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We report a 20-year-old woman with Crohn's disease (CD) who developed anterior neck pain while being treated with the anti-tumor necrosis factor (TNF)-alpha monoclonal antibody, infliximab. She showed no symptoms suggestive of active CD except for tenderness along the left common carotid artery with marked increases in serum TNF-alpha and inflammatory reactions. Based on thickened walls of large vessels with enhancement effects on computed tomography, she was diagnosed as having associated Takayasu's arteritis (TA), which was successfully treated with corticosteroid. Even if CD is controlled by infliximab, other autoimmune disorders, such as TA, may develop as a complication.

We report a patient with stiff-person syndrome and insulin-dependent diabetes mellitus with anti-glutamic acid decarboxylase (GAD) antibody, who suddenly complained of diplopia due to dysthyroid ophthalmopathy. Therapeutic efficacy of plasmapheresis and high-dose intravenous immunoglobulin was transient. After starting administration of rituximab, the patient showed obvious improvement of muscle spasms due to stiff-person syndrome and ophthalmoplegia following quick depletion of CD20-positive cells in peripheral blood. The anti-GAD and anti-thyroid antibodies decreased slowly. This drug might be a potent therapeutic option for refractory patients with stiff-person syndrome, particularly in those associated with dysthyroid ophthalmopathy.

We report a patient with rheumatoid arthritis (RA) who developed cytomegalovirus (CMV)-induced infectious mononucleosis-like syndrome (IMLS) while being treated with methotrexate and infliximab. She suddenly developed intermittent high fever and general fatigue with liver dysfunction, remarkable lymphocytosis and laboratory data suggestive of CMV reactivation. Her clinical symptoms quickly improved after the cessation of methotrexate and infliximab without the use of anti-viral drugs such as ganciclovir. CMV-induced IMLS might be a cause of persistent fever in RA patients, particularly when biologics are used for treatment.

Objective: Tristetraprolin (TTP), T cell intracellular antigen 1 (TIA-1), and Hu antigen R (HuR) are adenine/uridine-rich element binding proteins (ABPs) that affect the production of tumor necrosis factor alpha (TNFalpha) by binding to TNF messenger RNA (mRNA). TTP promotes deadenylation, TIA-1 inhibits translation, and HuR stabilizes TNFalpha mRNA. The aims of this study were to understand the posttranscriptional control of TNFalpha production in patients with rheumatoid arthritis (RA), and to identify parameters that may predict the efficacy of anti-TNFalpha therapy., Methods: Peripheral blood mononuclear cells from 38 patients with RA were obtained before therapy and 2 weeks and 54 weeks after administration of the first dose of infliximab, and from 20 healthy control subjects. TNFalpha, TTP, TIA-1, and HuR gene expression levels were analyzed by real-time polymerase chain reaction., Results: At baseline, TTP and HuR gene expression levels, as well as the TTP:TNFalpha, TTP:HuR, and TIA-1:TNFalpha gene expression ratios were lower in patients with RA than in control subjects, while expression of TNFalpha, TIA-1, and TIA-1:HuR was higher in patients with RA. The TTP:HuR expression ratio decreased significantly after administration of infliximab. Positive correlations were observed between TNFalpha and TTP, TNFalpha and TIA-1, TIA-1 and HuR, and TNFalpha and HuR gene expression in both healthy control subjects and patients with RA. At baseline, the TIA-1:HuR ratio tended to be higher in patients who achieved 50% improvement according to the American College of Rheumatology criteria (ACR50) at week 54 than in those who did not achieve at least an ACR20 response., Conclusion: Differences in ABP gene expression may affect TNFalpha gene expression. A higher TIA-1:HuR expression ratio might correlate with the response to infliximab therapy.

We report a patient with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) who showed high titers of anti-sulfated glucuronyl paragloboside (SGPG) IgM antibody without M-protein in serum. The patient was resistant to corticosteroids and immunosuppressants, but after administration of rituximab, clinical symptoms improved and the patient remained in a stable state for approximately 10 months. Rituximab may be a potent therapeutic option for refractory cases of CIDP irrespective of detectable M-protein in either serum or urine.