Induction of TNF-alpha and proinflammatory secretory phospholipase A2 by intravenous administration of CAMPATH-1H in patients with rheumatoid arthritis

J Rheumatol. 1995 Oct;22(10):1816-9.


Objective: To test the effect of infusions of CAMPATH-1H on levels of proinflammatory secretory phospholipase A2 (sPLA2) and tumor necrosis factor alpha (TNF-alpha) in patients with rheumatoid arthritis (RA).

Methods: Two patients with RA were infused with CAMPATH-1H; extracellular nonpancreatic sPLA2 activity was tested using radiolabelled E. coli membrane phospholipid, and circulating TNF-alpha levels were tested by ultrasensitive immunoassay.

Results: Circulating TNF-alpha began to rise within the first 2 h after infusion, reaching > 1000-fold values compared to preinfusion levels. Circulating sPLA2 activity began to rise a few hours after the start of infusion and reached extremely high values in 12 h, concomitant with fever and hypotension. The activity of sPLA2 decreased to pretreatment values in 3-18 days after infusion.

Conclusion: The mechanism leading to the increase of TNF-alpha and hyperphospholipasemia A2 has not been elucidated. It is possible that CAMPATH-1H activates cells that synthesize and release TNF-alpha and sPLA2, and/or that it induces interleukin 2 release, which in turn activates TNF-alpha, with subsequent release of sPLA2.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Alemtuzumab
  • Antibodies, Monoclonal / pharmacology*
  • Antibodies, Monoclonal, Humanized
  • Antibodies, Neoplasm / pharmacology*
  • Arthritis, Rheumatoid / metabolism*
  • Enzyme Induction
  • Female
  • Fever / chemically induced
  • Humans
  • Hypotension / chemically induced
  • Inflammation Mediators / blood*
  • Injections, Intravenous
  • Phospholipases A / blood*
  • Phospholipases A / metabolism
  • Phospholipases A2
  • Tumor Necrosis Factor-alpha / metabolism*


  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antibodies, Neoplasm
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Alemtuzumab
  • Phospholipases A
  • Phospholipases A2