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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whether induced by infection, inflammation, ischemia, and/or surgical injury, peritoneal adhesions are the leading cause of pelvic pain, bowel obstruction and infertility. It is clear that while postsurgical peritoneal wounds heal without adhesions in some patients, others develop severe scarring from seemingly equal procedures; in addition, in the same patient, adhesions can develop at one surgical site and not in another. The mechanisms underlying the predisposition to form adhesions as well as their site specificity are completely unknown. However, a large number of intraperitoneal surgical procedures are performed each day in the USA, and thus many patients are at risk of developing postoperative adhesions. Therefore, understanding of adhesion formation at the molecular level is essential and in the absence of such information, attempts to prevent patients from developing adhesions will remain an empirical process. The unprecedented advancement in molecular biology during the past decade has led to the identification of many biologically active molecules with the potential of regulating inflammatory and immune responses, angiogenesis and tissue remodeling, events that are central to normal peritoneal wound healing and adhesion formation. Although, the insight into their importance in the development of tissue fibrosis has substantially increased, their major roles in peritoneal biological functions and adhesion formation remain at best speculative. This article reviews the clinical implications of adhesions and attempts to highlight some of the key molecules i.e. growth factors, cytokines, chemokines, proteases and extracellular matrix, that are recognized to regulate inflammation, fibrinolysis, angiogenesis, and tissue remodeling, events that are central to peritoneal wound repair and adhesion formation. Finally, the article discusses the potential application and site specific delivery of several active compounds that are developed to alter the local inflammatory and immune response i.e., cytokine/chemokine network, targeted gene delivery and development of a new generation of biomaterials to prevent adhesion formation. Such understanding of peritoneal biology not only assist us to better manage patients with adhesion, but also those with endometriosis and malignant diseases that affect the peritoneal cavity.
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PMID:Peritoneal molecular environment, adhesion formation and clinical implication. 1189 50

Improvement in the prognosis of SLE prognosis has led to considering infertility therapy. The earliest reports displayed complications such as SLE revealed by ovulation induction or thrombophlebitis. Fertility is known to be normal in women with SLE, excepting amenorrhea accompanying severe flare-ups, renal insufficiency-related hypofertility and ovarian failure secondary to cyclophosphamide therapy. Anti-phospholipid antibodies are suspected to cause defective nidation and placental ischemia. An exponential rise of serum estradiol is observed irrespective of the ovulation induction protocol used, leading to SLE flare-up and thrombosis. We have experience with 114 cycles in 21 women with SLE and/or APS. A complication (fetal loss, SLE flare-up, thrombophlebitis) revealed the underlying disease in 8 women. Eighteen pregnancies led to 9 live-births, 4 fetal deaths and 5 embryonic losses. Pregnancy rate was higher after ovulation induction using gonadotropins (25% per cycle), than clomiphene (4%). Pregnancy rate was similar after IVFETE, whether the protocol was planned or not. However, three-quarters of the pregnancies after unplanned IVFETE led to abortions. On the contrary, 6 out of 7 pregnancies after planned IVFETE led to live-births. Two women developed thrombophlebitis after gonadotropins therapy. A SLE flare-up appeared after 13 out of 62 cycles, with a flare-up rate higher after gonadotropins (27% per cycle) than clomiphene therapy (6%), and after an unplanned (30%) than a planned procedure (10%). In conclusion, ovulation induction therapy can reveal SLE or APS. Clomiphene complications are uncommon. When gonadotropin therapy is considered, a preventive anti-inflammatory therapy should be discussed in SLE patients, in conjunction with heparin and/or anti-aggregate therapy for those with asymptomatic anti-phospholipid antibodies or prior thrombotic events.
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PMID:[Ovulation induction therapy and systemic lupus erythematosus]. 1274 58

The purpose of this review is to summarize the available evidence on the effects of uterine fibroids on fertility, infertility and pregnancy outcomes, and the effects of parity on fibroids. Fibroids, found in approximately 4% of pregnant women, are associated with an increased risk of pregnancy complications. However, prophylactic myomectomy in asymptomatic women is not only unjustified, but it may have adverse effects on reproduction. Fibroids are found in 1% to 2.4% of women with unexplained infertility. Removal of fibroids that distort the uterine cavity may be beneficial in infertile women with unexplained infertility and in women undergoing in vitro fertilization. The pregnancy rate after hysteroscopic, laparoscopic or abdominal myomectomy appears to be the same. Laparoscopic myolysis appears to have adverse effects on pregnancy outcomes while uterine artery occlusion in infertile and fertile women requires urgent prospective evaluation. Parity appears to be a natural global killer of uterine fibroids, most likely, through transient uterine ischemia, similar to that of uterine artery occlusion.
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PMID:Uterine fibroids: relationships to reproduction. 1458 84

