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Gestational Diabetes Mellitus: Dr. Mazze replies
LETTERS
Mayo elin Proc, April 1993, Vol 68
6. Persson B, Stangenberg M, Hansson U, Nordlander E. Gestational diabetes mellitus (GDM): comparative evaluation of two treatment regimens, diet versus insulin and diet. Diabetes 1985; 34 (Supp12):101-105 7. Drexel H, Bichler A, Sailer S, Breier C, Lisch H-J, Braunsteiner H, et a1. Prevention of perinatal morbidity by tight metabolic control in gestational diabetes mellitus. Diabetes Care 1988; 11:761-768 8. Kjos SL, Buchanan TA, Greenspoon JS, Montoro M, Bernstein GS, Mestman JH. .Gestational diabetes mellitus: the prevalence of glucose intolerance and diabetes mellitus in the first two months post partum. Am J Obstet Gynecoll990; 163:9398 9. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Krolewski AS, Rosner B, et a1. A prospective study of maturity-onset diabetes mellitus and risk of coronary heart disease and stroke in women. Arch Intern Med 1991; 151:1141-1147
Dr. Mazze replies The comments in the letter from Dr. Greenspoon and colleagues highlight a growing concern for the underdetection of gestational diabetes mellitus (GDM). In our study, the detection rate was less than 2%. The causes were a combination of factors, the most important of which was the lack of universal screening. The authors rightfully indicate that many women who had large for gestational age (LGA) infants or infants with macrosomia might have had hyperglycemia during their pregnancy but because of the absence of universal screening, that condition was undetected. To overcome this problem, the authors not only agree that universal screening is necessary but also suggest a change in both the screening and the diagnostic criteria that might have detected some of the women in the study who ultimately were delivered of large infants. The changes proposed by these and other investigators include careful follow-up of women with high screening values on the glucose challenge test (between 120 and 140 mg/dl). Currently, only the women whose results on the glucose challenge test are more than 140 mg/dl (25% of those screened) undergo a 3-hour oral glucose tolerance test. The authors' suggestion would increase the number of women administered an oral glucose tolerance test (based on our data) to 35 to 45% of those screened. The test would also be modified to include follow-up for women with high normal values (within 5% of the upper limit of normal on two test values) and for women with one abnormal value on the glucose challenge test. This follow-up might include dietary interventions and glucose monitoring and, for some women, insulin therapy. These combined changes may result in the detection of an additional 50,000 to 100,000 cases of GDM each year (extrapolated from our findings). Part of the argument for more effort in the detection and the inclusion of a broader definition of GDM is based on a
409
generalized belief that early detection with rapid interventions should prevent fetal complications, most notably those related to intrauterine growth. The authors are correct in noting that with available technology, women detected with impaired glucose tolerance and overt GDM could be offered dietary interventions and insulin therapies that would safely and expeditiously achieve euglycemia during pregnancy. The maintenance of "normal" blood glucose levels (60 to 120 mg/dl) has been shown to decrease substantially the risk of LGA infants or those with macrosomia and consequently to decrease fetal hypoglycemia and other results of excessive intrauterine growth. The implementation of universal screening and application of a broadened definition of GDM seem desirable. The financial, social, psychologic, and medical burdens associated with LGA infants or those with macrosomia outweigh the cost of implementing changes in detection. A decrease in the reliance on cesarean section, an avoidance of the necessity of neonatal intensive care, and the prevention of childhood and adult obesity are potential benefits of universal screening and appropriate care for those women detected with diabetes. Although the current study did not review the management of diabetes or completely consider various criteria for diagnosis, concluding that many of the women who had LGA infants or infants with macrosomia may have had hyperglycemia during their pregnancy is straightforward. Therefore, the time for universal screening, intensified treatment, and postpartum follow-up is now. Roger S. Mazze, Ph.D. International Diabetes Center Minneapolis, Minnesota
Restenosis Comes of Age As an investigator of the problem of restenosis,' I particularly enjoyed reading the article by Schwartz and associates, which was published in the January 1993 issue of the Mayo Clinic Proceedings (pages 54 to 62), in which they proposed a new pathogenetic hypothesis of restenosis. After a lengthy era of repetitive publications by investigators who tried to "squeeze" the problem of restenosis into the current conventional concept of atherosclerosis, this article considers that the thrombus formed at the site of angioplasty injury is the main determinant of restenosis. Initially, this proposition is correct because the cells engaged in wound healing reaction are able to proliferate only in the environment of a provisional matrix, which is represented by the thrombus. Later, the situation becomes more complicated. A formation (and a
