An adverse food reaction is defined as clinical symptom soccurring in children, adolescents or adults after ingestion of a food or chemical food additives. This reaction does not occur in healthy subjects. In certain individuals it is a manifestation of hypersensitivity, i.e. qualitatively altered response to the consumed food. The disease symptoms observed after ingestion of the food can be triggered by two pathogenetic mechanisms; this allows adverse food reactions to be divided into allergic and non-allergic food hypersensitivity (food intolerance). Food allergy is defined as an abnormalimmune response to ingested food (humoral, cellularor mixed). Non-immunological mechanisms (metabolic, pharmacological, microbiological or other) are responsible for clinical symptoms after food ingestion which occur in non-allergic hypersensitivity (food intolerance). Food allergy is considered a serious health problem in modern society. The prevalence of this disorderis various and depends, among other factors, onthe study population, its age, dietary habits, ethnic differences, and the degree of economic development of a given country. It is estimated that food allergy occurs most often among the youngest children (about6–8% in infancy); the prevalence is lower among adolescents (approximately 3–4%) and adults (about1–3%). The most common, age-dependent cause of hypersensitivity, expressed as sensitization or allergic disease (food allergy), are food allergens (trophoallergens). These are glycoproteins of animal or plantorigine contained in: cow’s milk, chicken egg, soybean, cereals, meat and fish, nuts, fruits, vegetables, molluscs, shellfish and other food products. Some of these allergens can cause cross-reactions, occurring as a result of concurrent hypersensitivity to food, inhaled orcontact allergens. The development of an allergic processis a consequence of adverse health effects on thehuman body of different factors: genetic, environmentaland supportive. In people predisposed (genetically) to atopy or allergy, the development of food allergy is determined by four allergic-immunological mechanisms, which were classified and described by Gell‑Coombs. It is estimated that in approximately 48–50%of patients, allergic symptoms are caused only by typeI reaction, the IgEmediated (immediate) mechanism. In the remaining patients, symptoms of food hypersensitivity are the result of other pathogenetic mechanisms, non-IgE-mediated (delayed, late) ormixed (IgE-mediated, non-IgE-mediated). Clinical symptomatology of food allergy varies individually and depends on the type of food induced pathogenetic mechanism responsible for their occurrence. They relateto the organ or system in which the allergic reactionhas occurred (the effector organ). Most commonly the symptoms involve many systems (gastrointestinaltract, skin, respiratory system, other organs), and approximately 10% of patients have isolated symptoms. The time of symptoms onset after eatingthe causative food is varied and determined by the pathogenetic mechanism of the allergic immune reaction (immediate, delayed or late symptoms). In the youngest patients, the main cause of food reactions is allergy to cow’s milk. In developmental age, the clinical picture of food allergy can change, as reflected in theso-called allergic march, which is the result of anatomical and functional maturation of the effector organs, affected by various harmful allergens (ingested, inhaled, contact allergens and allergic cross-reactions). The diagnosis of food allergy is a complex, long-termand time-consuming process, involving analysis of the allergic history (personal and in the family), a thorough evaluation of clinical signs, as well as correctly plannedallergic and immune tests. The underlying cause ofdiagnostic difficulties in food allergy is the lack ofa single universal laboratory test to identify bothIgE‑mediated and non-IgE-mediated as well as mixedpathogenetic mechanisms of allergic reactions triggeredby harmful food allergens. In food allergy diagnosticsis only useful to identify an IgE-mediated allergicprocess (skin prick tests with food allergens,levels of specific IgE antibodies to food allergens). This allows one to confirm the diagnosis in patients whose symptoms are triggered in this pathogenetic mechanism (about 50% of patients). The method allow ingone to conclude on the presence or absence of food hypersensitivity and its cause is a food challenge test (open, blinded, placebo-controlled). The occurrence of clinical symptoms after the administration of food allergen confirms the cause of food allergy (positive test) whereas the time elapsing between the triggering doseingestion and the occurrence of clinical symptoms indicate the pathogenetic mechanisms of food allergy (immediate, delayed, late). The mainstay of causal treatment is temporary removal of harmful food from the patient’s diet, with the introduction of substitute ingredients with the nutritional value equivalent to the eliminated food. The duration of dietary treatment should be determined individually, and the measures of the effectiveness of the therapeutic elimination diet should include the absence or relief of allergic symptoms as well as normal physical and psychomotor development of the treated child. A variant alternative for dietary treatment of food allergy is specific induction of food tolerance by intended contact of the patient with the native or thermally processed harmful allergen (oral immunotherapy). This method has been used in the treatment of IgE-mediated allergy (to cow’smilk protein, egg protein, peanut allergens). The obtained effect of tolerance is usually temporary. In order to avoid unnecessary prolongation of treatment ina child treated with an elimination diet, it is recommended to perform a food challenge test at least oncea year. This test allows one to assess the body’s currentability to acquire immune or clinical tolerance. A negative result of the test makes it possible to return toa normal diet, whereas a positive test is an indication for continued dietary treatment (persistent food allergy). Approximately 80% of children diagnosed with food allergy in infancy “grow out” of the disease before the age of 4–5 years. In children with non-IgE‑mediated food allergy the acquisition of food tolerance is faster and occurs in a higher percentage of treated patients compared to children with IgE-mediated food allergy. Pharmacological treatment isa necessary adjunct to dietary treatment in food allergy. It is used to control the rapidly increasing allergic symptoms (temporarily) or to achieve remission andto prevent relapses (long-term treatment). Preventivemeasures (primary prevention of allergies) are recommended for children born in a “high risk” group for the disease. These are comprehensive measures aimed at preventing sensitization of the body (an appropriate way of feeding the child, avoiding exposure to some allergens and adverse environmental factors). First ofall, the infants should be breast-fed during the first4–6 months of life, and solid foods (non milk products, including those containing gluten) should be introduced no earlier than 4 months of age, but no later than 6 months of age. An elimination diet is not recommended for pregnant women (prevention of intrauterine sensitization of the fetus and unborn child). The merits of introducing an elimination diet in mothers of exclusively breast-fed infants, when the child responds with allergic symptoms to the specific dietof the mother, are disputable. Secondary prevention focuses on preventing the recurrence of already diagnosed allergic disease; tertiary prevention is the fight against organ disability resulting from the chronic and recurrent allergic process. Food allergy can adversely affect the physical development and the psycho-emotional condition of a sick child, and significantly interfere with his social contacts with peers. A long-termdisease process, recurrence of clinical symptoms, and  difficult course of elimination diet therapy are factors that impair the quality of life of a sick child and his family. The economic costs generated by food allergies affect both the patient’s family budget (in the household), and the overall financial resources allocated to health care (at the state level). The adverse socioeconomic effects of food allergy can be reduced by educational activities in the patient’s environment and dissemination of knowledge about the disease in the society.

