Clinical Briefs
February 29, 2016 4 minutes read
Can Vitamin D Deficiency Cause Hypertension?
SOURCE: Chen S, et al. Vitamin D deficiency and essential hypertension. J Am Soc Hypertens 2015;9:885-901.
Should we just cut to the chase and accept that vitamin D deficiency causes everything? That’s the way it seems these days. Chen et al made a convincing case for at least a potential etiologic role of vitamin D in development of hypertension.
Premises for consideration of vitamin D in relationship to hypertension include the observation that persons with less opportunity for vitamin D metabolism as a result of living in higher latitudes, having skin of color, or living in a colder climate with less outdoor sun exposure manifest a higher prevalence of essential hypertension. As part of “proof of concept,” one clinical trial enhanced vitamin D through ultraviolet B radiation in vitamin D-deficient patients, resulting in lower blood pressure.
While it should seem simple to test the vitamin D-hypertension relationship hypothesis, the results of 40 randomized trials addressing the issue have been mixed. The authors provided some explanation for this by noting that younger hypertensives (< 45 years of age) have more effective counterregulatory mechanisms for maintaining vascular tone than older patients, and, hence, vitamin D repletion in younger patients has less effect on blood pressure. Since most trials have incorporated populations of diverse age, younger patients may have diluted potential blood pressure effects of vitamin D repletion.
The authors noted that vitamin D deficiency tends to lead toward vasoconstriction, a common component of essential hypertension. Perhaps identification of particular populations that are strong responders (and elimination of non-responder groups from clinical trials) will define better a therapeutic role for the prevention or treatment of hypertension with vitamin D.
Why We Can’t Allow Physical Exam Skills to Languish
SOURCE: Verghese A, et al. Inadequacies of physical examination as a cause of medical errors and adverse events: A collection of vignettes. Am J Med 2015;128:1322-1324.
With more highly evolved and readily available technology at our fingertips, it is sometimes tempting to let the echocardiogram sort out the abnormal heart sounds we detected, or allow the pelvic ultrasound to inform whether the uterus is enlarged, or short-cut parts of the physical exam we anticipate to be unlikely sources of pertinent information. At the same time, there may not be large-scale clinician awareness that a textbook of Evidence-based Physical Diagnosis even exists. (McGee, S. Evidence-based Physical Diagnosis, 3rd Edition. Philadelphia: Elsevier Saunders Publishers; 2012.) Could over-reliance on technology lead to meaningful errors?
Verghese et al reported on 208 vignettes that were volitionally reported to them in response to a survey soliciting instances of oversights related to the physical exam. The most common consequence of an inadequate physical exam was missed/delayed diagnosis. However, unnecessary treatment, delay in treatment, unnecessary exposure to radiation or contrast, and complications related to treatment were also reported.
Commonly missed items included abdominal masses, pregnancy, neurologic findings, murmurs, adenopathy, breast masses, heart failure, and herpes zoster. The authors reported that most of the cases in which inadequate physical examination led to consequences were the result of simply not performing the appropriate physical exam (rather than, for example, misinterpretation of an appropriately performed exam).
The authors made a case for reminding clinicians that appropriate physical examination skills need to be taught and maintained. Inadequate performance of the physical exam, as documented here, can lead to important consequences.
Teasing Relationships: Uric Acid, Fructose, and Hypertension
SOURCE: Madero M, et al. A pilot study on the impact of a low fructose diet and allopurinol on clinic blood pressure among overweight and prehypertensive subjects: a randomized placebo controlled trial. J Am Soc Hypertens 2015;9:837-844.
Uric acid has been under scrutiny for decades since its identification as a cardiovascular risk factor in the Framingham Heart Study. Whether elevations in uric acid are causally related to cardiovascular disease continues to be hotly debated. Elevations of plasma and intracellular uric acid are associated with higher blood pressure. Similarly, fructose, especially high-fructose corn syrup, has been suspect for its contribution to metabolic syndrome. Since fructose leads to increased intracellular and serum uric acid, a plausible pathologic pathway is evident.
Madero et all performed a two-step, controlled trial among 72 obese prehypertensive patients to examine the sequential effect of restricted dietary fructose for 4 weeks, followed by the addition of allopurinol 300 mg/day for another 4 weeks, compared to a control group. All subjects were advised to restrict sodium.
There was a trend for greater blood pressure reduction in the low-fructose diet group that did not achieve statistical significance. A post-hoc analysis of the second step of the trial (adding allopurinol to the diet) produced a reduction in office systolic blood pressure compared to the control group, but not in systolic blood pressure as measured by ambulatory blood pressure monitoring, which is considered more accurate and a better predictor of adverse effects of blood pressure. The roles of fructose restriction and allopurinol need more clarification.
In this section: another reason to take vitamin D supplements; polishing physical exam skills; and comparing the relationship between uric acid, fructose, and hypertension.
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