Skip to main content

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.