The aim of this study was to present the role and tasks of EFSA in providing food safety. The European Food Safety Authority (EFSA) provides the European Commission with independent scientific advice on all the matters that have a direct or indirect impact on food safety. It is a separate legal entity, independent from the other EU institutions. The establishment of EFSA was one of the key measures contained in the Commission’s White Paper on Food Safety, which was published in January 2000. The Regulation 178/2002/EC providing a legal basis for the Authority was formally adopted on 28 January 2002.

One of the most common causes of constipation in children is decreased intake of fiber in diet. Fiber consists of these elements of plants which are resistant to digestive enzymes. The fiber includes water-insoluble compounds (cellulose, lignin, some hemicellulose) and water-soluble compounds, like pectins, gums, some hemicellulose, agar, vegetable mucilages. This group also includes fructo-, gluco- and galactosaccharides. Insoluble fiber has greater impact on weight and stool consistency, it occurs mainly in cereal products. The main source of soluble fiber are fruits and vegetables, and its fundamental role is the stimulation of growth of the intestinal microflora, especially fermenting bacteria, such as Lactobacillus and Bifidobacteria (prebioticfunction). Insoluble fiber is metabolized to short chain fatty acids.Children that avoid fiber rich foods, lucomannan was successfully used. It has got properties of binding waterand multiplication of fermenting bacteria, there by facilitating the treatment of constipation in children.

Rare diseases (orphan diseases) are rare disorders, mostly, but not always, of genetically order, of sever, chronic course. They are the problem of public health, demanding coordination between national and abroad centers. Authors discussed problems of multidisciplinary medical care and actions to improve the situation of those patients in Poland.

Potassium is the major intracellular ion, even smallchanges in the distribution of potassium between extracellular and intracellular spaces can cause significant hypokalemia or hyperkalemia. Potassium homeostasis depends on complex renal and extrarenal regulatory mechanisms and factors affecting the intracellula rdistribution of potassium. Factors stimulating a shiftof potassium into cells include aldosterone, insulin, beta-adrenergic receptor stimulation, alkalosis. Potassiumim balance is one of the most common electrolyte disorder in children. The proper level of potassium isessential for normal organ function and neuromuscular transmission. Both hypokalemia and hyperkalemia can be life-threatening conditions which require immediatemedical intervention. This article describes the causes, clinical manifestations and therapeutic management in potassium imbalance in children.

The pathogenesis of inflammatory bowel diseases (IBD), comprised of Crohn’s disease (CD) and ulcerative colitis (UC) is still unknown. Various theories on the etiology of IBD have been entertained. The postulated concepts include an autoimmune background, disturbance in intestinal microbiota and environmental factors, which leads to conclusion that the pathogenesis of IBD is most likely compound. Recent studies have raised evidence that supports an intersection between 3 fundamental cell biologic pathways of chronic inflammationin IBD, comprised of autophagy, intracellural bacterial sensing and endoplasmic reticulum stress.

