To the Editor:
We read with interest the report by Guo et al (July 2001) (1) of a patient with hepatitis B-related polyarteritis nodosa (PAN) complicated by pulmonary hemorrhage. Pulmonary involvement, which is rare in patients with PAN, seems to be more frequent in patients with hepatitis B-related PAN, and endothelial cell damage by immune complex deposition could play a role.
We provided care for a 37-year-old African-American man who had experienced recent infection with hepatitis B. He presented with mononeuritis multiplex, significant weight loss, and fever. A sural nerve biopsy showed necrotizing vasculitis involving medium-sized arteries. He was diagnosed with PAN and was treated with high-dose corticosteroids, lamivudine and plasmapheresis. In the course of treatment, the patient developed respiratory distress requiring mechanical ventilation. Chest radiographs showed bilateral patchy alveolar infiltrates, and his hemoglobin and hematocrit levels had dropped from 13.9 g/dL and 43% to 11 g/dL and 32%, respectively. There was no evidence of hemolysis or GI bleeding. Over the next few days, there was progression of alveolar infiltrates associated with a further drop in hemoglobin and hematocrit levels to 6.5 g/dL and 19%, respectively, which is suggestive of alveolar hemorrhage. After about 3 weeks of continued treatment with corticosteroids and plasmapheresis, the patient's condition clinically improved, with clearing of the infiltrates on the chest radiographs.
Pulmonary involvement, although rare in cases of PAN, can occur in the form of alveolar hemorrhage or diffuse alveolar damage and can often be fatal. (2,3) Hepatitis B surface antigen, the trigger for the immune complex disease, results in the activation of the complement cascade and, in turn, neutrophil activation, is thought to play an important pathogenic role. Anti-endothelial cell antibodies also have been shown to play a role in endothelial damage, though they lack disease specificity. Immunohistochemical studies in PAN patients have shown inflammatory infiltrates with macrophages and T lymphocytes. (4) Some patients respond to aggressive therapy with corticosteroids and plasmapheresis, supporting the notion that immune complex-induced endothelial cell damage may indeed play a role in its pathogenesis.
Correspondence to: Luis R. Espinoza, MD, Professor and Chief, Section of Rheumatology, LSU Health Sciences Center, 1542 Tulane Ave, New Orleans, LA 70112-2822.
REFERENCES
(1) Guo X, Gopalan R, Ugbarugba S, et al. Hepatitis B-related polyarteritis nodosa complicated by pulmonary hemorrhage. Chest 2001; 119:1608-1610
(2) Bocanegra TS, Espinoza LR, Vasey FB. Pulmonary hemorrhage in systemic necrotizing vasculitis associated with hepatitis B. Chest 1981; 80:102-103
(3) Nick J, Tuder R, May R, et al. Polyarteritis nodosa with pulmonary vasculitis. Am J Respir Crit Care Med 1996; 153:450-453
(4) Matsumoto T, Homma S, Okada M, et al. The lung in polyarteritis nodosa, a pathologic study of 10 cases. Hum Patrol 1993; 24:717-724
COPYRIGHT 2002 American College of Chest Physicians
COPYRIGHT 2003 Gale Group
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