NDT Advance Access originally published online on August 3, 2006
Nephrology Dialysis Transplantation 2006 21(10):2993-2994; doi:10.1093/ndt/gfl152
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Anti-neutrophil cytoplasmic antibody (ANCA)-associated microscopic polyangiitis following a suppurative wound infection
Email: jasavige{at}unimelb.edu.auSir,
There is strong circumstantial evidence for the role of infections in the development of anti-neutrophil cytoplasmic antibody (ANCA) and ANCA-associated vasculitis. We describe here, a 74-year-old man who developed a wound infection after surgery for cancer and who was subsequently diagnosed with ANCA-associated microscopic polyangiitis.
The patient presented with 2 months of frequent bowel actions, bright blood per rectum and weight loss. Physical examination including digital rectal examination was normal but colonoscopy demonstrated a mass in the sigmoid colon. Urinalysis and serum creatinine (0.093 mmol/l and 10.5 mg/dl, respectively) were normal. The patient underwent surgery and a 6.5 x 8 cm mass occupying two-thirds of the bowel circumference was removed by anterior resection. Histology confirmed an adenocarcinoma of the sigmoid colon with full thickness penetration of the wall, but had spread no further (Duke's B).
One month after surgery, the patient began treatment with 5-fluorouracil. Within days of his second course, he developed pain in the abdominal wound and a purulent haemoserous discharge. A CT scan demonstrated a rectosigmoid abscess draining through the cutaneous fistula (Figure 1). A swab grew Escherichia coli, and the patient was treated with various antibiotics including ampicillin, gentamicin and metronidazole, as well as cefotaxime and ciprofloxacin. The amount of discharge lessened and the sinus closed over the following 6 weeks. The patient was not treated with further 5-fluorouracil.
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Four months after surgery, the patient was re-admitted with a painful knee, a temperature of 38.5°C and elevated C-reactive protein (123 mg/l, normal <10). Abdominal CT scan showed no collection nor metastases. However, his creatinine had deteriorated to 0.223 mmol/l (25.1 mg/dl), urinary phase contrast microscopy demonstrated >500 000 glomerular RBC/ml (normal <12 000/ml), and he had a perinuclear ANCA 3+ with strongly positive myeloperoxidase (MPO)-ANCA. A renal biopsy demonstrated a pauci-immune segmental proliferative necrotizing glomerulonephritis and the patient was treated with high dose prednisolone and cyclophosphamide. Six months after starting this treatment he was admitted to the hospital with a small bowel infarction and subsequently died.
The close temporal relationship in this patient suggests the infection had a precipitating and probably pathogenetic role in the development of the ANCA-associated microscopic polyangiitis. The association of infection, ANCA and vasculitis is well-recognized. Patients with Wegener's granulomatosis and microscopic polyangitiis often have preceding bacterial pulmonary infections [1,2], and those with nasal Staphylococcus aureus are more likely to relapse [3] unless they are treated [4]. In an experimental system, the immunization of rats with pasteurized sonicated proteins from E. coli and S. aureus resulted in circulating ANCA as well as a pauci-immune segmental necrotizing glomerulonephritis and mesenteric arteritis [5]. How infections produce ANCA is not clear but chronic suppurative infections comprise mainly neutrophils, and the injection of rats with apoptotic (but not non-apoptotic) neutrophils generate ANCA [6]. Furthermore, infections themselves result in the surface expression of proteinase 3 and myeloperoxidase, and ANCA binds to these and activates the neutrophils resulting in a damaged vascular endothelium [7].
ANCA sometimes occur with malignancy or after antibiotics, but the temporal relationship in this patient is inconsistent with these as pathogenetic factors. The presence of arteriolitis in the initial renal biopsy, and the demonstration of an ischaemic bowel without atherosclerosis or embolism are more consistent with an overlap syndrome with polyarteritis nodosa rather than the diagnosis of microscopic polyangiitis alone.
Conflict of interest statement. None declared.
Department of Medicine
(Austin Health/Northern Health)
University of Melbourne
The Northern Hospital, Epping VIC 3076
Australia
References
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- Pinching AJ, Lockwood CM, Pussell BA, Sweny P, Evans DJ, Peters DK. (1983) Wegener's granulomatosis: observations on 18 patients with severe renal disease. Q J Med 208:435–460.
- Stegeman CA, Cohen Tervaert JW, Sluiter WJ, Manson WL, de Jong PE, Kallenberg CGM. (1994) Association of chronic nasal carriage of Staphylococcus aureus and higher relapse rates in Wegener's granulomatosis. Ann Intern Med 120:12–17.
[Abstract/Free Full Text] - Stegeman CA, Cohen Tervaert JW, de Jong PE, Kallenberg CGM. (1996) Trimethoprim-sulphamethoxazole for the prevention of relapses of Wegener's granulomatosis. New Engl J Med 335:16–20.
[Abstract/Free Full Text] - Savige JA, Nassis L, Cooper T, Paspaliaris B, Martinello P, MacGregor D. (2002) Antineutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis after immunisation with bacterial proteins. Clin Exp Rheumatol 20:783–790.[Medline]
- Patry YC, Trewick DC, Gregoire M, et al. (2001) Rats injected with syngenic rat apoptotic neutrophils develop antineutrophil cytoplasmic antibodies. J Am Soc Nephrol 12:1764–1768.
[Abstract/Free Full Text] - Csernok E, Ernst M, Schmitt W, Bainton DF, Gross WL. (1994) Activated neutrophils express proteinase 3 on their plasma membrane in vitro and in vivo. Clin Exp Immunol 95:244–250.[Web of Science][Medline]
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