Exp Clin Endocrinol Diabetes 2004; 112 - P112
DOI: 10.1055/s-2004-819230

Lack of relevant association between prolactin and immune responses in patients with chronic heart failure

H Wallaschofski 1, C Stumpf 2, WG Daniel 1, CD Garlichs 1, T Lohmann 3
  • 1Department of Medicine I
  • 2Department of Medicine II*, Medizinische Klinik I, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen
  • 3City Hospital of Dresden-Neustadt; Germany

Recently an association between decreased activation of T-lymphocytes reflected by hyperprolactinemia and left ventricular systolic function in CHF has been suggested. PRL is a pluripotent hormone which interferes with immune regulation as well as angiogenesis. Furthermore, PRL enhances platelet activation, especially CD62p expression. In our series of 50 patients with CHF (66.9±12.6 years; EF: 22±9%), we demonstrated significantly reduced serum levels of IL-10, an anti-inflammatory cytokine, revealing the inflammatory milieu in CHF. To further elucidate the influence of hyperprolactinemia in CHF on platelet activation we retrospectively studied PRL values in the sera of our patients and compared these results with CD62p expression on platelets. In contrast to previous findings we detected no hyperprolactinemia in our CHF patients (PRL: 6.2±4.3 ng/ml, normal range of our assay: in females <24.2ng/ml and in males <18.7ng/mL). There were no significant differences between patients with EF>30% (n=19; PRL: 5.6±3.2 ng/ml) and EF<30% (n=31; PRL; 6.5±4.8 ng/ml; p>0.05). Moreover, we found no significant correlation between PRL and left ventricular function (r2=-0.008; p>0.05) and the pro-inflammatory cytokines IL-6 (r2=0.036; p>0.05), TNFa (r2=0.0034; p>0.05) or the anti-inflammatory cytokine IL-10 (r2=0.002; p>0.05). However, patients with CHF showed significant enhanced expression of CD62p on platelets compared to healthy control subjects. CD62p was not correlated to PRL values (r2=-0.012; p>0.05). This finding contrasts to our results in other patient-groups but can be explained by the low PRL values in our patients with CHF. Therefore, our data suggest that PRL- independent activation of the pro-inflammatory milieu in CHF may play a pathogenic role in the development and progression of CHF. In conclusion, PRL was neither associated with left ventricular function nor correlated with pro- or anti-inflammatory cytokines in CHF patients.