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Diagnostic dilemma: drug-induced vasculitis versus systemic vasculitis
  1. Indira Acharya1,
  2. David S Weisman1,
  3. Lanaya Williams Smith2,
  4. Lois Johanna Arend3
  1. 1Department of Internal Medicine, MedStar Union Memorial Hospital, Baltimore, Maryland, USA
  2. 2Department of Internal Medicine, MedStar Good Samaritan Hospital, Baltimore, Maryland, USA
  3. 3Department of Pathology, Johns Hopkins University, Baltimore, Maryland, USA
  1. Correspondence to Dr David S Weisman; david.s.weisman{at}medstar.net

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In conjunction with BMJ Case Reports, DTB will feature occasional drug-related cases that are likely to be of interest to readers. These will include cases that involve recently marketed drugs for which there is limited knowledge of adverse effects and cases that highlight unusual reactions to drugs that have been marketed for several years.

Summary

Drug-induced vasculitis can rarely cause inflammation and necrosis of blood vessel walls of both kidney and lung tissue. Diagnosis is challenging because of the lack of difference between systemic and drug-induced vasculitis in clinical presentation, immunological workup and pathological findings. Tissue biopsy guides diagnosis and treatment. Pathological findings must be correlated with clinical information to arrive at a presumed diagnosis of drug-induced vasculitis. We present a patient with hydralazine-induced antineutrophil cytoplasmic antibodies-positive vasculitis with a pulmonary-renal syndrome manifesting as pauci-immune glomerulonephritis and alveolar haemorrhage.

BACKGROUND

Vasculitis is defined as the presence of inflammation in a blood vessel wall. The subsequent reactive damage to mural structures leads to loss of vessel integrity, bleeding and compromise of the lumen. Incidence of antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis is 33.0 per million in the USA,1 but there are no clear data on the prevalence of drug-induced or hydralazine-induced vasculitis.

Drug-induced vasculitis (DIV) is related to exposure to a particular drug with rapid resolution of symptoms on discontinuation of the offending agent.1 It has variable clinical features including fever, arthritis and serositis with involvement of the pleura and/or pericardium.1 It occurs as small-vessel vasculitis (cutaneous leucocytoclastic vasculitis, IgA vasculitis, ANCA vasculitis), medium-vessel vasculitis and large-vessel vasculitis.2

Hydralazine most commonly causes ANCA vasculitis, resulting in pauci-immune glomerulonephritis.3 Simultaneous lung involvement is strikingly rare.4 5 We present a patient who developed pauci-immune glomerulonephritis accompanied by alveolar haemorrhage in the context of chronic use of hydralazine.

Case presentation

A woman in …

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Footnotes

  • Contributors IA: care of patient, collection of patient data for case report, writing of original manuscript, approval of final manuscript. DW: supervision of patient care, care of patient, supervision of writing, critical review of manuscript and approval of final manuscript. LWS: rheumatology clinician advised on case and approved final manuscript. LJA: clinical pathologist supplied the images, reviewed manuscript, approved final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.