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Clinical Assistant Professor, University of Florida, Gainesville
Dr. Kuritzky is a retained consultant for AbbVie, AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Chelsea, Daiichi Sankyo, Forest Pharmaceuticals, Janssen, Lilly, Novo Nordisk, Pfizer, and Sanofi.
Source: Mohebi R, et al. J Am Soc Hypertens 2014;8:491-497.
The Joint National Committee (for purists, AKA "the group originally assigned to create JNC8") suggests that for persons aged ≥ 60 years, systolic blood pressure (SBP) should be lowered to < 150 mmHg. Is this the right number? After all, the relationship between SBP and cardiovascular disease (CVD) demonstrated in epidemiologic observational studies appears to be linear, so might CVD risk be better reduced by achieving lower SBP than simply "< 150 mmHg"?
To address this question, Mohebi et al followed a population of senior citizens (n = 1845) for approximately 10 years, looking at the hazard ratio for suffering a CVD event or mortality when comparing various levels of BP to a BP of 120/80 (which they designate as ideal BP). All study participants were aged ≥ 60 years at baseline (mean age = 66 years), and ostensibly free of CVD.
In this population, persons with prehypertension were not at demonstrably greater risk than persons with ideal BP. However, when SBP was 140-150 mmHg, risk for CV events was more than 1.5 times as great as SBP 120 (even though there was no increased mortality signal).
Based on these observations, the authors suggest that the risk of CV events even at a SBP of 140-150 is substantially greater than "ideal BP." At the same time, they acknowledge that clinical trials in senior citizens attempting to clarify whether lower BP levels will improve outcomes more than simply attaining < 150 mmHg have been inconsistent.
Source: Fischer M, et al. J Clin Psychiatry 2014;75: 7:728-730.
The approach to management of a patient who incurs a positive urine drug test (UDT) screen for an illicit substance is complex. It is even more complex, however, if false positives could be the explanation.
Fischer et al report on their experience with 40 psychiatric patients found to be phencyclidine (PCP, also called "angel dust") positive on UDT. Out of this population, only one patient confirmed taking PCP. The others were receiving psychiatric medications known to potentially produce a false-positive result for PCP such as venlafaxine. The authors report that the list of medications potentially causing a false-positive PCP UDT — most of which are used for psychiatric disorders — is substantial, and includes lamotrigine, tramadol, ibuprofen, imipramine, diphenhydramine, and others.
This particular report, however, draws attention to another psychiatric medication, chlorprothixene, which they found to be the most common cause of a false-positive UDT for PCP, being associated with 16 of the 40 cases (venlafaxine was associated with 14 cases). Chlorprothixene has not previously been reported as a cause of false-positive PCP UDT.
These results must be considered preliminary because the investigators did not confirm the absence/presence of actual PCP by a highly sensitive method such as liquid chromatography. Nonetheless, these findings support consideration of chlorprothixene and other commonly used psychiatric drugs as the cause of false-positive PCP UDT results. Positive PCP results on UDT in a patient who denies using PCP may require confirmation with more sensitive assays than are typically used in routine UDT.
Source: Mente A, et al. N Engl J Med 2014;371: 601-611.
If you thought that another very large clinical trial would finally settle uncertainties about salt — well, I hate to disappoint you. Opinions about the role of salt in cardiovascular disease range from "there is little relationship" to "the relationship is strong and consistent," with all sorts of conjecture in between.
Mente et al report on data obtained from 18 different countries in which a single morning urine specimen measurement of sodium and potassium was used as a metric for dietary ingestion of those same electrolytes. They found a positive linear relationship between salt ingestion and blood pressure (BP), such that every 1 g/d increase in sodium was associated with a 2.11 mmHg increase in SBP.
Their data did not, however, demonstrate a "one size fits all" linearity. Persons with the highest sodium ingestion (> 5 g/d) demonstrated an almost 4-fold greater increment in BP per gram of sodium consumption than persons at the lowest levels (< 3 g/d sodium). Also, older persons and persons with pre-existing hypertension were more sensitive to BP-raising effects of sodium.
Potassium ingestion was inversely associated with BP. So are we finally finished with this roller coaster-like journey about sodium? Yes — well, that is until you turn the page on that article in the New England Journal of Medicine to find that the very next article also examined sodium in more than 100,000 persons, and did not come up with the same answer — oh well, we’ll keep searching.