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At least 19 recordsLinked to original sources

PubMed2002

A case of cerebral infarct in combined antiphospholipid antibody and ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome is a serious complication of ovulation induction and has a diverse clinical spectrum from edema to thromboembolism. Antiphospholipid antibody syndrome, one of the well known hypercoagulable states, can be also manifested as an arterial or venous thrombosis and recurrent spontaneous abortion. Sometimes a patient with antiphospholipid antibodies might not notice a miscarriage and seek for assisted reproduction treatment, which harbors a chance of developing ovarian hyperstimulation syndrome. If this happens, the ovarian hyperstimulation syndrome can exacerbate the thrombotic complication of underlying antiphospholipid antibody syndrome, resulting in a catastrophic vascular event. The authors experienced a case of middle cerebral artery infarct, which developed during ovarian hyperstimulation syndrome in a 33-yr-old woman with a previous history of fetal loss. An elevated titer of anticardiolipin antibodies was noticed and persisted thereafter. The authors suggest screening tests for the presence of antiphospholipid antibodies before controlled ovarian hyperstimulation.

Adult↗

PubMed2002

Current management of ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome is an iatrogenic and usually self-limiting condition which can occasionally be life threatening. This article reviews methods of prevention and management of ovarian hyperstimulation syndrome.

Analgesia↗

PubMed1996

Elevated liver function tests in a case of moderate ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome is a recognized complication of ovulation induction. Abnormalities in liver function have been considered to be a rare manifestation of the severe form of ovarian hyperstimulation syndrome (OHSS). A 28 year old woman with primary infertility underwent ovulation induction and intrauterine insemination. She was diagnosed with moderate OHSS and was followed as an outpatient. Early in her course of treatment she complained of upper right quadrant pain. Her work-up included an upper right quadrant ultrasound which showed only moderate ascites. Liver function tests at that time were elevated in a hepatocellular damage pattern. Liver function test elevations, as well as the ovarian hyperstimulation, resolved spontaneously in 10 days. Transient abnormalities in liver function do not appear to be limited to the most sever forms of OHSS.

Adult↗

PubMed2004

Ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication that is associated with modern techniques for in vitro fertilization. Extensive efforts have been made to understand the pathophysiology and to improve the management of this entity. The severe and life-threatening forms of the ovarian hyperstimulation syndrome are still challenging for critical care physicians. This article reviews the pathogenesis, epidemiology, classification, clinical manifestations, and complications of these forms of OHSS. The different therapeutic options currently available are reviewed, and a stepwise approach for the management of these patients is provided.

Female↗

PubMed2005

Ruptured ovarian cysts and bilateral ectopic pregnancy complicating a case of severe ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS), ruptured ovarian cysts and bilateral ectopic pregnancies are all well-recognized entities occurring in association with infertility treatment. We are reporting a case of severe OHSS which was complicated initially by ruptured ovarian cysts and later by bilateral ectopic pregnancy. Diagnosis of tubal pregnancy was obscured by stimulated ovaries, which prevented accurate ultrasound definition. The role of transvaginal ultrasound, serial beta human chorionic gonadotropin and the place of paracentesis in diagnosing these cases are discussed.

Adult↗

PubMed1983

Serotonin and the ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome was induced in rabbit by administration of human menopausal gonadotropin (HMG) and human chorionic gonadotropin (HCG). In an attempt to establish whether serotonin plays a part in the induction of this syndrome, the hyperstimulated rabbits were divided into two groups and were administered known anti-serotonin drugs, cyproheptadine and methysergide, respectively. The group treated with cyproheptadine, a non-specific serotonin antagonist, exhibited significant acceleration in the regression of the syndrome. Methysergide, a specific serotonin antagonist, administered to the second group, neither prevented the occurrence of the syndrome nor accelerated its regression. The results of this work indicate that serotonin does not seem to be directly involved in the production of the ovarian hyperstimulation syndrome in rabbits.

Animals↗

PubMed1998

The kallikrein-kinin system, but not vascular endothelial growth factor, plays a role in the increased vascular permeability associated with ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is a severe complication arising from controlled stimulation treatment. Vascular endothelial growth factor (VEGF) has recently emerged as an important factor which may be responsible for the hyperpermeability seen in OHSS. The purpose of the present study was to investigate and compare the mechanisms by which ascites in patients with OHSS and ovarian carcinoma induce increases in vascular permeability in an in vitro assay and an in vivo animal experiment. We found 8-fold lower VEGF levels in ascites from patients with OHSS than in those from patients with ovarian carcinoma. Although VEGF is produced by the ovaries, it is not necessarily the factor responsible for hyperpermeability. We also demonstrated that the vascular hyperpermeability produced by OHSS ascites was not abolished by specific neutralizing anti-VEGF antibodies, and that not all of the VEGF found in the ascites fluid is biologically active. Moreover, our results strongly suggest that the vascular permeability produced by OHSS ascites may depend on activation of the kallikrein-kinin system. Possible evidence for this phenomenon was obtained by demonstrating that the hyperpermeability caused by the ascites could be blocked by Trasylol (known to inhibit bradykinin synthesis) and potentiated by captopril (a kininase II inhibitor). Taken together, the results suggest that, although VEGF is found in ascites fluid from patients with OHSS, it is unlikely that the cause of OHSS involves VEGF production by the ovaries. The kallikrein-kinin system may be more important in the hyperpermeability seen in OHSS.

