Primary and myoma‐associated menorrhagia: role of prostaglandins and effects of ibuprofen

Mäkäräinen, Leo; Ylikorkala, Olavi

doi:10.1111/j.1471-0528.1986.tb08019.x

Cited by 91 publications

(33 citation statements)

References 15 publications

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“…This observation may be a consequence of increased PGF 2a production as explants from women with dysmenorrhoea produce more PGF 2a in response to arachidonic acid compared with normal endometrial explants (Lundstrom & Green 1978). Further evidence of the role of PGs comes from the administration of COX enzyme inhibitors such as ibuprofen, which have been demonstrated to reduce menstrual blood flow (Makarainen & Ylikorkala 1986) and selective COX2 inhibitors that have been used in the treatment of dysmenorrhoea and heavy menstrual blood loss (Daniels et al 2002).…”

Section: Menstrual Disordersmentioning

confidence: 99%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

295

226

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Inflammation involves alterations to vascular and immune cell function. It is well recognised that many physiological reproductive events such as ovulation, menstruation, implantation and onset of labour display hallmark signs of inflammation. These are orchestrated by specific molecular pathways involving a host of growth factors, cytokines, chemokines and lipid mediators. Resumption of normal reproductive function involves prompt and proper resolution of these inflammatory pathways. Recent literature confirms that resolution of inflammatory pathways involves specific biochemical events that are activated to re-establish homeostasis in the affected tissue. Moreover, initiation and maintenance of inflammatory pathways are the key components of many pathologies of the reproductive tract and elsewhere in the body. The onset of reproductive disorders or disease may be the result of exacerbated activation and maintenance of inflammatory pathways or their dysregulated resolution. This review will address the role of inflammatory events in normal reproductive function and its pathologies.

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Section: Menstrual Disordersmentioning

confidence: 99%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

295

226

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“…COX-2 and PGE 2 are also elevated in uterine tissue of women with menorrhagia (excessive menstruation), a known risk factor for endometrial cancer (123). PGE 2 is also commonly elevated in malignant endometrial epithelial cells (113).…”

Section: Interrelationship Of Sex Hormones With Cytokines Andmentioning

confidence: 99%

Inflammation and Endometrial Cancer: A Hypothesis

Modugno

Ness

Chen

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

229

201

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Endometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E 2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk factors for endometrial cancer-unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early menarche, and late menopause-may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14 (12):2840 -7)

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“…COX enzyme inhibitors such as ibuprofen reduce menstrual blood loss (Makarainen and Ylikorkala, 1986). A dual mode of action has been demonstrated for fenamates such as sodium meclofenamate and mefenamic acid which reduce prostaglandin synthesis and inhibit binding of PGE 2 to its receptor (Rees et al, 1988).…”

Section: Europe Pmc Funders Author Manuscriptsmentioning

confidence: 99%

“…Synthesis of PGI 2 and nitric oxide are also high in menstrual blood collected from menorrhagic endometrium of women presenting with excessive menstrual bleeding (Smith et al, 1981b;Makarainen and Ylikorkala, 1986). This finding indicates that the degree or duration of menstrual bleeding in women diagnosed with menorrhagia may be augmented after an increase in vasodilatatory factors.…”

Section: Europe Pmc Funders Author Manuscriptsmentioning

confidence: 99%

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

Sales¹

2003

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Prostaglandins are bioactive lipids produced from arachidonic acid by cyclooxygenase (COX) enzymes and specific terminal prostanoid synthase enzymes. After biosynthesis, prostaglandins exert an autocrine-paracrine function by coupling to specific prostanoid G protein-coupled receptors to activate intracellular signalling and gene transcription. For many years, prostaglandins have been recognized as key molecules in reproductive biology by regulating ovulation, endometrial physiology and proliferation of endometrial glands and menstruation. More recently, a role for COX enzymes and prostaglandins has been ascertained in reproductive tract pathology, including carcinomas, menorrhagia, dysmenorrhoea and endometriosis. Although the mechanism by which prostaglandins modulate these pathologies is still unclear, a large body of evidence supports a role for COX enzymes, prostaglandins and prostaglandin receptor signalling pathways in angiogenesis, apoptosis and proliferation, tissue invasion and metastases and immunosuppression. Here, an overview is provided of some of the findings from these studies with specific emphasis on the role of COX enzymes, prostaglandin E 2 and F 2α in disorders of endometrial proliferation and menstruation in non-pregnant women.The arachidonic acid cascade generates a family of bioactive lipids, including prostaglandins, thromboxanes and leukotrienes that modulate diverse physiological and pathophysiological responses in the reproductive tract. There has been a great deal of interest over the past few years in the involvement of arachidonic acid metabolites in pathology. However, there is still much uncertainty about the manner in which they contribute to specific phenotypic cellular changes that may precipitate pathophysiology. The focus of this review is to provide some insight into the role of cyclooxygenase (COX) enzymes, prostaglandin E 2 (PGE 2 ) and PGF 2α and their respective receptors in reproductive pathophysiology, with specific regard to disorders of endometrial proliferation and dysfunctional menstruation.The kinetics of the prostaglandin biosynthetic pathway is driven by the availability of free arachidonic acid. When released from plasma membrane phospholipids or dietary fatty acids, after activation of phospholipase A2 (PLA2) or PLC, arachidonic acid is cyclized and oxygenated by COX enzymes by addition of the 15-hydroperoxy group to form prostaglandin G 2 (PGG 2 ). The hydroperoxy group of PGG 2 is reduced to the hydroxy group of PGH 2 (Marnett, 1992) (Fig. 1). This intermediate serves as the substrate for terminal prostanoid synthase enzymes. These enzymes are named according to the prostaglandin they produce, such that prostaglandin D 2 is synthesized by prostaglandin-D-synthase (PGDS), prostaglandin E 2 (PGE 2 ) by prostaglandin-E-synthase (PGES); prostaglandin F 2α by

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Primary and myoma‐associated menorrhagia: role of prostaglandins and effects of ibuprofen

Cited by 91 publications

References 15 publications

Inflammatory pathways in female reproductive health and disease

Inflammatory pathways in female reproductive health and disease

Inflammation and Endometrial Cancer: A Hypothesis

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

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