Children born small for gestational age (SGA) are an important group of patients coming to an endocrinologist due to short stature. Last years several papers presenting results of growth hormone (GH) treatment in children with short stature and SGA were published. Most of SGA children compensate growth deficiency by the end of second year oflife. This phenomenon is called “catch-up growth”. In children who did not show “catch-up growth”there is a possibility to improve final height by GH therapy. The aim of the treatment is not only to improve final height but also to decrease risk of developing many diseases significantly increased in this group of children. In the article diagnostic schedule, indications for therapy, criteria for the start and end of the treatment are discussed. Contraindications, GH dosing, follow-up and adverse events of GH therapy in children with short stature due to SGA are presented. In Poland this therapy is not refunded. In the world GH therapy is indicated in children with growth deficiency and SGA for many years (approvedin USA since 2001, in Europe since 2003).

Ankyloglossia (tongue-tie) in breastfeeding infantscan cause problems in achieving proper latch what can lead to inadequate nutrition, maternal nipple painand trauma, and early weaning. Frenotomy can prevent these disadvantageous consequences of tongue‑tie. The assessment of the newborn’s frenum for this surgical procedure requires good knowledge of the anatomy of lingual frenum, tongue and mouth, physiology of breastfeeding and mechanism of sucking. The article presents the most relevant information in these field sand regarding the functional tongue development. Subsequently, the article describes diagnostic criteria for frenotomy in newborn infants (assessed by parental interview, examinations of the infant mouth and maternal breasts, observation of breastfeeding), thead visability of frenotomy supported by scientific research, methods of frenotomy, contraindications forthis procedure, and rare complications. Possible developmental consequences of the lingual constraint after failure to perform frenotomy when indicated in infants with tongue-tie are also described.

Cohen syndrome is a rare, recessively inherited condition with the broad, changing with age clinical spectrum. It is characterized by mental retardationac companied by specific sociable behavior, postnatal microcephaly, facial dysmorphism, muscle hypotonia/joint laxity, retinitis pigmentosa and progressive myopia. Additional characteristics include truncal obesity with comparatively slender limbs and intermittent neutropenia. The gene responsible for Cohen syndrome, COH 1 (defined also as VPS13B), was mapped to a region 8q22-8q23. The diagnosis could be very difficult, especially in very young children, due to age-dependent manifestation of some significant symptoms (ophthalmologic signs, truncal obesity) or intermittent appearance of the others (neutropenia). Since anearly diagnosis is important both for a patient and the family and the molecular tests are very expensive, we decided to delineate the clinical picture and etiology of this syndrome which, in our opinion, is recognized too rarely.

Each child’s immunization may be associated with the risk of adverse reaction. Severe post-vaccination reactions are very rare. Among the large group of children with varying severity of allergy to eggs, the reactions after MMR vaccination can happen, but they are not associated with hypersensitivity to egg protein antigens. The processed protein antigens and their minimum concentration in the MMR vaccine do not causeany allergic reaction. The fixed stereotype thinking of many doctors and parents is disqualification from the MMR vaccination of children allergic to eggs, especially with severe course of allergy. In this paper we present standards of vaccination of children allergic to eggs developed on the basis of the recommendations of the American Academy of Pediatrics in 2009 and the British Society for Allergy and Clinical Immunology in 2010, which are used in everyday practice 1, 2, 3. The cautionin the implementation of influenza vaccination in children with allergy to eggs show recently published recommendations of the Center for Disease Control and Prevention published in the MMWR/August 26, 2011/Vol. 60/No. 33, 1129–11324.

Neisseria menigitidis is the major cause of infection sand deaths worldwide. Meningococcal infections arethe most common in children up to 5 y.o., teenager sand young adolescents, as well as in special risk groups. Serogroups A, B, C, W135 and Y are responsible for approximately 90% of infections . Polysaccharide vaccine for serogroup A and C has been use since years, and effective and conjugated vaccines are available for serogroups A, C, W135 and Y. Development of broadly protective vaccine against Men B has been difficult and unmet challenge for decades. The “reverse vaccinology” methods let develop novel vaccine using the genome from MenB strain MC58. Several preclinical and clinical trials demonstrated immunogenicity, safety and tolerability of that vaccine in different age groups.

Since 2007, the main objective of the Pediatric Experts Group on Immunization Programme has been to include pneumococcal vaccination in the routine vaccination schedule in children under 2 years of age. Vaccination schedule of the Ministry of Health does not include universal pneumococcal vaccination this year. However the National Immunization Programme for 2012 includes pneumococcal vaccination programme for the larger risk groups, targeting those groups of children in epidemiological situations of risk (Table 1). In Poland, Streptococcus pneumoniae was the mainetiologic agent of community-acquired of invasive pneumococcal diseases (PID) in 2010, especially in the extreme age groups. Neonates, infants and the elderly have higher vulnerability to PID, because immune responsesare transient or insufficient for immune protection (Table 2). Vaccination with 13-valent pneumococcal conjugate vaccine (PCV 13) and after that with 23-valent pneumococcal polysaccharide vaccine (PPSV23) presents the new possibility of providing long-termprotection against PID.