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At least 631 records · Page 35Linked to original sources
PubMed1990

Prostaglandins: PGF2 alpha, PGE2, 6-keto-PGF1 alpha and TXB2 serum levels in dysmenorrheic adolescents before, during and after treatment with oral contraceptives.

Ten adolescents with primary dysmenorrhea (PD) were treated with the oral contraceptive (OC) Lyndiol 2.5 mg (R) for one cycle. The levels of PGF2 alpha, PGE2 and the metabolites of PGI2 and TXA2: 6-keto-PGF1 alpha and TXB2 were tested by a radioimmunoassay method during the 1st and 23rd day of the pre-treatment cycle (PrTC), the 23rd day of treatment (TC) and the 1st day of the post-treatment cycle (PoTC). The ratios PGF2 alpha/PGE2 and TXB2/6-keto-PGF1 alpha were also tested and compared during the above-mentioned days. Analytical comparison was made, for each Prostaglandin (PG) separately, between the 1st day of the PrTC and PoTC as well as the 23rd day of the PrTC and TC, respectively. All PG levels during TC and PoTC were found significantly lower, compared to those of the PrTC respectively. With regard to the ratios mentioned above, no statistically significant differences were found on the same days and cycles as previously stated. The reduction of the PG levels in PD patients after treatment with oral contraceptives, together with an improvement of the clinical findings of the disease, support the theory that oral contraceptives can be used for the treatment of PD cases, especially for those adolescents who also desire a contraceptive method.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Melatonin: a contraceptive for the nineties.

The hypothalamic GnRH pulse generator activates the pituitary-gonadal reproductive axis, and contraceptive techniques have advanced to the point where GnRH analogues can block this effect. However, nature has an even finer form of contraception, whereby the GnRH pulse generator is activated or inactivated at different seasons of the year. Darkness affects the retino-pineal nervous pathway to cause the synthesis and release of melatonin from the pineal gland at night. The duration of the night time release of melatonin is longer in winter than in summer; and it is the prolongation in the duration of the night time release of melatonin, with the change of season from summer to winter, which acts as the endocrine signal for inactivating the hypothalamic GnRH pulse generator. Humans are not seasonal breeders, and evidence is presented to indicate that this is due to an impairment of the retino-pineal pathway rather than an impairment of melatonin hypothalamic function. Thus the way is open for utilising melatonin as a human contraceptive, and a melatonin-based contraceptive is at present undergoing phase III clinical trials. The challenge is to develop more refined methods for administering (or releasing) melatonin, so that it has a night time amplitude and duration which mimics that seen in long day breeders.

Amenorrhea↗
PubMed1978

The effect of ibuprofen on the intrauterine pressure and menstrual pain of dysmenorrheic patients.

In 12 dysmenorrheic patients we examined the therapeutic action of the Prostaglandin-synthesis inhibitor: Ibuprofen, a non-steroidal analgesic agent. Ibuprofen highly significantly reduced the resting pressure (P less than 0.001), active pressure (P less than 0.001) and frequency (P less than 0.05) of cyclic activity of the uterus, as well as menstrual pain (P less than 0.001). Since these effects occurred after a single oral dose of 800 mg Ibuprofen, without side effects or complications, extensive field trials are recommended with this and other PG-synthesis inhibitors, to assess their therapeutic benefits.

Administration, Oral↗
PubMed1979

The refief of primary dysmenorrhea by ketoprofen and indomethacin.

The prostaglandin biosynthesis inhibitors ketoprofen and indomethacin were compared in the treatment of primary dysmenorrhea in a double-blind, cross-over trial involving 23 patients. Each drug was used for 2-4 days during 3 consecutive menstruations in randomized order. Good or moderate overall relief was obtained in 60 of the 68 ketoprofen-treated menstruations (88%). A dysmenorrhea score, based on subjective estimations of 8 symptoms, similarly decreased from a mean (+/- S.E.M.) basal level of 9.6 +/- 0.6 to 3.6 +/- 0.3 during ketoprofen treatment and to 4.0 +/- 0.3 during indomethacin. Both drugs relieved pelvic and lower back pains and eliminated vomiting and diarrhea in 82-97% of the cycles whereas headache, fatigue and nervousness were less frequently alleviated (40-67%). Eighteen of the 23 women (78%) had been unable to work during the first day of menstruation, the rate of working days lost was reduced to 4% with ketoprofen and 9 with indomethacin. Mild side-effects occurred during 12 ketoprofen and 14 indomethacin therapies. Ketoprofen thus seems to be as effective and tolerable as indomethacin in the treatment of primary dysmenorrhea.

Adolescent↗
PubMed1979

Prostaglandin biosynthesis inhibitors and endometriosis.

Prostaglandins (PGs) may be involved in the development of the symptoms of endometriosis. Therefore 18 patients with pelvic endometriosis were treated in placebo controlled double-blind trial with different prostaglandin biosynthesis inhibitors. These drugs were: acetylsalicylic acid (0.5 g x 3) exerting a weak PG-synthetase inhibition, indomethacin (25 mg x 3) inhibiting PG-synthetase, and as a representative of fenamates, tolfenamic acid (200 mg x 3), which both inhibits PG-synthetase and antagonizes PGs at the target level. The therapeutic effect was evaluated using a specific endometriosis score separately during menstruation and in premenstrum. Prostaglandin biosynthesis inhibitors did not alleviate premenstrual complaints better than placebo. During menstruation tolfenamic acid relieved endometriotic symptoms more effectively than placebo while indomethacin and acetylsalicylic acid did not differ from placebo. A drug which inhibit both the synthesis and action of PGs can thus be used in the alleviation of secondary dysmenorrhea due to endometriosis.

