Ali Islek

The role of Bifidobacterium lactis B94 plus inulin in the treatment of acute infectious diarrhea in children

BACKGROUND/AIMS In contrast to many other studies of probiotic species, the number of publications evaluating Bifidobacterium lactis and its combinations with prebiotics as treatments for acute infectious diarrhea is limited. We investigated the synbiotic effects of B. lactis B94 plus inulin on acute infectious diarrhea. MATERIALS AND METHODS The study was conducted on children with acute diarrhea between the ages of 2 and 60 months. The patients were administered 5×1010 colony-forming units (CFU) of B. lactis B94 plus 900 mg inulin or placebo, once a day for five days. Stools were examined for Rotavirus, Adenovirus, Entamoeba histolytica, Salmonella, Shigella, Campylobacter, Clostridium difficile, Cryptosporidium, and parasites. RESULTS We examined 79 patients in the synbiotic group and 77 patients in the placebo group. The duration of diarrhea was significantly reduced in the synbiotic group in comparison with the placebo group (3.9±1.2 days vs. 5.2±1.3 days, respectively; p<0.001). Moreover, the number of diarrheal stools on the third day was significantly lower in the synbiotic group than in the placebo group (5.5±2.9 vs. 8.3±3.01, respectively; p<0.001). Diarrhea in the synbiotic-group patients with rotavirus infection was of a significantly shorter duration (3.2±1.3 days vs. 5.2±1.3 days, respectively; p=0.001). Duration of diarrhea in patients who started the synbiotic treatment within the first 24 h was shorter than that in the patients who started the treatment later (3.9±1.1 days vs. 4.8±1.8 days, respectively; p=0.002). CONCLUSION Treatment with 5 × 1010 CFU of B. lactis B94 plus 900 mg inulin shortened the duration of acute watery diarrhea by an average of 31 h. This decrease was most pronounced in cases of Rotavirus diarrhea.

Extremely rare cause of congenital diarrhea: enteric anendocrinosis.

Congenital diarrheal disorders consist of a variety of chronic enteropathies. There are approximately 30 different diseases that can be classified into four groups according to the mechanisms involved in pathogenesis: (i) absorption and transport of nutrients and electrolytes; (ii) enterocyte differentiation and polarization; (iii) enteroendocrine cell differentiation; and (iv) modulation of the intestinal immune response. Affected patients often present with life‐threatening diarrhea, in the first few weeks of life. A new disorder, enteric anendocrinosis, which is characterized by severe malabsorptive diarrhea and a lack of intestinal enteroendocrine cells has recently been described in six patients with recessively inherited mutations in the Neurogenin‐3 gene. In this report we describe a seventh case with a review of the literature.

A rare outcome of iron deficiency and pica: Rapunzel syndrome in a 5-year-old child iron deficiency and pica

Bezoar is defined as the accumulation of organic or nonbiological substances inside the gastrointestinal system. Trichobezoars are the most frequently detected ones and are mostly present in patients with neuropsychiatric disorders. The continuance of the trichobezoar tail-shaped extension over the duodenum and jejunum is described in Rapunzel syndrome. Both conditions are rarely reported in children. The present case submitted here is related to a 5-year-old girl referred with an abdominal mass and anemia, diagnosed with Rapunzel syndrome and developing trichobezoar due to iron deficiency and pica.

Percutaneous endoscopic gastrostomy in children: Is early feeding safe?

