Differential Gene Expression Among Patients With Heart Failure Experiencing Pain.
Asa B Smith, Miyeon Jung, Susan J Pressler and 2 others
PMID 36920122WHAT IT FOUND
Patients with heart failure who had pain showed different blood gene expression than those without pain in a 40-patient sample, but the seven candidate genes were not confirmed in a 24-patient validation sample.
Key findings
01From 115 eligible patients, the 40-patient primary sample (20 with pain, 20 without) showed 334 differentially expressed genes: 279 upregulated and 55 downregulated.
02Seven candidate genes were upregulated in the pain group in the primary sample, but only three (CTSG, MMP8, and DEFA3) were also upregulated in the validation sample.
03In the 24-patient validation sample (10 with pain, 14 without), gene expression differences between pain and no-pain groups were not statistically significant.
STILL TO COME
How it was doneWhat they foundWhat it means for RNs
Read the rest of this summary
You get three full summaries a month, free, and we do not ask for a card. Search, the TL;DRs and your library stay unlimited either way.
What it does not show
The study was exploratory and small: the primary analysis had 40 patients and the validation analysis had 24. Pain was measured with a yes/no question, so the groups did not capture pain cause, location, severity, or pattern. The parent study did not collect pain cause or actively measure pain location, so the findings describe a mixed pain group rather than a specific pain phenotype. Comorbid arthritis and other inflammatory conditions may explain some gene differences; the study did not determine whether inflammation causes pain or results from other conditions. Only three of seven candidate genes were replicated in direction, and the validation sample did not show statistically significant differences. No clinical outcome, treatment, or nursing care was tested.
Declared interests
The authors declared no conflicts of interest. The parent study was NIH-funded.
The easy way to misread this
Do not read these gene differences as proof of a pain mechanism or a clinical biomarker. The validation sample did not confirm the differences, and pain cause and location were not measured.