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INTERFERON, BETA 1
LATEST LITERATURE
1: Multiple sclerosis (Houndmills, Basingstoke, England), 2009 Dec 7,
Neutralizing antibodies to 500 {micro}g interferon beta-1 b: 28-month results of the IDEAS extension trial.
[Abstract]The Interferon Dose Escalation Assessment of Safety extension trial monitored neutralizing antibodies to interferon beta-1b in patients who currently or had previously received the double dose (500 microg) for up to 28 months. Fifteen patients entered the extension trial; five patients were neutralizing antibody-positive at the start of the trial. The present study demonstrates that when neutralizing antibodies develop in patients receiving higher doses of interferon beta-1b they tend to persist for a prolonged period, although neutralizing antibody titers tend to decrease over time and some patients may revert to neutralizing antibody-negative status.
2: The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses, 2008 Dec, 40(6)
A prospective baseline versus on-treatment study assessing patient perceptions of using a smaller needle when injecting intramuscular interferon beta-1 a (Avonex).
[Abstract]This study assessed patient perceptions of using a smaller needle (1-inch, 25-gauge) to administer weekly intramuscular (IM) interferon beta-1 a (IFNbeta-1 a [Avonex]) injections. Patients received 1 IM IFNbeta-1 a injection at baseline using the standard needle (1.25-inch, 23-gauge), followed by 4 weekly injections using the smaller needle. The primary end points were change in self-reported visual analog scale scores for preinjection anxiety and postinjection pain, assessed at baseline and once weekly during the 4 weeks of therapy with the smaller needle. Secondary evaluations included assessment of patient perception of ease of use and fear of self-injection with 2 questionnaires, and changes in the number of injection-site reactions. Patients had a mean decrease of 25 +/- 31 mm (baseline mean, 46 mm; 4-week mean, 21 mm; p = .0002) in anxiety score and a mean decrease of 22 +/- 29 mm (baseline mean, 41 mm; 4-week mean, 19 mm; p = .0003) in pain score. Overall, patients thought the smaller needle was easier to use than the standard needle. Qualitative measurements suggested patients who self-injected IM IFNbeta-1 a experienced less fear when using the smaller needle. Preinjection preparation parameters decreased throughout the course of the treatment period. No patients experienced injection-site reactions with the smaller needle. Patients preferred using a smaller needle to administer their weekly IM IFNbeta-1 a injection.
3: Multiple sclerosis (Houndmills, Basingstoke, England), 2007 Apr, 13(3)
Prospective clinical and electrophysiological follow-up on a multiple sclerosis population treated with interferon beta-1 a: a pilot study.
[Abstract]OBJECTIVE: To analyse transcranial magnetic stimulation (TMS) variables in a prospective six-month follow-up pilot study on patients suffering from relapsing-remitting multiple sclerosis (RRMS), satisfying inclusion criteria for interferon (IFN) beta-1a treatment. BACKGROUND: So far, no predictive factors are available as to the course of RRMS treated with IFN beta-1 a. DESIGN/METHODS: Fifteen RRMS patients were studied before (month 0 (M0)) and after IFN beta-1a onset (M3, M6). The parameters analysed were motor functional score (mFS), Expanded Disability Status Scale (EDSS), and TMS variables - central motor conduction time (CMCT) and amplitude ratio (AR). RESULTS: Four of the six patients with no motor signs at inclusion, subsequently showed signs of pyramidal dysfunction. All had abnormal M0_TMS variables. The number of M0_TMS abnormalities per patient was greatest in the group that showed mFS worsening, and was significantly correlated with M6_EDSS. The M0_CMCT was significantly correlated with M6_EDSS. During follow-up, the number of patients with abnormal TMS variables decreased from 12/15 to 4/15, and the total number of abnormalities decreased from 33.3 to 16.7%. CONCLUSIONS: TMS variables might be predictive of disease progression. The improvement observed here in the TMS variables may reflect an improvement in MS patients undergoing IFN beta treatment.
