Volume 134 Number 6
Correspondence 727
In the ai"tide by Kauraniemi and associates, the risk of malignant or premalignant lesions was lower than in the rest of the population. They believe that the cautery and we believe the hydrogen ions destroyed the atypical epithelium at some stage of the natural progression of the disease. They also stated that even if it is impossible to prove cauterization of benign cervical lesions is the reason for the reduction of cervical cancer. the treatment should be seriously considered as a means of prev'enting cervical cancer. In our gynecology clinics we think the most important procedures in gynecology are cauterization, conization, coagulation, and cryocauterization of benign cervical lesions. Now with this powder the patient can destroy all benign cervical lesions. This powder is prescribed in all sexually active women. instead of water-made douches, so that any dysplastic lesion or carcinoma in situ will not become malignant and 'A'i!! revert back into normal vaginal cells. The acid environment has definitely been shown to cause endocervical cells to remain high in the cervical canal where they normally thrive in the alkaline environment, thereby maintaining the cenix free of dysplasia and carcinoma in situ and, in so doing, preventing the development of cervical cancer. l{arl John .l.:.arnaky, A1.J). The Obstetrical arzd Gynerulogi.-al Research Foundation and Research Institute 2164 Addison Houston, Texas 77030
tion and evaluation by additional methods, such as an oxytocin challenge test and a fetal nonstress reactive test. In cases in which fetal bradycardia follows amniocentesis, maternal hypotension due to a maternal "vasovagal" reflex should be ruled out as the cause of fetal bradycardia. 3 Maternal "vasovagal" reflex can be observed dinicaliy during the procedure. Another helpful point in recognizing this apparently harmless and transient cause of fetal bradycardia is a "normal" acceleration which precedes the bradycardia. By recognizing this cause of fetal bradycardia (which occurred in 6.6% of our second series) false positive results can be minimized. We fully agree with the authors that in any amniocentesis procedure continuous FHR monitoring can contribute additional valuable inforn1ation, as suggested by us in 1974. 4 · 5 Moshf' Ron; M.D. Departrnmt of Obstetrics and Gynecology H adassa University Hospital jerusalem, Israel
Fetal heart rate response to amniocentesis To the Editors:
4.
I read with interest the article, HFeta! heart rate reaction to amniocentesis as an indicator of fetal wellbeing" by John T. Harrison, M.D., F.A.C.O.G., and Joseph F. Marino, D.O., in the JouRNAL (132:49, 1978). I wish to add to their interesting findings our own experience of a study of 107 amniocenteses under continuous fetal heart rate (FHR) monitoring which was published in 1976 1 and since then has grown to 250 cases, being a roucine procedure in our Department for assessment of fetal well-being in any case in which amniocentesis is indicated. The two typical patterns of reaction, namely, tachycardia and bradycardia, correspond well with the findings of Harrison and Marino. I. 2 There are, however, two points which should be clarified according to our experience. As the "normal" response of the fetus to the stimulus of amniocentesis is tachycardia (82.2% in our first series) "no response" or an "equivocal" response should be regarded as a sign of the existence of some degree of fetal jeopardy (proved in 42.2% of the cases of our first series), and sometimes as an indication of severe distress as in these cases which show a response ofbradycardia. 2 Therefore, those cases in which an "equivocal" response is found need close observa-
REFERENCES I. Ron, M., and Polishuk, W. E.: The response to the fetal
2. 3.
5.
heart rate to amniocentesis, Br. j. Obstet. Gynaecoi. 83:758, 1975. Ron, M., Yaffe, H., and Sadosky, E.: Fetal heart rate response to amniocentesis in cases of decreased fetal movements, Obstet. Gynecol. 48:457, 1976. Ron, M., Yaffe, H., and Polishuk, W. E.: Fetal heart rate response to maternal hypotension during amniocentesis, Int. J. Gynaecol. Obstet. 14:503, 1976. Ron, M., Anteby, S., Diamant, Y. Z., and Polishuk, W. Z.: Int.]. Gynaecol. Obstet. 12:172,1974. Danforth, D. N.: Obstetrics and Gynecology, ed. 3, New Yotk, 1977, Harper & Row Publishers, pp. 748 and 760.
