- Meeting abstract
- Open Access
Hormones and not gender influences outcome in severe infection
© The Author(s) 2001
- Received: 15 January 2001
- Published: 2 March 2001
Previous clinical and experimental studies examining gender-related differences in infectious complications and mortality have provided inconsistent results. Some have shown a better, some a worse prognosis in women. In a small study an increase in β-estradiol has been demonstrated in men. Therefore our purpose was to study gender hormones in patients with severe infection with regard to 28 day mortality in a prospectively study.
Methods and results
We have included 145 patients (39.3% women) with a median age of 60 years, APACHE II Score of 19 and a survival rate of 64.7% in men and 62.1% in women. At admission, there was no significant difference in demographic data, laboratory signs of infection (temperature, C-reactive protein, procalcitonin, leukocyte count, platelets), location of infection or incidence of chronic immunosuppression, APACHE score or outcome between men and women. In addition hormonal analysis revealed no difference between sexes in β-estradiol, testosterone, cortisole, thyroidea stimulating hormone, whereas the gonadotropines were significantly higher in women, indicating that they were post menopausal (67% older than 55 years).
In a univariant analysis we found significant difference between survivor and non-survivor in β-estradiol (P < 0.001) without difference between gender, in temperature, C-reactive protein and procalcitonin at the day of admission, whereas testosterone, cortisone, dehydroepiandrostendiole, thyroidea stimulating hormone, gonadotropines or prolactin were not different between groups. We have compared the results of the radio-immuno-assay with HPLC and found perfectly matched results. β-Estradiol was elevated up to 25-times the normal range even at day of admission. β-Estradiol increased further in the next days reaching a maximum at day 4–7 and decreased thereafter. Patients on chronic steroid therapy had no different β-estradiol level than untreated patients. β-Estradiol was not influenced by body weight. Even women after hysterectomy and ovarectomy had elevated β-estradiol levels in plasma indicating that the gonads are not the source of β-estradiol.
In the survival analysis with Kaplan–Mayer analysis, increasing β-estradiol was highly associated with increasing mortality for both sexes, men and women (P < 0.001).
Men and women had similar survival rates. In men and women β-estradiol influence outcome.