Zolimomab aritox

Mycobacterium tuberculosis can cause significant infections in liver transplant candidates and recipients. Its nonspecific clinical features and prolonged growth time in culture make the diagnosis difficult, and treating tuberculosis (TB) remains challenging because of significant toxicities and drug-drug interactions. The diagnosis of a latent TB infection may be accomplished with tuberculin skin testing and with the newer interferon-γ release assays, although this infection may be underrecognized because of host factors. Latent TB should be treated, but the degree of liver failure and the likelihood of progression to active TB will dictate whether this should occur before or after transplantation. Patients who have a history of TB, have used muromonab-CD3 or anti-T lymphocyte antibodies, or have experienced allograft rejection or coinfection with cytomegalovirus, Pneumocystisjiroveci, or Nocardia are at the greatest risk of developing active TB. Active TB in transplant patients is difficult to treat because of drug-induced hepatotoxicity and the significant interaction between rifampin and calcineurin inhibitors. In this article, we review the epidemiology, clinical features, and evaluation of transplant candidates and recipients. In addition, we offer recommendations on the appropriate diagnostic and treatment regimens for patients with latent and active TB infections. Liver Transpl 16:1129–1135, 2010. © 2010 AASLD.

Muromonab-CD3 is a murine monoclonal antibody (MoAb) that is used in the prophylaxis and treatment of acute graft rejection. Activation of coagulation and fibrinolysis following anti-CD3 administration have been reported in some patients to lead to irreversible intragraft thrombosis.

We have studied the effect of muromonab-CD3 infusion on platelets using flow cytometry in six patients who received three daily doses of muromonab-CD3 as prophylaxis of rejection before receiving a living donor renal transplant. Samples were collected before, 15 and 60 min after muromonab-CD3 infusion. Immunolabeling of platelets was performed in whole blood using dual-color analysis. The following conjugated MoAb were used: anti-CD41a, -CD36, -CD42b, -CD62P, -CD63, -factor V/Va and nonspecific Ig. Samples were analyzed with a FACScan flow cytometer (Becton Dickinson, Mountain View, CA, USA).

After muromonab-CD3 infusion, an increase in the binding of MoAb anti-factor V/Va to platelets was seen, which was only statistically significant (2.2% vs. 12.8%, P=.04) after 15 min of the second dose. No significant changes were seen in the other MoAbs studied. No thrombotic complications were observed after transplantation.

In uremic patients receiving muromonab-CD3 infusion as prophylaxis of graft rejection, an increase in the binding of anti-factor V/Va, denoting an increased exposure of anionic phospholipids in platelets, was seen. This increase in platelet procoagulant activity might contribute to the appearance of thromboses within renal graft seen in some patients who received muromonab-CD3.