To evaluate the influence of maternal smoking on antioxidative capacity and intensity of oxidative damage in breast milk. The study group (n=30) was comprised of postpartum women who declared smoking more than five cigarettes per day during pregnancy and lactation (confirmed by the urinalysis of cotinine concentration), and their newborns. Control group included 29 non-smoking postpartum women and their newborns. Colostrum samples were collected on the 3rd day after delivery and breast milk samples between the 30th and the 32nd day after delivery. Morning maternal and neonatal urine samples were obtained on the day of the mature milk sampling. Isoprostane concentrations in colostrum/mature milk and urine were determined immunoenzymatically. Total Antioxidant Status (TAS) of colostrum/breast milk was determined by Rice–Evans and Miller method. Colostrum TAS in smokers was significantly lower than in non-smokers (P=0.006). In both groups, the TAS of mature milk was higher compared with colostrum, but significant differences were observed amongst smokers only (P=0.001). In smokers the isoprostane concentration of mature milk was significantly higher than the colostrum concentration (P=0.001). Significant inverse correlation between maternal urinary isoprostane concentration and the TAS of mature breast milk was observed in smokers (R=−0.525, P=0.023), but not in non-smokers (R=0.161, P=0.422). This study revealed that maternal smoking triggers harmful effects on an infant by impairing pro-oxidant–antioxidant balance of breast milk.

Elevated gastrin concentration leading to gastritis is explained as the effect of change in the density of D and G cells. The aim of the study was to determine and compare fasting serum gastrin concentrations, G and D cell densities in gastric antrum mucosa in children with chronic gastritis and in children with no gastritis or Helicobacter pylori infection. A total of 184 patients aged 6-18 years, with chronic abdominal pain underwent endoscopic examination. We created three groups: I - patients with chronic gastritis and H. pylori infection; II - patients with chronic gastritis but no H. pylori infection; III - patients with neither gastric mucosal abnormalities nor H. pylori infection. G and D cell densities were determined in the biopsy specimens (using Rb alpha H Gastrin & Somatostatin antibodies). Fasting serum gastrin concentrations were measured using a Beckmann gamma-counter and a GASK-PR kit. The mean serum gastrin concentration in group I was higher when compared with group II (p = 0.04) and group III (p = 0.019). No statistically significant differences were found between groups II and III (p = 0.91). There were no statistically significant differences in G and D cell densities between groups. The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.

