- Email: [email protected]
Hypocalcemia in infants of diabetic mothers
Volume 81 Number 3
Letters to the Editor
REFERENCES 1. Frasler, S. D., and Ralllson, M. L.: Growth retardation and emotional deprivation: Relative resistance to treatment with human growth hormone, J. PZI~IATR.80: 603, 1972. 2. Patton, R. G., and Gardner, L. I.: Growth failure in maternal deprivation, Springfield, Ili., 1963, Charles C Thomas, Publisher, p. 75. 3. Widdowson, E. M.: MentaI contentment and physical growth, Lancet 1: 1316, 1951. 4. Youlton, R., Kaplan, S. L., and Grumbach, M. M.: Growth and growth hormone. IV. Limitation of growth hormone response m insulin and arginlne and of the immunoreactive insulin response to arglnlne in the assessment of growth hormone deficiency in children, Pediatrics 43: 989, 1969. 5. Lippe, B., Wong, S-L. R., and Kaplan, S. A.: Simultaneous assessment of growth hormone and ACTH reserve in children pretreated with diethylstilbestrol, J. Clin. Endocrinol. Metab. 33: 949, 1971.
Reply To the Editor: The question regarding changes in our patient's weight during her hospitalization can not be answered on the basis of available information. All of her hospitalizations were short term, and no significant weight gain was observed. Whether or not significant change in weight would have been noted had the hospitalizations been for several weeks remains moot.
S. Douglas Frasler, M.D. Los Angeles County-University o'[ Southern Cali]ornia 1129 N. State St. Medical Center Los Angeles, Cali[. 90033
Hypocalcemia in infants of diabetic mothers To the Editor: Dr. Tsang and co-workers,1 in their article, "Hypocalcemia in infants of diabetic mothers," suggest that relative maternal hyperparathyroidism leading to fetal hypoparathyroidism may be the cause of hypocalcemla in h~fants of diabetic mothers. I should like to propose an alternate mechanism. The etiology could be explained by a hypersecretion of glucagon, due to both antenatal and
63 3
postnatal responses of the neonate. AntenataIly there might be hypertrophy of the alpha cells, occurring along with beta call hypertrophy. Dr. Tsang showed that lower serum calcium levels were assoslcated with more severe degrees of maternal diabetes. This might be due to a greater degree of alpha cell hypertrophy in infants of severely ill diabetic mothers. Postnatally there might be hypersecretion of glucagon in response to the neonatal hypoglycemia. The authors found that five of eight infants with hypoglycemia had hypocalcemia, whereas only one of 15 infants without hypoglycemia had hypocalcemia. Since glucagon decreases the serum calcium, possibly due to direct ~ and indirect mcchanismsfl "6 a hypersecretion of glucagon in infants of diabetic mothers might expIain the hypocalcemia. The authors showed no significant difference in tubular reabsorption of phosphorus between treated and untreated infants of diabetic mothers, or between infants of diabetic mothers and control subjects. The higher serum phosphorus levels in infants of diabetic mothers might be due to an inability to handle an endogenous phosphate load. This implies that the parathyroid glands are not directly involved.
Lorne Katz, M.D. Mount Sinai School o[ Medicine Filth Ave. and lOOth St. New York, N. Y. 10029
REFERENCES 1. Tsaxxg, R. C., Kleinman, L. I., Sutherland, J. M., and Light, I. J." Hypocalcemia in infants of diabetic mothers, J. PrnIATR. 80: 384, 1972. 2. Hattner, R. S., Bernstein, D. S., Aliapoulios, M. A., et al.- The hypocalcemlc activity of glueagon: Demonstration of independence from endogenous caleltonin secretion in the rat, Acta Endocrinol. 64: 726, 1970. 3. Avioli, L. V., Birge, S. J., Scott, S., et aI.: Role of the thyroid gland during glucagon-induced hypocalcemia in the dog, Am. J. Physlol. 216: 939, 1969. 4. Miiller, W. A., Faloona, G. R., Agailar-Parada, E., et al.: Abnormal alpha-cell function in diabetes. Response to carbohydrate and protein ingestion, N. Engl. J. Med. 283: 109, 1970. 5. Unger, R. H., Aguilar-Parada, E., Miiller, W. A., et al.: Studies of pancreatic alpha-cell function in normal and diabetic subjects, J. Clin. Invest. 49: 837, 1970. 6. Unger, R. H.: Glucagon physiology and pathophysiology, N. Engl. J. Med. 285" 343, 1971.
