Pneumocystis carinii Pneumonia Associated With Solid Ectopic Corticotropin-Producing Tumors-Reply
John W. Henson, MD
Neurology Service Molecular Neuro-oncology Laboratory Massachusetts General Hospital Fruit St Boston, MA 02114
Russell W. Walker, MD
Department of Neurology Memorial Sloan-Kettering Cancer Center 1275 York Ave New York, NY 10021
Diane E. Stover, MD
Pulmonary Division Memorial Sloan-Kettering Cancer Center 1275 York St New York, NY 10021
Anna O. S. Fels, MD
Department of Psychiatry New York Hospital-Cornell Medical Center 1300 York Ave New York, NY 10021
Jai K. JALAJ, MD
97 Main St, Suite A Fishkill, NY 12524
Arch Neurol. 1992;49(10):1012.
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In Reply.
—The occurrence of Pneumocystis carinii pneumonia (PCP) in patients with endogenous hypercortisolemia, as pointed out by McQuillen and Sugar, supports the hypothesis that our patients with brain tumors were predisposed to develop PCP because of glucocorticoid-induced alterations in their cellular immunity. Since our article was published, we have seen four additional cases of PCP in patients with brain tumor who were receiving high-dose steroid treatment. A second series of brain tumor patients with PCP is soon to be published.1
Another line of evidence implicating glucocorticoids in the abrogation of normal T-cell function is emerging from an understanding of their molecular pharmacology. Glucocorticoid receptors are ligand-binding transcription factors. Following steroid binding, they regulate transcription of specific cellular genes. The ability of dexamethasone to activate programmed T-cell death (apoptosis) is associated with transcriptional activation of TGF-β1 (a potent T-cell inhibitor),2 and suppression of interleukin 2 (T-cell growth factor)
. . . [Full Text PDF of this Article]
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