1314 Correspondence

Marc S. ArkovitzPatricia Devine

Mark RussoNancy BudhorickCharles J.H. Stolar

Columbia University College of Physicians and SurgeonsMorgan Stanley Children's Hospital of

New York–PresbyterianNew York, NY

E-mail address: ma2161@columbia.edu

doi:10.1016/j.jpedsurg.2007.04.004

References

[1] Boloker J, Bateman DA, Wung JT, et al. Congenital diaphragmatichernia in 120 infants treated consecutively with permissive hypercap-nea/spontaneous respiration/elective repair. J Pediatr Surg 2002;37(3):357-66.

[2] Harrison MR, Keller RL, Hawgood SB, et al. A randomized trial of fetalendoscopic tracheal occlusion for severe fetal congenital diaphragmatichernia. N Engl J Med 2003;349(20):1916-24.

[3] Jani J, Keller RL, Benachi A, et al. Prenatal prediction of survival inisolated left-sided diaphragmatic hernia. Ultrasound Obstet Gynecol2006;27:18-22.

Letter to the editor

References

To the Editor,

We have read with interest the article concerning a

neuroendocrine tumor of the pancreas resulting in precociouspuberty by Schutte and Knight [1] that was recentlypublished in your journal. Although their patient is ofinterest, we have a few comments regarding the diagnosticprocess. In the initial evaluation of the patient 4 monthspreviously, they mentioned several signs of puberty precox(ie, pubic hair, breast bud development, and vaginalbleeding), increased estradiol level (165 pg/mL), andadvanced bone age. These signs show probability ofperipheral precocious puberty in the patient. In such cases,a more extensive investigation including gonadotropin-releasing hormone testing is recommended to rule out adiscrete lesion affecting some part of the hormonal axiscontrolling puberty [2-4]. Furthermore, an estradiol level atthe upper end of the premenarcheal normal range (75 pg/mL)necessitates a prompt workup to distinguish a tumoral lesion[4,5]. The authors reported that an initial abdominalultrasonography had been unremarkable for a mass lesion,and they also noted that the pediatric endocrinologist whohad first seen the patient thought that a specific hormone-

secreting source was not apparent. On the other hand, themass could have only been disclosed after it was palpated byphysical examination after 4 months. Herein, we would liketo imply that despite an initial noncontributory ultrasono-graphic examination, the authors must have performedfurther abdominal imaging with the above-mentionedclinical and laboratory findings for the patient who mostprobably has peripheral precocious puberty [4,5]. Keeping inmind the 33% possibility of ultrasonography not detectingsuch a lesion, we call this to the attention of clinicians forearly diagnosis of relevant tumors [6]. Fortunately, theauthors did not uncover any metastatic lesion, but they couldhave eventually found otherwise after a 4-month delay in themanagement of a pancreatic malignancy. In this regard,gonadotropin-releasing hormone testing and detailed abdom-inal imaging seem to be paramount.

Ediz YeşilkayaPeyami Cinaz

Department of Pediatric Endocrinology and MetabolismGazi University Medical School

Ankara, TurkeyE-mail address: eyesilkaya@yahoo.co.uk

doi:10.1016/j.jpedsurg.2007.04.005

[1] Schutte WP, Knight PJ. Precocious puberty because of a pancreaticneuroectodermal tumor. J Pediatr Surg 2006;41:1916-8.

[2] Rodriguez H, Pescovitz OH. Precocious puberty: clinical management.In: Radovick S, MacGillivray MH, editors. Pediatric endocrinology: apractical clinical guide. New Jersey: Humana Pres Inc; 2004.p. 399-428.

[3] Lee PA, Kerrigan JR. Precocious puberty. In: Pescovitz OH, EugsterEA, editors. Pediatric endocrinology: mechanisms, manifestations, andmanagement. Philadelphia: Lippincott Williams and Wilkins; 2004.p. 316-33.

[4] Rosenfield RL. Puberty in the female and its disorders. In: Sperling MA,editor. Pediatric endocrinology. Philadelphia (Pa): Saunders; 2002.p. 455-518.

[5] Wheeler MD, Styne DM. Diagnosis and management of precociouspuberty. Pediatr Clin North Am 1990;37:1255-71.

[6] Rosch T, Lorenz R, Braig C, et al. Endoscopic ultrasound in pancreatictumor diagnosis. Gastrointest Endosc 1991;37:347-52.

