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Results for “Ovarian hyperstimulation syndrome”

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PubMed1979

Histamine levels in ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome was produced in rabbits by administration of human menopausal gonadotropin (hMG) and human chorionic gonadotropin (hCG). Histamine levels in the animals' plasma were determined by an enzymatic-isotopic assay. The results of this study show that there is no statistically significant difference between histamine levels in ovarian hyperstimulated animals as compared with control animals. Furthermore, no differences in the number of mast cells in the ovaries could be demonstrated between the 2 groups. It is concluded that histamine probably does not play a role in the pathogenesis of this syndrome. The relevance of this suggestion to other proposed mechanisms on the etiology of ovarian hyperstimulation syndrome is discussed.

Animals↗
PubMed1976

Treatment of ovarian hyperstimulation syndrome by antihistamine.

Ovarian hyperstimulation was produced by human menopausal gonadotropin and chorionic gonadotropin in rabbits. A more rapid regression of the hyperstimualted ovaries was observed in an antihistamine-treated group than in a control group. The difference in regression was found to be statistically significant. The possibility of treating the ovarian hyperstimulation syndrome by antihistamine is cited.

Animals↗
PubMed1975

Antihistamine blockade of the ovarian hyperstimulation syndrome. II. Possible role of antigen-antibody complexes in the pathogenesis of the syndrome.

Antihistamine can prevent the ovarian hyperstimulation syndrome in the rabbit. The mechanism underlying this experimental observation has not been elucidated. Our experiments were directed at the question of whether antigen-antibody complexes are a factor in the development of the ovarian hyperstimulation syndrome. The results do not support the theory that antigen-antibody complexes play a role in the pathogenesis of this syndrome.

Animals↗
PubMed2025

Potential therapeutic targets for ovarian hyperstimulation syndrome revealed by proteome-wide mendelian randomization and colocalization analysis.

Ovarian hyperstimulation syndrome (OHSS) is a severe complication associated with assisted reproductive technologies, characterized by metabolic, immune and vascular disorders. Understanding the molecular mechanisms underlying OHSS could reveal potential therapeutic targets and improve patient outcomes. In this study, We aimed to utilize proteome-wide Mendelian randomization (MR) and colocalization analysis to identify plasma proteins associated with OHSS and evaluate their potential as therapeutic targets through druggability assessment. We employed proteome-wide MR analysis summary data-based Mendelian randomization (SMR) analysis and phenome-wide association study (PheWAS) analysis to establish causal relationships between plasma proteins and OHSS. Colocalization analysis confirmed overlaps between proteins and genetic signals associated with OHSS. Pathway and network analyses were conducted to explore biological functions and protein interactions, while drug-target databases were queried for potential therapeutic interventions. Our results showed that 4 key proteins, including Suprabasin (SBSN), SLAMF4 (CD244), Enolase 3 (ENO3) and Thioredoxin domain-containing protein 12 (TXNDC12) were identified as significant contributors to OHSS. Pathway enrichment and interaction analyses further supported their involvement in metabolic, immune and structural pathways related to OHSS. Drug availability for colocalized proteins reveled potential drug targets for ENO3 (2-deoxy-D-glucose), CD244 (lenalidomide) and TXNDC12 (Auranofin), while no potential drug targets were identified for SBSN. Over all, our study identified15 plasma proteins, including SBSN, CD244, ENO3, and TXNDC12, as key contributors to the risk of OHSS through MR and colocalization analysis. These proteins were involved in metabolic regulation, immune response and antioxidant pathways, highlighting potential therapeutic targets and suggesting new directions for treatment strategies.

Humans↗
PubMed1979

Plasma prolactin, human chorionic gonadotropin, estradiol, testosterone, and progesterone in the ovarian hyperstimulation syndrome.

Plasma prolactin, estradiol, progesterone, and testosterone, but not HCG-beta levels, were higher in a patient who developed the ovarian hyperstimulation syndrome while undergoing ovulation induction with human gonadotropins than in two other women who also became pregnant after similar treatment without complications. These results suggest that hyperprolactinema, in association with elevated ovarian steroid levels, may be factors in the pathogenesis of this disorder.

