Introduction Migration refers to the movement of persons or children from an origin place to a destination place across some pre-defined, political boundary. Since the 1995s after war, Bosnia and Herzegovina has continued being a country of mass children immigration from Sandjak, Kosovo, Serbia, Monte Negro and sporadic immigration from China. Methods The presence of tuberculosis disease in the Immigrants children or foreign-born child should prompt the pediatricians to collect appropriate specimens to recover an organism. We conducted a secondary data analysis focusing on immigrants children sampled in the 1995 through 2010 versions of the National Bosnian Children Health Records Survey. Results The increase in tuberculosis among Gypsy children in Sarajevo coincided with similar increases in immigration into Bosnia and Herzegovina. Medical records were available for review to assess adequately potential missed opportunities to prevent tuberculosis in children from Sandjak in only 1.5% of cases and Gypsies in 33% cases. Most children with drug-resistant tuberculosis were Gypsy (18.1%) or Chinese Asian (11.2%), and 16.4% of children or their parents were from a Bosnia and Herzegovina regions in which tuberculosis is highly endemic as Sarajevo Canton mountain area. Conclusions Pediatricians should be aware of the special health problems as tuberculosis for which immigrant children are at risk. Immigration poses unique stresses on children and families. There were no significance difference between incidence of tuberculosis and resistence on therapy between children from Sandjak and Bosnia but that differences were higher in case of Gypsies children.

Background: Mutations in the LPL gene cause familial lipoprotein lipase deficiency. Symptoms of familial LPL deficiency usually begin in childhood and include abdominal pain, acute and recurrent inflammation of the pancreas, skin lesions called eruptive cutaneous xanthoma and an enlargement of the liver and spleen. The risk for two carrier parents to both pass the defective gene and, therefore, have an affected child is 25% with each pregnancy. Aims: Early diagnosis, routine surveillance and treatment of familial LPL deficiency may help to manage some of the symptoms and sometimes prevent related problems. Methods: Clinical genetic testing for familial lipoprotein lipase deficiency may be available through an in person genetic consultation for children who are considered at risk. Triglycerides and total cholesterol were measured using commercially available kits (Boehringer Mannheim). Results: Episodes of abdominal pain are common. Intensity, duration, and localization of episodes are variable. Enlargement of the liver and spleen occurs particularly among affected infants and children. The enlargement of these organs may vary, often in parallel with the fat content of the diet. The risk is the same for boys and girls. Conclusions: Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body. It is characterized by absence of lipoprotein lipase activity and a massive accumulation of chylomicrons in plasma and a corresponding increase of plasma triglyceride concentration. Higher levels of plasma LPL activity are associated with decreased TG and increased HDL cholesterol levels in children.