Iona M. Monteiro

Aberrant responses to TLR agonists in pediatric IBD patients; the possible association with increased production of Th1/Th17 cytokines in response to candida, a luminal antigen

Jyonouchi H, Geng L, Cushing‐Ruby A, Monteiro IM. Aberrant responses to TLR agonists in pediatric IBD patients; the possible association with increased production of Th1/Th17 cytokines in response to candida, a luminal antigen.
Pediatr Allergy Immunol 2010: 21: e747–e755.
© 2009 John Wiley & Sons A/S

Precocious enhancement of intestinal fructose uptake by diet in adrenalectomized rat pups.

Intestinal fructose transport typically increases 3-fold after completion of weaning (>28 d of age) in rats allowed to wean normally. Precocious enhancement of fructose transport has been demonstrated in rats fed high fructose diets during early weaning. To determine the role of corticosterone in the enhancement of fructose uptake by diet, we fed 17-d-old rat pups, previously adrenalectomized or sham-operated at 10 d of age, high (65%) fructose or fructose-free diets for 3 d. Corticosterone levels in 20-d-old sham-operated and unoperated controls were 2.2-3.3-fold higher than those in adrenalectomized littermates and in unoperated 10-d-old pups. Fructose uptake per mg and per cm were each 2.0-2.5-fold higher in adrenalectomized and sham-operated pups fed high fructose diets compared with those in adrenalectomized and sham-operated littermates fed fructose-free diets or to those in unoperated littermates allowed to wean normally with the dam. An increase in levels of GLUT5 mRNA in pups fed high fructose diets paralleled the increase in rates of fructose uptake. Intestinal glucose uptake was independent of corticosterone levels and of diet. Thus, the corticosterone surge is not necessary for the precocious enhancement of intestinal fructose transport and of GLUT5 mRNA expression by dietary fructose during weaning.

Dietary modulation of intestinal fructose transport and GLUT5 mRNA expression in hypothyroid rat pups.

BACKGROUND Intestinal fructose transport rates or GLUT5 mRNA levels typically show a two- to threefold increase after weaning in rats allowed to wean normally but can be enhanced precociously by high-fructose diets during early weaning. Developmental increases in serum thyroxine levels coincide with the onset of weaning and have been linked to changes in intestinal sucrase and lactase activities. METHODS Rat pups were made hypothyroid by giving the dam 0.01% propylthiouracil as drinking water from day 18 of gestation. The hypothyroid pups and age-matched euthyroid control pups were then fed high-fructose or high-glucose solutions by gavage, twice a day starting at 17 days of age for 3 days, and then killed at 20 days of age. RESULTS Serum thyroxine levels were five times lower in the hypothyroid pups. Rates of intestinal fructose uptake in the proximal and middle small intestine were 2.0 to 2.5 times higher in the hypothyroid and euthyroid pups fed high-fructose solution than in littermates fed high-glucose solution or those allowed to wean normally with the dam. Intestinal glucose uptake also increased in hypothyroid but not in euthyroid pups fed high-fructose or high-glucose solutions. GLUT5 mRNA levels increased in euthyroid and hypothyroid pups fed high fructose and paralleled the increase in fructose uptake. CONCLUSION During weaning, dietary fructose can precociously enhance intestinal fructose uptake and GLUT5 mRNA expression, independent of developmental increases in serum thyroxine levels. Modest changes in glucose transport rates indicate that nonspecific mechanisms may provide a minor contribution to diet-induced changes in nutrient absorption in hypothyroid pups.

Ontogenetic development of rat intestinal bile acid transport requires thyroxine but not corticosterone.

Absorption of bile acids by the distal ileum is an essential component of the enterohepatic circulation. In neonatal rats, the appearance of the apical sodium-dependent bile acid transporter (ASBT) at 17 d of age coincides with increases in serum corticosterone and thyroxine. We tested the hypothesis that these hormones modulate ASBT expression during ileal development. Taurocholate uptake into the isolated ileum of normal 20-d-old pups exhibited saturable (Km = 0.52 mM, Jmax = 0.34 pmol mg/min) and nonsaturable (Kdiff = 0.015 min−1) components and was two to five times greater than uptake in the proximal intestine. Hypothyroid or euthyroid pups received daily thyroxine injections starting at 6 d of age. At 12 d of age, serum concentrations of thyroxine, ileal abundance of ASBT mRNA, and ileal rates of taurocholate uptake were low in hypothyroid pups that received an injection of vehicle (HT−) or thyroxine (HT+) and in euthyroid pups that received an injection of vehicle (ET−) or thyroxine (ET+). At 20 and 26 d, ileal ASBT mRNA abundance and taurocholate uptake rate remained low in HT− pups but increased dramatically in ET− and ET+ pups, paralleling the increase in serum thyroxine. Restoration of normal plasma thyroxine in HT− pups by thyroxine injections (HT+) restored normal ASBT development. Sodium-glucose co-transporter activity and mRNA expression were independent of serum thyroxine levels. Corticosterone levels were significantly lower in pups that were adrenalectomized at 10 d of age. ASBT mRNA abundance and taurocholate uptake rate increased markedly with age but were the same in adrenalectomized, sham-operated, and nonoperated pups. Hence, endogenous thyroxine but not corticosterone regulates the developmentally timed appearance of ASBT.

