title: Prolactin and growth hormone responses to hypoglycemia in patients with rheumatoid arthritis and ankylosing spondylitis.
abstract: OBJECTIVE
  Prolactin (PRL) and growth hormone (GH) are pituitary hormones with immunomodulating properties. Their upregulated secretion may play a role in the pathogenesis of chronic inflammatory diseases. We evaluated PRL and GH responses to secretion stimulus in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS).
  
  
  METHODS
  Insulin hypoglycemia (0.1 IU/kg) was induced in 15 women with RA, 18 men with AS, and healthy controls matched for age, sex and body mass index. Plasma concentrations of glucose, PRL, GH, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-a) were analyzed.
  
  
  RESULTS
  RA patients had significantly lower area under the curve (AUC) of PRL (p = 0.049) compared to RA controls. During hypoglycemia double or higher increase of plasma PRL occurred in 5 RA (33%) patients and in 8 RA controls (57%). Using the General Linear Model procedure, no significant differences in PRL or GH responses were observed in patients with RA and AS. TNF-a was higher in patients with RA compared to RA controls (p < 0.05). There was no significant difference in TNF-a concentrations between AS patients and AS controls. IL-6 was higher in RA patients compared to controls (p < 0.05) and in AS patients compared to controls (p < 0.01). Significant positive correlation was found between TNF-a levels and AUC of PRL in AS patients (r = 0.46, p = 0.047), but not in the 2 control groups or in RA patients.
  
  
  CONCLUSIONS
  Our results indicate no upregulated PRL or GH responses to stimulation in premenopausal women with RA or men with AS.
authors.affiliation: National Institute of Rheumatic Diseases, Nabr. I. Krasku 4, 921-23 Piestany, Slovakia. rovensky@vurch.sk
authors.forename: Jozef
authors.initials: J
authors.lastname: Rovensky
authors.forename: Richard
authors.initials: R
authors.lastname: Imrich
authors.forename: Frantisek
authors.initials: F
authors.lastname: Malis
authors.forename: Martin
authors.initials: M
authors.lastname: Zlnay
authors.forename: Ladislav
authors.initials: L
authors.lastname: Macho
authors.forename: Juraj
authors.initials: J
authors.lastname: Koska
authors.forename: Milan
authors.initials: M
authors.lastname: Vigas
mesh_terms: D000328:Adult; D019540:Area Under Curve; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000175:diagnosis*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D013006:Growth Hormone / Q000097:blood* / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia; D007328:Insulin / Q000494:pharmacology; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011336:Probability; D011379:Prognosis; D011388:Prolactin / Q000097:blood* / Q000378:metabolism; D012016:Reference Values; D018570:Risk Assessment; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000175:diagnosis*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D011388:Prolactin; D013006:Growth Hormone