4: Seminars in ophthalmology, 2007 Jan-Mar, 22(1)
Cotton wool spots associated with interferon beta-1 alpha therapy.
[Abstract]PURPOSE: To describe a case of cotton wool spots associated with interferon beta-1a treatment. METHODS: Observational case report. RESULTS: A 40-year-old man with a history of multiple sclerosis was on interferon beta-1a. He presented with cotton wool spots on fundus exam, which resolved and then recurred all while on therapy. Interferon was discontinued after the second episode and again the cotton wool spots resolved. Upon restarting the interferon, no further cotton wool spots have recurred. CONCLUSION: To our knowledge this represents only the third case of interferon beta-1a associated cotton wool patches and the first in the English-language ophthalmic literature. Unlike interferon alpha therapy, interferon beta 1-a retinopathy is presumed to be extremely rare and more common etiologies for cotton wool spots should be excluded in these patients. Given this limited number of cases versus the relatively frequent use of interferon beta-1a in the management of multiple sclerosis, no conclusions regarding causality or screening can be made but the issue probably deserves further study.
5: Journal of drugs in dermatology : JDD, 2006 Apr, 5(4)
Recurrent injection site reactions from interferon beta 1-b.
[Abstract]Recombinant human interferon beta-1b is an immune-modulatory drug used for a variety of conditions including multiple sclerosis (MS). Skin reactions to therapeutic use of injectable interferon beta-lb are relatively common, including injection site reactions and exacerbation of underlying skin disease. Injection site reactions are seen much more frequently in females. We discuss a case of prolonged susceptibility to injection site reaction with over a decade of use of interferon beta 1-b for MS. Given the prevalence of such reactions, the dermatologist should be aware of the phenomenon and that it frequently does not necessitate discontinuation of therapy.
6: Medicina cl¨ªnica, 2005 Feb 5, 124(4)
[Long-term effect of neutralizing antibodies to interferon beta-1 b in patients with multiple sclerosis]
[Abstract]BACKGROUND AND OBJECTIVE: Our goal was to evaluate the relation between the presence of neutralizing antibodies (NABs) to interferon beta-1b in multiple sclerosis (MS) patients and the clinical evolution in the following years. PATIENTS AND METHOD: As we previously reported, we tested NABs in 68 patients treated with interferon beta-1b after 2 years of treatment. We prospectively followed this cohort every three months for a minimum period of 6 years collecting data about relapses, disability, secondary effects and dropouts. RESULTS: During the 6 year follow-up period, the annualized relapse rate did not differ between patients with and patients without NABs. A sustained progression was observed in 33% of positive patients and in 38% of patients without NABs. No differences were found in the proportion of patients who reached an EDSS score of 6. Secondary effects were similar in both groups. CONCLUSIONS: Although our results do not vouch for a negative effect of the presence of NABs on the clinical evolution of MS patients treated with interferon beta, further longitudinal studies to clarify the real effect of the presence of NABs in these patients are still much needed.
7: Journal of neurology, 2003 Oct, 250(10)
Interferon-beta-1 b decreased matrix metalloproteinase-9 serum levels in primary progressive multiple sclerosis.