Placental vascular diseases consist of obstetrical pathologies assumed to be linked to placental ischemia. Preeclampsia, defined as the association of hypertension, proteinuria and edema, occur in 3% of deliveries, in a non-selected population. Eclampsia, defined as the occurrence of convulsions in preeclamptic women, occur in 5 per 10,000 deliveries. Risk factors for preeclampsia are: preeclampsia in the previous pregnancy, maternal age <20 years, multiple pregnancies, and nulliparity. Placenta abruption, defined as premature separation of the placenta before delivery, occur in 5 to 15 per 1,000 deliveries. Risk factors are smoking, infertility, and preeclampsia or placental abruption in the previous pregnancy. Stillbirth, defined as fetal death between 24 weeks of gestation and delivery, occur in 1.5 per 1,000 deliveries, with a higher frequency in case of placental abruption, intrauterine growth restriction or preeclampsia.
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PMID:[Epidemiology of vascular placental disease]. 1502 84

Mammalian testes are highly sensitive to oxidative free radical damage. Acute scrotum is a clinical syndrome mainly caused by torsion of the spermatic cord that constitutes a surgical emergence affecting newborns, children and adolescents. This syndrome often leads to infertility of the ipsilateral (torted) and contralateral (not torted) testis, an outcome that makes surgical intervention mandatory. There is a controversy involving the effects of ischemia and reperfusion on ipsilateral and contralateral testes after unilateral torsion and detorsion of the spermatic cord. Conflicting reports have led to two distinct and opposite recommendations regarding surgical intervention: detortion and preservation of the ipsilateral testis, or ipsilateral orchiectomy to preserve contralateral fertility. Early detortion surgery in humans preserves fertility, but after prolonged torsion periods followed by preservation of the ipsilateral fertility of both testis is jeopardized. Lowered contralateral blood flow after unilateral testicular torsion is associated with reactive oxygen species (ROS) overgeneration and therefore with the corresponding tissue damage. Reperfusion time appears to be determinant of contralateral testes damage due to the consequent oxidative insult that accompanies the rise in ROS following ischemia-reperfusion. Nevertheless, more investigations on the molecular mechanisms and the antioxidant status in testis are necessary to ascertain the contribution of ROS to the tissue damage produced by spermatic cord torsion in experimental animals and humans.
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PMID:Spermatic cord torsion, reactive oxygen and nitrogen species and ischemia-reperfusion injury. 1505 28

Testicular microlithiasis is a well-defined clinical and pathologic entity easily diagnosed through testicular echography; however, its association with cancer and infertility is now under debate. Many efforts have been done in recent years to clarify the spectrum of lesions observed in testicular microlithiasis, but no published data as to the existence of a possible microlithiasis of the epididymis and the rete testis have been found. We have observed microlithiasis of the epididymis and the rete testis in surgical (8 epididymis and 6 testis) and autopsy specimens (12 cases). In decreased order of frequency, microliths of the proximal spermatic way were seen in rete testis, epididymal duct, and efferent ducts. Intraluminal, subepithelial, and interstitial microliths were localized along these segments of the spermatic way. Subepithelial microliths were the most frequently found. A granulomatous reaction around the interstitial epididymal microliths, mimicking malacoplakia, was observed in 1 case. The differential diagnosis of microliths includes corpora amilacea, Michaelis-Gutmann bodies, calcium deposits, hyaline globules, and parasites, like the giant kidney worm Dioctophyme renale. In infants and young adults, microlithiasis of the epididymis and the rete testis is frequently associated with alterations in the development of the proximal spermatic way. In elderly adults, it is related to ischemia and obstruction of the spermatic way.
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PMID:Microlithiasis of the epididymis and the rete testis. 1508 71

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a nuclear hormone receptor super family that has recently been implicated in atherosclerosis, inflammation, cancer, infertility, and demyelination. Oxidative stress, neutrophil infiltration, proinflammatory cytokines, and the exhibition of luminal acid play a role in the pathogenesis of gastric injury induced by ischemia-reperfusion. Rosiglitazone, a specific PPAR-gamma ligand, has been shown to have antiinflammatory activity, but its effects on experimental ischemia-reperfusion gastric injury remain unknown. We have investigated the effects of the rosiglitazone on gastric injury caused by ischemia following reperfusion in rats. Tumour necrosis factor-alpha (TNF-alpha) levels and changes in enzymatic activities of myeloperoxidase, as a marker of neutrophils infiltration, xanthine oxidase, superoxide dismutase, and glutathione peroxidase, were determined. Histological analysis of the lesions was also carried out. Pretreatment with 1 or 4 mg/kg of rosiglitazone ameliorated the gastric damage induced by clamping the celiac artery for 30 min followed by 60 min of reperfusion. It significantly (P<0.05) reduced the index of neutrophil infiltration and the levels of the cytokine. Rosiglitazone did not revert the reduced glutathione peroxidase activity but enhanced significantly (P<0.01) the decreased xanthine oxidase and superoxide dismutase activities in gastric mucosa of ischemic rats. In conclusion, rosiglitazone reduces the damage in ischemia-reperfusion gastric injury and alleviates the inflammatory response and the oxidative events.
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PMID:Rosiglitazone, an agonist of peroxisome proliferator-activated receptor gamma, protects against gastric ischemia-reperfusion damage in rats: role of oxygen free radicals generation. 1555 53