Perinatal mortality rate associated with diabetic pregnancy To the Editors: In their stimulating article entitled "Diabetic pregnancy and perinatal morbidity," published in the "Current Developments" section in THE jOURNAL (131:560, 1978), Kitzmiller and associates have provided a wealth of information helpful to any endocrinologist caring for pregnant diabetic patients. However, one finds it difficult to accept that the perinatal mortaility rate was 3.4o/c, particularly when the authors deleted seven patients who underwent elective abortions (4%), including three women (2%) in whom pregnancy was terminated after antenatal diagnosis of fetal anencephaly. Their deJection cannot be justified since these patients were registered with the pregnancy clinic of the Joslin Foundation and must have been provided the same kind of antenatal care as the others received. Apparently the authors deleted this group of patients to achieve an impressive perinatal mortality figure of
728 Correspondence Am.
· _ .· r one mcmaes tms group orr pauents ror purposes of cakulating the perinatal mortality rate, the true figures would be 5.4%, which is still impressive but takes away the claim of best figures from the authors, since a rate of 5% or less has been already reported bv various centers. 1
o
Arrl
rr
.::>.'±7o. 1I
1
1
.1
•
Romesh Khardori, M.D. Fellow, Endocrinology and Metabolism Room #831, Medical Research Building UniveTsity of Oregon 1'v1.edical School 3181 S.W. Sam jackson Park Road Portland, Oregon 97201
REFERENCE I. Gabbe, S. G.: Diabetes in pregnancy: clinical controversies,
Jul~
15, 1979
ObsteL Gvn('coi.
agemem of diabetic patients before pregnane} anct m early pregnancy. For this reason, our three ca~cs of anencephaly were included in our incidence or ~Y7, major congenital anomalies. In the article 1n· emphasized that the relationship of the metabolic perturbations of maternal diabetes to birth defects in the offspring is a very important area for research. Finally, I believe it is demeaning and trivial to claim the best record for anything in this complicated and changing \Vorid. In the paper
\Ve
stated that
"llH~
peri-
natal mortality rate in this [ 1975 to I 976) 'eries (34/ 1,000) is among the best reported to date for large groups of women with severe diabetes." Over the four years, 1975 to 1978, our perinatal mortalitv rate for 270 diabetic women was 36/1,000.
Clin. Obstet. Gynecol. 21:443, 1978.
Reply to Or. Khardori
J
fohn L 1\.itzmi/ln, M.D. Basion Hospitalfor fVomen 250 Longwood A1•nzuc Boston, A1assachusetts ()2! I 1
To the Editors:
In the closing paragraph of our article, we tried to emphasize the many factors which play a role in improved perinatal survival in pregnancies attaining a stage of viability in women with insulin-dependent diabetes. We cited a high proportion of cooperative, weii-motivated patients, a iow incidence of pyelonephritis and pre-eclampsia, application of measures that can assess fetal \vell-being, prediction of fetal pulmonary maturity by amniotic fluid analysis, and advances in neonatal care. We also stated that "the availability of the a-fetoprotein assay and ultrasonography has allowed the early diagnosis of anencephaly so that pregnancies may be terminated." This is an example of the application of new medical technology to reduce the mcidence of severely abnormal infants delivered after 24 weeks' gestation. We also would not include pregnancies aborted due to the diagnosis of Down's syndrome in our perinatal mortality figures-they would be considered in our abortion statistics. On the other hand, we completely agree with Dr. Khardori that congenital anomalies are a very important outcome variable to consider when assessing man-
Prior immunization by herpeevirus To the Editors:
In their article concerning the effects of prior immunization by herpesvirus type 1, Asher and his coworkers were not abie to demonstrate protection from challenge with herpesvirus type 2 (AM. J. 0BSTET. GYNECOL.