[Abstract]Recent reports have shown that matrix-metalloproteinases (MMPs) facilitate T-cell migration into the CNS and play a role in disruption of the blood-brain-barrier and myelin break-down. An increase of MMP-9 serum levels predicts disease activity in relapsing remitting multiple sclerosis (RRMS). Interferon-beta (IFN-beta), which is an established treatment for RRMS, inhibits T-cell migration in vitro in parallel with the downregulation of MMP expression. Only limited data are available for primary progressive multiple sclerosis (PPMS) which differs in demographic and immunological aspects as well as in MRI criteria from RRMS. In this study, 19 patients with laboratory-supported definite PPMS were treated with 8 x 10(6) IU IFN-beta1b (Betaferon) subcutaneously every other day. Serum was collected before treatment and on months 1, 2, 3, 6 and 9 during treatment. Levels of MMP-9 and of its natural inhibitor known as tissue-inhibitor of matrix-metalloproteinase-1 (TIMP-1) were quantified by ELISA. In addition MMP-2 serum levels were determined by zymography. 19 healthy volunteers served as controls. Before treatment serum levels of MMP-9 were elevated in patients with PPMS compared with controls, whereas there was no difference in TIMP-1 serum levels. During treatment with IFN- beta1b the concentration of MMP-9 in the serum of 18 out of 19 PPMS patients decreased,whereas serum levels of MMP-2 and TIMP-1 remained nearly unaffected. Our results demonstrate that the MMP-9 to TIMP-1 ratio in patients with PPMS is elevated in comparison with healthy controls. The suppression of MMP-9 by IFN-beta1b indicates that this drug is immunomodulatory active in PPMS patients. Further studies are necessary to test if IFN-beta exerts a beneficial effect in PPMS.
8: Multiple sclerosis (Houndmills, Basingstoke, England), 2001 Aug, 7(4)
Interferon beta-1 a and depression in relapsing-remitting multiple sclerosis: an analysis of depression data from the PRISMS clinical trial.
[Abstract]Depression is a suspected side effect of multiple sclerosis (MS) treatment with interferon beta-1a. However, this has not been confirmed by rigorous studies. Several psychological symptom rating scales were completed during the PRISMS clinical trial of subcutaneous interferon beta-1a (Rebif) for relapsing-remitting MS. We conducted an analysis of these data in order to determine whether symptom elevations were associated with treatment. The PRISMS clinical trial included 560 subjects from 22 centres in nine countries. There were two active treatment arms (44 mcg x 3 and 22 mcg x 3 subcutaneously three times per week) and a placebo group. Two hundred and sixty-seven of these subjects were enrolled at English speaking study centres, where psychiatric symptom ratings were obtained at baseline, 6, 12, 18 and 24 months using the Center for Epidemiological Studies Depression Rating Scale (CES-D), the General Health Questionnaire (GHQ) and the Beck Hopelessness Scale (BHS). After randomization, the groups completing these scales were similar in terms of age, gender, EDSS, duration of illness and employment status. Median CES-D scores in the high dose, low dose and placebo groups at baseline were also similar: 8.0, 7.0 and 8.0, respectively. After 6 months of treatment the median change in CES-D score was zero in all three groups. The proportion of subjects exceeding the traditional CES-D cut-point for clinically significant depression (> 15) after 6 months of treatment was strongly associated with pre-treatment depression (RR 2.9, 95% C.I.: 1.8-4.7), but not with treatment group (chi-square=1.64, d.f.=2, P=0.44). The results were comparable at 12, 18 and 24 months and when ratings from the other scales were evaluated. This analysis confirms that depression is common in persons with MS: the incidence of CES-D depression in the first 6 months of follow-up was 15.6%. However, no evidence of increased depressive symptomatology was observed in association with interferon beta-1a (Rebif).
9: Arquivos de neuro-psiquiatria, 2000 Jun, 58(2B)
[Interferon beta 1-a in multiple sclerosis: 1-year experience in 62 patients]
[Abstract]We report the results of a trial of interferon beta 1-a in 62 ambulatory patients with relapsing-remitting multiple sclerosis. Entry criteria included EDSS of 0 to 5.5 and at least two exacerbations in the previous 2 years. The patients received 3 million international units by subcutaneous injections three times a week. The end points were differences in exacerbation rate and treatment effect on disease progression. The annual exacerbation rate for patients that did not take the interferon beta 1-a was 1.32 and for the patients under medication 0.63. The EDSS score in patients that did not take the mediaction was 4.7 and 2.0 for the patients with interferon beta 1-a. Interferon beta 1-a was well tolerated and 85% of patients completed 1 year treatment.
