Dehydroepiandrosterone response to the adrenocorticotropin test and the combined dexamethasone and corticotropin-releasing hormone test in patients with multiple sclerosis.

TL;DR: This article uses exemplary testosterone and cortisol data to illustrate that one major concern of ratios lies in their distribution and inherent asymmetry, and suggests the use of non-parametric methods as well as the log-transformation of hormone ratios as appropriate methods to deal with these statistical problems.

TL;DR: In this article, the authors explored the feedback mechanism of the hypothalamic pituitary adrenocortical (HPA) system in epilepsy and found that there is a lack of inhibitory control of the HPA system in patients with epilepsy, also in the absence of enzyme inducing medication.

TL;DR: Current data on sex steroid hormones provide no straightforward explanation for the male predominance in Ankylosing spondylitis and there is no rationale to treat AS patients withsex steroid hormones.

TL;DR: Serum levels of DHEA in relation to serum levels of other adrenal hormones are completely different in patients with an acute inflammatory stressful disease state compared with patients with chronic inflammation, indicating that TNF and IL-6 play a predictive role for changes.

TL;DR: The data indicate that a deficiency in sulpho-conjugated steroids is a permanent feature of patients with SLE and that this is accentuated by the administration of corticosteroid derivatives.

TL;DR: Steroid synthesis in times of chronic illness may be diverted from adrenal androgen to corticosteroid pathways ensuring maintained secretion of cortisol, which is essential to the health of ill patients.

TL;DR: The data show that chronically elevated central CRH levels as occurring during chronic stress result in defective central nervous system and immune system responses to an acute (inflammatory) challenge, and provide evidence that chronic CRH hypersecretion is an important factor in the etiology of stress‐related disorders.

TL;DR: Two lines of evidence are obtained that neurosteroids do not inhibit TNF via the glucocorticoid receptor, and the inhibitory effect of dexamethasone, a classical glucoc Corticoid and inhibitor of TNF synthesis, was completely reversed by RU38486.