Blood Proteins↗
PubMed1976

Therapeutic use of gonadoliberin (follicle-stimulating hormone/luteinizing hormone-releasing hormone) in women.

Certain conclusions may be drawn from the present review: 1. Synthetic FSH/LH-RH may induce ovulation; therefore, a therapeutic effect has been established in some cases of anovulatory infertility, but it is still difficult to assess the correct dose of FSH/LH-RH because of individual variations in response. 2. Gonadoliberin may also be used to induce ovulation after follicular maturation has been evoked by other agents. FSH/LH-RH can be utilized for supplementing the LH surge after clomiphene therapy in cases of clomiphene failure. When associated with HMG, the synthetic decapeptide may be helpful in avoiding the ovarian hyperstimulation syndrome. 3. The "triggering" of ovulation by a continuous infusion of FSH/LH-RH might be a convenient means of controlling the timing of ovulation. 4. It is expected that FSH/LH-RH blocking analogs may be used to inhibit both LH and FSH release induced by endogenous gonadoliberin in women seeking contraception.

Anovulation↗
PubMed1978

Observations on 320 infertile patients treated with human gonadotropins (human menopausal gonadotropin/human chorionic gonadotropin).

From 1964 to 1975, 320 patients with failure of ovulation were treated with human gonadotropins (human menopausal gonadotropin [HMG]/human chorionic gonadotropin [HCG]). Estimation of the pituitary and ovarian function of each patient rather than classification into clinical groups contributed positively to the selection of patients. The dosage schedules used for the patients should be considered conservative, insofar as the amount of HMG and HCG administered per treatment cycle is concerned. The response to human gonadotropins was evaluated mainly according to excretion levels of estrogen and pregnanediol. Of the 320 patients, 256 ovulated at least once during treatment with gonadotropins (80%). Ovarian hyperstimulation syndrome was encountered in 22 patients (6.8%). Pregnancy occurred in 163 patients (50.9%) and in some of them twice, so that the total number of pregnancies was 206. Fifteen pregnancies were multiple (all of them twins). Of 197 pregnancies followed, 43 ended in abortion and 36 in premature labor. Cesarian section was performed in 21 cases.

Chorionic Gonadotropin↗
PubMed1978

[Spontaneous hyperstimulation of the ovaries with luteal cysts and ascites during a twin pregnancy-extreme case of the syndrome of painfull early pregnancy (author's transl)].

Laparotomy was performed in a para II gravida II of 28 years in an early twin pregnancy. The left ovary was enlarged to 18 X 8 cm, the right ovary to 1i X 8 cm by luteal cysts. The abdominal cavity contained an ample amount of peritoneal fluid. The history is understood as spontaneous ovarian hyperstimulation, and as an extreme case of the relatively common syndrome of painfull early pregnancy, occasionally leading to unnecessary surgical intervention.

Abdomen, Acute↗
PubMed2026

Epigenetic safety of in vitro maturation in PCOS: genome-wide DNA methylation profiling of cord blood from a randomized controlled trial.

BACKGROUND: In vitro maturation (IVM) provides a safer alternative to conventional in vitro fertilization (IVF) for women with polycystic ovary syndrome (PCOS) by mitigating the risk of ovarian hyperstimulation. However, concerns persist regarding whether IVM perturbs epigenetic reprogramming in the offspring. Current evidence is constrained by candidate-gene approaches or a lack of parental controls. This study aimed to evaluate the genome-wide DNA methylation safety of IVM compared with conventional IVF using a rigorous trio-based design. METHODS: This secondary epigenetic analysis was nested within a randomized controlled trial (RCT) (ClinicalTrials.gov: NCT03463772). We included 10 nuclear families (trios), comprising five IVM-conceived and five IVF-conceived singleton offspring alongside their biological parents. Both groups utilized a uniform freeze-only single-blastocyst transfer strategy to minimize hormonal confounding. Genomic DNA from umbilical cord blood (UCB) and parental peripheral blood was analyzed using reduced representation bisulfite sequencing (RRBS). Genome-wide methylation patterns and differentially methylated regions (DMRs) were subsequently compared between the groups. RESULTS: Clinical characteristics were comparable between the IVM and IVF groups. Genome-wide analyses demonstrated high concordance in UCB methylation patterns, revealing no significant differences in global CpG methylation levels or distributions across key genomic features (promoters, CpG islands, and gene bodies). Only three rare DMRs were identified in UCB (representing ~ 0.0001% of the genome), none of which mapped to imprinted or developmentally critical loci. Furthermore, methylation variability remained consistent between the groups. CONCLUSIONS: Our findings provide robust mechanistic evidence supporting the epigenetic safety of IVM. The remarkable stability of the neonatal methylome confirms that specific IVM conditions do not compromise early developmental programming, thereby endorsing IVM as a safe and viable alternative for women with PCOS. TRIAL REGISTRATION: ClinicalTrials.gov registry, NCT03463772. Registered on March 13, 2018.