10: Annales de dermatologie et de v¨¦n¨¦r¨¦ologie, 2000 Feb, 127(2)
[Subacute cutaneous lupus erythematosus and interferon beta-1 a]
[Abstract]We report the results of a trial of interferon beta 1-a in 62 ambulatory patients with relapsing-remitting multiple sclerosis. Entry criteria included EDSS of 0 to 5.5 and at least two exacerbations in the previous 2 years. The patients received 3 million international units by subcutaneous injections three times a week. The end points were differences in exacerbation rate and treatment effect on disease progression. The annual exacerbation rate for patients that did not take the interferon beta 1-a was 1.32 and for the patients under medication 0.63. The EDSS score in patients that did not take the mediaction was 4.7 and 2.0 for the patients with interferon beta 1-a. Interferon beta 1-a was well tolerated and 85% of patients completed 1 year treatment.
11: Perceptual and motor skills, 1998 Jun, 86(3 Pt 1)
Interferon beta 1-b in verbal memory functioning of patients with relapsing-remitting multiple sclerosis.
[Abstract]The effects of interferon Beta 1-b (Betaseron) on verbal memory functioning was examined in 167 patients with relapsing-remitting multiple sclerosis and 112 matched normal controls. Subjects were administered 10 verbal memory tests from the Memory Assessment Scales and the Verbal subtests from the Wechsler Adult Intelligence Scale. Analysis showed subjects treated with Betaseron (n = 73) did not perform significantly better on measures of verbal memory or verbal ability than subjects not receiving the drug (n = 94), although the mean performance of treated subjects was higher across all verbal memory tests. Both groups of patients performed significantly worse on verbal memory subtests measuring list acquisition, delayed list recall, delayed cued recall, and the immediate and delayed recall of names and faces than control subjects. Although patients had lower performance scores across all memory tests than the control subjects, their scores were not within the impaired range. These results do not permit a clear conclusion about the effects of Betaseron on verbal memory for any effect is probably obscured by the relatively preserved cognitive functioning of this outpatient sample.
12: Journal of neuroimmunology, 1998 Mar 1, 82(2)
Interferon-beta-1-b (IFN-B) decreases induced nitric oxide (NO) production by a human astrocytoma cell line.
[Abstract]Inducible nitric oxide synthase (iNOS) is expressed by astrocytes in demyelinating regions of multiple sclerosis (MS) brain plaques, suggesting that NO contributes to MS pathology. Since the immunosuppressive cytokine IFN-B ameliorates MS disease activity, it is of interest to assess the modulatory role of IFN-B on NO production. We studied the effects of IFN-B, as well as dexamethasone, IL-10, and transforming growth factor-beta (TGF-B), on cytokine-induced NO production by the human astrocytoma cell line, A172. L-NMMA and aminoguanidine, competitive inhibitors of iNOS suppressed NO production as measured by the NO byproduct, nitrite, as did IFN-B. Dexamethasone enhanced NO production, and IFN-B decreased the amount of the enhancement. Neither IL-10 nor TGF-B inhibited nitrite production. The therapeutic effect of IFN-B in MS may be partly due to suppression of pathogenic NO production.
13: Neurology, 1997 Aug, 49(2)
Treatment of multiple sclerosis with interferon beta-1 b.
[Abstract]Inducible nitric oxide synthase (iNOS) is expressed by astrocytes in demyelinating regions of multiple sclerosis (MS) brain plaques, suggesting that NO contributes to MS pathology. Since the immunosuppressive cytokine IFN-B ameliorates MS disease activity, it is of interest to assess the modulatory role of IFN-B on NO production. We studied the effects of IFN-B, as well as dexamethasone, IL-10, and transforming growth factor-beta (TGF-B), on cytokine-induced NO production by the human astrocytoma cell line, A172. L-NMMA and aminoguanidine, competitive inhibitors of iNOS suppressed NO production as measured by the NO byproduct, nitrite, as did IFN-B. Dexamethasone enhanced NO production, and IFN-B decreased the amount of the enhancement. Neither IL-10 nor TGF-B inhibited nitrite production. The therapeutic effect of IFN-B in MS may be partly due to suppression of pathogenic NO production.
