Preservation of Biomarkers Associated with Alzheimer's Disease (Amyloid Peptides 1-38, 1-40, 1-42, Tau Protein, Beclin 1) in the Blood of Neonates after Perinatal Asphyxia.

Perinatal asphyxia is a complex disease involving massive death of brain cells in full-term newborns. The most impressive consequence of perinatal asphyxia is a neurodegenerative brain injury called hypoxic-ischemic encephalopathy. Management of newborns after perinatal asphyxia is very difficult due to the lack of measurable biomarkers that would be able to assess the severity of the brain injury in the future, help in the selection of therapy, assess the results of treatment and determine the prognosis for the future. Thus, these limitations make long-term neurodevelopmental outcomes unpredictable during life. Quantifying biomarkers that can detect subclinical changes at a stage where routine brain monitoring or imaging is still mute would be a major advance in the care of neonates with brain neurodegeneration after asphyxia. Understanding the effect of perinatal asphyxia on changes in blood neurodegenerative biomarkers over time, which would be commonly used to assess the severity of postpartum encephalopathy, would be an important step in developing precision in predicting the consequences of brain injuries. We urgently need more accurate early predictive markers to guide clinicians when to use neuroprotective therapy. The needed neurodegenerative biomarkers may represent neuronal pathological changes that can be recognized by new technologies such as genomic and proteomic. Nevertheless, the simultaneous blood tau protein and various amyloid changes with the addition of an autophagy marker beclin 1 after perinatal asphyxia have not been studied. We decided to evaluate serum biomarkers of neuronal injury characteristic for Alzheimer's disease such as amyloid peptides (1-38, 1-40 and 1-42), tau protein and beclin 1, which can predict the progression of brain neurodegeneration in future. In this paper, we report for the first time the significant changes in the above molecules in the blood after asphyxia compared to healthy controls during the 1-7, 8-14 and 15+ days ELISA test.

Melatonin: A Potential Candidate for the Treatment of Experimental and Clinical Perinatal Asphyxia.

Perinatal asphyxia is considered to be one of the major causes of brain neurodegeneration in full-term newborns. The worst consequence of perinatal asphyxia is neurodegenerative brain damage, also known as hypoxic-ischemic encephalopathy. Hypoxic-ischemic encephalopathy is the leading cause of mortality in term newborns. To date, due to the complex mechanisms of brain damage, no effective or causal treatment has been developed that would ensure complete neuroprotection. Although hypothermia is the standard of care for hypoxic-ischemic encephalopathy, it does not affect all changes associated with encephalopathy. Therefore, there is a need to develop effective treatment strategies, namely research into new agents and therapies. In recent years, it has been pointed out that natural compounds with neuroprotective properties, such as melatonin, can be used in the treatment of hypoxic-ischemic encephalopathy. This natural substance with anti-inflammatory, antioxidant, anti-apoptotic and neurofunctional properties has been shown to have pleiotropic prophylactic or therapeutic effects, mainly against experimental brain neurodegeneration in hypoxic-ischemic neonates. Melatonin is a natural neuroprotective hormone, which makes it promising for the treatment of neurodegeneration after asphyxia. It is supposed that melatonin alone or in combination with hypothermia may improve neurological outcomes in infants with hypoxic-ischemic encephalopathy. Melatonin has been shown to be effective in the last 20 years of research, mainly in animals with perinatal asphyxia but, so far, no clinical trials have been performed on a sufficient number of newborns. In this review, we summarize the advantages and limitations of melatonin research in the treatment of experimental and clinical perinatal asphyxia.

Hypothermia after Perinatal Asphyxia Does Not Affect Genes Responsible for Amyloid Production in Neonatal Peripheral Lymphocytes.

In this study, the expression of the genes of the amyloid protein precursor, ß-secretase, presenilin 1 and 2 by RT-PCR in the lymphocytes of newborns after perinatal asphyxia and perinatal asphyxia treated with hypothermia was analyzed at the age of 15-21 days. The relative quantification of Alzheimer's-disease-related genes was first performed by comparing the peripheral lymphocytes of non-asphyxia control versus those with asphyxia or asphyxia with hypothermia. In the newborns who had perinatal asphyxia, the peripheral lymphocytes presented a decreased expression of the amyloid protein precursor and ß-secretase genes. On the other hand, the expression of the presenilin 1 and 2 genes increased in the studied group. The expression of the studied genes in the asphyxia group treated with hypothermia had an identical pattern of changes that were not statistically significant to the asphyxia group. This suggests that the expression of the genes involved in the metabolism of the amyloid protein precursor in the peripheral lymphocytes may be a biomarker of progressive pathological processes in the brain after asphyxia that are not affected by hypothermia. These are the first data in the world showing the role of hypothermia in the gene changes associated with Alzheimer's disease in the peripheral lymphocytes of newborns after asphyxia.

Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy: Possible Therapeutic Role of Curcumin.

For thousands of years, mankind has been using plant extracts or plants themselves as medicinal herbs. Currently, there is a great deal of public interest in naturally occurring medicinal substances that are virtually non-toxic, readily available, and have an impact on well-being and health. It has been noted that dietary curcumin is one of the regulators that may positively influence changes in the brain after ischemia. Curcumin is a natural polyphenolic compound with pleiotropic biological properties. The observed death of pyramidal neurons in the CA1 region of the hippocampus and its atrophy are considered to be typical changes for post-ischemic brain neurodegeneration and for Alzheimer's disease. Additionally, it has been shown that one of the potential mechanisms of severe neuronal death is the accumulation of neurotoxic amyloid and dysfunctional tau protein after cerebral ischemia. Post-ischemic studies of human and animal brains have shown the presence of amyloid plaques and neurofibrillary tangles. The significant therapeutic feature of curcumin is that it can affect the aging-related cellular proteins, i.e., amyloid and tau protein, preventing their aggregation and insolubility after ischemia. Curcumin also decreases the neurotoxicity of amyloid and tau protein by affecting their structure. Studies in animal models of cerebral ischemia have shown that curcumin reduces infarct volume, brain edema, blood-brain barrier permeability, apoptosis, neuroinflammation, glutamate neurotoxicity, inhibits autophagy and oxidative stress, and improves neurological and behavioral deficits. The available data suggest that curcumin may be a new therapeutic substance in both regenerative medicine and the treatment of neurodegenerative disorders such as post-ischemic neurodegeneration.

Is N-terminal pro-brain type natriuretic peptide a useful marker in newborns with heart defects?

BACKGROUND: Heart diseases are currently a significant cause of morbidity and mortality in newborns. The existing diagnostic methods are often not sufficient or, in many cases, cannot be used. Great advances have been achieved in medical knowledge concerning biomarkers for the diagnosis of circulatory system disorders in adult patients. Among these biomarkers, N-terminal pro-brain type natriuretic peptide (NT-proBNP) plays a main role. However, in the existing literature, there is not enough data concerning the physiological features of this biomarker in newborns and its potential use in neonatal cardiac diagnostics. OBJECTIVES: To evaluate the diagnostic usefulness of NT-proBNP measurements in correlation with other markers of circulatory failure and myocardial damage in newborns with heart defects. MATERIAL AND METHODS: This study involved 126 newborns. Patients were divided into 2 main groups: group I included infants with congenital heart defects (CHD) and group II (control) included healthy neonates. Newborns with CHD were further divided into 2 subgroups: group Ia with simple shunts and group Ib with combined heart defects. Patients in group I were further divided according to the hemodynamic significance of CHD. The NT-proBNP level was evaluated using the CARDIAC proBNP immunologic test (Cobas h232; Roche Diagnostics, Basel, Switzerland). RESULTS: The NT-proBNP concentrations were significantly higher in newborns with CHD compared to healthy ones. Newborns with combined heart defects had higher levels of NT-proBNP than newborns with simple shunts. The NT-proBNP concentrations in newborns with CHD correlated with echocardiographic parameters of hemodynamic significance and with left ventricular ejection fraction (LVEF). Additionally, NT-proBNP correlated with clinical symptoms of heart failure (HF; Ross classification, Reithmann's score). CONCLUSIONS: Statistically significant differences in NT-proBNP level between newborns with heart defects and healthy controls were shown. In newborns with heart diseases, significant correlations were found between NT-proBNP level and the type of heart defect (simple shunt or combined defects), the hemodynamic significance of the defect, LVEF, and the clinical intensity of HF.

Alzheimer's Disease Associated Presenilin 1 and 2 Genes Dysregulation in Neonatal Lymphocytes Following Perinatal Asphyxia.

