Disorders of signaling molecules controlling the migration of neural

crest cells result in Hirschsprung’s disease; AChE activity increases over

time after birth. The nerve pathology may be a direct result of increased

AChE expression. We do not have yet sufficient information on the

precise molecular mechanisms. Acetylcholinesterase in Hirschsprung’s

disease seems to function in its noncholinergic role as a signaling

molecule. Independent from that AChE staining is very helpful in

diagnosis.—P. Schmittenbecher

doi:10.1016/j.jpedsurg.2005.10.035

An abnormal distribution of C-kit positive cells in thenormoganglionic segment can predict a poor clinical outcomein patients with Hirschsprung’s diseaseTaguchi T, Suita S, Masumoto K, et al. Eur J Pediatr Surg 2005

(June);15:153-158.

The loss or decrease of intestinal cells of Cajal (ICCs) has been implicated in

several disorders of human intestinal motility. The authors have encountered

a few cases of patients suffering from severe constipation or enterocolitis,

resulting in death after a definitive operation for Hirschsprung’s disease,

even though the normoganglionic intestine had been successfully pulled

through. They investigated the distribution of ICCs using C-kit immunos-

taining in the normoganglionic segment and compared these findings with

the clinical outcome after a definitive operation in each case. These

investigations were performed in 15 cases with Hirschsprung’s disease. The

distributions of protein gene product 9.5 as general neuronal marker and of

nicotinamide adenine dinucleotide phosphate diaphorase as marker of nitric

oxide neurons were also examined. The numbers of ICCs and neurons were

evaluated quantitatively and C-kit immunoreactive cells showed a normal

distribution in the normoganglionic segment in 13 cases while they were

markedly (less than 50% compared with the other cases) decreased in 2

cases. The distributions of protein gene product 9.5 and nicotinamide

adenine dinucleotide phosphate diaphorase were almost the same in all

cases. The bowel movements of 13 cases showing normal C-kit distribution

were satisfactory, whereas they were impaired in 2 cases with decreased

number of C-kit cells. One infant suffered from severe persistent

constipation and had to undergo a resection of a dilated colon. The other

infant died of sepsis because of postoperative enterocolitis and had a

markedly dilated colon. It is concluded that fewer C-kit positive cells in

the normoganglionic segment can allow for a prediction of a poor

clinical outcome after definitive surgery, probably due to poor intesti-

nal motility.—Thomas A. Angerpointner

doi:10.1016/j.jpedsurg.2005.10.036

Abdomen

Peritoneal taurolidine lavage in children with localized peritonitis dueto appendicitisSchneider A, Sack U, Rothe K, et al. Pediatr Surg Int 2005 (June);21:

445-448.

Adjuvant strategies such as peritoneal saline lavage and drainage have

been recommended in intra-abdominal infection. Taurolidine should

inactivate proinflammatory modulators to prevent the onset of a systemic

inflammatory response syndrome. It binds to bacterial walls and inhibits

bacterial adherence, inactivates endotoxic lipopolysaccharides, decreases

tumor necrosis factor a and interleukin 1 secretion, and enhances

leukocyte activity. Intra-abdominal application was studied to determine

whether it might influence the clinical course in children with perforated

appendicitis and localized peritonitis.

A prospective, randomized, double-blind trial in children older than

6 years with perforated appendicitis and localized peritonitis was carried

out. Taurolin 2%, 25 to 100 mL of solution (according to the body weight),

or isotonic saline solution was applied as peritoneal lavage. Fifteen treated

children and 12 children in the control group were analyzed. The clinical

courses were without differences with one local abscess formation in each

group. One obstruction in the control group required a laparotomy, and an

incomplete obstruction in the treatment group was treated conservatively.

Leukocytes, C-reactive protein, endotoxin, and tumor necrosis factor aserum levels showed no difference. Interleukin 2 levels were markedly

increased in both groups as a sign of the inflammatory reaction. Interleukins

1 and 6 levels were comparatively elevated in both groups.

Clinical course and occurrence of complications were similar in both

groups. A beneficial effect of taurolidine could not be shown. A reduction

of serum endotoxin levels was not evident. The proinflammatory mediators

were not changed in a relevant amount. The study failed to demonstrate an

advantage of taurolidine lavage in children with localized peritonitis

because of appendicitis.—P. Schmittenbecher

doi:10.1016/j.jpedsurg.2005.10.037

Solitary liver abscess in a healthy child presenting with fever ofunknown originSakran W, Kawar B, Chervinsky L. Eur J Pediatr Surg 2005

(June);15:193 -195.

Pyogenic liver abscess is rarely encountered in normal children. The

authors report a case of solitary pyogenic liver abscess in a healthy

8-month-old boy who presented with fever of unknown origin and mild

hepatomegaly. Full recovery was achieved by surgical intervention and

prolonged antibiotic treatment.—Thomas A. Angerpointner

doi:10.1016/j.jpedsurg.2005.10.038

Infarction of an accessory spleen presenting as acute abdomenin a neonateGardikis S, Pitiakoudis M, Sigalas I, et al. Eur J Pediatr Surg 2005

(June);15:203 -205.

An accessory spleen is a relatively common condition, but the torsion thereof

is extremely rare, with only 9 cases reported in the pediatric literature. This

paper describes a case of an accessory spleen that was found necrotic during

an emergency laparotomy in a 14-day-old female infant with signs of an acute

abdomen. This is presumably the youngest reported patient. Etiology of the

necrosis was a thrombosis of its trophic vessels, secondary to pedicle torsion.

The mass was removed and the postoperative course was uneventful. The

literature is reviewed.—Thomas A. Angerpointner

doi:10.1016/j.jpedsurg.2005.10.039

Genitourinary Tract

Germ cell development in the descended and cryptorchid testis andthe effect of hormonal manipulationOng C, Hasthorpe S, Hutson JM. Pediatr Surg Int 2005 (April);21:240 -254.

The authors review the current knowledge of germ cell development in

normal and cryptorchid testis. Germ cell development starts in the fetus and is

completed at puberty. Fetal spermatogonia transform between 3rd and 12th

month postnatally into adult dark (Ad) spermatogonia, with coincident rise of

luteinizing hormone (LH), testosterone, and Mullerian inhibiting substance

as well as Leydig cell proliferation. By 3 to 4 years of age, Ad spermatogonia

further transform to B spermatogonia and primary spermatocytes. Sertoli

cells transform and decrease steadily from birth to puberty.

In cryptorchid testis, transformation into Ad spermatogonia and later

development of primary spermatocytes are affected, Leydig cell number is

reduced, and Sertoli cell transformation and development of seminiferous

International Abstracts 285