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Table 2 Changes of the hormonal systems in chronic inflammatory rheumatic diseases

From: Interaction of the endocrine system with inflammation: a function of energy and volume regulation

  Effect on immune system/inflammation Observed changes in chronic inflammatory rheumatic diseases Long-term consequences
Energy storage hormones    
Insulin Direct support of immune cells Hyperinsulinemia, insulin resistance Insulin resistance, cachexia,
Pro-inflammatory in a state of systemic insulin resistance Stimulation of sympathetic nervous systema
Leukocytes do not become insulin-resistant Immune activation
Insulin-like growth factor-1 Support of innate and adaptive immunity [83, 84] Low IGF-1, IGF-1 resistance Cachexia, osteoporosis, immune activation
Androgens Inhibition of immune system and inflammation [148] Hypoandrogenemia Cachexia, loss of fertility, osteoporosis
Insulin resistance, immune activation
Estrogens Bi-modal role: support of B lymphocytes and T helper type 2; inhibition of macrophages, natural killer cells, and T helper type 1 (see [27]) Normal peripheral and high local estrogen levels, high 16α-hydroxylated estrogensb Local juxtainflammatory fat deposition
Low 2-hydroxylated estrogensc Immune activation (16α-hydroxylated forms)
Vitamin D Bi-modal role: support of innate immunity and inhibition of adaptive immunity [149] Hypovitaminosis D is common Osteoporosis, cachexia
Immune activation toward Th1 and Th17
Osteocalcin Not known Little and ambiguous results Unclear
Vagus nerve Immunosuppressive in acute inflammation (TNF) Low activity Loss of appetite, gastrointestinal disturbances, immune activation
Energy expenditure hormones    
Cortisol Immunosuppressive Normal to slightly increased in GC-free patients, low levels in GC-pretreated patients Cachexia, osteoporosis
Volume overload
Not much influence on immune system
Sympathetic nervous system (noradrenaline/adrenaline) β-Adrenergic: suppressive for innate immunity and T helper type 1 lymphocytes, support of B lymphocytes High activity Cachexia, osteoporosis
α-Adrenergic: support of inflammation Hypertension, volume overload
Immune activation due to nerve fiber lossd
Growth hormone Immunostimulatory Little and ambiguous results Cachexia, osteoporosis
Thyroid hormones (T3) Directly immunostimulatory Low T3 levels, diminished activity of the hypothalamic-pituitary-thyroid gland axis but possibly normal T3 levels in muscle Cachexia
Indirectly via provision of inorganic iodide Immune activation in granulocytes
RAAS (angiotensin II) Directly immunostimulatory Elevated activity Volume overload, hypertension
Cachexia, insulin resistance, osteoporosis
Immune activation
  1. aThis will not lead to immunosuppression due to loss of sympathetic nerve fibers in inflamed tissue and secondary lymphoid organs. bThese are proproliferative mitogenic estrogens. cThese are anti-mitogenic estrogens. dSympathetic nerve fiber loss was described locally in inflamed tissue and in secondary lymphoid organs. GC, glucocorticoid; IGF-1, insulin-like growth factor-1; RAAS, renin-angiotensin-aldosterone system; T3, tri-iodothyronine; Th, T helper lymphocyte; TNF, tumor necrosis factor.