Perinatal asphyxia is mainly a brain disease leading to the development of neurodegeneration, in which a number of peripheral lesions have been identified; however, little is known about the expression of key genes involved in amyloid production by peripheral cells, such as lymphocytes, during the development of hypoxic-ischemic encephalopathy. We analyzed the gene expression of the amyloid protein precursor, ß-secretase, presenilin 1 and 2 and hypoxia-inducible factor 1-α by RT-PCR in the lymphocytes of post-asphyxia and control neonates. In all examined periods after asphyxia, decreased expression of the genes of the amyloid protein precursor, ß-secretase and hypoxia-inducible factor 1-α was noted in lymphocytes. Conversely, expression of presenilin 1 and 2 genes decreased on days 1-7 and 8-14 but increased after survival for more than 15 days. We believe that the expression of presenilin genes in lymphocytes could be a potential biomarker to determine the severity of the post-asphyxia neurodegeneration or to identify the underlying factors for brain neurodegeneration and get information about the time they occurred. This appears to be the first worldwide data on the role of the presenilin 1 and 2 genes associated with Alzheimer's disease in the dysregulation of neonatal lymphocytes after perinatal asphyxia.

Vitamin B12 deficiency as a cause of severe neurological symptoms in breast fed infant - a case report.

BACKGROUND: Vitamin B12 (cobalamin, cbl) deficiency in children is rare and may occurs in exclusively breast fed infants of mothers on vegetarian or vegan diet with lack of appropriate supplementation. The clinical manifestation of vitamin B12 deficiency include neurological disorders, megaloblastic anemia and failure to thrive. Routine and commonly used laboratory tests such as cell blood count (CBC) or serum vitamin B12 level are sufficient for appropriate diagnosis. Typical therapy is based on intramuscular cobalamin injections. Early diagnosis and early onset of treatment are crucial factors for long-term prognosis of patients as the duration of deficiency may be correlated with the development of long lasting changes in the nervous system. The purpose of this article is to present influence of maternal vitamin B12 deficiency as a cause of infant psychomotor retardation. CASE PRESENTATION: We report the case of a 7 months old girl whose parents sought medical advice due to pathological somnolence and developmental regression of their daughter with onset approximately 2 months prior to the visit. Following several diagnostic tests it was determined that the infant's symptoms were due to vitamin B12 deficiency which was secondary to the mother's latent Addison-Biermer disease. Apart from neurological symptoms the infant also showed megaloblastic anemia which is typical to cobalamin deficiencies. Intramuscular vitamin B12 supplementation resulted in instant improvement of the patient's general condition and blood morphology. Unfortunately, psychological examination indicated long-term psychomotor retardation due to delayed diagnosis of B12 deficiency. CONCLUSIONS: Vitamin B12 levels should be considered during differential diagnosis of neurological symptoms in exclusively breast-fed infants especially if they co-exist with megaloblastic anemia and psychomotor retardation.

The Evaluation of Cardiac Troponin T in Newborns.

INTRODUCTION: In this paper, we evaluated the physiologic ranges of cardiac troponin T (cTnT) serum concentrations in healthy newborns. This is significant because these ranges have not been determined yet, especially for newborns older than 7 days. Cardiac troponins are widely used as diagnostic markers in adults; however, they cannot be routinely used in infants due to lack of data concerning normal values in this age group. AIM: To determine the physiologic ranges of cTnT concentrations in newborns and to evaluate the influence of factors such as age, sex, and blood saturation. METHODS: The study involved 59 newborns up to 46 weeks of postmenstrual age (full-term and preterm). The exclusion criteria were severe perinatal asphyxia and presence of severe diseases. Troponin T concentrations were evaluated by the Roche CARDIAC T Quantitative Test. The obtained results were statistically analyzed by the use of the Statistica 9.0 computer program. RESULTS: The study revealed that cTnT levels in newborns correlate with postmenstrual age, but not with chronologic or fetal age. Sex, delivery mode, and blood oxygenation did not influence cTnT concentrations in the studied patients. CONCLUSIONS: (1) Cardiac troponin T concentration depends on postmenstrual age in newborns. (2) Cardiac troponin T concentration in newborns does not depend on sex, mode of delivery, or blood saturation.

Dysregulation of Autophagy, Mitophagy, and Apoptotic Genes in the Medial Temporal Lobe Cortex in an Ischemic Model of Alzheimer's Disease.

