Tumor necrosis factor alpha, interleukin 6, intracellular adhesion molecule-1 and uric acid levels in chronic heart failure

الملخص EN

Chronic heart failure is a model of systemic hypoxia This hypoxia is associated with activation of xanthine oxidase resulting in hyperuricemia, leucocytes and endothelial cell activation.

Circulating markers of inflammation include Tumor necrosis factor alpha, (TNF-a) interleukin 6,(IL-6) as well as Intracellular adhesion molecule-1 (ICAM-1) were measured, in addition to kidney, liver function tests and serum uric acid.

This study was conducted on forty patients with chronic heart failure class IV.

All the patients were under furosemide and digoxin therapy, the patients also received allopurinol 300 mg/day for one month.

Twenty healthy subjects were included as a control group (group I).

Patients were classified into 2 groups, group II: patients before allopurinal therapy and group III: the same patients one month after therapy.

Mean value of serum uric acid showed significant elevation in group II compared to controls and to patients group (III) (P<0.001 for both).

Mean values of TNF-a, 1L-6 and ICAM-1 revealed significant elevation in patient groups (II, III) before and after therapy compared to controls (P<0.001 for each).

In patients groups after therapy, TNF-a IL-6 and ICAM-1 showed significant reduction compared to patients group before therapy (P<0.001, <0.05 and<0.001 respectively).

Ejection fraction value (%) in patient groups before and after therapy (groups II, III) showed statistically insignificant reduction compared to controls (group I).

We concluded that: 1- There was strong association between hyperuricemia TNF-a, IL-6 and ICAM-1 in chronic heart failure.

These markers may play a role in the development and progression of heart failure through cardiac function impairment.

2- Low dose allopurinal therapy may have a beneficial effect for patients with chronic heart failure through inhibition of xanthine oxidase activity, so we suggest the following: 1- Inhibition of the synthesis, release or function of these cytokines might benefit the heart failure patients by using anticytokine therapy.

2- Inhibition of xanthine oxidase activity by long term high dose of allopurinol therapy.