Humans↗
PubMed1978

Serum 17beta-estradiol. Index of follicular maturation during gonadotropin therapy.

Thirteen patients with hypogonadotropic hypogonadism were treated with human menopausal gonadotropins (hMG) and human chorionic gonadotropin (hCG) to induce ovulation. Daily serum 17beta-estradiol (E2) assays were used to monitor the ovarian response to HMG. Apparent ovulation, documented by basal body temperatures, occurred in 41 of 53 hMG-hCG treatment cycles. Thirteen pregnancies occurred in 8 of the 13 patients. One twin pregnancy resulted. The hyperstimulation syndrome did not occur. Our data indicate that an optimal pregnancy rate with a minimum risk of hyperstimulation can be achieved when ovulation is induced 24 hours after the preovulatory serum E2 concentration has reached 500 to 900 pg/ml. Ovulation is induced by administering 10,000 IU and 5000 IU hCG on successive days. In addition, we now routinely give two or three injections of 2500 IU hCG at subsequent 3- to 4-day intervals to support the corpus luteum.

Adult↗
PubMed1977

Management of hyperstimulation syndrome.

A case of hyperstimulation syndrome secondary to Pergonal therapy is presented. Successful management was based principally on severe sodium and fluid restriction without the use of volume expanders. The rationale for this therapeutic approach is presented and discussed. Although this iatrogenic disease should be virtually eliminated with the monitoring of daily urinary estrogens, severe hyperstimulation may still occur as a result of laboratory error.

Adult↗
PubMed1979

Measurement of the ovarian follicle by ultrasound in ovulation induction.

Ultrasonic monitoring of ovarian follicles and estimation of serum estradiol were carried out in 12 patients with clomiphene therapy, in 5 patients with gonadotropin therapy, and in 7 normal controls. The average diameter of preovulatory follicles in normal controls was 12,8 mm; in ovulation induction groups it was 2 to 4 mm greater. The level of serum estradiol was also higher in ovulation induction groups than in normal controls. The combined use of these two methods is recommended: ultrasonic monitoring to minimize the risk of multiple pregnancies and estrogen level monitoring to minimize the risk of hyperstimulation. Ultrasound is also safe and practical in following the size of hyperstimulated ovaries.

Clomiphene↗
PubMed1977

The use of gonadotropins for the induction of ovulation in women with polycystic ovarian disease.

Ten infertile patients with polycystic ovarian disease were treated with 18 cycles of "pure" human pituitary follicle-stimulating hormone (HP-FSH) and 10 cycles of human menopausal gonadotropin (HMG) consisting of FSH and luteinizing hormone (LH) in a 1:1 ratio. Human chorionic gonadotropin was used to trigger ovulation when optimal follicular development was achieved as judged by urinary estrogen determinations. Of the 18 cycles utilizing HP-FSH, 14 were presumptively ovulatory, 2 were conceptual, and in 5 cycles ovarian enlargement was noted. Of the 10 HMG cycles, none was ovulatory, no conceptions resulted, and 6 instances of hyperstimulation were noted. Pretreatment serum LH levels were significantly higher than normal follicular phase values. These observations suggest that endogenous LH levels in patients with polycystic ovaries are quite adequate for follicular development so that the administration of exogenous LH is unwarranted. Furthermore, the data suggest that HP-FSH or low-LH-containing HMG may prove to be an additional safe and effective nonsurgical treatment modality for patients who are anovulatory because of polycystic ovaries.

Adult↗