Gamma‐glutamyl transferase (GGT) is a second‐generation enzymatic liver function test available for several decades, initially used as a sensitive indicator of alcohol ingestion, hepatic inflammation, fatty liver disease, and hepatitis. Longitudinal and cross‐sectional investigational studies since 1990 have associated GGT with an increase in all‐cause mortality, as well as chronic heart disease events such as congestive heart failure and components of the metabolic syndrome (abnormal body mass index and levels of high‐density lipoprotein cholesterol, glucose, triglycerides, and systolic and diastolic blood pressure). In the upper reference range, GGT was found to be an independent biomarker of the metabolic syndrome, with a 20% per GGT quartile trend rise. Additionally, GGT was positively correlated with an 18% per quartile risk of cardiovascular events and a 26% per quartile increased risk of all‐cause mortality. Furthermore, it may be considered a biomarker for “oxidative stress” associated with glutathione metabolism and possibly a “proatherogenic” marker because of its indirect relationship in the biochemical steps to low‐density lipoprotein cholesterol oxidation. GGT is becoming an important addition to the multimarker approach to cardiovascular risk evaluation. It should be considered a valuable adjunct in stratifying patient risk and in assessing the aggressiveness of appropriate treatment, with hopes of preventing unnecessary cardiac events and deaths in future years. Prev Cardiol. 2010;13:36–41.©2009 Wiley Periodicals, Inc.

OBJECTIVEWhile metformin is generally accepted as the first-line agent in treatment of type 2 diabetes, there are insufficient evidence and extensive debate about the best second-line agent. We aimed to assess the benefits and harms of four commonly used antihyperglycemia treatment regimens considering clinical effectiveness, quality of life, and cost. RESEARCH DESIGN AND METHODSWe developed and validated a new population-based glycemic control Markov model that simulates natural variation in HbA 1c progression. The model was calibrated using a U.S. data set of privately insured individuals diagnosed with type 2 diabetes. We compared treatment intensification of metformin monotherapy with sulfonylurea, dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, or insulin. Outcome measures included life-years (LYs), quality-adjusted lifeyears (QALYs), mean time to insulin dependence, and expected medication cost per QALY from diagnosis to first diabetes complication (ischemic heart disease, myocardial infarction, congestive heart failure, stroke, blindness, renal failure, amputation) or death. RESULTSAccording to our model, all regimens resulted in similar LYs and QALYs regardless of glycemic control goal, but the regimen with sulfonylurea incurred significantly lower cost per QALY and resulted in the longest time to insulin dependence. An HbA 1c goal of 7% (53 mmol/mol) produced higher QALYs compared with a goal of 8% (64 mmol/mol) for all regimens. CONCLUSIONSUse of sulfonylurea as second-line therapy for type 2 diabetes generated glycemic control and QALYs comparable with those associated with other agents but at lower cost. A model that incorporates HbA 1c and diabetes complications can serve as a useful clinical decision tool for selection of treatment options.Diabetes is one of the most prevalent and costly chronic medical conditions worldwide, incurring significant burdens on individuals, society, and the health care system. It is currently estimated that 25.8 million Americans, or 8.3% of the population, have diabetes (1). Glucose-lowering therapies are the cornerstone of diabetes management, with multiple epidemiological studies linking glycemic control to a lower risk of diabetes-related complications and mortality. Large randomized controlled trials have demonstrated a reduction in microvascular complications

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Until now, the mechanical properties of the microcalluses that form in human cancellous bone have been unexplained. We measured the microhardnesses of microcalluses in cancellous bone, of the trabeculae within the microcalluses, of the trabeculae adjacent to microcalluses, and of trabeculae lacking microcalluses in a human tibia and femur. We observed no important differences between materials at the four different sites. Because the microhardness of bone is very closely related to its stiffness, this finding indicates that microcalluses are likely to stiffen the trabeculae in which they are formed, even though they may surround unhealed fractures of the cancellous trabeculae.