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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

How a weakened immune system affects the female's reproductive system is explained. The female's endocrine system controls the menstrual and reproductive systems, and the immune system attacks harmful substances and organisms. The hypothalamus stimulates the pituitary gland to produce the hormones FSH and LH, which in turn signal the ovaries to produce estrogen and progesterone. These hormones cause a mature egg to be released. If fertilized, the egg remains within the uterus; if not, menstruation occurs. HIV-positive females often complain of menstrual cycle changes, such as irregular periods, depression, or pain. The virus, other complications, or medications, such as AZT, may cause these symptoms. Estrogen therapy may help those with suppressed immune systems who have premature menopause. Oral contraceptives offer protection against pregnancy, but not HIV. It is not known if the pill reacts adversely with AIDS treatment drugs. Lists are provided showing the pros and cons of oral contraceptives and hormone therapy.
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PMID:[Women, immunity and sexual hormones]. 1136 3

Women have a higher incidence of inflammatory disorders than men and also appear to perceive painful stimuli differently. It has been suggested that neuroinflammation plays a role in painful bladder disorders of uncertain etiology, such as interstitial cystitis. Nerve growth factor (NGF) is a neurotrophin produced in peripheral tissues that can also mediate pain and inflammation. We found that treatment of mice with the estrogen antagonist ICI 182,780 had no effect on bladder NGF content but decreased bladder NGF messenger RNA. Using immunohistochemistry, we demonstrated that the mucosa is the primary source of NGF in the mouse bladder, and the bladder mucosa also expresses estrogen receptor (ER)-alpha, ER-beta, and the high-affinity NGF receptor tyrosine kinase A. Estrogen may also modulate neurogenic inflammation by interaction with other substances and cells that participate in the pathogenesis of neurogenic inflammation, including substance P, bradykinin, and mast cells. Collectively, these observations indicate that estrogen has the capacity to influence the onset and course of neurogenic inflammation of the bladder.
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PMID:Estrogen and neuroinflammation. 1137 49

The vast majority of people experience tension-type headache during their lifetimes. Boys experience tension-type headache slightly more than girls during preadolescent years. During adolescence and adult years, tension-type headache occurs more commonly in females. Tension-type headache changes in women occur in relation to gynecologic changes, including menses, pregnancy, and menopause. These changes are related to estrogen fluctuations. Estrogen fluctuations cause changes in neurochemicals important for pain signal transmission, including serotonin, gamma-aminobutyric acid, and enkephalins.
Curr Pain Headache Rep 2001 Oct
PMID:Estrogen and tension-type headache. 1156 Aug 10

Besides their well-established actions on reproductive functions, estrogens exert a variety of actions on many regions of the nervous system that influence higher cognitive function, pain mechanisms, fine motor skills, mood, and susceptibility to seizures; they also appear to have neuroprotective actions in relation to stroke damage and Alzheimer's disease. Estrogen actions are now recognized to occur via two different intracellular estrogen receptors, ER-alpha and ER-beta, that reside in the cell nuclei of some nerve cells, as well as by some less well-characterized mechanisms. In the hippocampus, such nerve cells are sparse in number and yet appear to exert a powerful influence on synapse formation by neurons that do not have high levels of nuclear estrogen receptors. However, we also find nonnuclear estrogen receptors outside of the cell nuclei in dendrites, presynaptic terminals, and glial cells, where estrogen receptors may couple to second messenger systems to regulate a variety of cellular events and signal to the nuclear via transcriptional regulators such as CREB. Sex differences exist in many of the actions of estrogens in the brain, and the process of sexual differentiation appears to affect many brain regions outside of the traditional brain areas involved in reproductive functions. Finally, the aging brain is responsive to actions of estrogens, which have neuroprotective effects both in vivo and in vitro. However, in an animal model, the actions of estrogens on the hippocampus appear to be somewhat attenuated with age. In the future, estrogen actions over puberty and in pregnancy and lactation should be further explored and should be studied in both the hypothalamus and the extrahypothalamic regions.
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PMID:Invited review: Estrogens effects on the brain: multiple sites and molecular mechanisms. 1171 47

