Administration of testosterone to elderly hypogonadal men with Crohns disease improves their Crohns disease activity index: a pilot study
Farid Saad1,2, Ahmad Haider3, Winfred Kurtz4, Erik Giltay5 & Louis Gooren6
Objectives: To investigate effects of testosterone in hypogonadal men with Crohns disease (CD).
Design and methods: Thirteen men, aged 4567 years were diagnosed with subnormal plasma testosterone. They received treatment with parenteral testosterone undecanoate. They also suffered from CD. The Crohns disease activity index (CDAI) (1) was used to assess the severity of the disease. Levels of testosterone and C-reactive protein (CRP) were compared between the 13 men with CD and the other 109 hypogonadal men in this study.
Results: Levels of CRP were 22.7 mg/dl (95% confidence interval of the mean (CI): 14.934.3) in 13 men with CD versus 3.5 (2.941) in 107 control men (P=0.001). Levels of testosterone were lower in men with CD versus controls (2.6±0.4 ng/ml; 95% CI: 2.32.9 vs 2.9±0.4; 95% CI: 2.83.0; P=0.02). Upon normalization of testosterone, there was a significant decline in the CDAI occurring over the first 15 months, with stabilization of the improvement over the next 9 months. CRP levels declined progressively. Body mass index and waist circumference declined and the metabolic profile improved. Hemoglobin levels and the hematocrit increased significantly.
Conclusion: Upon normalization of plasma testosterone an improvement of the CDAI and CRP was noted. Also hemoglobin improved. The interpretation of the mechanism of this improvement is speculative. i) There is an inverse relationship between testosterone and levels of some inflammatory markers. ii) Endogenous cortisol combats inflammation. The local activation of glucocorticoids is mediated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) increasing cortisol, and 11β-HSD2 decreasing cortisol. Expression of 11β-HSD1 is elevated in inflamed tissue in CD, whereas 11β-HSD2 expression is decreased. Little is known about the effects of testosterone on local activation/deactivation of cortisol in the gut.