Claudia Pacchiarotti

Helicobacter pylori seropositivity in children with atopic dermatitis as sole manifestation of food allergy

A positive association between Helicobacter pylori antibodies and food allergy presenting with gastrointestinal symptoms has recently been reported. A subset of a H. pylori strain possesses an antigen, CagA, as a virulence factor. Anti‐H. pylori and anti‐CagA IgG titre have been determined in children with atopic dermatitis (AD) as the sole clinical manifestation of food allergy. In this study, thirty patients with AD as the sole clinical manifestation of food allergy were examined (group A). For comparative purposes, 30 patients affected by food allergy with gastrointestinal symptoms (group B) and 30 affected by atopic asthma (group C) were studied. Anti‐H. pylori and anti‐CagA immunoglobulin G (IgG) were determined in all individuals by means of the enzyme‐linked immunosorbent assay. The anti‐H. pylori IgG titre was significantly higher in group A and group B vs. group C (p < 0.05); no significant difference was detected between group A and group B (p > 0.05). No significant difference in anti‐CagA titre was found between the groups. These data demonstrate a positive association between H. pylori antibodies and AD as the sole manifestation of food allergy. Further investigations are needed to evaluate the cause–effect relationship between H. pylori seropositivity and AD.

Increased release of interleukin-6 by oesophageal mucosa in children with reflux oesophagitis.

OBJECTIVE To evaluate the release of interleukin-6 (IL-6) by oesophageal mucosa and to establish the serum levels of IL-6 and C-reactive protein (CRP), and plasma fibrinogen in children with reflux oesophagitis. DESIGN In a prospective study, IL-6 release by tissue fragments obtained from oesophageal biopsies was determined and serum IL-6 and CRP as well as plasma fibrinogen were analysed. METHODS The study population comprised ten children with reflux oesophagitis, diagnosed on the basis of 24 h oesophageal pH monitoring and endoscopy with biopsies. Ten children with recurrent abdominal pain were studied for comparative purposes. Biopsy tissue fragments were processed to obtain a cell suspension and the release of IL-6 was determined in culture medium. Serum IL-6 levels were measured by ELISA, serum CRP by turbidimetry, and plasma fibrinogen by spectrophotometry. RESULTS Oesophageal cells obtained from reflux oesophagitis patients synthesize and release in vitro a significantly higher amount of IL-6 than controls (71.26+/-19.5 versus 31.67+/-8.02 pg/10(6) cells; P<0.01). Serum IL-6, serum CRP and plasma fibrinogen levels were not statistically different between patients with reflux oesophagitis and controls. CONCLUSIONS These results suggest a short-term action of IL-6 since its effects could be exerted only in the microenvironment of the oesophageal mucosa.

Cyclic Vomiting Syndrome

Cyclic vomiting syndrome is a disorder characterized by recurrent episodes of nausea and vomiting with complete resolution of symptoms between attacks. Nitric oxide plays a critical role in regulating several components of gastrointestinal mucosal defense and injury. Interleukin-6 has a wide variety of actions in the gastrointestinal apparatus. The purpose of this study was to evaluate the synthesis and release of nitric oxide and interleukin-6 by the esophageal and gastric mucosa in 10 children with cyclic vomiting syndrome, during symptom-free periods, and in 10 controls. The nitric oxide and interleukin-6 release by esophageal mucosa cells obtained from cyclic vomiting patients was quite similar to that in controls, but the release of nitric oxide from gastric mucosa cells of patients was significantly higher than that of controls. Conversely, no interleukin-6 was detectable in gastric mucosa cell supernatants in any of the patients. Further studies are needed to evaluate the relationship between factors triggering cyclic vomiting syndrome and the release of nitric oxide and interleukin-6 by gastric mucosa.

“EEG abnormalities” may represent a confounding factor in celiac disease: A 4-year follow-up family report

Objective The occurrence of celiac disease (CD), electroencephalographic (EEG) abnormalities (with “subtle” seizures or even without any clinical seizures), and neurological disorders has been reported since the 1980s, though there has been no definitive consensus about the possible causal relationship. This topic is further complicated by the occurrence in infancy of ‘clinical–EEG pictures’ called ‘benign epilepsy of infancy’. Methods and results Here, we report a 4-year follow-up on two siblings with newly diagnosed biopsy-proven celiac disease showing EEG abnormalities not responsive to a gluten-free diet. Conclusions This family report indicates that in patients with neurologically asymptomatic CD and EEG abnormalities, it is advisable to make a differential diagnosis between EEG abnormalities associated with CD and an incidental association with cortical hyperexcitability, with “subtle” seizures or even without any clinical seizures. Practice implications A long follow-up may sometimes be required, as it was in the family described here, to clarify the etiopathogenetic and therapeutic relationships between clinical and EEG features in CD.

Irritable oesophagus: A new cause of Sandifer's syndrome

Sir, Sandifer’s syndrome is a rare paediatric manifestation of gastro-oesophageal reflux (GOR) disease characterized by distonic movements. GOR disease is characterized by pathological GOR and associated symptoms. In children, patients with normal oesophageal exposure to acid and a significant association between reflux episodes and symptoms have been identified and described as having ‘‘irritable oesophagus’’ [1,2]. A 1-y-old female was referred to our Paediatric Gastroenterology Unit because, from the tenth month of life, she experienced 8 12 daily episodes of abnormal movements (rotation of head and neck, and arching of the upper part of the trunk). A gastrointestinal barium study excluded the presence of hiatus hernia (HH). An oesophagogastroscopy with biopsies was normal. To detect pathological GOR as well as to investigate the relationship between GOR episodes and abnormal movements, the patient underwent 24-h gastro-oesophageal pH monitoring (Figure 1). Since all parameters were normal, GOR disease was excluded. In order to verify the relation between GOR episodes and abnormal movements, we calculated specificity and sensitivity indices as well as the binomial formula (references in [1]). On the basis of such investigations, irritable oesophagus was diagnosed and the patient was treated with omeprazole (1 mg/kg/d) for 4 wk. During the first week of therapy, the number of abnormal movements decreased, and thereafter no abnormal movements occurred. The patient was followed for 6 mo, and no abnormal movements have been reported. In 1964, Kinsbourne described Sandifer’s syndrome, characterized by abnormal movements and HH [3]. In 1977, Murphy and Gellis [4] reported that the abnormal movements were related to GOR disease and that the presence of HH was not necessary in this syndrome. This case report demonstrates that irritable oesophagus is a new cause of Sandifer’s syndrome.