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Prostaglandin-mediated dysmenorrhea
Volume Number
143 1
the partners
Correspondence
involved;
it simply will not sustain a rela-
tionship which depends for its continuance
upon fre-
quent acts of coitus. As well as that, and unlike Temperature-Rhythm, which concentrates on defining times of infertility, the Ovulation Method brings the partners into confrontation with their fertility in each cycle; this has profound psychological results, including an awakening of the suppressed desire for that fertility to become creative of human life. Those who are impressed by ideas reflected in statistics of “Use-Effectiveness” may see the differences in the total pregnancy rates reported in this trial as an encouragement to offer the Sympto-Thermal method to clients interested in natural family planning, rather than the Ovulation Method. This would have the good effect of leaving the teaching of the Ovulation Method to those people who are most likely to make a success of it. 1. J. Billings, M.D. I41 Grey St. East Melbourne 3002, Australia REFERENCES
1. Weissman, M. C., Foliaki, L., Billings, E. L., and Billings, J. J.: Lancet 1:613, 1972. 2. Billings, J. J.: AM. J. OBSTET. GYNECOL. 136:697, 1980.
Prostaglandin-mediated dysmenorrhea To the Editors: The concluding statements of Rosenwaks and associates (AM. J. OBSTET. GYNECOL. 140:592, 1981) seem a bit misleading by their overgeneralization and are not really supported by the data presented in the study. Indeed, it cannot be claimed that “the present study supports the hypothesis that primary dysmenorrhea is a prostaglandin-mediated phenomenon and that reduction of prostaglandin synthesis is accompanied by pain relief,” when, in fact, only 70% (not 100%) of patients experienced excellent and moderate relief. Although I share their enthusiasm for the prostaglandin theory of dysmenorrhea and for the valuable use of nonsteroidal anti-inflammatory drugs in treating many dysmenorrheic women, should we not cautiously avoid condoning the “empiric practice of treating primary dysmenorrhea with these substances” since 30% of these women may not respond to them? How do we identify the (70%) dysmenorrheic women who will be relieved by these agents? On the other hand, how can we explain the lack of relief in 30% of women despite a significant reduction in their PGF-M levels? Were the five women who had been “pregnant at least once but not more than four times,” in this group? I am also curious to know why treatment was started 1 to 5 days before onset of menses rather than at the
onset of menses, and why only two menstrual were studied. Roger Duuivier,
115
cycles M.D.
Gynecology-Obstetrics Diagnostic and Treatment Center Albert Einstein College of Medicine of Yeshiva University 1165 Morris Park Avenue Bronx, New York 10461
Reply to Dr. Duvivier To the Editors: The inquiry of Roger Duvivier has two aspects: semantic and scientific. Insofar as the first is concerned, the statement in the article is accurate, namely, “the study supports”not proves-“that primary dysmenorrhea is a prostaglandin-mediated phenomenon.” The scientific part of the inquiry is more taxing. The recognition of the role of prostaglandins in the pathogenesis of dysmenorrhea has become a dominant theme in recent writings on the syndrome. Successful clinical trials with prostaglandin synthetase inhibitors (PG.%) allowed formulation, perhaps for the first time, of a unified “prostaglandin theory” that explains the various aspects of menstrual distress, as well as its treatment. The introduction of a successful treatment, however, sometimes obviates further need for exploration into the origins of the disease. In the case of dysmenorrhea, the belief in the therapeutic efficacy of hormonal contraceptives had the undesirable effect of minimizing the amount of original research on the problem in the 1960s and early 197Os, with the exception of Vernon Pickles’ work on uterine prostaglandins.’ We face a related salient question now: Will the success of the new PGSIs lead to another pause in research on dysmenorrhea? Between 1970 and 1979, only about 10 scientific articles per year were published on dysmenorrhea. Of the grants awarded by the National Institutes of Health for research on the reproductive system, none was directed specifically to dysmenorrhea. Thus, our knowledge of dysmenorrhea remains sketchy. In relation to dysmenorrhea, prostaglandins F and E have been studied most extensively; however, embarrassingly little is known about other members of the arachidonic acid cascade, even such important ones as prostacyclin, which is produced in large amounts in the uterus. Are other hormones involved in dysmenorrhea? For instance, what is the significance of elevated levels of vasopressin in dysmenorrheic women?2 By stressing the role of prostaglandins in dysmenorrhea, we tend to forget that other substances are involved in the genesis of the main symptom-pain-and we still do not know why dysmenorrhea is absent in women with anovulatory cycles.