Endoscopic management of transanal protrusion of subdural peritoneal shunt in a child.

JPGN Volume 53, N The first case of transanal protrusion was reported in 1966 by Wilson and Bertran (20). Transanal protrusion of VP shunt S ubdural peritoneal shunts (SP shunts) are used in the management of chronic subdural collections. The basic objective is similar to that of ventriculoperitoneal shunts (VP shunts); namely, the excess fluid is drained into the peritoneal cavity and is absorbed. The equipment and techniques used in these 2 types of shunts are similar, which suggests similar complications may arise. Although there has been an extensive literature regarding VP shunts, there have been scant reports about SP shunts. Hence, the literature regarding VP shunts is incorporated in our case. Cases of bowel perforation have been reported in which anal protrusion of the distal part of the VP shunt was the initial presentation (1–15). Abdominal surgery was the approach used to manage most cases. Only a few cases reported in the literature were managed endoscopically. In 1996, Brown et al (1) reported the first case successfully managed by sigmoidoscopy, establishing this method to be an important option for uncomplicated cases. We report this case of anal protrusion of a SP shunt in a 30-month-old child managed by colonoscopy with a favorable outcome. A 30-month-old child with right SP shunt placed at 13 months of age because of an enlarged subdural space and increased head circumference presented to the hospital because of an extrusion of the shunt through the anus. He was in his usual state of health when approximately 12 cm of the shunt tubing was noted to be protruding from the child’s anus during defecation. The extruded shunt was cut at home and the child was brought to the emergency department. He was completely asymptomatic at the time of presentation. Physical examination, including a rectal examination, was unremarkable, with no tubing visible at the anus. He was admitted to the pediatric intensive care unit and placed on broad-spectrum antibiotics because of the concern of bowel perforation and possible peritonitis and shunt infection. His shunt was then externalized at the cervical level. Computed tomography scan of the abdomen showed the shunt entering the lumen of the transverse colon (Figs. 1 and 2), and hence an urgent unprepped colonoscopy was performed to visualize the shunt tubing in an attempt to remove it and assess possible bowel perforation. During colonoscopy, the shunt tubing was visualized in the stool in the colon (Figs. 3 and 4). The visualized mucosa appeared

Levetiracetam-associated acute pancreatitis in an adolescent with autism: a case report.

5. Ricordi C, Lacy PE, Scharp DW. Automated islet isolation from human pancreas. Diabetes. 1989;38(suppl 1):140. 6. Matsumoto S, Takita M, Chaussabel D, et al. Improving efficacy of clinical islet transplantation with iodixanol based islet purification, thymoglobulin induction and blockage of IL-1-beta and TNF-alpha. Cell Transplant. 2011;20:1641Y1647. 7. O’Connell FP, Pinkus JL, Pinkus GS. CD138 (syndecan-1), a plasma cell marker immunohistochemical profile in hematopoietic and nonhematopoietic neoplasms. Am J Clin Pathol. 2004;121:254Y263. 8. Conejo JR, Kleeff J, Koliopanos A, et al. Syndecan-1 expression is up-regulated in pancreatic but not in other gastrointestinal cancers. Int J Cancer. 2000;88:12Y20. 9. Kawakami H, Kuwatani M, Shinada K, et al. Autoimmune pancreatitis associated with hemorrhagic pseudocysts: a case report and literature review. Intern Med. 2008;47:603Y608.

ROLE OF THE PLASMA CORTICOSTERONE SURGE IN THE PRECOCIOUS ENHANCEMENT OF FRUCTOSE UPTAKE IN WEANING RATS. † 729

ROLE OF THE PLASMA CORTICOSTERONE SURGE IN THE PRECOCIOUS ENHANCEMENT OF FRUCTOSE UPTAKE IN WEANING RATS. † 729