[Overweight in primary school-age children. Prevalence and risk factors]. / Gewichtsentwicklung im frühen Grundschulalter. Prävalenz, Inzidenz und Risikofaktoren für Übergewicht und Adipositas.

BACKGROUND: Various studies show that pre-school age is a sensitive period for the development of overweight and obesity. During a longitudinal study between 2010 and 2013, the municipal health authority (city of Frankfurt) in cooperation with the university children's hospital investigated the development of weight in children aged 5 to 8. MATERIALS AND METHODS: The weight and height of a collective of 5720 children were measured (2010/11). In addition, nutritional and exercise habits, as well as media consumption was documented for 4758 children through a questionnaire during the school enrolment procedure. The weight and height of 3481 children were measured again in the second grade (2012/13). RESULTS: Over a period of 24 months, the percentage of overweight (not obese) children increased from 7.5 to 9.4 % and that of obese children from 4.5 to 5.0 %. 164 of 2818 children with a normal initial weight (5.8 %) changed to percentile class overweight or obese. 79 of 260 children who were initially overweight, not obese (30 %), changed to the group of normal weight, but only 4 out of 156 obese children (3 %). Increased TV consumption (> 1 h per day), availability of their own television, lack of physical activity, and consumption of high-calorie drinks were risk factors for the development of overweight during the primary school age. 72 % of parents of overweight children and 22 % of obese children falsely classified their children as normal weight. CONCLUSIONS: Targeted education about the risk of obesity in the primary school age and offers for early intervention should be established in the healthcare services concerned.

Risk of Pseudomonas aeruginosa cross-colonisation in patients with cystic fibrosis within a holiday camp--a molecular-epidemiological study.

OBJECTIVE: A study on the molecular epidemiology of Pseudomonas aeruginosa in patients with cystic fibrosis (CF) from Germany (N = 18) and Israel (N = 12) is presented. The aim is to provide an answer to the question as to whether or not social contact outside the hospital environment involves a potential risk for person-to-person spread of this pathogen. METHODS: Sputa from German and Israeli patients were obtained while these were attending a holiday camp in Israel. The sputum samples were analysed with regard to Pseudomonas aeruginosa. Strains dissimilar in macroscopic appearance and/or antibiotic resistance patterns were genotyped using pulsed-field gel electrophoresis after digestion of genomic DNA with restriction endonuclease Spel. The genetic polymorphism of DNA fragment patterns of all strains (N = 146) was studied for their overall relatedness using a fingerprint software system. RESULTS: Most of the German patients (77.7%) were colonised persistently by a unique clonal type during the four-week screening period. Isolates obtained from Israeli patients displayed a very close clonal relationship and a higher antibiotic resistance as a result of preceding epidemic spread of certain clones before the camp. Additionally, isolates showing identical PFGE patterns were demonstrated once in a single male Israeli patient and in one female German patient, suggesting previous cross-colonisation. CONCLUSION: The occurrence of person-to-person spread through social contact in patients with CF is supported by our findings, but remains a rare event outside the hospital environment, provided appropriate hygienic measures are applied.

Ultrasound studies of the intestinal wall in patients with cystic fibrosis.

BACKGROUND: In 1994, first published reports described cystic fibrosis patients who experienced a then unknown complication-ileocecal and colonic stenoses with submucosal proliferation requiring surgical intervention. To investigate a suspected correlation between increased intestinal wall diameter and high doses of pancreatic enzymes, we carried out a prospective study in our CF-outpatient clinic. METHODS: By ultrasound analysis we measured the intestinal wall diameter in 201 patients. One hundred ninety-three patients treated with pancreatic enzymes had pancreatic insufficiency. Eight patients showed normal pancreatic function, seven of them had never been treated with pancreatic enzymes. The control group included 12 healthy children. Measuring points were the distal ileum, cecum, ascending, and descending colon. Measurements were made by the longitudinal and cross sectional cut. The following aspects of the patients' history were recorded (a) current type of pancreatic enzyme medication; (b) total dosage per day (with reference to lipase units); (c) duration of therapy with standard-strength pancreatic enzyme (SSPE) preparations (< or = 10,000 lipase units per capsule) and HSPE preparations (> or = 20,000 lipase units per capsule); (d) gastrointestinal complication (distal intestinal obstruction syndrome, meconium ileus, abdominal surgery, intussusception), diabetes mellitus, and hepatobiliary complications. RESULTS: The intestinal wall diameter in patients receiving HSPE therapy was greater (with prominent submucosal layer) than that in patients receiving SSPE therapy or in patients with pancreatic sufficiency. Healthy subjects had the smallest intestinal wall diameter. There was no correlation between patient history and increased intestinal wall thickness. CONCLUSIONS: Ultrasound detects characteristic ileocecal wall lesions in the majority of cystic fibrosis patients on pancreatic enzymes. These lesions may lead to significantly increased ileocecal wall thickness, which is correlated but not restricted to HSPE.

