Trial reportThe Journal of clinical endocrinology and metabolism2016
N-Terminal Prosomatostatin as a Risk Marker for Cardiovascular Disease and Diabetes in a General Population.
Trial report in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Vasoactive Biomarkers Associated With Long-Term Incidence of Symptomatic Peripheral Arterial Disease and Mortality.Angiology · 2021Article
- Somatostatin and Neuropeptide Y in Cerebrospinal Fluid: Correlations With Amyloid Peptides AβFrontiers in aging neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextSomatostatin inhibits a range of hormones, including GH, insulin, and glucagon, but little is known about its role in the development of cardiometabolic disease.
objectiveThe objective of the study was to investigate whether fasting plasma concentration of N-terminal prosomatostatin (NT-proSST) is associated with the development of diabetes, coronary artery disease (CAD), and mortality. DESIGN, SETTING, AND
participantsNT-proSST was measured in plasma from 5389 fasting participants of the population-based study Malmö Preventive Project, with a mean baseline age of 69.4 ± 6.2 years. Cox proportional hazards models adjusted for traditional cardiovascular risk factors were used to investigate the relationships between baseline NT-proSST and end points, with a mean follow-up of 5.6 ± 1.4 years.
main outcome measuresCAD, diabetes, and mortality were measured.
resultsOverall, NT-proSST (hazard ratio [HR] per SD increment of log transformed NT-proSST) was unrelated to the risk of incident diabetes (220 events; HR 1.05; 95% confidence interval [CI] 0.91-1.20; P = .531) but was related to the risk of incident CAD (370 events; HR 1.17; 95% CI 1.06-1.30; P = .003), all-cause mortality (756 events; HR 1.24; 95% CI 1.15-1.33; P < .001), and cardiovascular mortality (283 events; HR 1.33; 95% CI 1.19-1.43; P < .001). The relationships were not linear, with most of the excess risk observed in subjects with high values of NT-proSST. Subjects in the top vs bottom decile had a severely increased risk of incident CAD (HR 2.41; 95% CI 1.45-4.01; P < .001), all-cause mortality (HR 1.84; 95% CI 1.33-2.53; P < .001), and cardiovascular mortality (HR 2.44; 95% CI 1.39-4.27; P < .001).
conclusionNT-proSST was significantly and independently associated with the development of CAD, all-cause mortality, and cardiovascular mortality.
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