Mayo elin Proc, April 1993, Vol 68
6. Persson B, Stangenberg M, Hansson U, Nordlander E. Gestational diabetes mellitus (GDM): comparative evaluation of two treatment regimens, diet versus insulin and diet. Diabetes 1985; 34 (Supp12):101-105 7. Drexel H, Bichler A, Sailer S, Breier C, Lisch H-J, Braunsteiner H, et a1. Prevention of perinatal morbidity by tight metabolic control in gestational diabetes mellitus. Diabetes Care 1988; 11:761-768 8. Kjos SL, Buchanan TA, Greenspoon JS, Montoro M, Bernstein GS, Mestman JH. .Gestational diabetes mellitus: the prevalence of glucose intolerance and diabetes mellitus in the first two months post partum. Am J Obstet Gynecoll990; 163:9398 9. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Krolewski AS, Rosner B, et a1. A prospective study of maturity-onset diabetes mellitus and risk of coronary heart disease and stroke in women. Arch Intern Med 1991; 151:1141-1147
Dr. Mazze replies The comments in the letter from Dr. Greenspoon and colleagues highlight a growing concern for the underdetection of gestational diabetes mellitus (GDM). In our study, the detection rate was less than 2%. The causes were a combination of factors, the most important of which was the lack of universal screening. The authors rightfully indicate that many women who had large for gestational age (LGA) infants or infants with macrosomia might have had hyperglycemia during their pregnancy but because of the absence of universal screening, that condition was undetected. To overcome this problem, the authors not only agree that universal screening is necessary but also suggest a change in both the screening and the diagnostic criteria that might have detected some of the women in the study who ultimately were delivered of large infants. The changes proposed by these and other investigators include careful follow-up of women with high screening values on the glucose challenge test (between 120 and 140 mg/dl). Currently, only the women whose results on the glucose challenge test are more than 140 mg/dl (25% of those screened) undergo a 3-hour oral glucose tolerance test. The authors' suggestion would increase the number of women administered an oral glucose tolerance test (based on our data) to 35 to 45% of those screened. The test would also be modified to include follow-up for women with high normal values (within 5% of the upper limit of normal on two test values) and for women with one abnormal value on the glucose challenge test. This follow-up might include dietary interventions and glucose monitoring and, for some women, insulin therapy. These combined changes may result in the detection of an additional 50,000 to 100,000 cases of GDM each year (extrapolated from our findings). Part of the argument for more effort in the detection and the inclusion of a broader definition of GDM is based on a
409
generalized belief that early detection with rapid interventions should prevent fetal complications, most notably those related to intrauterine growth. The authors are correct in noting that with available technology, women detected with impaired glucose tolerance and overt GDM could be offered dietary interventions and insulin therapies that would safely and expeditiously achieve euglycemia during pregnancy. The maintenance of "normal" blood glucose levels (60 to 120 mg/dl) has been shown to decrease substantially the risk of LGA infants or those with macrosomia and consequently to decrease fetal hypoglycemia and other results of excessive intrauterine growth. The implementation of universal screening and application of a broadened definition of GDM seem desirable. The financial, social, psychologic, and medical burdens associated with LGA infants or those with macrosomia outweigh the cost of implementing changes in detection. A decrease in the reliance on cesarean section, an avoidance of the necessity of neonatal intensive care, and the prevention of childhood and adult obesity are potential benefits of universal screening and appropriate care for those women detected with diabetes. Although the current study did not review the management of diabetes or completely consider various criteria for diagnosis, concluding that many of the women who had LGA infants or infants with macrosomia may have had hyperglycemia during their pregnancy is straightforward. Therefore, the time for universal screening, intensified treatment, and postpartum follow-up is now. Roger S. Mazze, Ph.D. International Diabetes Center Minneapolis, Minnesota
Restenosis Comes of Age As an investigator of the problem of restenosis,' I particularly enjoyed reading the article by Schwartz and associates, which was published in the January 1993 issue of the Mayo Clinic Proceedings (pages 54 to 62), in which they proposed a new pathogenetic hypothesis of restenosis. After a lengthy era of repetitive publications by investigators who tried to "squeeze" the problem of restenosis into the current conventional concept of atherosclerosis, this article considers that the thrombus formed at the site of angioplasty injury is the main determinant of restenosis. Initially, this proposition is correct because the cells engaged in wound healing reaction are able to proliferate only in the environment of a provisional matrix, which is represented by the thrombus. Later, the situation becomes more complicated. A formation (and a