Aspirin↗
PubMed1985

Treatment of premenstrual symptoms.

The etiology of premenstrual syndrome is unknown. A wide variety of etiological explanations has been suggested, but controlled studies based on these theories have generally failed to provide confirmation. This article reviews the literature on treatment of premenstrual symptoms and provides some practical suggestions for clinical management.

Bromocriptine↗
PubMed1985

Menstrual cycle patterns and the risk of breast disease.

The relationship between menstrual cycle patterns and the risk of breast disease was evaluated using data from a hospital-based case-control study of 288 women with benign breast disease (203 chronic cystic diseases and 85 benign tumours), 317 with breast cancer and 602 age-matched controls with a spectrum of acute conditions unrelated to any of the established or potential risk factors for breast disease. A lifelong irregular menstrual pattern [defined as frequent occurrence of menstrual-like episodes of bleeding less than 21 or more than 35 days apart) was negatively associated with the risk of benign breast lesions (relative risk, RR = 0.6, with 95% confidence interval = 0.4-1.0) and of breast cancer (RR = 0.4, with 95% confidence interval = 0.3-0.8]. This inverse association could not be explained by any of the identified potential confounding factors, including the major risk factors for breast disease. The findings of this study, showing that a lifelong history of irregular (and hence more likely anovular) cycles was less frequent among women with benign and malignant breast diseases, support the hypothesis that frequent ovular cycles might be more carcinogenic than anovular ones.

Adolescent↗
PubMed1985

Methodological issues in studies of premenstrual changes.

The main methodological issues that should be considered in studies of premenstrual changes are discussed. They include: the selection of well-defined groups of subjects who reflect the diversity of subtypes of premenstrual changes (PMC); the confirmation of retrospective reports through daily monitoring of changes by ratings, or by objective procedures when possible; the need to consider the diversity of premenstrual biological changes instead of comparing average levels, since there is a likelihood that different pathophysiological changes are connected with diverse behavioral and mood changes; application of a multivariate, time-related approach to explore the pathophysiology of PMC; the need to exclude placebo responders prior to the active drug phase in treatment trials and the need for such trials to be double-blind, placebo-controlled and, if possible, of a cross-over design. Attention to such issues should lead to increased consistency of findings across studies and eventually to a better understanding of the pathophysiology of PMC and to a rational, effective treatment.

20-alpha-Dihydroprogesterone↗
PubMed1993

The relationship between mood and sexuality in women using an oral contraceptive as a treatment for premenstrual symptoms.

This study investigated the effects of a triphasic oral contraceptive (OC) on mood and on sexual interest in a group of 45 women with premenstrual complaints. Subjects made daily ratings of mood and sexual interest for one baseline cycle and were then randomly assigned to receive either placebo or OC for 3 mo. Women who received the OC reported decreased sexual interest during the menstrual and postmenstrual phases of the cycle. The predominant effect of both the OC and the placebo on mood was one of improvement, particularly during the premenstrual phase. There was little evidence of co-variation of mood and sexual interest in either group. Although the mechanism for the adverse effects of the OC on levels of sexual interest in unknown, it is clear that this effect was not simply a consequence of pill-induced negative mood change. The findings provide evidence that mood and sexual desire are dissociable and suggest that OCs can have direct effects on women's sexuality.

Adolescent↗
PubMed1991

The descriptive epidemiology of hysterectomy, Province of Quebec, 1981-1988.

This study reports the descriptive epidemiology of hysterectomy in the Province of Quebec, Canada, from 1981 to 1988. Data on hysterectomies (n = 150,849) among women 15 years and older were obtained from MED-ECHO, a computerized database of hospital discharge summaries. Hysterectomy rates were established, with denominators consisting of the estimated female populations with a uterus. From 1981 to 1988, the age-adjusted rate for hysterectomy declined from 100.4 to 67.4 per 10,000 women with a uterus. Curves representing age-specific rates of hysterectomy revealed a consistent bimodal pattern over time, a first peak occurring in women aged 40 to 44 years, and a second in women aged 65 to 69. Hysterectomy rates for elective conditions such as leiomyoma, endometriosis, disorders of menstruation, and prolapse decreased consistently over time. The proportion of women who had a hysterectomy and simultaneous bilateral oophorectomy declined from 35% in 1981 to 30% in 1988. Despite the substantial decline in the frequency of hysterectomy over the 8-year period, at rates prevailing in 1988, three of ten women would have had a hysterectomy by the age of 60.

Adolescent↗
PubMed1993

Contraceptive choices for women with endocrine complications.

Previous confusion regarding the interference by oral contraceptives in measurements of endocrine function have been largely eliminated by the advent of improved, more sensitive assays. There are few if any contraindications to oral contraceptive use in patients with thyroid disease. Patients with prolactinoma can be treated with bromocriptine to restore fertility and prevent mineral loss. However, as a less expensive alternative, oral contraceptives can be prescribed to correct mineral loss, because there is no convincing evidence of an adverse effect on prolactinomas by the steroidal content of the pill. Oral contraceptives comprise a near ideal treatment modality for women with polycystic ovary disease because, among other effects, oral contraceptives reduce synthesis of androgen by inhibiting pituitary gonadotropin secretion.

Contraception↗