Current interceptive methods of contraception utilizable between ovulation and nidation include hormonal methods and IUDs. Since the 1st clinical study of the use of high doses of estrogen as a postcoital contraceptive appeared in 1967, the remarkable efficacy of the method has been confirmed by numerous other studies. The most important series used 50 mg diethylstilbestrol (DES) or 5 mg ethinyl estradiol (EE) per day for 5 days beginning within 72 hours of unprotected intercourse. The mechanism by which estrogens exercise their interception are unclear, but there are probably several factors involved including luteolysis and anomalies in endometrial development. The method is highly effective but rates of nausea, vomiting, breast tenderness, and to a lesser degree menorrhagia are high. The incidence of extrauterine pregnancy is about 1 per 10 intrauterine pregnancies for any postcoital method. Estrogen postcoital contraception is preferable to DES because of the fear of genital adenosis or vaginal adenocarcinoma in case of failure of DES. Opinion is divided as to the teratogenic risks of high doses of estrogens in general. Postcoital contraception with a progestin, levonorgestrel, which renders the endometrium inhospitable to nidation, was 1st described in 1973. The efficacy of norgestrel alone depends on the dose used. The most common secondary effects are spotting and cycle shortening. The method has the advantage of requiring a very small dose, but the disadvantage of requiring administration in the 12 hours following intercourse. Several combinations of estrogens and progestins have been proposed for postcoital use, of which the most interesting consists of 1 mg of dl-norgestrel and 100 mcg of EE repeated exactly 12 hours later. The treatment should be administered within 12 hours of unprotected intercourse. A multicenter study of 692 women treated with this method gave a pregnancy rate of 1.6%, which would have been lower if 4 women not meeting the conditions of treatment had been excluded. 52.7% of women treated had nausea or vomiting. Compared to estrogens alone, the EE-Norgestrel combination takes less time, requires 4 pills instead of 50 or 60, is better tolerated overall, and requires much less estrogen. Postcoital insertion of an IUD is very effective and has the advantages that it can be used later than 72 hours following intercourse, it is the only method currently available in case OCs are contraindicated, it allows subsequent longterm effective contraception, and it is 100% effective. The major disadvantages are pain on periovulatory or postovulatory insertion and the risk of infection. Possible future hormonal methods of postcoital contraception based on use of anti-progesterone steroids, especially RU486, or of luteinizing hormone releasing hormone agonist are currently under development.
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PMID:[Post-coital contraception]. 1228 Feb 7

The therapeutic use of estrogens for more than 25 years made it possible to examine evidence of their safety and effectiveness in a study of 292 postmenopausal women who had undergone prolonged estrogen therapy. Diethylstilbestrol and conjugated equine estrogens have been used most frequently since 1945. The study showed that only 5% of patients necessitated discontinuation from severe side effects; the latter of the 2 compounds was tolerated without side effects among almost all patients. Hot flashes were completely relieved in 93 of 94 patients. Prolonged estrogen therapy was the treatment for postmenopausal osteoporosis in 119 patients, 103 of whom had suffered collapse of vertabrae. Either complete or significant relief from pain occurred in 90%. A group of 27 women showed evidence that estrogen is a prophylactic against postmenopausal osterporosis. Justification for the fear that mammary and cervical carcinoma may result from this therapy is absent. When combined with periodic pelvic and vaginal cytological examinations, prolonged cyclic oral estrogen therapy is safe and effective treatment for postmenopausal women with disabling symptoms or osteoporosis.
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PMID:Prolonged estrogen therapy in postmenopausal women. 1230 88

Estrogen has been implicated in modulation of pain processing. Although this modulation occurs within the CNS, estrogen may also act on primary afferent neurons whose cell bodies are located within the dorsal root ganglia (DRG). Primary cultures of rat DRG neurons were loaded with Fura-2 and tested for ATP-induced changes in intracellular calcium concentration ([Ca(2+)](i)) by fluorescent ratio imaging. ATP, an algesic agent, induces [Ca(2+)](i) changes via activation of purinergic 2X (P2X) type receptors and voltage-gated Ca(2+) channels (VGCC). ATP (10 microM) caused increased [Ca(2+)](i) transients (226.6+/-16.7 nM, n = 42) in 53% of small to medium DRG neurons. A 5-min incubation with 17 beta-estradiol (100 nM) inhibited ATP-induced [Ca(2+)](i) (164+/-14.6 nM, P<0.05) in 85% of the ATP-responsive DRG neurons, whereas the inactive isomer 17 alpha-estradiol had no effect. Both the mixed agonist/antagonist tamoxifen (1 microM) and specific estrogen receptor antagonist ICI 182780 (1 microM) blocked the estradiol inhibition of ATP-induced [Ca(2+)](i) transients. Estradiol coupled to bovine serum albumin, which does not diffuse through the plasma membrane, blocked ATP-induced [Ca(2+)](i), suggesting that estradiol acts at a membrane-associated estrogen receptor. Attenuation of [Ca(2+)](i) transients was mediated by estrogen action on VGCC. Nifedipine (10 microM), an L-type VGCC antagonist mimicked the effect of estrogen and when co-administered did not increase the estradiol inhibition of ATP-induced [Ca(2+)](i) transients. N- and P-type VGCC antagonists omega-conotoxin GVIA (1 microM) and omega-agatoxin IVA (100 nM), attenuated the ATP-induced [Ca(2+)](i) transients. Co-administration of these blockers with estrogen induced a further decrease of the ATP-induced [Ca(2+)](i) flux. Together, these results suggest that although ATP stimulation of P2X receptors activates L-, N-, and P-type VGCC, estradiol primarily blocks L-type VGCC. The estradiol regulation of this ATP-induced [Ca(2+)](i) transients suggests a mechanism through which estradiol may modulate nociceptive signaling in the peripheral nervous system.
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PMID:Estradiol inhibits atp-induced intracellular calcium concentration increase in dorsal root ganglia neurons. 1273 39

