Although treatment with immunosuppressive regimens can prevent or minimize the need for BMT, acute GVHD remains a significant complication that may prove fatal in most patients. There is an urgent clinical need for therapies that minimize GVHD while preserving BMT availability for GVHD prophylaxis and/or therapy.
GvHD is a common and often severe manifestation of post-thymus transplant infection. GvHD, which typically strikes children 3 to 6 weeks after transplant with a high incidence over time, is a clinical entity that affects both immunologic and immunosuppressive therapy. It is often triggered by an antigen-presenting cell (APC) triggering T-cell activation. In contrast, the immunosuppressive drugs used to prevent GvHD have been shown to alter the number and functions of GVHD APCs. Understanding the APC and T-cell activation is therefore important to understand any future drug development for GvHD and is the focus of much current research.
The signs and symptoms of GvHD frequently overlap with acute graft rejection, but they are not exactly the same. Symptoms vary according to the organ being affected. GvHD symptoms can be classified as systemic or localised symptoms.\n
Treatment is highly individualised based on the characteristics of both the graft donor and the recipient. These include the underlying condition of each patient, their physical abilities and their preferences. The mainstay of treatment is supportive treatment including measures to reduce the severity of symptoms. Potential transplant-related immunosuppressive drugs, such as azathioprine or mycophenolate mofetil, are used to prevent organ rejection after the transplant..
This article presents how many people have graft vs host disease and what conditions may be associated with an increased risk of developing this condition.
GvHD affects > 10,000 patients annually in the U.S. alone. In most patients, it is of the B cell or T cell-dependent, and therefore graft specific. In other cases, it is not graft directed. The immune system's T cell-mediated response is critical, because it enables the immune system to discriminate between host and foreign materials. Immune system abnormalities are the most important variables in determining what type of GVHD develops.
T-guard significantly reduced the occurrence and severity of acute graft-versus-host disease when compared with a placebo. In addition, T-guard significantly increased the probability of grafting-versus-host disease resolution. ClinicalTrials.gov number: NCT00505845.
Despite their use in the past, the T-guard has low compliance in clinical circumstances. In recent years, many new indications were developed to extend the indications for T-guard, which showed a positive impact on the use of the device. However, no single new indication has changed the use of T-guard in patients with hematopoietic stem cell transplantation.
There has been no breakthrough discovery for treating GvHD. Despite this, there have been some recent advances and some hope for future treatments.\n...this chapter contains an update of treatments for GvHD and recommendations for when to start treatment. There are several treatments in the pipeline that are being tested such as [bortezomib, donor specific transfusions, and rituximab]. None of these therapies have been proven to be effective. Many more projects are being done for GvHD. It is likely that many treatments will be [developed], but the lack of progress to date suggests that more research may be needed before improvements in treatment can be achieved.
T-guard does not provide any clinical benefit when used during the first post-transplant week. However, in patients who receive a heart transplant from grafts who have not received t-GVHD prophylactic treatment, T-guard may significantly reduce the risk of developing t-GVHD, particularly acute t-GVHD. This is particularly important given that tnT-pro-B cytokines are thought to be important mediators of the development of t-GVHD in graft recipients without a matching donor, and because an earlier start of T-cell immunosuppression post transplant may also decrease the risk of development of t-GVHD.
T-Guard is a form of skin graft made up of a blend of silicone and liquid silicone. The silicone, unlike most other silicone-based products, is non-allergic. T-Guard is routinely used in skin transplantation today both in USA and in Europe, although it is still technically a “semisolid silicone” product (i.e., it contains some liquids), and therefore has not been allowed in all countries as a “medical grade silicone”.
Graft vs host disease has many causes. A significant share of these causes can be controlled by the GVHD prevention measures for the transplanted organ. To prevent and control these causes, clinicians should be aware of the relevant measures.