TY - JOUR
T1 - Neither exogenous nor endogenous GnRH stimulation alters the bio/immuno ratio of serum LH in healthy women and in polycystic ovarian disease
AU - Ding, Ying‐Qing ‐Q
AU - Anttila, Leena
AU - Ruutiainen, Kristiina
AU - Erkkola, Risto
AU - Irjala, Kerttu
AU - Huhtaniemi, Ilpo
PY - 1991/1
Y1 - 1991/1
N2 - The purpose of this study was to re‐evaluate the quantitative and qualitative responses of LH to exogenous and endogenous GnRH stimulation in normally cycling women and in polycystic ovarian disease (PCOD). Responses of serum LH to GnRH (100g i.v.) and the opioid antagonist naloxone (10 mg i.v.) were determined in healthy women in the early (n = 5) and late (n = 4) follicular phase, and in patients with PCOD (n = 20). Serum bioactive (B) LH was determined by a mouse interstitial cell in vitro bioassay, and immunoreactive LH by a conventional RIA (I‐LH) and a novel sensitive (0.05 IU/I) and specific immunofluorimetric assay (F‐LH). The B/I (2.4 ± 0.1) and B/F (2.7 ± 0.6) ratios in basal serum samples of the PCOD patients were significantly higher (p < 0.05) than the corresponding ratios (1.6‐1.8 and 1.8‐2.0) of the control women. GnRH stimulated the secretion of I‐LH (2‐4‐fold), F‐LH and B‐LH (3‐5‐fold each) in all groups studied. There were no apparent changes of the BII and BIF ratios in normal women during early follicular phase or in patients with PCOD. However, the normal women during late follicular phase displayed a significant (pCO.05) increase in the BII ratio, albeit no change was found in the BIF ratio. During naloxone‐induced endogenous GnRH responses, the control women during late follicular phase showed a %‐fold increase in B‐LH, I‐LH and F‐LH, with unchanged B/I and B/F ratios. No LH responses to naloxone were found in normal women during early follicular phase or in patients with PCOD. We conclude that, hy utilizing an immunofluorimetric assay, the basally elevated biohmmuno ratio of LH could be confirmed in PCOD patients. However, there were no qualitative changes in LH during the response to GnRH stimulation in normal women or in PCOD. 1991 Acta Obstet Gynecol Scand
AB - The purpose of this study was to re‐evaluate the quantitative and qualitative responses of LH to exogenous and endogenous GnRH stimulation in normally cycling women and in polycystic ovarian disease (PCOD). Responses of serum LH to GnRH (100g i.v.) and the opioid antagonist naloxone (10 mg i.v.) were determined in healthy women in the early (n = 5) and late (n = 4) follicular phase, and in patients with PCOD (n = 20). Serum bioactive (B) LH was determined by a mouse interstitial cell in vitro bioassay, and immunoreactive LH by a conventional RIA (I‐LH) and a novel sensitive (0.05 IU/I) and specific immunofluorimetric assay (F‐LH). The B/I (2.4 ± 0.1) and B/F (2.7 ± 0.6) ratios in basal serum samples of the PCOD patients were significantly higher (p < 0.05) than the corresponding ratios (1.6‐1.8 and 1.8‐2.0) of the control women. GnRH stimulated the secretion of I‐LH (2‐4‐fold), F‐LH and B‐LH (3‐5‐fold each) in all groups studied. There were no apparent changes of the BII and BIF ratios in normal women during early follicular phase or in patients with PCOD. However, the normal women during late follicular phase displayed a significant (pCO.05) increase in the BII ratio, albeit no change was found in the BIF ratio. During naloxone‐induced endogenous GnRH responses, the control women during late follicular phase showed a %‐fold increase in B‐LH, I‐LH and F‐LH, with unchanged B/I and B/F ratios. No LH responses to naloxone were found in normal women during early follicular phase or in patients with PCOD. We conclude that, hy utilizing an immunofluorimetric assay, the basally elevated biohmmuno ratio of LH could be confirmed in PCOD patients. However, there were no qualitative changes in LH during the response to GnRH stimulation in normal women or in PCOD. 1991 Acta Obstet Gynecol Scand
KW - GnRH stimulation
KW - in vitro bioassay
KW - luteinizing hormone
KW - naloxone
KW - polycystic ovarian disease
KW - serum LH
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U2 - 10.3109/00016349109006212
DO - 10.3109/00016349109006212
M3 - Article
C2 - 1927298
AN - SCOPUS:0025942989
SN - 0001-6349
VL - 70
SP - 211
EP - 217
JO - Acta Obstetricia et Gynecologica Scandinavica
JF - Acta Obstetricia et Gynecologica Scandinavica
IS - 3
ER -