Ischemic brain damage is a pathological incident that is often linked with medial temporal lobe cortex injury and finally its atrophy. Post-ischemic brain injury associates with poor prognosis since neurons of selectively vulnerable ischemic brain areas are disappearing by apoptotic program of neuronal death. Autophagy has been considered, after brain ischemia, as a guardian against neurodegeneration. Consequently, we have examined changes in autophagy (BECN 1), mitophagy (BNIP 3), and apoptotic (caspase 3) genes in the medial temporal lobe cortex with the use of quantitative reverse-transcriptase PCR following transient 10-min global brain ischemia in rats with survival 2, 7, and 30 days. The intense significant overexpression of BECN 1 gene was noted on the 2nd day, while on days 7-30 the expression of this gene was still upregulated. BNIP 3 gene was downregulated on the 2nd day, but on days 7-30 post-ischemia, there was a significant reverse tendency. Caspase 3 gene, associated with apoptotic neuronal death, was induced in the same way as BNIP 3 gene after brain ischemia. Thus, the demonstrated changes indicate that the considerable dysregulation of expression of BECN 1, BNIP 3, and caspase 3 genes may be connected with a response of neuronal cells in medial temporal lobe cortex to transient complete brain ischemia.

Discrepancy in Expression of ß-Secretase and Amyloid-ß Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia.

Brain ischemia may be causally related with Alzheimer's disease. Presumably, ß-secretase and amyloid-ß protein precursor gene expression changes may be associated with Alzheimer's disease neuropathology. Consequently, we have examined quantitative changes in both ß-secretase and amyloid-ß protein precursor genes in the medial temporal lobe cortex with the use of quantitative rtPCR analysis following 10-min global brain ischemia in rats with survival of 2, 7, and 30 days. The greatest significant overexpression of ß-secretase gene was noted on the 2nd day, while on days 7-30 the expression of this gene was only modestly downregulated. Amyloid-ß protein precursor gene was downregulated on the 2nd day, but on days 7-30 postischemia, there was a significant reverse tendency. Thus, the demonstrated alterations indicate that the considerable changes of expression of ß-secretase and amyloid-ß protein precursor genes may be connected with a response of neurons in medial temporal lobe cortex to transient global brain ischemia. Finally, the ischemia-induced gene changes may play a key role in a late and slow onset of Alzheimer-type pathology.

Alzheimer-associated presenilin 2 gene is dysregulated in rat medial temporal lobe cortex after complete brain ischemia due to cardiac arrest.

BACKGROUND: Brain ischemia may be causally related with Alzheimer's disease. Probably, presenilin gene dysregulation may be associated with Alzheimer's disease neuropathology. Consequently, we have examined quantitative changes in both presenilin 1 and 2 genes in the medial temporal lobe cortex following 10-min global brain ischemia in rats. METHODS: Global brain ischemia was induced by cardiac arrest in female rats that were allowed to survive for 2, 7 and 30 days. The expression of presenilin genes was evaluated in the rat medial temporal lobe cortex with the use of quantitative RT-PCR analysis. RESULTS: Presenilin 1 gene expression tended to be downregulated from days 2 to 7 postischemia but at day 30, there was a reverse tendency. The greatest overexpression of presenilin 2 gene was noted at 2-nd day whilst on day 7, the expression of this gene was only modestly elevated. Eventually, at day 30 expression of presenilin 2 gene was modestly downregulated. Alterations of presenilin 2 gene expression between 2 and 7 days and between 2 and 30 days were statistically significant. CONCLUSIONS: Thus, presented changes suggest that the significant dysregulation of presenilin 2 gene may be connected with a response of neuronal cells to transient global brain ischemia due to cardiac arrest. Finally, the ischemia-induced gene dysregulation may play a key role in the late onset of Alzheimer's-type dementia.

Dysregulation of Amyloid-ß Protein Precursor, ß-Secretase, Presenilin 1 and 2 Genes in the Rat Selectively Vulnerable CA1 Subfield of Hippocampus Following Transient Global Brain Ischemia.

The interaction between brain ischemia and Alzheimer's disease (AD) has been intensively investigated recently. Nevertheless, we have not yet understood the nature and mechanisms of the ischemic episodes triggering the onset of AD and how they influence its slow progression. The assumed connection between brain ischemia and the accumulation of amyloid-ß (Aß) peptide awaits to be clearly explained. In our research, we employed a rat cardiac arrest model to study the changes in gene expression of amyloid-ß protein precursor (AßPP) and its cleaving enzymes, ß- and γ-secretases (including presenilins) in hippocampal CA1 sector, following transient 10-min global brain ischemia. The quantitative reverse-transcriptase PCR assay demonstrated that the expression of all above genes that contribute to Aß peptide generation was dysregulated during 30 days in postischemic hippocampal CA1 area. It suggests that studied Aß peptide generation-related genes can be involved in AßPP metabolism, following global brain ischemia and will be useful to identify the molecular mechanisms underpinning that cerebral ischemia might be an etiological cause of AD via dysregulation of AßPP and its cleaving enzymes, ß- and γ-secretases genes, and subsequently, it may increase Aß peptide production and promote the gradual and slow development of AD neuropathology. Our data demonstrate that brain ischemia activates delayed neuronal death in hippocampus in an AßPP-dependent manner, thus defining a new and important mode of ischemic cell death.

Neurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?

For thousands of years, humankind has used plants for therapeutics. Nowadays, there is a renewed public interest in naturally occurring treatments with minimal toxicity and diets related to health. Alterations in hippocampal neurogenesis have been recognized as an integral part of brain ischemia. Neuronal stem/progenitor cells in the hippocampus are positively and negatively regulated by intrinsic and extrinsic agents. One positive regulator of neurogenesis in the hippocampus is curcumin in the diet. This review provides an assessment of the current state of the field in hippocampal neurogenesis and neuroprotection studies in brain ischemia and focuses on the role of curcumin in the diet. Data suggest that dietary intake of curcumin enhances neurogenesis. Recent studies performed in ischemic models have suggested that curcumin also has neuroprotective features. One potential mechanism to explain several of the general health benefits associated with curcumin is that it may prevent ageing-associated changes in cellular proteins that lead to protein insolubility and aggregation after ischemia such as ß-amyloid peptide and tau protein. Here, we also review the evidence from ischemic models that curcumin improves cognition and health span by overexpression of life supporting genes and preventing or delaying the onset of neurodegenerative changes. Available data provide evidence that curcumin induces neurogenesis and neuroprotection and may provide a novel therapeutic agent for both regenerative medicine and for the treatment of neurodegenerative diseases such as postischemic brain neurodegeneration with Alzheimer phenotype.

Neuronal autophagy: self-eating or self-cannibalism in Alzheimer's disease.

Autophagy is a major intracellular degeneration pathway involved in the elimination and recycling of damaged organelles and long-lived proteins by lysosomes. Many of the pathological factors, which trigger neurodegenerative diseases, can perturb the autophagy activity, which is associated with misfolded protein aggregates accumulation in these disorders. Alzheimer's disease, the first neurodegenerative disorder between dementias, is characterized by two aggregating proteins, ß-amyloid peptide (plaques) and τ-protein (tangles). In Alzheimer's disease autophagosomes dynamically form along neurites within neuronal cells and in synapses but effective clearance of these structures needs retrograde transportation towards the neuronal soma where there is a major concentration of lysosomes. Maturation of autophago-lysosomes and their retrograde trafficking are perturbed in Alzheimer's disease, which causes a massive concentration of autophagy elements along degenerating neurites. Transportation system is disturbed along defected microtubules in Alzheimer's disease brains. τ-protein has been found to control the stability of microtubules, however, phosphorylation of τ-protein or an increase in the total level of τ-protein can cause dysfunction of neuronal cells microtubules. Current evidence has shown that autophagy is developing in Alzheimer's disease brains because of ineffective degradation of autophagosomes, which hold amyloid precursor protein-rich organelles and secretases important for ß-amyloid peptides generation from amyloid precursor. The combination of raised autophagy induction and abnormal clearance of ß-amyloid peptide-generating autophagic vacuoles creates circumstances helpful for ß-amyloid peptide aggregation and accumulation in Alzheimer's disease. However, the key role of autophagy in Alzheimer's disease development is still under consideration today. One point of view suggests that abnormal autophagy induction causes a concentration of autophagic vacuoles rich in amyloid precursor protein, ß-amyloid peptide and the elements crucial for its formation, whereas other hypothesis points to marred autophagic clearance or even decrease in autophagic effectiveness playing a role in maturation of Alzheimer's disease. In this review we present the recent evidence linking autophagy to Alzheimer's disease and the role of autophagic regulation in the development of full-blown Alzheimer's disease.

Sporadic Alzheimer's disease begins as episodes of brain ischemia and ischemically dysregulated Alzheimer's disease genes.