To the Editor: The high prevalence of tuberculosis (TB) underlines the important role of BCG (bacillus Calmette-Guerin) immunization. The vaccine, however, is not free from complications, which could be local or disseminated. Disseminated BCG infection as a result of TB vaccination is a rare complication with an incidence of 0.06 to 1.56 cases per million vaccinations; it occurs exclusively in patients with immune deficits. However, in these cases, the prognosis is unfavorable; up to 70% of patients die, despite intensive antituberculous treatment (1–4). A 4-month-old-girl exhibited enlargement of left axillary lymph nodes during a 1.5-month period. She was the second child of healthy parents, with no family history of genetic disorders or TB. She was vaccinated according to the regimen compulsory in Poland: the first dose of BCG and anti–hepatitis B virus (HBV) vaccination on the first day of life, followed by vaccination against diphtheria, tetanus, pertussis, poliomyelitis, and the second dose of anti-HBV after 6 weeks. BCG vaccination was performed intradermally in the upper part of left arm by administration of 0.1 mL Brazilian Moreau strain (Biomed, Lublin, Poland). On hospital admission, the patient was in reasonably good condition but pale, with grossly enlarged, adjacent left axillary lymph nodes and hepatosplenomegaly. Laboratory tests showed anemia, thrombocytopenia, elevated transaminase activity, a high C-reactive protein level, and high level of immunoglobulin M (IgM) class anti-cytomegalovirus (CMV) reactive antibodies. Based on clinical manifestations and biochemical and serologic signs, CMV infection was suspected. The patient was administered a 14-day regimen of ganciclovir (10 mg/kg/day); results of liver function tests and blood count normalized, and hepatosplenomegaly decreased. However, the lymph nodes continued to enlarge, and diagnostic excision and bone marrow aspiration were performed to exclude a neoplastic process. A histopathologic image of the excised lymph nodes showed caseating granulomas, and tuberculous lymphadenitis was suggested (Figure). Figure Digitally processed hematoxylin-eosin staining of the excised lymph nodes, showing caseating, tuberculosislike granulomas (original magnification ×100). At that time, a diagnosis of disseminated BCG infection as a complication of TB vaccination in a presumed immunocompromised patient was proposed. This idea was based on suggestive lymph node pathology, which showed caseating granulomas, a history of TB vaccination, and the exclusion of other pathologic changes. Flow cytometry measurements showed abnormally low expression of the α chain of the interferon (IFN)-γ receptor on peripheral blood lymphocytes. Only 20% lymphocytes expressed CD 119 (IFN-γ receptor outer subunit R1). Three-drug anti-tuberculous therapy (with rifampin, isoniazid, and streptomycin) was introduced despite chest and bone radiographs that were negative for infection, no abnormalities found on funduscopy, and negative results of Ziehl-Neelsen staining of lymph node tissue. Despite this therapy, the child's condition worsened; she exhibited a high temperature, hemolysis, and progressive neutropenia, thrombocytopenia, cholestasis, and renal failure. Uncontrolled sepsis developed, and she died. At postmortem examination, the diagnosis of disseminated BGC infection was made on the basis of multiple TB-like granulomas in the lungs, lymph nodes, meninges, liver, spleen, and kidneys. However, direct microbiologic confirmation of BCG infection was lacking because cultures were negative and Ziehl-Neelsen and periodic acid–Schiff staining did not show acid-fast bacilli, other bacteria, or fungi in these specimens. This case represents a rare complication of antituberculous vaccination, that is a progressive, disseminated BCG infection in a patient with deficiency of IFN-γ receptor. Concomitant CMV infection was diagnosed by positive IgM antibody response. Transient response to the ganciclovir treatment made the final diagnosis of BCG infection more difficult and probably postponed implementation of the anti-TB therapy. Until now ≈100 cases have been reported in the literature, most of them in infants and young children. These patients also had clear predisposition to other severe infections with intracellular microorganisms such as atypical mycobacteria, Salmonella spp., Listeria monocytogenes, and Leishmania spp (1–5). The INF-γ receptor is present on many cell types; however, its deficiency on macrophages may be responsible for the inhibition of phagocytosis and intracellular killing and the observed deficit of an antimycobacterial immunity. Among children with a clinical syndrome of IFN- γ–receptor deficiency, a clear genetic defect was identified in ≈20%. In our patient, the diagnosis was made by detection by flow cytometry of abnormally low expression of the α chain of the IFN-γ receptor on peripheral blood lymphocytes. This method appears to have high diagnostic value, given the fact that genetic methods are not always available and are expensive and often insensitive. The prognosis in patients with BCG infection secondary to IFN-γ–receptor deficiency is unfavorable. A few cases of successful treatment with allogenic bone marrow transplantation have been reported with long-term improvement of general condition and stable receipt of the graft as shown by molecular analysis of peripheral leukocytes (4,6–8). However, as specific and efficient therapy for this condition has not been as yet proposed, supportive measures with early diagnosis and institution of anti-TB and antimicrobial drug treatment appear to be important in managing this rare immune deficiency. The level of IFN-γ-receptor expression in populations known to be susceptible to TB, and its potential role in this phenomenon, appears to be a promising area of study.

1689 children (M/F 1169/520 mean age 6.5 +/- 3 years) with chronic HBV infection were treated with low doses of Interferon alfa (3 MU TIW for 20 weeks). We recalculated the dose to body surface area and checked the HBeAg clearance rate in children receiving dose < 3 MU/m(2) (group 1), 3-4 MU/m(2) (group 2), 4-5 MU/m(2) (group 3) and dose > 5 MU/m(2) (group 4). End of treatment and end of one year follow-up HBeAg clearance rate was highest in group 4 (42,1 and 66,2%). The HBeAg clearance rate did not differ among the other three groups of children (group 1 - 27,9 and 50,2%, group 2 - 27,6 and 43,9%, group 3 - 28 and 51,8%). Higher ALT activity and shorter duration of HBV infection could contribute to the better results in group 4. We showed that the efficacy of the low interferon dose schedule is similar to the efficacy of recommended treatment with 5 MU/m(2) for 6 months.

Introduction: The course of HBV infection and the outcome of interferon alpha (IFNα) therapy of patients with chronic hepatitis B, is determined by the antiviral immune response of the host. The aim of the study was to investigate 1) the correlation between IL-6 and IL-12 serum levels and biochemical and histopathological changes in children with chronic hepatitis B, 2) predictive value of pre-treatment serum levels of these cytokines in patients treated with interferon alpha and 3) changes in serum levels of these cytokines after interferon alpha treatment. Methods: Serum levels of IL-6, IL-12 (heterodimer p70) and IL-12 (heterodimer p70 & p40 subunit) were determined by specific ELISA in 39 children with chronic hepatitis B on the first and the last day of IFNα therapy. Results: Serum levels of IL-6, IL-12 (p70) and IL-12 (p70&p40) were respectively within the following ranges of values: 0-1.7 pg/mL, 3.0-85.1pg/mL, 93.7-442.7 pg/mL and they showed no correlation with biochemical and histopathological changes. The pre-treatment cytokines levels in patients who responded and those who did not respond to IFNα therapy did not differ statistically. There was no statistical difference between the end and pre-treatment cytokines levels in both groups. Conclusions: Serum levels of IL-6 and IL-12 do not reflect the inflammatory activity of hepatitis and have no predictive value of positive response to the IFNα therapy in children with chronic hepatitis B. Serum IL-6 and IL-12 levels at the end of INFa treatment do not inform of their role in immunological changes which take place while inhibition of HBV replication or virus clearance.

