- Email: [email protected]
Maternal cocaine use and risk of sudden infant death
Volume 115 Number 2
3.
4.
5.
deficiency: adenosine deaminase (ADA) and purine nucleotide phosphorylase (PNP) deficiencies. Clin Immunol Immunopathol 1986;40:157-65. McGeady SJ. Transient hypogammaglobulinemia of infancy: need to reconsider name and definition. J PEDIATR 1987; 110:47-50. Tiller TL, Buckley RH. Transient hypogammaglobulinemia of infancy: review of the literature, clinical and immunologic features of 11 new cases and long-term follow-up. J PEDIATR 1978;92:347-53. Benderly A, Pollack S, Etzioni A. Transient hypogammaglobulinemia of infancy with severe bacterial infections and persistent IgA deficiency. Israel J Med Sci 1986;22:393-6.
Reply To the Editor: Dr. Etzioni suggests that the hypogammaglobulinemia observed in our patient with hereditary orotic acidura may have been a manifestation of transient hypogammaglobulinemia of infancy. The rapidity with which normalization of serum lgG and the marked increase in serum IgM concentrations occurred in our patient after the institution of uridine replacement strongly suggests a causal relationship. Moreover, transient hypogammaglobulinemia of infancy is a very rare condition when strict criteria for its diagnosis are used1; it appears highly improbable that two rare entities occurred simultaneously. Not mentioned in Dr. Etzioni's letter is the fact that the patient's lymphocyte response to pokeweed mitogen also increased substantially with uridine therapy. Furthermore, repeat studies using a flow cytometry method to count the number of blast cells present after mitogen stimulation, performed 13 months after the start of treatment, showed the patient's response to both concanavalin A and pokeweed mitogen to be in the low range of normal (data not shown in article). We agree with Dr. Etzioni's suggestion that more patients with orotie aciduria need to be studied to better define the immunologic abnormalities associated with this rare condition. Carlos A. Alvarado, MD John R. MeKolanis, PhD Department o f Pediatrics Emory University School o f Medicine Atlanta, GA 30322 REFERENCE
1.
Tiller TL, Bucley RH. Transient hypogammaglobulinemia of infancy: review of the literature, clinical and immunologic features of 11 new cases, and long-term follow-up. J PEDIATR 1978;92:347-53.
Maternal c o c a i n e use and risk of
sudden infant death To the Editor." The recent article by Bauchner et al. (J PEDIATR 1988;113:8314) regarding the risk of sudden infant death syndrome (SIDS) among infants with in utero exposure to cocaine suggests that there is no increased risk of SIDS among infants exposed in utero to
E d i t o r i a l correspondence
.3 3 3
cocaine. Subjects were included in the cocaine-negative group on the basis of self-reported drug history and urinalysis. Self-reported drug histories are often inaccurate because the subjects may deny their use of drugs. 1 Urinalysis generally detects drug use in the previous 2 to 3 days, so many users have negative drug test results if they have abstained in recent days. Therefore it is possible that some of those who denied cocaine use and had negative urinalysis results were misclassified as nonusers of cocaine. A way to obviate the shortcoming of urinalysis is to analyze the hair, where the drug accumulates for many months.2 We have applied this technique successfully to human hair samples, as small as 10 mg, from admitted cocaine users who had negative urine test results for cocaine. Hair samples of only 1.5 mg from babies of women who used cocaine during pregnancy have also proved positive for cocaine. No cross reactivity occurs with hair from individuals not using cocaine? Because the reproductive effects of cocaine use cause high levels of public anxiety, the method of hair analysis for cocaine use in previous months should be used for unequivocal verification of maternal nonexposure. Karen Graham, MD Gideon Koren, MD The Motherisk Program The Hospital for Sick Children Toronto, Ontario M5G 1X8, Canada REFERENCES
1.
2.
3.
Single E, Kandel D, Johnson BD. The reliability and validity of drug use responses in a large-scale longitudinal survey. J Drug Issues 1975;426:426-43. Valente D, Cassini M, Pigliapochi M, Vansetti G. Hair as the sample in assessing morphine and cocaine addiction. Clin Chem 1981;27:1952-3. Graham K, Koren G, Klein J, Schneiderman J. Detecting maternal exposure to cocaine by hair analysis [Abstract 442]. Pediatr Res 1989;25(4, pt 2).
Lactose tolerance in colicky infants To the Editor." We were disappointed that Moore et al. (J PEDIATR 1988;113:979-84) failed to cite our recent article on infantile colic, 1 in which we did what they suggested: we modified both the protein and the carbohydrate intakes of formula-fed infants with severe colic. We did a double-blind crossover study on 10 formula-fed infants with severe colic. The effect of food on the symptoms were studied during a period of 4 weeks; during this time, infants were exclusively fed the milk preparations provided by us. We used an adapted cow milk formula with a lactose concentration of 7.5 gm/dl, pooled human milk, and preparations made from these two by hydrolyzing more than 90% of lactose by insolubilized laetase. Combining the weeks in which preparations with untreated or hydrolyzed lactose were given, we found no significant difference in the symptoms of colic: while receiving preparations with untreated lactose, infants had colic on 107 (82%) of 131 days, and the mean duration of colic was 4.8 hours; during feeding of preparations with hydrolyzed lactose, colic occurred on 87 (76%) of 115 days, and the mean duration was 6.0 hours. Combining the
3.