Incidence of development of factor VIII and factor IX inhibitors in haemophiliacs.

The development of factor VIII:C inhibitors remains one of the most serious complications of repeated transfusion in patients with haemophilia A. The proportion of patients affected has been reported to range from 3.6% to 25%, but these figures have been derived mainly from retrospective data and from total numbers of known haemophiliacs instead of number at true risk. The assessment here is based on a prospective study, started in 1976, on the incidence of inhibitor development in haemophiliacs born after 1970 whose FVIII or FIX activity was 5% or less, and who had received replacement therapy at least once. 46 of 63 children with haemophilia A and 13 of 17 with haemophilia B fulfilled the enrollment criteria. Inhibitors developed only in haemophilia A patients who had previously been treated with FVIII products--inhibitor concentrations were high in 12 and low in 3. Inhibitors developed in 24% (15/63) of all haemophilia A patients, and in 52% (14/27) of those with severe disease. The incidence of inhibitor development for all haemophilia patients was 39.1 per 1000 patient-years of observation. All inhibitors were first detected when patients were aged 0.08-5.2 years. The cumulative risk was 33% at age 6 years. The findings indicate that previous reports have underestimated the risk of acquiring FVIII inhibitors. Prospective, standardised studies, especially in children, are needed for the assessment of the true risk of this complication.

[Thrombocyte function in children with Type I diabetes mellitus. Cross-sectional study]. / Thrombozytenfunktion bei Kindern mit Diabetes mellitus Typ I. Querschnittstudie.

Platelet count, spontaneous platelet aggregation, ADP- and collagen-induced platelet aggregation platelet adhesion, platelet volume, shape change, beta-thromboglobulin and von-Willebrand-factor have been investigated in 51 insulin dependent diabetic children without clinical signs of diabetic angiopathy. Compared to an age matched healthy control group diabetic children showed a significant enhancement of spontaneous platelet aggregation, elevated plasma levels of von-Willebrand-factor, increased platelet shape change and adhesion. No alterations could be found in ADP--and collagen--induced platelet aggregation and in beta-thromboglobulin levels. Significant correlations could be found between the total glycosylated haemoglobin concentrations (Hb A1) and spontaneous platelet aggregation, as well as between duration of diabetes Hb A1, and platelet volume. In this study we could demonstrate changes in platelet function in diabetic children without clinical signs of diabetic angiopathy. However these changes could be due to metabolic adjustment and may precede diabetic vasculopathy.

[Physiologic blood coagulation studies in idiopathic arterial thrombosis]. / Gerinnungsphysiologische Untersuchungen bei idiopathischen arteriellen Thrombosen.

QUESTIONING: The prevalence of inherited thrombotic syndromes in the general population appears to be higher than that of inherited bleeding disorders. However, the most important candidates for screening are patients with unexplained thromboembolism at ages of less than 40 years: In 19 children suffering from "idiopathic" arterial thrombosis laboratory screening has been performed. METHODS: PT, PTT, TT, platelet count, spontaneous platelet aggregation, von Willebrand-factor, fibrinogen, plasminogen, antithrombin III, protein C, C1-inactivator, alpha-1-antitrypsin, alpha-1-antichymotrypsin, alpha-2-antiplasmin and alpha-2-macroglobulin have been investigated. RESULTS: Compared to an age matched healthy control group we could demonstrate in children with arterial thrombosis in vitro platelet activation with significant enhanced platelet aggregation, elevated levels of von Willebrand-factor and alpha-1-antichymotrypsin at the onset of disease. Protein C and alpha-2-antiplasmin were significantly decreased. These changes turned back to normal in the following 6 to 9 months. PT, PTT, TT, platelet count, plasminogen, alpha-1-antitrypsin, c1-inactivator and alpha-2-macroglobulin showed no alterations compared to controls. CONCLUSIONS: Platelet activation and alteration of platelet function have been shown in vivo and in vitro to initiate thrombosis. The von Willebrand's VIII molecule is involved in this step. The lowering of protein C levels at the onset of thrombotic diseases is discussed to be due to an increased turnover, whereas the decreased levels of alpha-2-antiplasmin might be a counter-regulation to the thrombotic event, showing an "activated" fibrinolytic system.