131 :788) 1978). They attributed this to -pos-
sible strain difference among type 2 virus. As reported previously (AM. J. Ossn:T. GvNECOL. 125:41. 1976), we werr able to demonstrate protection of newborn mice from lethal infection due to maternal vaginal challenge with type 2 herpesvirus after maternal immunization with type l virus. Perhaps this is an exam pie of strain differences suggested by the authors. I would encourage them to continue with their model of latent infection to test this hypothesis. Man•in S. Amstr.v. M.D. Department of Obstetrics-Gynecology School of Medicine and Dentistry The University of Rochester Medical Center Rochesi•'r, New York 14620
Correspondence 727
In the ai"tide by Kauraniemi and associates, the risk of malignant or premalignant lesions was lower than in the rest of the population. They believe that the cautery and we believe the hydrogen ions destroyed the atypical epithelium at some stage of the natural progression of the disease. They also stated that even if it is impossible to prove cauterization of benign cervical lesions is the reason for the reduction of cervical cancer. the treatment should be seriously considered as a means of prev'enting cervical cancer. In our gynecology clinics we think the most important procedures in gynecology are cauterization, conization, coagulation, and cryocauterization of benign cervical lesions. Now with this powder the patient can destroy all benign cervical lesions. This powder is prescribed in all sexually active women. instead of water-made douches, so that any dysplastic lesion or carcinoma in situ will not become malignant and 'A'i!! revert back into normal vaginal cells. The acid environment has definitely been shown to cause endocervical cells to remain high in the cervical canal where they normally thrive in the alkaline environment, thereby maintaining the cenix free of dysplasia and carcinoma in situ and, in so doing, preventing the development of cervical cancer. l{arl John .l.:.arnaky, A1.J). The Obstetrical arzd Gynerulogi.-al Research Foundation and Research Institute 2164 Addison Houston, Texas 77030
tion and evaluation by additional methods, such as an oxytocin challenge test and a fetal nonstress reactive test. In cases in which fetal bradycardia follows amniocentesis, maternal hypotension due to a maternal "vasovagal" reflex should be ruled out as the cause of fetal bradycardia. 3 Maternal "vasovagal" reflex can be observed dinicaliy during the procedure. Another helpful point in recognizing this apparently harmless and transient cause of fetal bradycardia is a "normal" acceleration which precedes the bradycardia. By recognizing this cause of fetal bradycardia (which occurred in 6.6% of our second series) false positive results can be minimized. We fully agree with the authors that in any amniocentesis procedure continuous FHR monitoring can contribute additional valuable inforn1ation, as suggested by us in 1974. 4 · 5 Moshf' Ron; M.D. Departrnmt of Obstetrics and Gynecology H adassa University Hospital jerusalem, Israel
Fetal heart rate response to amniocentesis To the Editors:
4.
I read with interest the article, HFeta! heart rate reaction to amniocentesis as an indicator of fetal wellbeing" by John T. Harrison, M.D., F.A.C.O.G., and Joseph F. Marino, D.O., in the JouRNAL (132:49, 1978). I wish to add to their interesting findings our own experience of a study of 107 amniocenteses under continuous fetal heart rate (FHR) monitoring which was published in 1976 1 and since then has grown to 250 cases, being a roucine procedure in our Department for assessment of fetal well-being in any case in which amniocentesis is indicated. The two typical patterns of reaction, namely, tachycardia and bradycardia, correspond well with the findings of Harrison and Marino. I. 2 There are, however, two points which should be clarified according to our experience. As the "normal" response of the fetus to the stimulus of amniocentesis is tachycardia (82.2% in our first series) "no response" or an "equivocal" response should be regarded as a sign of the existence of some degree of fetal jeopardy (proved in 42.2% of the cases of our first series), and sometimes as an indication of severe distress as in these cases which show a response ofbradycardia. 2 Therefore, those cases in which an "equivocal" response is found need close observa-
REFERENCES I. Ron, M., and Polishuk, W. E.: The response to the fetal
2. 3.
5.
heart rate to amniocentesis, Br. j. Obstet. Gynaecoi. 83:758, 1975. Ron, M., Yaffe, H., and Sadosky, E.: Fetal heart rate response to amniocentesis in cases of decreased fetal movements, Obstet. Gynecol. 48:457, 1976. Ron, M., Yaffe, H., and Polishuk, W. E.: Fetal heart rate response to maternal hypotension during amniocentesis, Int. J. Gynaecol. Obstet. 14:503, 1976. Ron, M., Anteby, S., Diamant, Y. Z., and Polishuk, W. Z.: Int.]. Gynaecol. Obstet. 12:172,1974. Danforth, D. N.: Obstetrics and Gynecology, ed. 3, New Yotk, 1977, Harper & Row Publishers, pp. 748 and 760.
