Pityriasis rosea-like drug eruption due to bupropion: a case report.

Pityriasis rosea (PR) is a common, acute, and self-limited inflammatory skin disease. The typical clinical presentation includes the appearance of a primary "herald" patch followed within days to weeks by the onset of secondary scaly skin eruptions distributed along the skin tension line in most cases. Although PR is a well-known and relatively common disease, its cause is still not completely understood. However, viral agents, autoimmunity, psychogenic status, and numerous drugs have been proposed as possible factors to PR. Bupropion is known to cause hypersensitivity reactions. We present a clinical case of PR eruption caused by the use of bupropion. To the best of our knowledge, this is the first published case of PR associated with bupropion use.

The stromal gene encoding the CD274 antigen as a genetic modifier controlling survival of mice with γ-radiation-induced T-cell lymphoblastic lymphomas.

Using an inter-specific subcongenic strain, Nested Recombinant Haplotype 3 (NRH3), generated between two mouse strains showing extreme differences in γ-radiation-induced thymic lymphoma susceptibility (SEG/Pas and C57BL/6J), we have identified a critical region on chromosome 19 that regulates survival of mice suffering from T-cell lymphoblastic lymphomas. Mapped on this region, the gene encoding the Cd274 ligand is able to trigger an inhibitory effect that modulates T-cell receptor (TCR) signalling and affects thymocyte maturation. Interestingly, this gene shows differential expression between thymic stromal cells from both strains in early response to a single sublethal γ-ray dose, but is inhibited in T-cell lymphoblastic lymphomas. Furthermore, we have identified several polymorphisms in the complementary DNA sequence of this gene that affect the affinity for its Cd279 receptor and are able to induce a differential rate of thymocyte apoptosis. Taken together, our data are consistent with Cd274 acting as a genetic modifier that influences the survival of γ-radiation-induced T-cell lymphoma-bearing mice. The data similarly support the idea of a co-evolution of tumour cells and associated stromal cells to generate a favourable microenvironment for T-cell lymphoma growth.