Many gastrointestinal pain syndromes are more prevalent in women than men, suggesting a gonadal steroid influence. We characterized the effects of estrogen on two responses to colorectal distention (CRD) in the rat: the visceromotor reflex (vmr) and L6-S1 dorsal horn neuron activity (ABRUPT and SUSTAINED neurons). Ovariectomized rats were injected with estrogen, and responses to innocuous and noxious intensities of CRD were measured between 4 hr and 14 d after injection and compared with ovariectomized and intact, cycling rats. Plasma estrogen levels were determined at each time point. Ovariectomy significantly decreased the magnitude of the vmr and ABRUPT neuron response to CRD compared with cycling rats. Four and 48 hr after estrogen injection (10 microg), the magnitude of the vmr and ABRUPT neuron response returned to the level or greater than that of cycling rats. All responses were comparable with ovariectomized rats by 7 d. These results paralleled the plasma estrogen concentration. Fifty micrograms of estrogen did not further increase the magnitude of the vmr or neuronal response 48 hr after estrogen but did extend the period of the increased ABRUPT neuron response to 14 d. Estrogen did not affect the response of SUSTAINED neurons. In a separate experiment, the response to innocuous CRD was sensitized in estrogen-treated rats but not ovariectomized or cycling rats. The present data suggest that estrogen modulates the spinal cord processing and reflex responses to innocuous and noxious colorectal stimuli in female rats and may contribute to alterations in sensory processing associated with irritable bowel syndrome.
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PMID:Estrogen modulates the visceromotor reflex and responses of spinal dorsal horn neurons to colorectal stimulation in the rat. 1273 60

Cyclooxygenase inhibitors demonstrate effective antinociception in many clinical and experimental pain models. Acute uterine cervical distension (UCD) forms the basis for obstetric and some gynecologic pain, and acute UCD in rats results in nocifensor reflexes which are inhibited by morphine in animals lacking, but not in animals with circulating estrogen. We studied the antinociceptive effect of intravenous and intrathecal injection of the cyclooxygenase inhibitor, ketorolac in acute UCD rats and its dependency on estrogen. Virgin rats received estrogen or placebo treatment for 1 week following oviarectomy. An intrathecal catheter was inserted for drug administration. Rats were anesthetized, then the electromyographic response in the rectus abdominus muscle and mean arterial blood pressure change to UCD was recorded before and with cumulative dosing of intravenous or intrathecal ketorolac. Intravenous ketorolac produced dose dependent inhibition of the responses to UCD, but intrathecal ketorolac was ineffective at the maximum test dose (300 microg). Estrogen replacement did not affect the stimulus response or maximum efficacy of ketorolac. Unlike morphine, which reduces response to UCD by spinal and supraspinal mechanisms and whose action is blocked by estrogen, the cyclooxygenase inhibitor, ketorolac acts at an estrogen-independent, non spinal site.
Pain 2003 Sep
PMID:Systemic, but not intrathecal ketorolac is antinociceptive to uterine cervical distension in rats. 1449 26

Estrogen exerts a strong influence on episodic headaches, such as migraine and tension-type headache. A relationship between sex hormones and chronic daily headache (CDH) is less well established. However, similarities between episodic and CDH suggest that estrogen also may significantly influence CDH. Pathophysiologic studies of CDH identify neurochemical abnormalities similar to those influenced by estrogen in episodic headache, such as aberrant 5-hydroxytryptamine activity. In addition, gender differences in CDH prevalence in pediatric and adult populations support a hormonal influence. Few studies have evaluated the ability of gynecologic events, such as menses, to influence CDH.
Curr Pain Headache Rep 2004 Feb
PMID:Estrogen and chronic daily headache. 1473 85


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