The study of sporadic Alzheimer's disease etiology, now more than ever, needs an infusion of new concepts. Despite ongoing interest in Alzheimer's disease, the basis of this entity is not yet clear. At present, the best-established and accepted "culprit" in Alzheimer's disease pathology by most scientists is the amyloid, as the main molecular factor responsible for neurodegeneration in this disease. Abnormal upregulation of amyloid production or a disturbed clearance mechanism may lead to pathological accumulation of amyloid in brain according to the "amyloid hypothesis." We will critically review these observations and highlight inconsistencies between the predictions of the "amyloid hypothesis" and the published data. There is still controversy over the role of amyloid in the pathological process. A question arises whether amyloid is responsible for the neurodegeneration or if it accumulates because of the neurodegeneration. Recent evidence suggests that the pathophysiology and neuropathology of Alzheimer's disease comprises more than amyloid accumulation, tau protein pathology and finally brain atrophy with dementia. Nowadays, a handful of researchers share a newly emerged view that the ischemic episodes of brain best describe the pathogenic cascade, which eventually leads to neuronal loss, especially in hippocampus, with amyloid accumulation, tau protein pathology and irreversible dementia of Alzheimer type. The most persuasive evidences come from investigations of ischemically damaged brains of patients and from experimental ischemic brain studies that mimic Alzheimer-type dementia. This review attempts to depict what we know and do not know about the triggering factor of the Alzheimer's disease, focusing on the possibility that the initial pathological trigger involves ischemic episodes and ischemia-induced gene dysregulation. The resulting brain ischemia dysregulates additionally expression of amyloid precursor protein and amyloid-processing enzyme genes that, in addition, ultimately compromise brain functions, leading over time to the complex alterations that characterize advanced sporadic Alzheimer's disease. The identification of the genes involved in Alzheimer's disease induced by ischemia will enable to further define the events leading to sporadic Alzheimer's disease-related abnormalities. Additionally, knowledge gained from the above investigations should facilitate the elaboration of the effective treatment and/or prevention of Alzheimer's disease.

Brain ischemia activates ß- and γ-secretase cleavage of amyloid precursor protein: significance in sporadic Alzheimer's disease.

Amyloid precursor protein cleavage through ß- and γ-secretases produces ß-amyloid peptide, which is believed to be responsible for death of neurons and dementia in Alzheimer's disease. Levels of ß- and γ-secretase are increased in sensitive areas of the Alzheimer's disease brain, but the mechanism of this process is unknown. In this review, we prove that brain ischemia generates expression and activity of both ß- and γ-secretases. These secretases are induced in association with oxidative stress following brain ischemia. Data suggest that ischemia promotes overproduction and aggregation of ß-amyloid peptide in brain, which is toxic for ischemic neuronal cells. In our review, we demonstrated the role of brain ischemia as a molecular link between the ß- and the γ-secretase activities and provided a molecular explanation of the possible neuropathogenesis of sporadic Alzheimer's disease.

[Exposure to carbon monoxide toxicity as a cause for hospitalization of patients in the Children's Clinical Hospital in Lublin in the years 2006-2012]. / Narazenie na toksyczne dzialanie tlenku wegla jako przyczyna hospitalizacji pacjentów w Dzieciecym Szpitalu Klinicznym w Lublinie w latach 2006-2012.

Exposure to carbon monoxide (CO) accounts for a frequent cause for patient hospitalization in the Children's Clinical Hospital (DSK). The most common source of exposure includes the use of defective heating appliances operating on gas or coal and less frequently the fire toxic fumes. The purpose of the present study was to estimate the number of hospitalized patients in DSK in Lublin between the years 2006-2012 according to age, sex, urban-rural residence, season, carboxyheamoglobin (COHb) levels and hospitalization period. The subjects were assigned to three age groups: I - neonates and infants, II - children from 1 to 6 years of age, III - children aged between 7 to 17 years. In total 99 patients (50 female, 49 male) were admitted to hospital on account of carbon monoxide intoxication. Children aged 6 years and above constituted the most numerous age group. Furthermore 1 neonate and 5 infants (6.1%) and 43 children aged 1 to 6 years (43.4%) were hospitalized. The intoxications were visibly season-related. The highest frequency of CO poisoning lasted from October until March. The largest incidence was recorded in December and January. The majority of the children were urban residents - 67%, 33% were from rural areas. Carboxyhaemoglobin levels upon admission ranged from 0 to 26.7%. The average hospitalization lasted 2.4 days. Carbon monoxide intoxication remains a pressing health concern. The awareness of CO intoxication hazards among general public, application of appropriate first aid techniques, identification of clinical symptoms and treatment methods present the opportunity to save lives and reduce the long-term effects of CO poisoning.