Background: Percutaneous endoscopic gastrostomy (PEG) is the preferred method to provide nutritional support for patients with normal gastrointestinal function but cannot be fed orally for a variety of reasons. Owing to safety concerns, the first feeding after PEG tube placement is generally delayed. Early feeding may be an option; however, childhood studies regarding early feeding after the PEG procedure are highly insufficient. Methods: A prospective randomized controlled study was conducted to compare early (4th hour) and late (12th hour) feeding after the PEG procedure. The PEG process was performed with the standard pull technique. Prophylactic antimicrobial drugs were not used. Complications such as gastric residue after feeding, vomiting, fever, systemic signs of infection, and duration of hospital stay were recorded. Tube feeding training was given to parents during their stay in the hospital in both groups. In the first and third days following PEG, the patients were visited by an experienced nurse in their homes and evaluated in terms of potential complications. Results: The study was completed with a total of 69 patients: 35 in the early feeding group and 34 in the late feeding group. The demographic characteristics of the groups were similar. Vomiting was rare and detected as similar in both groups (early feeding group 8.5% [3/35], late feeding group 8.8% [3/34], P = 1.00). Rarely, minor gastric residue was observed in both groups (early feeding group 11.4%, late feeding group 8.8% [P = 1.00]). The amount of gastric residue in the early feeding group was a maximum of 13.2 mL, whereas the late feeding group had a maximum of 14.3 mL. The average duration of stay in the hospital for the early and late feeding groups was calculated as 6.7 ± 0.64 and 28.3 ± 3.74 hours, respectively (P < 0.001). Leakage from gastrostomy fistulas, peritonitis, and aspiration were not observed in any patients. Conclusions: The feeding at the fourth hour after PEG placement was safe and well tolerated by patients and shortened the duration of the hospital stay. The use of prophylactic antibiotics seems to be unnecessary before the procedure.

Intestinal dysfunction in APECED syndrome could mimic IPEX syndrome.

T o the Editor: Classical diagnosis of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome depends on the appearance of 2 of its 3 major criteria: mucocutaneous candidiasis, autoimmune hypoparathyroidism, and adrenal failure. A variety of clinical components may be seen in the clinical picture, however, and they may occur before onset of the 3 major criteria, resulting in diagnostic delay (1). Intestinal dysfunction is one such component of APECED syndrome and is observed in 18% to 22% of patients with APECED syndrome. A variety of causes are attributed to this intestinal dysfunction, such as celiac disease, cystic fibrosis, pancreatic insufficiency, intestinal infections with candida albicans, and loss of enteroendocrine cells caused by autoimmune attack (2,3). Mutations of the forkhead box P3 (FoxP3) gene result in impaired function of regulatory T cells, which leads to immune dysregulation, polyendocrinopathy, enteropathy, and X-linked (IPEX) syndrome. In about one-third of patients, with clinical symptoms resembling IPEX syndrome, no mutation was found in the FoxP3 gene (4). So far, only 2 articles have been published about these IPEX-like patients. One of them suggested improvement of clinical symptoms with sirolimus usage in 2 IPEX and 5 IPEX-like patients (5). And a recently published article showed significant reduction in peripheral regulatory T cells in an impressive cohort of 28 IPEX-like patients (4). In that report, the authors declared exclusion of the Wiskott-Aldrich syndrome, Omenn syndrome, hyper-immunoglobulin E syndrome, and autoimmune lymphoproliferative syndrome, which were originally included in the differential diagnosis; however, APECED syndrome was not included in the differential diagnosis, despite its involvement in

Pentoxifylline therapy attenuates intestinal injury in rat pups with hypoxic ischemic encephalopathy

Abstract Aim: The aim of this study was to evaluate the effects of post-ischemic pentoxifylline (PTX) therapy on the gut injury in neonatal rat model of hypoxic ischemic encephalopathy (HIE). Methods: Seven-day-old Wistar rat pups (n = 24) of either sex, delivered spontaneously, were used in this experimental study. Seven-day-old rat pups were randomly divided into three groups. Control group (n = 8): after median neck incision was made, neither ligation nor hypoxia was performed. Hypoxia group (n = 8): 0.5 ml of saline was injected intraperitoneally immediately after hypoxia. Pentoxifylline + Hypoxia group (n = 8): the rat pups were administered intraperitoneally 60 mg/kg of PTX immediately after hypoxia. Eight rats from all groups were sacrificed 24 h after drug administration. The ischemic injury was scored at least six sections at three different levels using histopathologic injury scores (HIS). Results: Induction of hypoxia/reoxygenation (H/R) increased mean HIS levels significantly at 24 h in the intestinal tissue samples in the hypoxia group as compared with the control group. Induction of H/R decreased means HIS levels significantly at 24 h in the intestinal tissue samples in the PTX + hypoxia group as compared with the hypoxia group. Conclusion: In this experimental study, PTX significantly attenuated H/R-induced intestinal injury in neonatal rat model of HIE. These findings indicate that PTX can reduce the intestinal H/R injury.

