bean town babes beats u penn murderers

the proper methodology for treating pdoriasis is to increase the level of tnf alpha and not decrease it. see faustman''s work  pubmed.org faustman me hanism tnf


what has faustman patented or published about castleman disease?

increase the levels of tnf alpha and save lives?


relax the iranians and north koreans will soon be here with the launch of a cobalt jsvked nuke into the jet stream,

you don't need a weatherman to tell you whivh way the eind blows death


walk el chapo and  distribute morphine producing yeast


the end of life will soon be here when the iranians and north koreans fire cobslt jacked nukes at you


 

Diagnosis of Castleman disease in a patient treated with prolonged anti-TNF biologic therapy for psoriasis and psoriatic arthritis

DOI: http://dx.doi.org/10.1016/j.jaad.2015.02.648

Article Infoclick to collapse contents 

© 2015 Published by Elsevier Inc. 

We present the case of a 50-year-old man with severe chronic plaque psoriasis and psoriatic arthritis treated with anti-TNF biologic therapy for 5 years. He received infliximab infusions 8 weekly from 2008 to 2012, and was switched to adalimumab due to secondary treatment failure in January 2013. He presented in January 2014 with anorexia, unintentional weight loss, and lymphadenopathy. This was followed by an episode of acute illness comprising spiking fevers, malaise, and joint symptoms, with raised inflammatory markers, neutrophilia, and a negative septic screen. Adalimumab was stopped while he underwent further investigations. Serum electrophoresis showed polyclonal increase in the gamma region. Serum kappa and lambda light chain levels were elevated, with preservation of a normal ratio, suggestive of a polyclonal increase in immunoglobulins. Elispot was negative. CT scan of the chest, abdomen and pelvis showed generalised lymphadenopathy in the mediastinum, abdomen and pelvis, concerning for lymphoma. Histologic examination of an inguinal lymph node demonstrated atretic follicles with hyalinized germinal centers, stromal hyalinisation and an increased number of plasma cells, which appeared polytypic. Immunohistochemistry demonstrated strongly positive kappa, lambda and CD138 stains. Immunohistochemical staining for EBV and HHV8 was negative. The clinicohistopathologic features were in keeping with a diagnosis of multicentric plasma cell variant of Castleman disease (CD). CD is a nonclonal lymphoproliferative disorder, characterized by follicular hyperplasia of lymph nodes. Multicentric CD usually presents with lymphadenopathy, and there may be hepatosplenomegaly. Multicentric plasma cell type CD is frequently associated with systemic symptoms, as in our patient, and may progress to non-Hodgkin lymphoma. The pathogenesis is not fully understood. In some patients, it is virally driven, for example by HHV8, which is well recognized in HIV-positive patients. In our patient, the etiology of CD is uncertain. Although lymphomas arising in the setting of anti-TNF biologic therapy have been reported, to the best of our knowledge, this is the first reported case of CD arising following anti-TNF biologic therapy. Although there was no evidence of viral reactivation, we wonder whether the emergence of CD may be linked to his prolonged anti-TNF biologic therapy.