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Acute Spontaneously Resolving Pulmonary Vasculitis: A Case Report

DOI: 10.1155/2012/706838

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Abstract:

This is the first description that we are aware of describing the spontaneous resolution of an acute pulmonary vasculitis, possibly secondary to microscopic polyangiitis. Haemoptysis is a common symptom for patients presenting to primary and tertiary referral centres, and pulmonary vasculitis is one of a variety of aetiologies that should always be considered. The pulmonary vasculitides are difficult diagnostic and management problems. They are encumbered by a relative paucity of level 1 evidence addressing their diagnosis, classification, and treatment. This is therefore an important paper to publish because it adds to the global breadth of experience with this important clinical condition. In July 2010 a 43-year-old female presented with a 24-hour history of 30?mL of frank haemoptysis. There were no symptoms suggestive of a respiratory infection. She worked as an office manager and had no relevant occupational or environmental exposures. She had ceased smoking ten years previously having accumulated a ten-pack-year history. She had hypertension treated with amlodipine and perimenstrual migraines. Both parents and her brother were alive without any significant medical diseases. On presentation peripheral arterial oxygen saturation was 85% on room air, respiratory rate was 24 per minute, blood pressure was 200/100, and temperature was 38.5°C. She remained afebrile thereafter. An ECG demonstrated sinus rhythm, 100 beats per minute. A chest X-ray demonstrated bilateral perihilar infiltrates. A CTPA confirmed diffuse bilateral alveolar infiltrates (Figure 1). No vascular filling defects were identified. Haemoglobin was 99?g/L (115–160). MCV (mean cell volume) was 67?fL (81–96), and the film was suggestive of iron deficiency. White cell count was mildly elevated at 137/nL (3.5–11). Other inflammatory markers were also mildly elevated. ESR (erythrocyte sedimentation rate) was 29?mm (<15). CRP (C-reactive protein) was 68.1?mgl/L (<8). Creatinine was 65?μmol/L (50–100). Urea was 48?μmol/L (2.7–7.8). Electrolytes were within normal limits. INR (international normalised ratio) was 1.1 (0·9–1.2). APTT (activated partial thromboplastin time) was 28 seconds (25–34). Testing for antiglomerular basement membrane, antiuclear cytoplasmic antibodies (cANCA and pANCA), antinuclear antibodies, and extractable nuclear antigens (ENA) were all negative. Rheumatoid factor was <10?IU/mL (<30). Several sputum samples were sent. No pathogens were identified on standard bacterial and mycobacterial cultures. There was no cytological evidence of malignancy. Urinalysis was normal.

References

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[3]  L. Guillevin, B. Durand-Gasselin, R. Cevallos et al., “Microscopic polyangiitis: clinical and laboratory findings in 85 patients,” Arthritis & Rheumatism, vol. 42, pp. 421–430, 1999.
[4]  P. J. Klemmer, W. Chalermskulrat, M. S. Reif, S. L. Hogan, D. C. Henke, and R. J. Falk, “Plasmapheresis therapy for diffuse alveolar haemorrhage in patients with small-vessel vasculitis,” American Journal of Kidney Diseases, vol. 42, no. 6, pp. 1149–1153, 2003.

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