Somatotropic, lactotropic and adrenocortical responses to insulin-induced hypoglycemia in patients with rheumatoid arthritis.
Neuroendocrine mechanisms have been suggested to play an important role in the onset and progression of rheumatoid arthritis (RA). The aim of this study was to evaluate hypothalamic-pituitary functions in RA patients by measurement of hormone responses to insulin-induced hypoglycemia. Insulin-hypoglycemia (Actrapid HM 0.1 IU/kg, i.v. as a bolus) was induced in 17 male patients and in 11 age-, gender-, and weight-matched healthy subjects. Concentrations of growth hormone (GH), prolactin (PRL) and cortisol were analyzed in plasma. PRL release after thyreoliberin stimulation (TRH, 200 g, i.v.) was determined in 21 patients with active forms of RA and in 12 control subjects to evaluate pituitary lactotropic response. In RA patients, basal concentrations of glucose, GH, PRL, and cortisol were in the normal range and they were comparable to those in the control group. Stress of hypoglycemia induced significant elevation of GH, PRL, and cortisol concentrations in all groups. Cortisol responses to hypoglycemia were comparable in patients and in control subjects. GH release during hypoglycemia was increased (p < 0.05) and PRL response was attenuated (p < 0.05) in RA patients versus control subjects. After TRH administration, PRL response was the same in patients as in healthy subjects. In conclusion, the present study revealed an altered hypothalamic-pituitary function in patients with RA, namely, an enhanced somatotropic and reduced lactotropic activation in response to insulin-induced hypoglycemia. Basal hormone levels and cortisol release during hypoglycemia were similar to those in healthy subjects.
Research Institute of Rheumatic Diseases, Piest'any, Slovak Republic. rovensky@vurch.sk
Jozef
J
Rovensky
Jana
J
Bakosová
Juraj
J
Koska
Lucia
L
Ksinantová
Daniela
D
Jezová
Milan
M
Vigas
D000302:Adrenal Cortex / Q000187:drug effects / Q000378:metabolism; D000328:Adult; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D001327:Autoimmune Diseases / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D001786:Blood Glucose / Q000187:drug effects; D005260:Female; D019382:Human Growth Hormone / Q000097:blood / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000503:physiopathology; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D012636:Secretory Rate / Q000187:drug effects; D013973:Thyrotropin-Releasing Hormone
D001786:Blood Glucose; D007328:Insulin; D019382:Human Growth Hormone; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D006854:Hydrocortisone