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Clinical Resistance (clinical + resistance)

Distribution by Scientific Domains
Medical Sciences80%

Selected Abstracts

Long-term treatment with botulinum toxin type A in cervical dystonia has low immunogenicity by mouse protection assay,

MOVEMENT DISORDERS, Issue 10 2008
Mitchell F. Brin MD
Abstract To evaluate the immunogenicity of botulinum toxin type A (BoNTA; BOTOX) in cervical dystonia (CD). Subjects diagnosed with CD for ,1 year and previously naïve to BoNTs were treated with BoNTA in a prospective, open-label, multicenter study. Serum samples were analyzed for BoNTA neutralizing antibodies using the Mouse Protection Assay (MPA). Clinical resistance was assessed with a test injection of 20 U BoNTA placed unilaterally into the frontalis (Frontalis Antibody Test; FTAT) or corrugator muscle (Unilateral Brow Injection; UBI). Efficacy was assessed and adverse events were recorded. Of 326 subjects enrolled, 251 (77%) completed the study. Subjects received a median of 9 BoNTA treatments (mean dose per session ranged from 148.4 to 213.0 U over a mean of 2.5 years [range: 3.2 months,4.2 years]). Only 4 of 326 subjects (1.2%) tested positive for antibodies in the MPA; three of these subjects stopped responding clinically to BoNTA (of whom one also showed clinical resistance in the FTAT) and one continued to respond. Consistent improvements in the signs/symptoms of CD were noted. The most frequent treatment-related adverse events were mild to moderate weakness, dysphagia, neck pain, and injection-site pain. The current formulation of BoNTA rarely causes neutralizing antibody formation in CD subjects treated ,4 years. © 2008 Movement Disorder Society [source]

Acyclovir-resistant varicella infection with atypical lesions in a non-HIV leukemic infant

ACTA PAEDIATRICA, Issue 12 2000
N Crassard
ABSTRACT An HIV-negative infant presented with VZV primary infection during the maintenance therapy for mega-karyoblastic leukaemia. The lesions were initially vesicular and necrotic but became verrucous and hyperkerato tic. A clinical resistance to acyclovir was suspected and confirmed by histologic and virologic studies. The patient was successfully treated by foscarnet. Conclusion: resistance of VZV to acyclovir may occur after a short treatment in a non-AIDS patient. ± Acute leukaemia, acyclovir, foscarnet, Varicella zoster virus [source]

Long-term treatment with botulinum toxin type A in cervical dystonia has low immunogenicity by mouse protection assay,

MOVEMENT DISORDERS, Issue 10 2008
Mitchell F. Brin MD
Abstract To evaluate the immunogenicity of botulinum toxin type A (BoNTA; BOTOX) in cervical dystonia (CD). Subjects diagnosed with CD for ,1 year and previously naïve to BoNTs were treated with BoNTA in a prospective, open-label, multicenter study. Serum samples were analyzed for BoNTA neutralizing antibodies using the Mouse Protection Assay (MPA). Clinical resistance was assessed with a test injection of 20 U BoNTA placed unilaterally into the frontalis (Frontalis Antibody Test; FTAT) or corrugator muscle (Unilateral Brow Injection; UBI). Efficacy was assessed and adverse events were recorded. Of 326 subjects enrolled, 251 (77%) completed the study. Subjects received a median of 9 BoNTA treatments (mean dose per session ranged from 148.4 to 213.0 U over a mean of 2.5 years [range: 3.2 months,4.2 years]). Only 4 of 326 subjects (1.2%) tested positive for antibodies in the MPA; three of these subjects stopped responding clinically to BoNTA (of whom one also showed clinical resistance in the FTAT) and one continued to respond. Consistent improvements in the signs/symptoms of CD were noted. The most frequent treatment-related adverse events were mild to moderate weakness, dysphagia, neck pain, and injection-site pain. The current formulation of BoNTA rarely causes neutralizing antibody formation in CD subjects treated ,4 years. © 2008 Movement Disorder Society [source]

Resampling-Based Multiple Testing Methods with Covariate Adjustment: Application to Investigation of Antiretroviral Drug Susceptibility

BIOMETRICS, Issue 2 2008
Yang Yang
Summary Identifying genetic mutations that cause clinical resistance to antiretroviral drugs requires adjustment for potential confounders, such as the number of active drugs in a HIV-infected patient's regimen other than the one of interest. Motivated by this problem, we investigated resampling-based methods to test equal mean response across multiple groups defined by HIV genotype, after adjustment for covariates. We consider construction of test statistics and their null distributions under two types of model: parametric and semiparametric. The covariate function is explicitly specified in the parametric but not in the semiparametric approach. The parametric approach is more precise when models are correctly specified, but suffer from bias when they are not; the semiparametric approach is more robust to model misspecification, but may be less efficient. To help preserve type I error while also improving power in both approaches, we propose resampling approaches based on matching of observations with similar covariate values. Matching reduces the impact of model misspecification as well as imprecision in estimation. These methods are evaluated via simulation studies and applied to a data set that combines results from a variety of clinical studies of salvage regimens. Our focus is on relating HIV genotype to viral susceptibility to abacavir after adjustment for the number of active antiretroviral drugs (excluding abacavir) in the patient's regimen. [source]

Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571

BRITISH JOURNAL OF HAEMATOLOGY, Issue 1 2002
Christophe Barthe
Summary. The Abl kinase inhibitor STI571 (imatinib mesylate) induces haematological remissions in many patients with chronic myeloid leukaemia (CML) but advanced stage CML usually becomes resistant to STI571. We describe a patient in whom progressive resistance to STI571 correlated with the appearance of a mutation in the Bcr-Abl kinase domain. This was a G to A transition that resulted in a glutamic acid to lysine substitution at position 255 (E255K) in the Abl type 1a protein. We suggest that the acquisition of point-mutations in the tyrosine kinase domain of Bcr-Abl may cause progressive clinical resistance to STI571. [source]