We propose that inadequate sympathetic bias and Th2 bias in the uterine environment contributes to the formation of fibroids, independent of the sex steroid status. We also propose that fibroids represent a modern maladaptation that partly results from decreasing exposure to seminal fluid, which contains catecholalmines, transforming growth factor beta1 (TGFbeta1), aldosterone, prostaglandins, and other factors that shift the uterine environment to sympathetic and T helper (Th)2 bias. Lower risk of fibroids is associated with pre-menarche, post-menopause, pregnancy, exposure to contraceptives, smoking, earlier age of first pregnancy, shorter interval since last pregnancy, higher parity, and non-obesity. These associations are currently attributed to alterations of sex steroids. However, the association may also be explained by the observation that pre-menarche, post-menopause, pregnancy, and smoking represent periods of sympathetic and Th2 bias. Furthermore, use of contraceptives, early age of first pregnancy, short interval since last pregnancy, high parity, abnormal pap smear, and non-obesity may represent surrogates for increased sexual activity and increased exposure to seminal fluid. Catecholalmines, aldosterone, TGF, and prostaglandins are among the seminal fluid components that promote sympathetic and Th2 bias. Vasectomized copulations protect against fibroids, an observation that undermines the steroid hypothesis and supports our hypothesis. The putative mechanism of action of uterine artery embolization (UAE) for fibroid treatment is starvation of blood supply, but the extensive collaterals that protect uterine perfusion would presumably also buffer against fibroid hypoperfusion. Instead, the sympathetic and Th2 responses to UAE-related ischemia may contribute to fibroid regression. A potential explanation for the association of fibroids with intrauterine devices may be a Th1 cell-mediated immune response to the foreign body, which may also enhance the contraceptive effect. Novel methods of preventing and treating fibroids by promoting sympathetic and Th2 shift through natural, pharmacologic, and neuromodulatory means are envisioned. Fibroids are likely a modern dysfunction given the high Darwinian fitness cost of fibroid-related infertility, and may be attributable to reduced intercourse frequency. Fibroids have been observed among animals in captivity that are presumably reproductively isolated.
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PMID:Sympathetic and T helper (Th)2 bias may ameliorate uterine fibroids, independent of sex steroids. 1621 89

Testicular torsion is a serious problem in male children and, if not treated at the right time, can lead to subfertility and infertility. The main reason for testicular damage is ischemia-reperfusion injury. A number of chemical substances have been used to protect testes against ischemia-reperfusion injury in experimental animals. The possible protective effect of N-acetylcysteine on testicular tissue after testicular detorsion was examined in the current study. Twenty-four rats were divided into four groups: sham operation, torsion, detorsion, and NAC + detorsion groups (n = 6 for each group). Excluding sham operation group, the rats were subjected to unilateral torsion (720-degree rotation in clockwise direction). After torsion (5 h) and detorsion (2 h), unilateral orchidectomy was performed. Malondialdehyde levels and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were determined in testicular tissue. Administration of N-acetylcysteine caused a decrease in malondialdehyde levels and an increase in glutathione peroxidase levels compared to detorsion group. The results suggest that N-acetylcysteine may be a potential protective agent for preventing the negative biochemical changes related to oxidative stress in testicular injury caused by testis torsion.
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PMID:The effects of N-acetylcysteine on antioxidant enzyme activities in experimental testicular torsion. 1641 70

Antiphospholipid syndrome (APS) is a cause of infertility and fetal loss. Ovarian stimulation can induce previously unknown APS. Ovarian hyperstimulation syndrome (OHS) is uncommon but potentially life-threatening, as well as catastrophic APS. A woman that simultaneously developed a severe OHS and a catastrophic APS is described in this paper. Both entities produced thrombotic cardiac and brain thrombosis. A peculiar mechanism of cardiac ischemia is also described. In spite of the life-threatening risk of this situation, the indication for preventive anti-aggregation and/or anticoagulation is not clear.
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PMID:Catastrophic antiphospholipid syndrome related to severe ovarian hyperstimulation. 1653 87


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