Clinical Briefs
May 15, 2017 3 minutes read
Achieving Depression Remission
SOURCE: Zimmerman M, et al. J Clin Psychiatry 2017;78:2:177-183.
Few clinicians doubt that pharmacotherapies for depression usually are beneficial. On the other hand, many of us probably were too quick to endorse antidepressants based on improvements in symptom scores, without looking at the most important bottom line: attainment of remission. Clinical trial data indicate that for any typical initial antidepressant monotherapy, remission is achieved in only about 30% of patients, thus requiring either substitution or augmentation with another agent. Additionally, whereas clinicians probably assess depression status based on improvements using the “thumbnail sketch” approach, clinical trials employ validated scales, such as Hamilton Depression Rating Scale (HAM-D), Patient Health Questionnaire (PHQ-9), and others.
Zimmerman et al compared three different depression scales to the HAM-D (used as the gold standard) in adults treated as outpatients (n = 153) in the department of psychiatry at Brown University. The three comparator scales were Clinically Useful Depression Outcome Scale (CUDOS), Quick Inventory of Depressive Symptomatology Self Report (QUIDS-SR), and PHQ-9.
By effect size, all four scales showed comparable efficacy of antidepressant treatment. On the other hand, patients were significantly more likely to be scored as in remission by the HAM-D than QUIDS-SR and PHQ-9, and significantly less likely than CUDOS.
Clinicians recently have been advised to consider using formal treatment scores to follow depression, similar to our monitoring of A1c for diabetes or TSH for hypothyroidism. Noting the discrepancy between individual scoring systems, more work may be needed to determine which depression scale fits a particular clinical setting.
Antithrombotics and Subdural Risk
SOURCE: Gaist D, et al. JAMA 2017;317:836-846.
Before you digest the somewhat concerning observations of the Danish case-control data discussed below, it is important to remember that the risk of intracerebral hemorrhage in patients taking long-term anticoagulation (most commonly for atrial fibrillation) is < 0.5% per year, and for atrial fibrillation patients appropriately stratified by CHA2DS2-VASC, consistently outweighed by the beneficial risk reduction of thrombotic episodes.
That said, Gaist et al reported on a database of patients in Denmark (n = 10,100) with first subdural hematoma (SDH) compared to controls (n = 484,386). Included in the authors’ definition of antithrombotics were warfarin, aspirin, clopidogrel, the dipyridamole/aspirin combination capsule, and direct anticoagulants (dabigatran, apixaban, and rivaroxaban). Perhaps not surprisingly, almost half the subjects who incurred a SDH were receiving some antithrombotic medication, either alone or in combination.
Overall, the risk for SDH was greatest when antithrombotic medications were combined, especially with warfarin/antiplatelet combinations (odds ratios, 4.0-7.9). The only exception to this range of increased risk with combinations was the dipyridamole/aspirin combination treatment (that is, dipyridamole/aspirin alone), for which the odds ratio for SDH risk was not statistically significantly increased. Intracranial bleeding is more frequent in patients who take antithrombotic treatments. However, for appropriately selected users, the benefits of thrombosis risk reduction generally outweigh bleeding risks.
Health Consequences of What We Eat vs. What We Should Eat
SOURCE: Micha R, et al. JAMA 2017;317:912-924.
If you were asked to compile a balance sheet for which foods/nutrients should be maximized vs. minimized, there probably would be few differences from 10 items evaluated by Micha et al seeking a relationship between dietary components and cardiovascular mortality.
The 10 items included in their dietary analyses were fruits, vegetables, nuts/seeds, whole grains, unprocessed red meats, processed meats, sugar-sweetened beverages, polyunsaturated fats, seafood omega-3 fats, and sodium.
Based on 702,308 cardiometabolic deaths in U.S. adults in 2012, these data suggest that almost half of such deaths in men and women were associated with suboptimal intake of critical nutrients. According to these authors, the single largest contributor to cardiometabolic deaths was high intake of sodium, which, of course, has been variously associated (or not) with hypertension and heart failure. Next in the “deficit in the diet” category was nuts/seeds, followed by low seafood omega-3 fats, low vegetables, and low fruits. Consistent with recent health warnings, high intake of processed meats and sugar-sweetened beverages also was identified to be health culprits.
Consequences of suboptimal diet were more dramatic within the demographic communities of African Americans and Hispanics, as well as those with lesser education. Changing dietary intake on a population-wide basis is a challenging task, but perhaps these associations of specific identified nutrient imbalances with adverse cardiovascular outcomes will help us shape that change.
In this section: treating depression; the subdural risk of antithrombotics; and the health consequences of a poor diet.
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