Three recent hypertension trials have pointed out a disparity in the likelihood of diabetes developing when ramipril, 1 captopril, 2 or losartan 3 are used in comparison with either conventional β blocker therapy, 3 diuretic therapy, 2 or placebo. 1 In the treatment of high blood pressure the recognition that insulin resistance, a precursor to type 2 diabetes, commonly occurs in hypertensive patients 4 represents more evidence in favor of a greater chance of diabetes if a person is hypertensive. But, how often do patients with hypertension develop diabetes?
The reason we muse about such issues relates to the well‐known and substantial additional cardiovascular risk that the presence of diabetes attaches to the hypertensive patient.
In a recent prospective cohort study that included more than 12,000 adults, the development of type 2 diabetes was nearly 2.5‐times more likely in patients with hypertension compared with normotensive counterparts. 5 Other studies, such as those of Hayashi et al. 6 and Grodzicki et al. 7 corroborate this finding on different continents.
This isn't all that surprising when we consider that a large number of patients with hypertension are above ideal body weight and often have evidence of insulin resistance. 4 However, more distressing is the concern regarding how often diabetes develops as a result of antihypertensive therapy and whether the background of the patients (overweight, insulin resistant) places them at higher risk of drug‐induced (or is it drug enabling?) diabetes. This is a much more challenging question. In the afterglow of the Antihypertensive and Lipid‐Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), this probably is not the best time to resurrect an old controversy about the effect of diuretics (and β blockers) on glucose metabolism; however, there does appear to be a relationship between diuretic 8 and β blocker 4 usage and diabetes development. In ALLHAT it was evident that diuretic‐based therapy did have somewhat higher glucose levels at the end of the study compared with either calcium channel blocker or angiotensin‐converting enzyme (ACE)‐inhibitor treatment. 8
What do we do with this information? There are several possibilities. First, we share this knowledge with patients hoping it motivates them when we suggest they make lifestyle changes that could both reduce blood pressure levels and diabetes risk. Second, we make a mental note to watch their biochemical values a little more closely (and perhaps more often) after initiating therapy and avoid the tendency to attribute complaints of urinary frequency to the diuretic without at least considering that the diuretic effect may be osmotic rather than thiazide‐based. Whether the use of an ACE inhibitor or an angiotensin receptor blocker should be preferred in the hypertensive at risk for diabetes is best left for the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII). But we should remember the ALLHAT results, which reported benefit of diuretic therapy in both diabetics and nondiabetics.
References
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