This article discusses how the newest smallpox vaccine has been approved for testing in patients with eczema or atopic dermatitis.
Between 1 and 6 percent of patients vaccinated with the original smallpox vaccine had eczema vaccinatum (EV), where the live virus vaccine actually caused a smallpox infection. The mortality rate for EV is 1%. This article explains why people with atopic dermatitis may have this response. The vaccine is administered via the lower epidermis, which has proven to have the best immune response. Individuals with atopic dermatitis have an altered epidermis that does not produce the same quantity of anti viral and anti bacterial proteins. Further, with the dermatitis, there is an exagerrated Th2 response, but Th1 cells are the primary cell-mediated immune cells. Basically, patients with atopic dermatitis could not safely be vaccinated with the original vaccine. In fact, exposure to someone who was vaccinated was enough to give some patients EV. Because over 50% of the population has eczema or comes in direct contact with someone who does, it is an important step for a vaccine to reduce the risk of EV.
Engler RJ, Kenner J, Leung DY. Smallpox vaccination: Risk considerations for patients with atopic dermatitis. J Allergy Clin Immunol. 2002 Sep;110(3):357-65.
Showing posts with label new medicines. Show all posts
Showing posts with label new medicines. Show all posts
Monday, October 15, 2007
Friday, October 5, 2007
New psoriasis drug in the news
The World Congress of Dermatology met this past week in Argentina, and this story made international news. It is about the new biologic drug used to treat psoriasis, Ustekinumab. I found this study detailing its mechanism of action
Reddy M, Davis C, Wong J, Marsters P, Pendley C, Prabhakar U. Modulation of CLA, IL-12R, CD40L, and IL-2Ralpha expression and inhibition of IL-12- and IL-23-induced cytokine secretion by CNTO 1275. Cell Immunol. 2007 May;247(1):1-11.
This drug works by targeting IL-12 and IL-23. Current medications such as Adalimumab (Humira), Etanercept (Enbrel), Efalizumab (Raptiva), and Infliximab (Remicade) work similarly by targeting other types of cell messangers. All but Efalizumab work by blocking TNF alpha, an inflammation-causing mediator. Efalizumab binds to CD11a and prevents T cell functioning. Because psoriasis is mediated by T cells, these biologic drugs can work. Further, IL-12 is one of the key mediators in T cell activation.
Part of the problem with the current biologics is that they are extremely expensive (which I'm sure Ustekinumab will be also), and they require weekly injections or infusions. This new drug promises to only require monthly self injections, which is far more convenient and less painful than the weekly administrations. It should also help reduce cost compared to a drug like remicade, which requires infusions at specialty pharmacies or a hospital.
Reddy M, Davis C, Wong J, Marsters P, Pendley C, Prabhakar U. Modulation of CLA, IL-12R, CD40L, and IL-2Ralpha expression and inhibition of IL-12- and IL-23-induced cytokine secretion by CNTO 1275. Cell Immunol. 2007 May;247(1):1-11.
This drug works by targeting IL-12 and IL-23. Current medications such as Adalimumab (Humira), Etanercept (Enbrel), Efalizumab (Raptiva), and Infliximab (Remicade) work similarly by targeting other types of cell messangers. All but Efalizumab work by blocking TNF alpha, an inflammation-causing mediator. Efalizumab binds to CD11a and prevents T cell functioning. Because psoriasis is mediated by T cells, these biologic drugs can work. Further, IL-12 is one of the key mediators in T cell activation.
Part of the problem with the current biologics is that they are extremely expensive (which I'm sure Ustekinumab will be also), and they require weekly injections or infusions. This new drug promises to only require monthly self injections, which is far more convenient and less painful than the weekly administrations. It should also help reduce cost compared to a drug like remicade, which requires infusions at specialty pharmacies or a hospital.
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