Letters to the Editor
REFERENCES 1. Frasler, S. D., and Ralllson, M. L.: Growth retardation and emotional deprivation: Relative resistance to treatment with human growth hormone, J. PZI~IATR.80: 603, 1972. 2. Patton, R. G., and Gardner, L. I.: Growth failure in maternal deprivation, Springfield, Ili., 1963, Charles C Thomas, Publisher, p. 75. 3. Widdowson, E. M.: MentaI contentment and physical growth, Lancet 1: 1316, 1951. 4. Youlton, R., Kaplan, S. L., and Grumbach, M. M.: Growth and growth hormone. IV. Limitation of growth hormone response m insulin and arginlne and of the immunoreactive insulin response to arglnlne in the assessment of growth hormone deficiency in children, Pediatrics 43: 989, 1969. 5. Lippe, B., Wong, S-L. R., and Kaplan, S. A.: Simultaneous assessment of growth hormone and ACTH reserve in children pretreated with diethylstilbestrol, J. Clin. Endocrinol. Metab. 33: 949, 1971.
Reply To the Editor: The question regarding changes in our patient's weight during her hospitalization can not be answered on the basis of available information. All of her hospitalizations were short term, and no significant weight gain was observed. Whether or not significant change in weight would have been noted had the hospitalizations been for several weeks remains moot.
S. Douglas Frasler, M.D. Los Angeles County-University o'[ Southern Cali]ornia 1129 N. State St. Medical Center Los Angeles, Cali[. 90033
Hypocalcemia in infants of diabetic mothers To the Editor: Dr. Tsang and co-workers,1 in their article, "Hypocalcemia in infants of diabetic mothers," suggest that relative maternal hyperparathyroidism leading to fetal hypoparathyroidism may be the cause of hypocalcemla in h~fants of diabetic mothers. I should like to propose an alternate mechanism. The etiology could be explained by a hypersecretion of glucagon, due to both antenatal and
63 3
postnatal responses of the neonate. AntenataIly there might be hypertrophy of the alpha cells, occurring along with beta call hypertrophy. Dr. Tsang showed that lower serum calcium levels were assoslcated with more severe degrees of maternal diabetes. This might be due to a greater degree of alpha cell hypertrophy in infants of severely ill diabetic mothers. Postnatally there might be hypersecretion of glucagon in response to the neonatal hypoglycemia. The authors found that five of eight infants with hypoglycemia had hypocalcemia, whereas only one of 15 infants without hypoglycemia had hypocalcemia. Since glucagon decreases the serum calcium, possibly due to direct ~ and indirect mcchanismsfl "6 a hypersecretion of glucagon in infants of diabetic mothers might expIain the hypocalcemia. The authors showed no significant difference in tubular reabsorption of phosphorus between treated and untreated infants of diabetic mothers, or between infants of diabetic mothers and control subjects. The higher serum phosphorus levels in infants of diabetic mothers might be due to an inability to handle an endogenous phosphate load. This implies that the parathyroid glands are not directly involved.
Lorne Katz, M.D. Mount Sinai School o[ Medicine Filth Ave. and lOOth St. New York, N. Y. 10029
REFERENCES 1. Tsaxxg, R. C., Kleinman, L. I., Sutherland, J. M., and Light, I. J." Hypocalcemia in infants of diabetic mothers, J. PrnIATR. 80: 384, 1972. 2. Hattner, R. S., Bernstein, D. S., Aliapoulios, M. A., et al.- The hypocalcemlc activity of glueagon: Demonstration of independence from endogenous caleltonin secretion in the rat, Acta Endocrinol. 64: 726, 1970. 3. Avioli, L. V., Birge, S. J., Scott, S., et aI.: Role of the thyroid gland during glucagon-induced hypocalcemia in the dog, Am. J. Physlol. 216: 939, 1969. 4. Miiller, W. A., Faloona, G. R., Agailar-Parada, E., et al.: Abnormal alpha-cell function in diabetes. Response to carbohydrate and protein ingestion, N. Engl. J. Med. 283: 109, 1970. 5. Unger, R. H., Aguilar-Parada, E., Miiller, W. A., et al.: Studies of pancreatic alpha-cell function in normal and diabetic subjects, J. Clin. Invest. 49: 837, 1970. 6. Unger, R. H.: Glucagon physiology and pathophysiology, N. Engl. J. Med. 285" 343, 1971.