Pneumocoocal infection and haemolytic uremic syndrome

Hemolytic uremic syndrome, one of the common causes of acute renal failure in children, is characterized by the triad of microangiopathy, haemolytic anemia, thrombocytopenia and acute renal failure. The diarrhoea-associated Hemolytic uremic syndrome is usually termed as a typical Hemolytic uremic syndrome. Streptococcus pneumoniae is an uncommon etiological pathogen for inducing Hemolytic uremic syndrome, and Streptococcus pneumoniae associated Hemolytic uremic syndrome is also termed as atypical hemolytic uremic syndrome. To report two pediatric cases of invasive S pneumoniae complicated with hemolytic uremic syndrome HUS. The first patient presented with pneumococcal pneumonia and empyema and the second patient presented with pneumococcal pneumonia and meningitis. The two patients were under one year of age and required peritoneal dialysis with improvement of renal function in one; the other died. Pneumococcal invasive disease may be a cause of severe 1-IUS, so a high index of suspicion is mandatory to prompt appropriate diagnosis and management

[Chronic gastritis in children]

Active gastritis, atrophic gastritis [AG] and intestinal metaplasia are lesions associated with Helicobacter pylon [H. pylon] infection in adults. To assess the prevalence of chronic gastritis, its histological characteristics and clinical features in children. 345 children [M/F: 151/194, mean age: 8.6 +/- 3.7 years; range: 1-18 years] were enrolled, referred for upper gastrointestinal endoscopy [UGI endo] with clinical manifestations of gastritis, i.e., recurrent abdominal pain [n=232, 67.2%], upper gastrointestinal bleeding [n=59, 17.1%] and miscellaneous [n=53, 15.3%]. Four per-endoscopic gastric biopsy specimens [antrum: 2, fundua: 2] were taken. Biopsies were assessed and graded according to the updated Sydney system. H. pylon infection was considered if 2 out 3 tests were positive [culture, histology and rapid unease teat], whereas 3 concordant negative results identified H. pylon negative children. H. pylon infection and chronic gastritis were detected in 215/345 [62.3%] [M/F. 104/1 17, sex ratio M/F=0.89] and 221/345 [64.05%] children, respectively. Recurrent abdominal pain [n=149, 67.4%] was the main clinical features of chronic gastritis followed by vomiting [n=43, 19.5%] and upper gastrointestinal bleeding [n=4l, 18.6%]. Any clinical features were however found to be specific. UGI endo showed; nodular gastritis [n=90, 40.72%], congestive gastnitis [n=84, 38%], gastric ulcer [n=9], bulbar ulcer [n=5] and normal [n=47, 21 2%]. Chronic gastritis was active in 115 cases [52%] and was significantly associated with nodular gastritis [p<0.05]. Thirty two chronic gastnitis [14.4%] exhibited AG [M/F: 16/16, mean age: 9.4 +/- 3.4 years] and 30/32 [93.7%] were H. pylon positive. AG was significantly associated with H. pylon infection [p<0.0001] and nodular gastritis [p<0.005]. Active, follicular and AG were significantly associated with H. pylon infection [p <0.00001]. Three patients exhibited intestinal metaplasia. Chronic gastnitis is frequent in children. Any clinical features were found to be specific. It significantly associated H. pylon infection and nodular gastnitis. Atrophic gastnitis was found in 145%of children

[Congenital hepatic fibrosis in children: about 9 cases and review of the literature]

Congenital hepatic fibrosis is a recessive autosomic disease with two major risks: gastrointestinal haemorrhage caused by portal hypertension and cholangitis related to bacterial infection of dilated intrahepatic bile ducts. The aim of our study is to define epidemiological features, the presenting symptoms, the diagnosis, the evolution and the management of this disease. Between January 1990 and December 2000, we reported the cases of nine children with this disease at children hospital of Tunis.Three were male and six female. The mild age was three years and six months. Consanguinity was present in five cases and similar cases were found in six cases. The FHC was revealed by portal hypertension in five cases, angiocholitis in one case and by portal hypertension and angiocholitis in three cases. Liver biopsy was done in seven children. Ultrasound examination of the liver and kidney revealed caroli syndrome in five cases and polykystose renal in two cases The intravenous pyelography was performed in four cases showing precalicial canalicular ectasia in four cases. Eosophageal endoscopy had shown oesophageal varices in six patients. The follow up had shown that three patients had gastrointestinal bleeding, three had angiocholitis. One patient died with multivisceral failure. The treatment of acute bleeding has needed blood transfusion in four cases. Primary prevention of bleeding was done by endoscopic sclerosis alone in one case and associated to betablokers in two cases. Secondary prevention of varices bleeding was done by sclerotherapic in two cases, by beta blokers alone in one case and by betablokers associated to elastic ligation of oesophageal varices in one case