4.
5.
deficiency: adenosine deaminase (ADA) and purine nucleotide phosphorylase (PNP) deficiencies. Clin Immunol Immunopathol 1986;40:157-65. McGeady SJ. Transient hypogammaglobulinemia of infancy: need to reconsider name and definition. J PEDIATR 1987; 110:47-50. Tiller TL, Buckley RH. Transient hypogammaglobulinemia of infancy: review of the literature, clinical and immunologic features of 11 new cases and long-term follow-up. J PEDIATR 1978;92:347-53. Benderly A, Pollack S, Etzioni A. Transient hypogammaglobulinemia of infancy with severe bacterial infections and persistent IgA deficiency. Israel J Med Sci 1986;22:393-6.
Reply To the Editor: Dr. Etzioni suggests that the hypogammaglobulinemia observed in our patient with hereditary orotic acidura may have been a manifestation of transient hypogammaglobulinemia of infancy. The rapidity with which normalization of serum lgG and the marked increase in serum IgM concentrations occurred in our patient after the institution of uridine replacement strongly suggests a causal relationship. Moreover, transient hypogammaglobulinemia of infancy is a very rare condition when strict criteria for its diagnosis are used1; it appears highly improbable that two rare entities occurred simultaneously. Not mentioned in Dr. Etzioni's letter is the fact that the patient's lymphocyte response to pokeweed mitogen also increased substantially with uridine therapy. Furthermore, repeat studies using a flow cytometry method to count the number of blast cells present after mitogen stimulation, performed 13 months after the start of treatment, showed the patient's response to both concanavalin A and pokeweed mitogen to be in the low range of normal (data not shown in article). We agree with Dr. Etzioni's suggestion that more patients with orotie aciduria need to be studied to better define the immunologic abnormalities associated with this rare condition. Carlos A. Alvarado, MD John R. MeKolanis, PhD Department o f Pediatrics Emory University School o f Medicine Atlanta, GA 30322 REFERENCE
1.
Tiller TL, Bucley RH. Transient hypogammaglobulinemia of infancy: review of the literature, clinical and immunologic features of 11 new cases, and long-term follow-up. J PEDIATR 1978;92:347-53.
Maternal c o c a i n e use and risk of
sudden infant death To the Editor." The recent article by Bauchner et al. (J PEDIATR 1988;113:8314) regarding the risk of sudden infant death syndrome (SIDS) among infants with in utero exposure to cocaine suggests that there is no increased risk of SIDS among infants exposed in utero to
E d i t o r i a l correspondence
.3 3 3
cocaine. Subjects were included in the cocaine-negative group on the basis of self-reported drug history and urinalysis. Self-reported drug histories are often inaccurate because the subjects may deny their use of drugs. 1 Urinalysis generally detects drug use in the previous 2 to 3 days, so many users have negative drug test results if they have abstained in recent days. Therefore it is possible that some of those who denied cocaine use and had negative urinalysis results were misclassified as nonusers of cocaine. A way to obviate the shortcoming of urinalysis is to analyze the hair, where the drug accumulates for many months.2 We have applied this technique successfully to human hair samples, as small as 10 mg, from admitted cocaine users who had negative urine test results for cocaine. Hair samples of only 1.5 mg from babies of women who used cocaine during pregnancy have also proved positive for cocaine. No cross reactivity occurs with hair from individuals not using cocaine? Because the reproductive effects of cocaine use cause high levels of public anxiety, the method of hair analysis for cocaine use in previous months should be used for unequivocal verification of maternal nonexposure. Karen Graham, MD Gideon Koren, MD The Motherisk Program The Hospital for Sick Children Toronto, Ontario M5G 1X8, Canada REFERENCES
1.
2.
3.
Single E, Kandel D, Johnson BD. The reliability and validity of drug use responses in a large-scale longitudinal survey. J Drug Issues 1975;426:426-43. Valente D, Cassini M, Pigliapochi M, Vansetti G. Hair as the sample in assessing morphine and cocaine addiction. Clin Chem 1981;27:1952-3. Graham K, Koren G, Klein J, Schneiderman J. Detecting maternal exposure to cocaine by hair analysis [Abstract 442]. Pediatr Res 1989;25(4, pt 2).
Lactose tolerance in colicky infants To the Editor." We were disappointed that Moore et al. (J PEDIATR 1988;113:979-84) failed to cite our recent article on infantile colic, 1 in which we did what they suggested: we modified both the protein and the carbohydrate intakes of formula-fed infants with severe colic. We did a double-blind crossover study on 10 formula-fed infants with severe colic. The effect of food on the symptoms were studied during a period of 4 weeks; during this time, infants were exclusively fed the milk preparations provided by us. We used an adapted cow milk formula with a lactose concentration of 7.5 gm/dl, pooled human milk, and preparations made from these two by hydrolyzing more than 90% of lactose by insolubilized laetase. Combining the weeks in which preparations with untreated or hydrolyzed lactose were given, we found no significant difference in the symptoms of colic: while receiving preparations with untreated lactose, infants had colic on 107 (82%) of 131 days, and the mean duration of colic was 4.8 hours; during feeding of preparations with hydrolyzed lactose, colic occurred on 87 (76%) of 115 days, and the mean duration was 6.0 hours. Combining the