Adult↗

PubMed1985

Pathophysiology of the ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome occurred after induction of ovulation with menotropins (follicle-stimulating hormone and luteinizing hormone) and implantation of an intrauterine pregnancy. Serial determinations of aldosterone, deoxycorticosterone, 17 beta-estradiol, progesterone, human chorionic gonadotropin, urinary and plasma electrolytes, and fluid balance were obtained. Plasma renin activity, aldosterone, deoxycorticosterone, and antidiuretic hormone rose markedly. Hydration for four days improved urinary output but also accelerated sodium and fluid retention. Subsequent restriction of salt and water stabilized the patient. Spontaneous abortion was followed by prompt diuresis without a change in therapy. Regression analysis of the authors' data, the clinical observations, and other data in the literature suggest that the ovarian hyperstimulation syndrome is produced by excessive secretion of an unknown hormone that regulates peritoneal fluid during the normal menstrual cycle, and that elevations of plasma renin, aldosterone, and antidiuretic hormone are secondary.

Adult↗

PubMed2006

Vascular endothelial growth factor response to exogenous chorionic gonadotropic hormone in the luteal phase of women with a history of severe ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is a severe complication of ovarian stimulation. No reliable test exists to predict the syndrome. The objective of the present prospective observational study was to examine vascular endothelial growth factor (VEGF) secretion after human chorionic gonadotropin (hCG) administration in the luteal phase of a spontaneous cycle of women with a history of severe OHSS. Five women with a history of severe OHSS were administered 250 mug recombinant hCG intravenously on day 21 of a spontaneous menstrual cycle. Plasma samples were collected at regular intervals from 15 min before hCG to 6 h thereafter and the free VEGF plasma concentrations were determined. Plasma levels of free VEGF remained at the lower detection limit of the assay throughout the observational period. Women with previous severe OHSS do not show a significant short-time response of VEGF secretion upon hCG administration. No evidence was found to support the notion that women inclined to develop a severe form of the syndrome after ovarian stimulation could possibly be identified by the VEGF short-time secretory response to exogenous hCG in the luteal phase of a spontaneous cycle.

Adult↗

PubMed1999

Human albumin enhances expression of vascular endothelial growth factor in cultured human luteinizing granulosa cells: importance in ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is a severe complication of ovarian stimulation for assisted reproductive techniques. Clinical manifestations are massive extravascular fluid accumulation and haemoconcentration. Vascular endothelial growth factor (VEGF) has been demonstrated to mediate the development of OHSS. Intravenous albumin at the time of oocyte aspiration has been suggested as an effective prophylactic treatment against the occurrence of severe OHSS. Here it is reported that in cultured human luteinizing granulosa cells, VEGF mRNA expression was enhanced by human albumin and maximum expression was observed in cultured granulosa cells obtained from patients with serum oestradiol concentrations >2000 pg/ml on the day of human chorionic gonadotrophin injection (P < 0. 05).

Albumins↗

PubMed2003

Clinical and laboratory evaluation of hospitalized patients with severe ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is an important complication of ovarian stimulation and IVF that enhances patients' morbidity. To evaluate any increased incidence of hospitalization from severe OHSS during 2000, this study analysed certain clinical, ultrasound and laboratory characteristics of hospitalized patients with severe OHSS. These studies were carried out on women undergoing IVF who were hospitalized because of severe OHSS between 1996 and 2000 at the Hôpital Antoine Béclère. Patients' ages and serum hormone concentrations were collected on day 3 of ovarian stimulation for various assays, and laboratory and ultrasound measurements taken during ovarian stimulation for IVF were compared. An increase was noted during last year in the frequency of the severe form of OHSS requiring hospitalization (0.9 versus 1.8%, P < 0.05). Patients' ages and hormonal characteristics on day 3 of menstrual cycle, and laboratory and ultrasound variables were similar between the two groups. In addition, the increased incidence of OHSS during 2000 was not associated with any special laboratory or ultrasound parameter, and the policy of ovarian induction had not changed. It is essential to introduce a simple ovarian stimulation protocol providing acceptable IVF results with a minimum of risk.

Adult↗

PubMed1996

Prevention and treatment of ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is the most serious complication of ovarian stimulation. Although the milder form is more common, particularly among patients undergoing gonadotropin stimulation for assisted reproductive technology, the severe form is rare. Classification schemes are clinically directed and useful in diagnosis and management of moderate and severe cases. The ovarian renin-angiotensin system, as well as vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF) offers attractive theories as to the pathogenesis of this disorder. Unfortunately, clinical applications of these findings are not yet available. Possible prevention measures would include identification of patients at high risk, withholding human chorionic gonadotropin (hCG), using a gonadotropin-releasing hormone agonist to trigger ovulation, using a smaller dose of hCG, controlled gonadotropin drift, or avoidance of fresh embryo transfer by cryopreservation and frozen embryo transfer at a later date. Management of moderate to severe OHSS rests upon the principles of expanding intravascular volume and maintaining adequate urine output.