14: American journal of veterinary research, 1994 Aug, 55(8)
Kinetics of inhibition of replication of vesicular stomatitis virus in blood mononuclear cells of horses after in vitro and in vivo treatment with recombinant equine interferon-beta 1.
[Abstract]Recombinant equine interferon-beta 1 (reqIFN-beta 1) induces an antiviral state in blood mononuclear cells (BMC) of horses. Maximal protection against replication of vesicular stomatitis virus is achieved 6 hours after treatment with IFN in vitro and in vivo. Duration of the protective effect depends on the dose of IFN in vitro and in vivo. Availability of reqIFN-beta 1 in cultures of BMC for up to 48 hours does not prolong the antiviral state. The protective effect on BMC after treatment with IFN has similar duration in vivo and in vitro. Monitoring of the effect of IFN in vivo is, thus, simplified because the antiviral state may be recorded by testing cells twice (ie, before and 6 hours after application of interferon). All further tests may be performed in vitro. Multiple administration of reqIFN-beta 1 do not prolong duration of the protective phases after each administration. Duration of the antiviral state depends only on the dose of reqIFN-beta 1.
15: Journal of interferon research, 1990 Jun, 10(3)
Recombinant equine interferon-beta 1: purification and preliminary characterization.
[Abstract]Equine interferon-beta 1 (EqIFN-beta 1) was purified from extracts of recombinant Escherichia coli by sequential chromatography on hydroxylapatite, anion-, and cation-exchangers. The resulting protein was greater than 98% pure as determined by sodium dodecylsulfate gel electrophoresis, gel permeation HPLC, and reverse-phase HPLC. Amino-terminal amino acid sequencing revealed that essentially all molecules contained an additional amino-terminal methionine. The specific antiviral activity of EqIFN-beta 1 determined on equine dermal fibroblasts challenged with vesicular stomatitis virus (VSV) was approximately 5 X 10(8) U/mg. Less than 0.001% of this activity was observed in antiviral assays using human (A549), murine (L-M), ovine (SCP), or bovine (MDBK and BT) cells challenged with VSV or encephalomyocarditis virus. A series of monoclonal murine IgG antibodies were developed which neutralize the antiviral activity of EqIFN-beta 1. None of these antibodies nor rabbit antiserum to EqIFN-beta 1 were able to neutralize human IFN-beta; antiserum to human IFN-beta did not neutralize EqIFN-beta 1. Two of the monoclonal antibodies were used to establish a rapid one-step solid-phase enzyme immunoassay for EqIFN-beta 1.
16: Cancer research, 1991 Mar 15, 51(6)
Chromosome 9 deletion mapping reveals interferon alpha and interferon beta-1 gene deletions in human glial tumors.
[Abstract]We have applied restriction fragment length polymorphism analysis to a 30-member panel of primary glioma DNAs, which had been previously examined for loss of genetic information (C. D. James, E. Carlbom, J. P. Dumanski, M. Hansen, M. Nordenskjold, V. P. Collins, and W. K. Cavenee, Cancer Res., 48:5546-5551, 1988), to determine the frequency and sublocalization of loss of genetic information from chromosome 9. We have also utilized scanning densitometry for dosage determination of the 9p-localized interferon alpha and interferon beta-1 genes among these same tumors. Our results reveal the following: (a) for those cases in which loss has occurred, the region of common loss lies on the short (p) arm of the chromosome; (b) loss of genetic information from the short arm of chromosome 9 occurs frequently in glial tumors of intermediate (anaplastic, grade III) and high (glioblastoma, grade IV) histological malignancy (10 of 20 cases) but not in tumors of low (grade II) histological malignancy (0 of 10 cases); (c) tumors with 9p deletions are hemi- or nullizygous for interferon beta-1 and the interferon alpha gene cluster; (d) cases of interferon nullizygosity occur exclusively among tumors of highest histological malignancy (glioblastoma). These data, especially the determination of a region of nullizygosity, suggest proximity to or residence within a gene(s) whose function(s) is (are) critical to the suppression of the malignant evolution of glial tumors.
