The American journal of managed care
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Multiple sclerosis (MS) is a chronic immune-mediated disease that potentially requires symptomatic and disease-modifying therapies. Numerous symptoms (eg, fatigue, spasticity, depression, bowel and bladder dysfunction, pain, and impaired mobility) are associated with the neurologic damage that results from MS. Several therapies (eg, modafinil, dalfampridine, baclofen, diazepam, gabapentin, opioids) are used for symptomatic treatment of disability and symptoms, but these do not improve disease outcome. ⋯ A more definitive therapy for MS should reduce relapse rate, prolong remission, limit the onset of new MS lesions, and postpone the development of long-term disability. The currently available MS disease-modifying therapies have been shown to reduce relapse rate, have beneficial effects on magnetic resonance imaging measures, and delay accumulation of disability. In addition, a number of agents are in development, but thus far no beneficial agent has been established in primary-progressive MS.
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Type 2 diabetes mellitus (T2DM) is a multisystem disease comprising numerous metabolic defects that contribute to the development of hyperglycemia. Although insulin resistance in the skeletal muscle and liver together with progressive beta cell failure are traditionally thought of as the core defects responsible for the development and progression of hyperglycemia, research over the past 2 decades has revealed a far more complex interaction of organs and tissues, with consequences for the fundamental understanding of the mechanisms of glucose disequilibrium and the nature of T2DM itself. ⋯ The function of the kidneys in abnormal glucose homeostasis is a striking example of this evolution in T2DM knowledge, as the role of glucose transporters in regulating plasma glucose levels and producing hyperglycemia has enhanced current understanding of T2DM. As pathophysiologic mechanisms and defects continue to be discovered, they offer an expansion of potential targets for treatment of T2DM.