Pathophysiology and management strategies for hyperglycemia for patients with acute illness during and following a hospital stay.

Hyperglycemia in the inpatient setting is associated with poor clinical outcomes and is often suboptimally managed. This review addresses the pathophysiology of hyperglycemia, current recommendations for management of inpatient hyperglycemia in the general medical and surgical care setting, the transition between different diabetes treatments, and the transition from inpatient to outpatient therapy. The preferred drug for management of inpatient hyperglycemia is insulin. Successful use of intravenous and subcutaneous insulin in the hospital is based on the implementation of standardized protocols. Current guidelines recommend basal-bolus subcutaneous insulin in non-critically ill patients. The methods of switching from intravenous to subcutaneous, sliding-scale to basal-bolus, and biphasic to basal-bolus are discussed. Transition from an inpatient to an outpatient insulin regimen, especially in patients new to insulin therapy, requires special attention to ensure that patients have the knowledge to administer insulin safely and effectively. The optimal regimen at discharge must be individualized. Patients with acute infections may benefit from insulin therapy until the infection is resolved. Strategies to optimize diabetes therapy after discharge are discussed. Prompt outpatient follow-up is crucial to ensure optimal glycemic control. Despite the challenges, improved glycemic control in individuals with acute illness has the potential to reduce morbidity and mortality in individuals with this widespread metabolic illness.

Alopecia areata: what to expect from current treatments.

Alopecia areata is relatively benign and often resolves on its own, although its psychosocial impact on children and young adults can be severe. Some form of treatment is usually required. Because current treatments may not show results for 3 to 6 months, reassuring the patient and the parents and informing them about the results that can be expected are an essential part of management. The choice of treatment depends on the patient's age and the extent of alopecia activity.

Distinct roles of the Ikappa B kinase alpha and beta subunits in liberating nuclear factor kappa B (NF-kappa B) from Ikappa B and in phosphorylating the p65 subunit of NF-kappa B.

Phosphatidylinositol 3'-kinase (PI3K) and the serine/threonine kinase AKT have critical roles in phosphorylating and transactivating the p65 subunit of nuclear factor kappaB (NF-kappaB) in response to the pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF). Mouse embryo fibroblasts (MEFs) lacking either the alpha or beta subunit of IkappaB kinase (IKK) were deficient in NF-kappaB-dependent transcription following treatment with IL-1 or TNF. However, in contrast to IKKbeta-null MEFs, IKKalpha-null MEFs were not substantially defective in the cytokine-stimulated degradation of Ikappabetaalpha or in the nuclear translocation of NF-kappaB. The IKK complexes from IKKalpha- or IKKbeta-null MEFs were both deficient in PI3K-mediated phosphorylation of the transactivation domain of the p65 subunit of NF-kappaB in response to IL-1 and TNF, and constitutively activated forms of PI3K or AKT did not potentiate cytokine-stimulated activation of NF-kappaB in either IKKalpha- or IKKbeta-null MEFs. Collectively, these data indicate that, in contrast to IKKbeta, which is required for both NF-kappaB liberation and p65 phosphorylation, IKKalpha is required solely for the cytokine-induced phosphorylation and activation of the p65 subunit of NF-kappaB that are mediated by the PI3K/AKT pathway.