Serum and follicular fluid (FF) estradiol (E2) levels in ovarian hyperstimulation syndrome (OHSS) during in vitro fertilization (IVF) and gamete intrafallopian transfer (GIFT) conception cycles after pituitary suppression

1991 ◽  
Vol 8 (3) ◽  
pp. 137-140 ◽  
Author(s):  
Joan Leya ◽  
Mary Wood Molo ◽  
Denise Olson ◽  
Ewa Radwanska
Keyword(s):  
In Vitro Fertilization ◽  
Follicular Fluid ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Gamete Intrafallopian Transfer ◽  
Vitro Fertilization ◽  
Pituitary Suppression

Administration of methylprednisolone to prevent severe ovarian hyperstimulation syndrome in patients undergoing in vitro fertilization

2002 ◽  
Vol 78 (3) ◽  
pp. 529-533 ◽  
Author(s):  
Trifon Lainas ◽  
Georgios Petsas ◽  
Georgia Stavropoulou ◽  
Efthymia Alexopoulou ◽  
George Iliadis ◽  
...  
Keyword(s):  
In Vitro Fertilization ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vitro Fertilization ◽  
Severe Ovarian Hyperstimulation Syndrome

scholarly journals A Mutation in the Follicle-Stimulating Hormone Receptor as a Cause of Familial Spontaneous Ovarian Hyperstimulation Syndrome

2004 ◽  
Vol 89 (4) ◽  
pp. 1255-1258 ◽  
Author(s):  
Lucia Montanelli ◽  
Anne Delbaere ◽  
Costantino Di Carlo ◽  
Carmine Nappi ◽  
Guillaume Smits ◽  
...  
Keyword(s):  
In Vitro Fertilization ◽  
Ovarian Hyperstimulation Syndrome ◽  
Follicle Stimulating Hormone ◽  
High Sensitivity ◽  
Ovarian Hyperstimulation ◽  
Satisfactory Explanation ◽  
Vitro Fertilization ◽  
Increased Sensitivity ◽  
Stimulation Of

Abstract Ovarian hyperstimulation syndrome (OHSS) occurs mainly after excessive stimulation of the ovaries by exogenous gonadotropins administrated in the context of in vitro fertilization procedures (iatrogenic OHSS). Recently, spontaneous and recurrent occurrence of the disease (spontaneous OHSS) was shown in two families to be caused by mutations affecting the follitropin receptor (FSHr). The two mutant FSHr (T449I, D567N) harbor aminoacid substitutions in the serpentine portion of the receptor and display abnormally high sensitivity to the pregnancy hormone hCG, thus providing a satisfactory explanation to the phenotype. In addition, mutant D567N showed also increased sensitivity to thyrotopin (TSH) and displayed increase in basal (ligand-independent) activity. In this report, we describe a new familial case of recurrent OHSS. The affected women were heterozygous for a different mutation involving codon 449, where an alanine was substituted for threonine. Similar to D567N, the T449A FSHr mutant shows an increase of its sensitivity to both hCG and TSH, together with an increase in basal activity. Together with the two previous studies, this report shows that inappropriate stimulation of the FSHr by hCG is a cause of spontaneous OHSS.

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