Multiple Sclerosis: Kachuck NJ

Frohman EM, Goodin DS, Calabresi PA, Corboy JR, Coyle PK, Filippi M, Frank JA, Galetta SL, Grossman RI, Hawker K, Kachuck NJ, Levin MC, Phillips JT, Racke MK, Rivera VM, Stuart WH, Anonymous00118. · University of Texas Southwestern Medical Center at Dallas, USA. · Neurology. · Pubmed #12963748 No free full text.

Abstract: Advancements in imaging technologies and newly evolving treatments offer the promise of more effective management strategies for MS. Until recently, confirmation of the diagnosis of MS has generally required the demonstration of clinical activity that is disseminated in both time and space. Nevertheless, with the advent of MRI techniques, occult disease activity can be demonstrated in 50 to 80% of patients at the time of the first clinical presentation. Prospective studies have shown that the presence of such lesions predicts future conversion to clinically definite (CD) MS. Indeed, in a young to middle-aged adult with a clinically isolated syndrome (CIS), once alternative diagnoses are excluded at baseline, the finding of three or more white matter lesions on a T2-weighted MRI scan (especially if one of these lesions is located in the periventricular region) is a very sensitive predictor (>80%) of the subsequent development of CDMS within the next 7 to 10 years. Moreover, the presence of two or more gadolinium (Gd)-enhancing lesions at baseline and the appearance of either new T2 lesions or new Gd enhancement on follow-up scans are also highly predictive of the subsequent development of CDMS in the near term. By contrast, normal results on MRI at the time of clinical presentation makes the future development of CDMS considerably less likely.

Kachuck NJ. · USC Keck School of Medicine, 1520 San Pablo Street, 3000 Los Angeles CA 90033, USA. · Expert Rev Neurother. · Pubmed #16162084 No free full text.

Abstract: The approval of natalizumab for relapsing forms of multiple sclerosis, and the subsequent voluntary suspension of its use due to an unexpected viral infection, is a cautionary tale of how much we have to learn about how to prioritize and perform the necessary research and development of novel therapeutics for human diseases, the ethics of placebo-controlled trials and the relationships between researchers, regulatory authorities and the pharmaceutical industry.

Weiner LP, Kachuck NJ, Gilmore W, Lund B. · USC Keck School of Medicine, Department of Neurology, Los Angeles, CA 90033, USA. · Mult Scler. · Pubmed #11936493 No free full text.

This publication has no abstract.

Kachuck NJ. · Multiple Sclerosis Comprehensive Care and Research Center, 1520 San Pablo Street, Suite 3000, Los Angeles, CA 90033, USA. · Expert Opin Pharmacother. · Pubmed #19586420 No free full text.

Abstract: BACKGROUND: Fampridine-SR is under submission as the first drug to be FDA approved with an indication specifically for multiple sclerosis symptoms. Compounded forms of the active agent of Fampridine-SR (4-aminopyridine) have been used in clinical practice for many years. Clinical trials have now been completed that demonstrate a robust capacity of the drug to meet stringent statistical and clinically meaningful end points. OBJECTIVE: To review the present understanding of multiple sclerosis, the proposed mechanism of action of Fampridine-SR in patients, the published data regarding its efficacy and safety in human clinical trials, and to discuss its potential clinical uses in MS. RESULTS/CONCLUSION: Fampridine-SR 10 mg twice a day has been shown to be safe and effective in improving the ambulation of patients with walking disability due to MS. It will probably find clinical application beyond this specific indication in a significant proportion of patients.

Lund BT, Ashikian N, Ta HQ, Chakryan Y, Manoukian K, Groshen S, Gilmore W, Cheema GS, Stohl W, Burnett ME, Ko D, Kachuck NJ, Weiner LP. · Department of Neurology, Keck School of Medicine, University of Southern California, MCH-142, Los Angeles, California 90033, USA. · J Neuroimmunol. · Pubmed #15342208 No free full text.

Abstract: Multiple Sclerosis (MS) is a chronic inflammatory disease of the CNS which is characterized by large mononuclear cell infiltration and significant demyelination. CXCL8 is a chemo-attractant for both neutrophils and monocytes and triggers their firm adhesion to endothelium. In this study, we demonstrate that serum CXCL8 and CXCL8 secretion from PBMCs are significantly higher in untreated MS patients compared to controls and are significantly reduced in MS patients receiving interferon-beta1a therapy. We suggest that CXCL8 may serve as a marker of monocyte activity in MS and may play a role in monocyte recruitment to the CNS.