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Tumour necrosis factor α (TNF α) gene polymorphism and non-ischaemic heart failure are linked, according to latest research by Densem et al, with the “TNF2” allele predominating in patients with this type of heart disease.
TNF α overexpression is linked with heart failure and its effects are reversible with TNF α binding protein in animal studies. TNF α concentrations in blood are raised in patients with heart failure and are proportional to severity of symptoms and survival. Early trials indicate that TNF α inhibition decreases symptoms. Healthy people vary in the amount of TNF α they produce—according to whether they have a G to A substitution at position−308 in the gene promoter. The TNF2 allele results in a six- or sevenfold increase in inducible synthesis.
Densem et al reasoned that frequency of the TNF2 genotype would be higher in patients who had a heart transplant for end stage heart failure than in the general population and compared expected against actual frequency in 175 transplant patients and 212 unrelated healthy controls.
TNF2 allele frequency was similar for the transplant patients and controls (31% v 27%). However, it was significantly higher in non-ischaemic (viral/idiopathic) than ischaemic heart failure (38% v 27%, p=0.03) and the controls (38% v 27%, p=0.05) when patients were grouped according to their diagnosis before transplantation. TNF2 frequency was similar in patients with ischaemic heart failure and controls.
If TNF α is a cause of non-ischaemic heart failure—currently unproved—anti-TNF α treatment would be beneficial.
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