Perinatal mortality rate associated with diabetic pregnancy To the Editors: In their stimulating article entitled "Diabetic pregnancy and perinatal morbidity," published in the "Current Developments" section in THE jOURNAL (131:560, 1978), Kitzmiller and associates have provided a wealth of information helpful to any endocrinologist caring for pregnant diabetic patients. However, one finds it difficult to accept that the perinatal mortaility rate was 3.4o/c, particularly when the authors deleted seven patients who underwent elective abortions (4%), including three women (2%) in whom pregnancy was terminated after antenatal diagnosis of fetal anencephaly. Their deJection cannot be justified since these patients were registered with the pregnancy clinic of the Joslin Foundation and must have been provided the same kind of antenatal care as the others received. Apparently the authors deleted this group of patients to achieve an impressive perinatal mortality figure of
728 Correspondence Am.
· _ .· r one mcmaes tms group orr pauents ror purposes of cakulating the perinatal mortality rate, the true figures would be 5.4%, which is still impressive but takes away the claim of best figures from the authors, since a rate of 5% or less has been already reported bv various centers. 1
o
Arrl
rr
.::>.'±7o. 1I
1
1
.1
•
Romesh Khardori, M.D. Fellow, Endocrinology and Metabolism Room #831, Medical Research Building UniveTsity of Oregon 1'v1.edical School 3181 S.W. Sam jackson Park Road Portland, Oregon 97201
REFERENCE I. Gabbe, S. G.: Diabetes in pregnancy: clinical controversies,
Jul~
15, 1979
ObsteL Gvn('coi.
agemem of diabetic patients before pregnane} anct m early pregnancy. For this reason, our three ca~cs of anencephaly were included in our incidence or ~Y7, major congenital anomalies. In the article 1n· emphasized that the relationship of the metabolic perturbations of maternal diabetes to birth defects in the offspring is a very important area for research. Finally, I believe it is demeaning and trivial to claim the best record for anything in this complicated and changing \Vorid. In the paper
\Ve
stated that
"llH~
peri-
natal mortality rate in this [ 1975 to I 976) 'eries (34/ 1,000) is among the best reported to date for large groups of women with severe diabetes." Over the four years, 1975 to 1978, our perinatal mortalitv rate for 270 diabetic women was 36/1,000.
Clin. Obstet. Gynecol. 21:443, 1978.
Reply to Or. Khardori
J
fohn L 1\.itzmi/ln, M.D. Basion Hospitalfor fVomen 250 Longwood A1•nzuc Boston, A1assachusetts ()2! I 1
To the Editors:
In the closing paragraph of our article, we tried to emphasize the many factors which play a role in improved perinatal survival in pregnancies attaining a stage of viability in women with insulin-dependent diabetes. We cited a high proportion of cooperative, weii-motivated patients, a iow incidence of pyelonephritis and pre-eclampsia, application of measures that can assess fetal \vell-being, prediction of fetal pulmonary maturity by amniotic fluid analysis, and advances in neonatal care. We also stated that "the availability of the a-fetoprotein assay and ultrasonography has allowed the early diagnosis of anencephaly so that pregnancies may be terminated." This is an example of the application of new medical technology to reduce the mcidence of severely abnormal infants delivered after 24 weeks' gestation. We also would not include pregnancies aborted due to the diagnosis of Down's syndrome in our perinatal mortality figures-they would be considered in our abortion statistics. On the other hand, we completely agree with Dr. Khardori that congenital anomalies are a very important outcome variable to consider when assessing man-
Prior immunization by herpeevirus To the Editors:
In their article concerning the effects of prior immunization by herpesvirus type 1, Asher and his coworkers were not abie to demonstrate protection from challenge with herpesvirus type 2 (AM. J. 0BSTET. GYNECOL.
131 :788) 1978). They attributed this to -pos-
sible strain difference among type 2 virus. As reported previously (AM. J. Ossn:T. GvNECOL. 125:41. 1976), we werr able to demonstrate protection of newborn mice from lethal infection due to maternal vaginal challenge with type 2 herpesvirus after maternal immunization with type l virus. Perhaps this is an exam pie of strain differences suggested by the authors. I would encourage them to continue with their model of latent infection to test this hypothesis. Man•in S. Amstr.v. M.D. Department of Obstetrics-Gynecology School of Medicine and Dentistry The University of Rochester Medical Center Rochesi•'r, New York 14620