Childhood chronic gastritis and duodenitis: Role of altered sensory neuromediators

AIM To investigate the roles of the neuropeptides vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) in chronic gastritis and duodenitis in children. METHODS Biopsy samples from the gastric and duodenal mucosa of 52 patients and 30 control subjects were obtained. Samples were taken for pathological examination, immunohistochemical staining, enzyme activity measurements and quantitative measurements of tissue peptide levels. RESULTS We observed differential effects of the disease on peptide levels, which were somewhat different from previously reported changes in chronic gastritis in adults. Specifically, SP was increased and CGRP and VIP were decreased in patients with gastritis. The changes were more prominent at sites where gastritis was severe, but significant changes were also observed in neighboring areas where gastritis was less severe. Furthermore, the degree of changes was correlated with the pathological grade of the disease. The expression of CD10, the enzyme primarily involved in SP hydrolysis, was also decreased in patients with duodenitis. CONCLUSION Based on these findings, we propose that decreased levels of VIP and CGRP and increased levels of SP contribute to pathological changes in gastric mucosa. Hence, new treatments targeting these molecules may have therapeutic and preventive effects.

HFE-Related Hereditary Hemochromatosis Is Not Invariably a Disease of Adulthood: Importance of Early Diagnosis and Phlebotomy in Childhood.

treatment with ustekinumab. The route of administration (subcutaneous and not intravenous) and the low dose of approximately 1 mg/kg per day were chosen because of the scarce data in the pediatric literature regarding that treatment. Our experience should encourage pediatric trials aimed at considering ustekinumab as a rescue therapy in anti-TNF refractory pediatric patients with CD. In summary, we describe a dramatic resolution of symptoms in a 7-year-old boy with refractory active CD treated with ustekinumab. In addition, we provide anecdotal data on dosage and scheduling of ustekinumab in pediatric CD. The effectiveness and safety of this drug in children should be studied prospectively.

A very rare cause of acute pancreatitis: Berardinelli-Seip congenital lipodystrophy

Pancreatitis is among rare diseases in pediatrics clinics. It is usually presented with a sign of underlying systemic disease. Berardinelli-Seip congenital lipodystrophy (BSCL) is a very rare disease characterized by near absence of adipose tissue resulting in apparent muscle hypertrophy from birth or early infancy associated with severe insulin resistance. Common clinical features are hypertriglyceridemia, acanthosis nigricans, hepatomegaly with or without splenomegaly and high stature. Acromegaloid features, cardiomyopathy and mental retardation can also be present. We describe a 7-year-old Turkish boy with these clinical features of BSCL and presented with acute pancreatitis.

Langerhans cell histiocytosis in IPEX syndrome: Possible role for natural regulatory T cells?

pletely inhibited after immunoabsorption of the antibodies on purified human epidermal filaggrin but not on bovine serum albumin used as a control [(6) and Fig. 1a]. In addition, it is now clear that at least part of the profilaggrin present in the human buccal mucosa epithelium is citrullinated. In fact, it is extracted in the absence of a denaturing agent, and it is recognized by the human autoantibody called ‘antiperinuclear factor’. The latter is specifically found in the serum of patients with rheumatoid arthritis and belongs to the family of autoantibodies that exclusively recognize epitopes generated by citrullination of arginine residues on the targeted antigenic proteins (8, 9). In conclusion, these data clearly demonstrate that profilaggrin is expressed by the most differentiated keratinocytes of the oral cavity mucosae, the filaggrin monomers being generated only in the orthokeratinized epithelium of the hard palate.