Reply

To the Editor,We thank Drs Yesilkaya and Cinaz, pediatric endocri-

nologists, for their letter emphasizing the importantdifference between central precocious puberty (CCP) and

1315Correspondence

peripheral precocious puberty (PPP). Central precociouspuberty is the more common type, is occasionallyassociated with a central nervous system mass lesion,and can be of interest to neurosurgeons. Peripheralprecocious puberty is less common, is caused by sexhormone production by a peripheral tumor or byexogenous hormone ingestion, and is of interest topediatric surgeons when caused by a hormone-secretingadrenal or gonadal tumor. Drs Yesilkaya and Cinaz pointout the pulsatile secretion of gonadotropin-releasinghormone (GnRH) should be elevated in CCP because ofexcess central nervous system secretion, but GnRH shouldbe suppressed in PPP. I know nothing about the sensitivityor specificity of GnRH testing. Perhaps a pediatricendocrinologist could add a short explanation on howuseful GnRH testing is in differentiating CPP from PPPbecause this is information pediatric surgeons probablyshould know.

We first saw this patient when she walked into our office,and her parents had the computed tomographic scans inhand; so, for us, as opposed to diagnosing endocrinologists,this was an interesting “no brainer.” The patient continues toremain tumor free at her 18-month follow-up examination.

Philip KnightUniversity of Kansas

Wichita, KS, USAE-mail address: molikka@wsspa.com

doi:10.1016/j.jpedsurg.2007.04.006

Letter to the Editor

To the Editor,

We read with interest the article concerning esophageal

substitution published by Tannuri et al [1]. An impressiveexperience on esophageal replacement in children waspresented. By comparing a group of patients submitted toesophagocoloplasty (EC) with a group submitted to gastrictransposition (GT), the authors concluded that the colonmust be the first-choice substitute. However, such astatement may not be correct because we believe themethodology was not adequate and may be unfairly biasedagainst GT, a technique we have found excellent forcaustic strictures (via posterior mediastinum after transhia-tal esophagectomy) and has been consistently reportedwith favorable outcome [2,3].

In fact, the patient population in the study was veryheterogeneous, and the surgical procedure did not differonly concerning the substitute; moreover, the length of

follow-up was not presented. Beyond the different samplesize, the groups were not characterized regarding age, dateof operation, and follow-up. The underlying condition, awell-known parameter influencing mortality and morbidityrates, is quite different (23/115 vs 3/34 for causticstrictures). If a group of infants with long gap esophagealatresia submitted to GT by retrosternal route in 1978presents a significant worse outcome than a group ofpreschool children with caustic stricture submitted to ECin the posterior mediastinum in 2005, it does not implythat the explanation resides in the different substitute. Inaddition, it should be emphasized that a similar distribu-tion of a variable between the 2 groups does not excludethe possibility that it could affect the outcome even morethan the type of substitute. The small proportion ofpatients (n = 8) submitted to GT in the esophageal bed,the preferred route for supporters of this technique, limitsa comparison.

The criteria adopted to differentiate between minor andmajor complications should be clear and justified. Whydid the authors classify abdominal evisceration (EC, 10cases; GT, 2) and cervical anastomotic stricture requiringsurgical repair (EC, 2; GT, 0) as minor complications butclassified delayed gastric emptying (EC, 0; GT, 3) andaxial torsion of stomach (EC, 0; GT, 3) as majorcomplications? There was no mention of colon redun-dancy; does it mean that none of the 115 EC patients(retrosternal in 95) developed it?

We are not sure that the different sample size andexperience did not have any influence. Would the sameresults of EC be expected in a series of 34 procedures? Themortality rate was quite different (EC, 0.9%; GT, 6.9%) butdid not reach statistical significance because of the relativelysmall number of GT cases. Indeed, it is likely that in a largerseries the mortality rate would decrease. The complicationrate would also be less with a greater experience in GT. Asstated by the authors, axial torsion of the stomach as well asdelayed gastric emptying can be prevented; so, according toauthors' classification the most frequent causes of majorcomplications of GT may be reduced.

Lastly, there was a critical limitation to proceed with acomparison; as the authors affirmed “…EC has been ourfirst choice…” and “…we started performing GT, mainlyin patients…with prior failed EC.” Therefore, the conclu-sion of the study should be descriptive; the authors mustnot state “…esophagocoloplasty must be the first choicefor esophageal replacement in children.” Because there isno sufficient evidence about the best substitute regardingoutcome, the choice of esophageal replacement should bedictated by the experience of the surgeon (colon,stomach, jejunum) or the simplicity of the technique(ie, gastric transposition).