{"id":49884,"date":"2021-03-19T19:06:28","date_gmt":"2021-03-19T18:06:28","guid":{"rendered":"https:\/\/blogs.bmj.com\/bmj\/?p=49884"},"modified":"2021-03-19T19:06:40","modified_gmt":"2021-03-19T18:06:40","slug":"alex-nowbars-journal-reviews-12-march-2021-2","status":"publish","type":"post","link":"https:\/\/blogs.bmj.com\/bmj\/2021\/03\/19\/alex-nowbars-journal-reviews-12-march-2021-2\/","title":{"rendered":"Alex Nowbar\u2019s journal reviews\u201419 March 2021"},"content":{"rendered":"

Alex Nowbar reviews the latest research from the top medical journals<\/em><\/p>\n

\"\"Thou shalt have a fishy<\/b><\/p>\n

Cardiovascular disease is less than desirable, but it does get tiresome hearing about one or other dietary thing that could reduce risk of it. Mohan and colleagues report that a fish intake of at least 175\u2009g (roughly two servings) a week is associated with a lower risk of major cardiovascular disease in people with prior cardiovascular disease, but not in the general population. This is based on large numbers of patients across the globe in a mixture of observational and randomised studies, but this analysis is not informative for changing practice. The authors write: \u201cThe consumption of fish (especially oily fish) should be evaluated in randomized trials of clinical outcomes among people with vascular disease.\u201d Well yes, but I\u2019m not sure such a trial would be practical, although there have been randomised trials of fish oil supplements (which have been a mixed bag). We\u2019ll probably never know if a fish diet in general is protective because those more likely to eat fish are also more likely to do all sorts of other things\u2014the classic nutrition research dilemma.<\/span><\/p>\n

JAMA Intern Med<\/span><\/i> doi:10.1001\/jamainternmed.2021.0036<\/span><\/a><\/p>\n

CNS drugs in dementia<\/b><\/p>\n

Maust and colleagues\u2019 prevalence study of over a million older adults with dementia in the community in the US found that 13.9% of them had prescriptions for three or more central nervous system (CNS)-active drugs for at least 30 days. These could include antidepressants, opioids, benzodiazepines, and antipsychotics. This won\u2019t come as much of a surprise, but it is worrying because these drugs can increase the risk of impaired cognition, falls, and death. More importantly, we don\u2019t know how best to manage these people\u2019s complex needs. The authors comment that they could not assess the appropriateness of the prescriptions. Even if these data had been available, it still would have been debatable whether reducing pain is worth an increased risk of falls, for example. A rate of 13.9% polypharmacy could well be achieving the best outcomes possible in this population\u2014these patients have pain and mental disorders among many other conditions\u2014but I find it hard to believe that three or more CNS drugs can be in many patients\u2019 best interests.<\/span><\/p>\n

JAMA <\/span><\/i>doi:10.1001\/jama.2021.1195<\/span><\/a><\/p>\n

STEMI without risk factors<\/b><\/p>\n

In a large Swedish registry, 14.9% of ST elevation myocardial infarctions (STEMIs) occurred in people without standard modifiable cardiovascular risk factors. The \u201cbig four\u201d of these risk factors (known as SmuRFs) are smoking, hypertension, hypercholesterolaemia, and diabetes. People without SmuRFs were less likely to receive statins, ACE inhibitors or angiotensin receptor blockers, or \u03b2\u2009blockers at discharge. This seems suboptimal. Worse still, 30 day mortality was higher in those without SMuRFs. This underlines the need for evidence based post-STEMI medication initiation even in people perceived to be low risk. People without SMuRFs who have STEMI must have a substrate for developing cardiovascular disease even if we don\u2019t yet know how to measure this.<\/span><\/p>\n

Lancet <\/span><\/i>doi:10.1016\/S0140-6736(21)00272-5<\/span><\/a><\/p>\n

Gestational diabetes screening<\/b><\/p>\n

Hillier and colleagues compared two gestational diabetes screening tests in a large randomised trial with the same subsequent guideline-directed management. The one-step approach (a fasting 2 hour oral glucose tolerance test) resulted in more diagnoses of gestational diabetes (16.5% <\/span>v<\/span><\/i> 8.5%) than the two-step approach (non-fasting 1 hour glucose tolerance followed by a 3 hour fasting test if positive), but there was no difference between the groups in subsequent perinatal or maternal complications from gestational diabetes. This suggests that there may be little advantage to the broader diagnostic approach compared with the two-step approach. This means that interventions can be targeted at the people identified in the two-step approach, and screening for the additional cases isn\u2019t beneficial. This is an example where the additional diagnoses detected by the one-step approach can be considered overdiagnosis\u2014where there was no advantage to knowing or treating the condition for maternal or perinatal outcomes. Perhaps these people are more likely to develop diabetes subsequently, but that doesn\u2019t mean we need to screen for it in pregnancy. There is already enough to worry about that has more immediate implications.<\/span><\/p>\n

N Engl J Med <\/span><\/i>doi:10.1056\/NEJMoa2026028<\/span><\/a><\/p>\n

New drug for early Alzheimer\u2019s disease<\/b><\/p>\n

Eli-Lily\u2019s new drug donanemab was tested in the 257-patient double-blind randomised TRAILBLAZER-ALZ trial. It was positive for the primary outcome of change in the Integrated Alzheimer\u2019s Disease Rating Scale at 76 weeks, but the aim to reduce disease progression by at least half was not achieved. Patients had to have early symptomatic Alzheimer\u2019s disease with evidence of tau and amyloid deposition on positron emission tomography to be eligible to receive the intravenous injections of donanemab or placebo every four weeks. There was no benefit of donanemab over placebo seen on the secondary outcomes, which further calls into question the significance of the positive primary endpoint. There were no safety concerns.<\/span><\/p>\n

N Engl J Med <\/span><\/i>doi:10.1056\/NEJMoa2100708<\/span><\/p>\n

Alex Nowbar<\/strong> is a clinical research fellow at Imperial College London.<\/span><\/i><\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

Alex Nowbar reviews the latest research from the top medical journals […]<\/p>\n

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