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By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is a consultant for GlaxoSmithKline and is on the speaker's bureau of GlaxoSmithKline, 3M, Wyeth-Ayerst, Pfizer, Novartis, Bristol-Myers Squibb, AstraZeneca, Jones Pharma, and Boehringer Ingelheim.
Bariatric surgery and reversal of dysglycemia
Source: Salinari S, et al. First-phase insulin secretion restoration and differential response to glucose load depending on the route of administration in type 2 diabetic subjects after bariatric surgery. Diabetes Care 2009; 32:375-380.
Most type 2 diabetics (DM2) who undergo bariatric surgery enjoy a prompt reversal or at least a substantial diminution of their dysglycemia. These salutary effects occur both after malabsorptive surgery (diverting the digestive tract around to bypass components of the small intestine) or restrictive surgery (diminishing gastric capacity). The mechanisms by which surgery improves glucose regulation appear to go beyond simple weight loss; indeed, glucose regulation improves well before meaningful weight loss has occurred, suggesting that some change in intestinal glucose modulation factors must be involved.
Salinari et al studied glucose metabolism in 9 DM2 subjects who underwent biliopancreatic diversion bariatric surgery, comparing their glucose metabolism with healthy, normal-weight controls.
The healthy pancreas provides a bolus of preformed insulin immediately in response to mealtime increases in plasma glucose. One of earliest manifestations of DM2 is loss of first-phase insulin secretion, leading to a consistent mismanagement of glucose, since early elevations of plasma glucose are not met with a prompt matching insulin bolus. In this trial, the first-phase insulin response was restored by 1 month after surgery. Similarly, b-cell responsiveness to glucose elevation was normalized; and lastly, insulin sensitivity was restored to essentially normal. Concordant with the concept that elimination of some intestinal component is central to these phenomena, sensitivity to oral glucose was improved to a greater degree than was intravenous glucose. Incretin levels (GLP, GIP), however, were unchanged.
Malabsorptive bariatric surgery provides prompt regression of DM2, apparently due (at least in part) to some as yet unidentified intestinal hormone, and independent of identified incretin hormones such as GLP and GIP.
Metabolic syndrome and salt sensitivity
Source: Chen J, et al. Metabolic syndrome and salt sensitivity of blood pressure in non-diabetic people in China: A dietary intervention study. Lancet 2009;373:829-835.
Although definitions of what constitutes metabolic syndrome (MBS) vary, there is general agreement that insulin resistance (IR) is a fundamental component. By leading to sodium retention, IR may contribute to the development of hypertension (HTN).
Blood pressure effects of salt restriction are highly variable, but one would anticipate that MBS subjects might respond more intensely based upon the IR-to-sodium retention link. To investigate this, Chen et al studied 1881 nondiabetic subjects, of whom 283 had MBS. All participants were fed a low-sodium diet (= 3 g NaCl/d) for 7 days, followed by a high-sodium diet (= 18 g NaCl/d) for 7 days. At baseline, the mean BP in the MBS group was 128/81 mmHg vs 115/72 mmHg in those without MBS.
High-salt sensitivity was defined as a BP change of 5 mmHg or more in response to dietary salt modulation. At the end of each diet period, MBS subjects had a threefold or greater odds ratio for high-salt sensitivity (both to a rise in BP with sodium load, as well as a reduction in BP with sodium restriction). The benefits of salt restriction in persons with MBS may be more substantial than the general population.
Herpes zoster in TNF-treated RA patients
Source: Strangfeld A, et al. Risk of herpes zoster in patients with rheumatoid arthritis treated with anti-TNF-a agents. JAMA 2009;301:737-744.
The evolution of pharmacotherapy for rheumatoid arthritis (RA) has led to the development of agents which, at least, offer major symptomatic improvement, and at best, promise remission. Because TNF agents involve modulation of steps critical to immune integrity, vigilance for serious bacterial infections is required. Yet, whether TNF agents impact the incidence of viral infections, which is also important, has been little-studied. Population studies on patients with RA have demonstrated a doubling of risk for herpes zoster compared to a control population.
Strangfeld et al enrolled RA patients (n = 5040) receiving either TNF agents or conventional DMARDS, such as methotrexate. Herpes zoster incidence was monitored over 36 months.
Overall, TNF agents were associated with an increased zoster incidence (hazard ratio = 1.82) compared to conventional treatment. Among the TNF agents, there was a distinct difference between etanercept, which did not show a statistically significant increase in zoster risk, vs infliximab and adalimumab, which did. The authors suggest that patients treated with the latter two agents merit particular vigilance for early signs and symptoms of herpes zoster to allow prompt intervention.