Rheumatic Manifestations of Endocrine Diseases

Joseph A. Markenson


Curr Opin Rheumatol. 2010;22(1):64-71. 

In This Article

Hypothalamic-gonadal Axis

Female-to-male ratios differ among connective tissues diseases. The ratio for RA is 3: 1 with the exception of juveniles and older adults. SLE has a female-to-male ratio of 9: 1 and in RA the incidence is higher in postmenopausal as opposed to premenopausal women.[81] Adult men have a significant delayed onset of disease. Masi and Kaslow[82] and Petri[83] have suggested that this may be due to gonadal hormones with protection of RA in younger men (testosterone) and predisposition to SLE in women (estrogens). A recent article studied longitudinally the levels of total testosterone, sex hormone-binding globulin (SHBG), and LH in 41 males with early RA (DMARD naïve at study entry) over 2 years. Only in male patients less than 50 years old were lower base line levels of testosterone found compared with controls. When treated with DMARDS those males who responded with decreased activity of disease (measured by DAS 28 and HAQ) also demonstrated significantly increased levels of testosterone. Changes in testosterone levels in patients more than 50 years were marginally better after DMARD treatment and LH levels in both groups were unchanged (although lower in men > 50). The consequence was improvement of the hypothalamic-pituitary-gonadal (HPG) axis at the gonadal level but not the hypothalamic-pituitary-adrenal (HPA) level.

In patients with RA both the HPG and the HPA axis have been reported to respond abnormally to inflammation and stress. The important question of whether inflammation decreased the HPA axis (increasing risk for RA) and if correction occurs with therapy, was not answered. As pointed out by Masi et al.[84••] one needed to be able to calculate baseline levels for these hormones prior to onset of disease to be able to answer this question


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