Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Pathophysiology of the ovarian hyperstimulation syndrome. 392 8

The overall incidence of clinically important (moderate to severe) OHSS ranges from 1% to 10% of IVF cycles, but only a small proportion (0.5% to 2%) of the cases are severe. In extreme but rare cases, secondary complications such as deep vein thrombosis, respiratory distress and acute hepato-renal failure may occur. The main risk factors are the presence of polycystic ovaries, high ovarian response to superovulation therapy, the use of hCG to trigger the ovulatory process or for luteal phase support, and the endogenous production of hCG by an early pregnancy. The pathogenesis of OHSS is unknown, although the predominant biochemical mediator is thought to be the renin-angiotensin system. Ovarian stimulation should always be carefully monitored to identify those women at risk. In IVF cycles, the hCG injection should be withheld if the risk is judged to be too great. Some women will benefit from a policy of proceeding to collect oocytes, but electively cryopreserving any resulting embryos, thus allowing the ovarian stimulation cycle not to be wasted. The administration of albumin at the time of oocyte collection will reduce the chance of severe OHSS occurring. If a decision is made to proceed with oocyte recovery and embryo transfer, it may be advisable to give 5000 IU of hCG, rather than 10,000 IU, as the ovulatory trigger. Progesterone, and not hCG, should be given in the luteal phase. Women developing mild or moderate OHSS should be kept under outpatient surveillance to detect the minority that may progress to severe OHSS. Those with severe OHSS should be hospitalised for fluid and electrolyte management. Paracentesis under ultrasound guidance is recommended where there are tense ascites, but further surgical intervention should rarely be undertaken and only when there is good clinical evidence of ovarian torsion or haemorrhage.
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PMID:Diagnosis, prevention and management of ovarian hyperstimulation syndrome. 862 33

The ovarian hyperstimulation syndrome is the most important iatrogenic complication of ovarian stimulation. Every drug used in the treatment of infertility such as FSH, HMG, CC, GnRHa, can lead to the syndrome. The authors of the article report the incidence of OHSS in their patients treated for an assisted conception program; the role of oestrogens, HCG and renin-angiotensin system; the classification, the therapy and how to prevent the syndrome.
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PMID:[The ovarian hyperstimulation syndrome]. 801 99

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.
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PMID:Prevention and treatment of ovarian hyperstimulation syndrome. 898 30

Ovarian hyperstimulation syndrome (OHSS) is a serious complication affecting ovulation induction. Its most severe manifestation takes the form of massive ovarian enlargement and multiple cysts, haemoconcentration and third-space accumulation of fluid. The full-blown clinical syndrome may be complicated by renal failure and oliguria, hypovolaemic shock, thromboembolic episodes, adult respiratory distress syndrome (ARDS), and death. Although the pathophysiology of this syndrome has not been completely elucidated, it seems likely that the increased capillary permeability triggered by the release of vasoactive substance secreted by the ovaries under human chorionic gonadotrophin (HCG) stimulation plays a key role in this syndrome. Several factors such as histamine, serotonin, prostaglandins, prolactin, and a variety of other substances have been implicated in this process in the past. At present, factors belonging to the renin-angiotensin system, cytokines including the interleukins, tumour necrosis factor alpha, endothelin-1 and vascular endothelial growth factor (VEGF) are thought to be involved in triggering increased vascular permeability after ovulation induction treatment. This manuscript summarizes the current knowledge of the pathophysiology of ovarian hyperstimulation syndrome with emphasis on the correlation of the various factors with the clinical phenomena of this iatrogenic syndrome.
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PMID:The pathophysiology of ovarian hyperstimulation syndrome--views and ideas. 957 53

Ovarian hyperstimulation syndrome (OHSS) is characterized by massive transudation of protein-rich fluid (mainly albumin) from the vascular space into the peritoneal pleural and to a lesser extent to the pericardial cavities. The intensity of the syndrome is related to the degree of the follicular response in the ovaries to the ovulation inducing agents. OHSS is still a threat to every patient undergoing ovulation induction. The pathophysiology of OHSS is of extreme importance in the face of the increased use of ovulation induction agents as well as the development of sophisticated assisted reproductive techniques. The correlation found between plasma cytokine activities and the severity of OHSS suggests that plasma cytokines may be involved in the pathogenesis of OHSS and may serve as a means of monitoring the syndrome during the acute phase and throughout convalescence. The interactions between cytokine and non-cytokine mediators of the syndrome, such as the renin-angiotensin system and vascular endothelial growth factor were recently clarified. Awareness of possible mechanisms and factors in the pathophysiology of OHSS will hopefully provide opportunities to design specific treatment regimens effective for both prevention and treatment of this potentially fatal iatrogenic condition. Among IVF patients with severe and critical OHSS, pregnancy rates, multiple gestations, miscarriage, preterm premature rupture of the membranes, prematurity, and low birth weight rates are significantly higher than those reported previously for pregnancies after assisted conception. The incidence of other obstetrical complications, as well as congenital malformations and Cesarean section rates are not significantly different.
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PMID:Clinical aspects of ovarian hyperstimulation syndrome. 1042 16

Ovarian Hyperstimulation Syndrome (OHSS) is a serious disorder complicating the use of ovary-stimulating drugs in assisted reproduction programs. While its pathogenesis is not fully understood, it is believed that human chorionic gonadotropin (hCG) stimulation is vital to the development of OHSS. Further evidence suggests that the renin-angiotensin pathway, vascular endothelial growth factor, endothelin-1, and cytokines all play a role in altering ovarian capillary permeability, leading to increased interstitial fluid. OHSS can produce a myriad of symptoms and signs involving numerous body systems, up to and including hypovolemic shock and acute renal failure. As growing numbers of women opt for assisted reproduction, it becomes increasingly important for emergency physicians to be able to recognize this condition. Clinical classification into mild, moderate, severe, and critical forms of OHSS can help the physician plan appropriate investigations, admission requirements, and acute management. Two cases of OHSS, representing the spectrum of this problem, are presented along with a review of the literature.
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PMID:Ovarian hyperstimulation syndrome: imperatives for the emergency physician. 1043 59

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.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17

Ovarian hyperstimulation syndrome (OHSS) is a rare and potentially life-threatening complication during controlled ovarian stimulation. It can be associated with severe morbidity and may even be fatal. The etiology of the condition and predisposing factors are still not fully understood. Data concerning pathophysiology in patients with OHSS were searched using PubMed and other medical data bases. The incidence of severe OHSS, as calculated by World Health Organization (WHO), is 0.2-1% of all stimulation cycles in assisted reproduction. Considerations on OHSS classifications and forms of manifestations are discussed in detail. New insights concerning genetics and altered FSH receptor are given. OHSS may involve, according to its grade of severity, elevated or decreased levels of growth factors, cytokines, mediators, changes in hormones, renin-angiotensin and kinin-kallikrein system. There are massive electrolytic imbalances and changes in hemodynamic and fluid metabolism. Furthermore, liver and pulmonary dysfunction is observed as well as increased coagulation with subsequent thromboembolism. The influence of OHSS on the pregnancy rate and outcome of pregnancy is a matter of controversy. Patients with OHSS have high pregnancy rates with a tendency to an increased incidence of abortion.
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PMID:Update on ovarian hyperstimulation syndrome: Part 1--Incidence and pathogenesis. 1798 84