Clinical Briefs
Choices in Addressing Postprandial Glucose Elevations
SOURCE: Aronoff SL. Rationale for treatment options for mealtime glucose control in patients with type 2 diabetes. Postgraduate Med 2017;129:231-241.
The philosophy of “fix the fasting first” seems both physiologically and functionally sound when initially addressing elevated A1c levels, since the greatest burden of excess glucose in most patients with A1c levels > 8 is from fasting and overnight glucose load (rather than postprandial). Once the fasting glucose has been corrected, if the A1c is not at goal postprandial glucose (PPG), excesses then must be addressed with treatments that preferentially reduce PPG.
Several classes of agents are appropriate to address PPG elevations, including alpha-glucosidase inhibitors, glinides (e.g., nateglinide, repaglinide), rapid-acting insulin, GLP-1 receptor agonists (e.g., exenatide, liraglutide, albiglutide), and pramlintide. Pramlintide is a parenteral analogue of the hormone amylin, which is co-secreted with insulin by beta-cells. In addition to facilitating insulin activity, pramlintide also demonstrates some GLP-1 receptor agonist-like activity (e.g., delayed gastric emptying, although through a hypothalamic mechanism rather than gastrointestinal mechanism).
Recent exploration of the GLP-1 receptor agonist class has suggested that it may be subclassified into short-acting and long-acting agents. Although all currently available GLP-1 receptor agonists affect both fasting and PPG, short-acting GLP-1 receptor agonist agents (exenatide and lixisenatide) appear to produce a more dominant effect on PPG, whereas the so-called long-acting GLP-1 receptor agonists produce a more dominant effect on fasting glucose.
Control of PPG sometimes is critical to attain A1c goals; additionally, there has been some literature support for an association between elevated PPG and adverse cardiovascular outcomes. Fortunately, there is a diversity of good choices available to address PPG elevations.
What if COPD Exacerbation Was Pulmonary Embolism?
SOURCE: Aleva FE, et al. Prevalence and localization of pulmonary embolism in unexplained acute exacerbations of COPD: A systematic review and meta-analysis. Chest 2017;151:544-554.
In contrast to most of the other top 10 causes of death, mortality from COPD has not declined in the past two decades. It now ranks as the number three cause of mortality worldwide. Exacerbations of COPD may be induced by viruses, bacteria, and inhaled toxins, but despite thorough evaluation as many as 30% of episodes lack a clear etiology. Might acute pulmonary embolism (PE) be mistaken for (or cause) a COPD exacerbation?
Aleva et al reviewed data from seven studies of patients admitted for acute COPD exacerbations (n = 880) who underwent pulmonary CT-angiography as part of their evaluation. Within the group lacking an identified etiology for their apparent COPD exacerbation, 16% were determined to have suffered a PE. Most of these emboli qualified for anticoagulant treatment.
When PE occurs in relation to apparent COPD exacerbations, pleuritic chest pain and heart failure signs were seen more often. D-dimer measurements might help exclude PE, as the authors clearly explained they are not suggesting pulmonary CT angiography become a routine part of evaluation. Rather, one hopes that awareness of PE as a cause of COPD exacerbations will be considered more routinely, especially in patients presenting with pleuritic chest pain and signs of heart failure.
What Is ‘Syndemics’?
SOURCE: Singer M, et al. Syndemics and the biosocial conception of health. Lancet 2017;389:941-950.
Unless one has studied sociology or anthropology extensively, “syndemics” probably is unfamiliar. Syndemics is the aggregation of two or more concurrent or sequential epidemics or disease clusters in a population with biological interactions that exacerbate the prognosis and burden of disease. Merrill Singer (a coauthor of the study under discussion here) has been credited with creating the term.
The reason one likely will hear much more about syndemics is that global health issues often are strongly driven by syndemics. For instance, the syndemic syndrome SAVA (substance abuse, violence, and AIDS) reflects the consequences of poverty, inner-city residence, unemployment, disrupted social networks, lack of social support, and ethnic inequalities that also result in endemic/epidemic status for disorders such as tuberculosis, sexually transmitted infections, hepatitis, infant mortality, suicide, and more.
Probably the closest terminology most have used is “biopsychosocial.” That is to say, it is becoming ever clearer that disease incidence, prevalence, comorbid disease, and disease outcomes are much more complex than the equation germ + host = disease. Hopefully, as policymakers become more aware of the wisdom of addressing public health issues from the perspective of syndemics, improved outcomes will occur.
In this section: Addressing postprandial glucose elevations; examining the possible connection between COPD and pulmonary embolisms; and defining healthcare's future reality.
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