17: Zentralblatt f¨¹r Veterin?rmedizin. Reihe B. Journal of veterinary medicine. Series B, 1992 Jul, 39(5)
Monitoring of effects induced by recombinant equine interferon-beta 1 in whole blood and separated fractions of peripheral blood of horses.
[Abstract]Interferon is known to induce antiviral mechanisms and to exert immunoregulatory capacities on various cell types. The antiviral capacity of recombinant equine interferon-beta 1 (rEqIFN-beta 1) is most sensitively monitored by indirect quantitation of multiplication of vesicular stomatitis virus (VSV) in blood cells of horses. As few as 0.5 pg rEqIFN-beta 1/ml can be assessed by means of 90% reduction of VSV-replication in whole blood (w.b.) as well as in isolated mononuclear blood cells (MNC) in spite of individual variations. The immunoregulatory influence of 20-50 pg rEqIFN-beta 1/ml is sufficient to cause at least a 50% reduction of mitogen-induced lymphocyte proliferation in MNC, while higher concentrations are needed in w.b. Of the mitogens tested the best stimulation of proliferation on the equine lymphoid cells was obtained with staphylococcal enterotoxin B (SEB). Release of reactive oxygen species (ROS) from phagocytic cells in w.b. or from isolated polymorphonuclear cells (PMN) as monitored by chemiluminescence (CL) does not seem suitable for evaluation of rEqIFN-beta 1-induced immunoregulation as only very high rEqIFN-beta 1-concentrations (10(3)-10(4) pg/ml) result in a minute increase (up to 20%) of CL. Comparative studies on w.b. and isolated leukocyte fractions from identical specimens of individual horses suggest that monitoring of antiviral and distinct immunoregulatory capacities of rEqIFN-beta 1 can be performed on w.b. without loss of information and sensitivity as compared to isolated MNC.
18: Journal of interferon research, 1992 Apr, 12(2)
A method for the assay of "difficult" interferons exemplified with recombinant equine interferon-beta 1.
[Abstract]We wished to assay recombinant equine interferon-beta 1 (rEqIFN-beta 1) but could not obtain satisfactory results with previously described methods. Therefore, we developed a yield-reduction assay, using primary horse peripheral blood mononuclear cells (PBMC) with vesicular stomatitis virus (VSV) for challenge, which proved consistently satisfactory and highly sensitive. It is suggested that this method of assay may be useful for IFNs from other animals where problems are encountered.
19: Journal of interferon research, 1992 Dec, 12(6)
"Discordant" influence of equine recombinant interferon-beta 1 on the cytotoxic capacity of equine polymorphonuclear neutrophils and peripheral blood mononuclear cells in vitro and in vivo.
[Abstract]The influence of recombinant equine interferon-beta 1 (rEqIFN-beta 1) on mononuclear cells of peripheral blood (PBMC) and polymorphonuclear neutrophilic granulocytes (PMN) was tested under in vitro and ex vivo conditions. Treatment of equine PBMC with IFN in vitro enhanced the antibody-independent cytotoxicity (AICC) and antibody-dependent cytotoxicity (ADCC) while there was no significant effect on the cytotoxic capacity of PMN treated with rEqIFN-beta 1 in vitro. Ex vivo there was an increased capacity of AICC and ADCC upon single or multiple application of rEqIFN-beta 1 in PMN, only. Treatment with rEqIFN-beta 1 thus induced an increased cellular cytotoxicity in vitro and in vivo but in different populations of peripheral blood cells. In vivo rEqIFN-beta 1 causes a pronounced activation of PMN but not of PBMC as cytotoxic effector cells. This might be achieved indirectly, e.g., by cytokines produced by IFN-sensitive cells.