Journal of Pediatric Gastroenterology and NutritionVolume 39, Issue S1 p. S319-S319 ABSTRACTS: Poster Session Abstracts P0689 POTENTIAL ROLE OF SULPHATE-REDUCING BACTERIA IN ETIOPATHOGENESIS OF INFLAMMATORY BOWEL DISEASE IN CHILDREN - PRELIMINARY STUDY B. Kaminska, B. Kaminska Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorP. Landowski, P. Landowski Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorM. Korzon, M. Korzon Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorA. Szlagatys, A. Szlagatys Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorZ. Kmiec, Z. Kmiec Department of Histology and Immunology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorD. Kartanowicz, D. Kartanowicz Department of Histology and Immunology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorJ. Kurlenda, J. Kurlenda Department of Microbiology, City Hospital, Gdansk, PolandSearch for more papers by this authorI. Aleksandrowicz, I. Aleksandrowicz Department of Microbiology, City Hospital, Gdansk, PolandSearch for more papers by this author B. Kaminska, B. Kaminska Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorP. Landowski, P. Landowski Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorM. Korzon, M. Korzon Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorA. Szlagatys, A. Szlagatys Department of Pediatrics, Pediatric Gastroenterology and Oncology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorZ. Kmiec, Z. Kmiec Department of Histology and Immunology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorD. Kartanowicz, D. Kartanowicz Department of Histology and Immunology, Medical University of Gdansk, Gdansk, PolandSearch for more papers by this authorJ. Kurlenda, J. Kurlenda Department of Microbiology, City Hospital, Gdansk, PolandSearch for more papers by this authorI. Aleksandrowicz, I. Aleksandrowicz Department of Microbiology, City Hospital, Gdansk, PolandSearch for more papers by this author First published: 01 June 2004 https://doi.org/10.1002/j.1536-4801.2004.tb13119.x Submitted by: [email protected] Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume39, IssueS1June 2004Pages S319-S319 RelatedInformation

excluded if tbey were < 65 years Diagnosis codes were used to exclude procedures being perthrmed tor signs or symptoms or for surveillance (histo D' of polyp, IBD, or cancer).Results: FS-SCR increased in all subgroups, ranging from 16% (65-69 years African American male [AAM]) to 82% (85+ years White female [WF]), with the most dramatic increases in the ->80 years age group.Changes in FOBT-SCR ranged from -9% (80-84 years AAM) to 36% (85 + WF), the largest incremem in older ages.The use of BE-SCR declined in almost all snbgroups, ranging from -31% (80-84 years AAM) to 12% (85 + ~VF).CY-SCR increased in virtually all subgroups with most of the increase occurring in the 65-69 years age group (from 7% in AAM to 27% in WF).Conch6tons: in general, increased CRC screening was seen in all age, race, and gender groups wath most of the COL-SCR increases occurring in younger patients.However, in the older age groups, particularly 85 +, dramatic increases in both FS-SCR and FOBT-SCR were noted.Thus, changes in reimbursement were most often associated w'ith large increases in the oldest age groups, which are least likely to benefit from these procedures in terms of prolonging life expeztancy.

One hundred children with chronic hepatitis B, aged 1-17.3 years participated in the study. The results of treatment with interferon alpha (IFN-alpha) were evaluated. An attempt was made to define the factors predicting positive response to treatment. Three million units of IFN-alpha 2a or 2b were given by subcutaneous injections to analysed patients 3 times a week for 20 weeks. Positive treatment outcome reflected in HbeAg elimination was observed in 46% of children. High AlAT activity preceding therapy had a statistically significant effect on positive treatment outcome. The inhibition of HBV replication caused by the treatment was permanent and it coexisted with the normalisation of AlAT activity in blood serum. Full response to therapy with IFN-alpha measured with the elimination of HbeAg and HbsAg was observed in 14% of children. It was favoured by high AlAT activity before treatment and short HBV duration.

Forty-seven children treated in various Polish centers between 1985 and 1995 for primary malignant liver tumors were retrospectively analyzed. Hepatoblastoma (HB) prevailed--it was found in 39 cases. There were 6 hepatocarcinoma (HCC) cases and 2 cases of undifferentiated sarcoma (UDS). In 44% of HB patients the tumor involved both liver lobes. 18% of children with HB presented with pulmonary metastases at diagnosis. Chemotherapy was applied in 92% of cases (preoperatively in 67%). Tumor resection was performed in 56% of HB patients. Overall survival of patients with hepatoblastoma was 43.6%, while it was 50% for hepatocarcinoma and 100% for undifferentiated sarcoma (2 cases only). Mean observation time was 58 months. The hepatoblastoma subgroup, being the largest (83% of all cases), was analyzed separately for prognostic factors. Completeness of tumor excision strongly influenced survival. Involvement of both lobes of the liver and multifocality of the tumor were other adverse prognostic factors.