptoms of bowel ischaemia or infarction is an exceedingly rare manifestation of giant cell arteritis. Nine cases of giant cell arteritis presenting with small bowel ischaemia or infarction have been reported in the English medical literature [19]. The case we present is what we believe to be the first reported case of giant cell arteritis presenting as infarction of the colon.

Notes

Correspondence to: M. A. Trimble, 101 Fieldcrest Street, Apt 101, Ann Arbor, MI 48103, USA. Back

References

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Accepted 14 June 2001





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