is a patent holder (EP0752884) with the European Patent Office. Adverse events occurred at similar rates in all treatment groups. CONCLUSIONS Ingested hrIFN- was safe at the doses used. Patients in the 5,000-unit hrIFN- treatment group maintained more -cell function 1 year after study enrollment than individuals in the placebo group, whereas this effect was not observed in patients who received 30,000 units hrIFN-. Further studies of low-dose ingested hrIFN- in new-onset type 1 diabetes are needed to confirm this effect. Residual -cell function was shown to correlate with decreased complication rates in the Diabetes Control and Complications Trial (1). As a result, preservation of -cell function is an important treatment goal in patients with type 1 diabetes. Over the past 25 years, multiple clinical trials attempted to prevent progressive -cell destruction after the diagnosis of type 1 diabetes using immunosuppressive or immunomodulatory agents such as cyclosporin (2,3), cyclosporin in combination with bromocriptine (4), azathioprine with or without glucocorticoids (5,6), nicotinamide with or without glucocorticoids (7,8), and parenteral interferon- (IFN-) (9). More recent intervention trials used monoclonal antibodyCbased therapies such as rituximab (anti-CD-20) (clinical trial reg. no. NCT00279205), daclizumab (anti-CD25) in combination with mycophenolate mofetil (clinical trial reg. no. “type”:”clinical-trial”,”attrs”:”text”:”NCT00100178″,”term_id”:”NCT00100178″NCT00100178), anti-CD3 (10C12), and GAD (13). Although several studies are still ongoing and thus the results p85 are pending, trials of anti-CD3 antibodies and GAD have demonstrated delayed decline of endogenous insulin secretion. However, none of these intervention trials have yet been translated into common clinical practice for two reasons: 0.05. Data processing and statistical evaluations were completed using SAS (version 9.1, SAS Institute, Cary, NC). RESULTS Of 128 subjects enrolled in the study, 107 received at least one dose of study drug, and 93 completed the follow-up (Fig. 1). Five patients who completed the study were Firategrast (SB 683699) excluded from the final analysis because they changed study centers (and thus C-peptide assays) during the study period. Thus, a total of 88 subjects generated data for the final analysis. Open in a separate window Figure 1 Patient flow diagram. ANA, anti-nuclear antibodies. Baseline characteristics of subjects included in the final analysis are shown in Table Firategrast (SB 683699) 1. Sensitivity analyses showed no significant differences between baseline characteristics of noncompleters and completers. Table 1 Baseline Firategrast (SB 683699) patient characteristics of 88 patients included in the final analysis (%). values are based on Pearson’s 2 test, Fisher’s exact test, Kruskal-Wallis test, Firategrast (SB 683699) or ANOVA as appropriate. Safety Three serious adverse events (SAEs) occurred during the study. An 18-year-old male patient developed septicemia during his 9th month of treatment with 30,000 units hrIFN-. His subsequent clinical course was complicated by multiple peripheral Firategrast (SB 683699) emboli, and he required prolonged hospitalization. The patient recovered fully but hrIFN- was discontinued. One placebo-treated patient developed medulloblastoma, and another placebo-treated patient developed gastroenteritis resulting in diabetic ketoacidosis requiring hospitalization. All SAEs and adverse events were reviewed by the data safety and monitoring board, and no SAE was considered to be related to therapy. There was no difference in the occurrence of adverse events among the three treatment groups. During the study, subjects had means SD of 2.1 2.4, 1.6 2.0, and 2.1 2.1 adverse events each in the placebo, 5,000-unit hrIFN-, and 30,000-unit hrIFN- groups, respectively. Other than the SAEs, all adverse events were rated as mild to moderate (grades 1 or 2 2). A summary of adverse.