143 1
the partners
Correspondence
involved;
it simply will not sustain a rela-
tionship which depends for its continuance
upon fre-
quent acts of coitus. As well as that, and unlike Temperature-Rhythm, which concentrates on defining times of infertility, the Ovulation Method brings the partners into confrontation with their fertility in each cycle; this has profound psychological results, including an awakening of the suppressed desire for that fertility to become creative of human life. Those who are impressed by ideas reflected in statistics of “Use-Effectiveness” may see the differences in the total pregnancy rates reported in this trial as an encouragement to offer the Sympto-Thermal method to clients interested in natural family planning, rather than the Ovulation Method. This would have the good effect of leaving the teaching of the Ovulation Method to those people who are most likely to make a success of it. 1. J. Billings, M.D. I41 Grey St. East Melbourne 3002, Australia REFERENCES
1. Weissman, M. C., Foliaki, L., Billings, E. L., and Billings, J. J.: Lancet 1:613, 1972. 2. Billings, J. J.: AM. J. OBSTET. GYNECOL. 136:697, 1980.
Prostaglandin-mediated dysmenorrhea To the Editors: The concluding statements of Rosenwaks and associates (AM. J. OBSTET. GYNECOL. 140:592, 1981) seem a bit misleading by their overgeneralization and are not really supported by the data presented in the study. Indeed, it cannot be claimed that “the present study supports the hypothesis that primary dysmenorrhea is a prostaglandin-mediated phenomenon and that reduction of prostaglandin synthesis is accompanied by pain relief,” when, in fact, only 70% (not 100%) of patients experienced excellent and moderate relief. Although I share their enthusiasm for the prostaglandin theory of dysmenorrhea and for the valuable use of nonsteroidal anti-inflammatory drugs in treating many dysmenorrheic women, should we not cautiously avoid condoning the “empiric practice of treating primary dysmenorrhea with these substances” since 30% of these women may not respond to them? How do we identify the (70%) dysmenorrheic women who will be relieved by these agents? On the other hand, how can we explain the lack of relief in 30% of women despite a significant reduction in their PGF-M levels? Were the five women who had been “pregnant at least once but not more than four times,” in this group? I am also curious to know why treatment was started 1 to 5 days before onset of menses rather than at the
onset of menses, and why only two menstrual were studied. Roger Duuivier,
115
cycles M.D.
Gynecology-Obstetrics Diagnostic and Treatment Center Albert Einstein College of Medicine of Yeshiva University 1165 Morris Park Avenue Bronx, New York 10461
Reply to Dr. Duvivier To the Editors: The inquiry of Roger Duvivier has two aspects: semantic and scientific. Insofar as the first is concerned, the statement in the article is accurate, namely, “the study supports”not proves-“that primary dysmenorrhea is a prostaglandin-mediated phenomenon.” The scientific part of the inquiry is more taxing. The recognition of the role of prostaglandins in the pathogenesis of dysmenorrhea has become a dominant theme in recent writings on the syndrome. Successful clinical trials with prostaglandin synthetase inhibitors (PG.%) allowed formulation, perhaps for the first time, of a unified “prostaglandin theory” that explains the various aspects of menstrual distress, as well as its treatment. The introduction of a successful treatment, however, sometimes obviates further need for exploration into the origins of the disease. In the case of dysmenorrhea, the belief in the therapeutic efficacy of hormonal contraceptives had the undesirable effect of minimizing the amount of original research on the problem in the 1960s and early 197Os, with the exception of Vernon Pickles’ work on uterine prostaglandins.’ We face a related salient question now: Will the success of the new PGSIs lead to another pause in research on dysmenorrhea? Between 1970 and 1979, only about 10 scientific articles per year were published on dysmenorrhea. Of the grants awarded by the National Institutes of Health for research on the reproductive system, none was directed specifically to dysmenorrhea. Thus, our knowledge of dysmenorrhea remains sketchy. In relation to dysmenorrhea, prostaglandins F and E have been studied most extensively; however, embarrassingly little is known about other members of the arachidonic acid cascade, even such important ones as prostacyclin, which is produced in large amounts in the uterus. Are other hormones involved in dysmenorrhea? For instance, what is the significance of elevated levels of vasopressin in dysmenorrheic women?2 By stressing the role of prostaglandins in dysmenorrhea, we tend to forget that other substances are involved in the genesis of the main symptom-pain-and we still do not know why dysmenorrhea is absent in women with anovulatory cycles.