Female↗

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↗

PubMed1995

Human chorionic gonadotropin-dependent expression of vascular endothelial growth factor/vascular permeability factor in human granulosa cells: importance in ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is a severe complication arising from controlled ovarian stimulation treatment. This iatrogenic condition is potentially lethal and occurs in 0.3-5% of stimulated ovarian cycles. hCG exacerbates OHSS. The pathophysiology of OHSS is still unknown; therefore, treatment regimens are aimed at ameliorating symptoms. Prominent features of OHSS are an elevated risk of thromboembolism due to enhanced production of von Willebrand factor by endothelial cells and ascites, or pulmonary edema due to increased vascular permeability followed by third space fluid accumulation. Both of these sequelae can be evoked by vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF). High concentrations of VEGF/VPF have been demonstrated in ascitic fluid from patients with OHSS, but the source of VEGF/VPF in these patients remained unidentified. Here we report that the messenger ribonucleic acid expression of VEGF/VPF in human luteinized granulosa cells (GCs) is dose and time dependently enhanced by hCG in vitro. Furthermore, VEGF/VPF proteins are produced by GCs. Our results suggest that the effects of hCG on the development and course of OHSS may be mediated by the production of VEGF/VPF by GCs.

Adult↗

PubMedDate not supplied

[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome].

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.

Capillary Permeability↗

PubMed1997

Serum estradiol level and oocyte number in predicting severe ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is a relatively common and potentially life-threatening complication of ovarian stimulation, the pathogenesis of which remains unclear. To clarify the predictive values of serum estradiol levels and oocyte number in severe OHSS, and to investigate the impact of high serum estradiol levels on pregnancy outcome, we retrospectively analyzed clinical data from 431 cycles of ovarian stimulation for assisted reproduction performed from 1993 through 1995. Receiver operating characteristic plots were used to estimate the predictive power of the measured variables. The overall frequency of severe OHSS was 5.5%. Using a serum estradiol level of 3,600 pg/mL as the minimum cut-off value, the sensitivity was 58%, with a specificity of 92%, a positive predictive value of 29%, and a negative predictive value of 97%. The predictive power was similar when a cut-off point of 20 oocytes retrieved was used. The two criteria together gave a sensitivity of 33%, a specificity of 92%, a positive predictive value of 40%, and a negative predictive value of 98%. One of seven oocyte donors developed severe OHSS. The pregnancy rate was higher in patients with severe OHSS than in patients who did not develop this syndrome (73.9% vs 32.5%) but the pregnancy outcomes were not significantly different. We conclude that elevated estradiol concentrations and oocyte number appear to be helpful in predicting severe OHSS, but neither parameter by itself is predictive. This syndrome is rare in the absence of luteal hCG support, either exogenous or pregnancy-derived; when it occurs, there are usually extremely high preovulatory estradiol concentrations and numerous oocytes retrieved. High serum estradiol levels are unlikely to have adverse effects on pregnancy outcome in patients with severe OHSS.

Adult↗

PubMed2000

Ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome is an iatrogenic complication of assisted reproduction. In its most severe form, it is potentially fatal. The major clinical components are marked ovarian enlargement and increased capillary permeability leading to ascites, hydrothorax and pericardial effusion. Severe cases are associated with thromboembolic phenomena, respiratory distress and renal failure. The definitive pathophysiology is unknown. The available evidence would support a central role for inflammatory cytokines and angiogenic growth factors. Ultrasound examination and serum oestradiol values are currently used to predict patients at risk. The ideal treatment is prevention, but there has been only limited success. The main aims of treatment are to correct fluid imbalance, maintain renal perfusion and support the patient until the condition resolves. Drug therapy has a limited role, although anticytokine agents may prove useful.

Chorionic Gonadotropin↗

PubMed2005

Case report: delirium associated with ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome (OHSS) is one of the most important complications of assisted reproductive technologies. Mild OHSS is characterized by ovarian enlargement and abdominal discomfort. In severe cases anasarca, hepatic dysfunction, reduced blood volume, electrolyte imbalance, organ failure and thromboembolic phenomena may be observed. Delirium is a syndrome, not a disease, and has many causes, all of which result in a similar pattern of signs and symptoms relating to a patient's level of consciousness and cognitive impairment. Delirium remains an under-recognized and under-diagnosed clinical disorder. The case is presented of a 30-year-old woman with OHSS and delirium. She underwent intracytoplasmic sperm injection (ICSI) for severe male factor infertility. Five days after oocyte retrieval, ascite formation was observed in ultrasonographic evaluation, and embryo transfer was cancelled. Twelve days after retrieval she came to the emergency clinic with abdominal distension and pain. She was hospitalized and paracentesis was performed every other day three times. She had altered consciousness and psychomotor hypoactivity 1 h after the last paracentesis. Psychiatric consultation revealed that she was in a state of delirium, and haloperidol was administered for treatment. Her symptoms disappeared within a week. Her medication was stopped when symptoms resolved and she was still asymptomatic in psychiatric evaluation 1 week later.

Adult↗