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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of pulmonary neuroendocrine cells (PNEC) was analyzed immunohistochemically in 14 victims of sudden infant death syndrome (SIDS), and 10 cases of infant death unrelated to SIDS, excluding congenital heart disease. Lung tissue sections were immunostained with antibodies against chromogranin A (CGA), calcitonin (CT) and gastrin-releasing peptide (GRP). CT/GRP immunoreactivity decreased in older infants of each group, while CGA immunoreactivity showed almost no decrease. Serial section analysis showed some PNEC produced CGA, CT and GRP. However, CGA-immunoreactive PNEC sometimes lacked of CT/GRP immunoreactivity. The difference of PNEC distribution between SIDS and the control cases could not be verified. To date, there have been no studies reported of PNEC distribution in infants by using CGA expression. CGA is considered to be the most useful marker for detecting PNEC in infant lung. Our findings suggest that substances produced by PNEC changed with postnatal development both in SIDS and the control group. This result may be one clue to clarifying the development and function of small airways in infants, allowing further progress in SIDS research.
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PMID:[Distribution of pulmonary neuroendocrine cells--an immunohistochemical study of the lung in autopsied infants including sudden infant death syndrome]. 780 12

A perinatal death presenting as a possible homicide is reported. An infant was born with a cleft palate, but without other apparent abnormality, to a mother who experienced postpartum depression. The infant apparently died during feeding. A death certificate, giving cot death and congenital malformations as the causes of death, was rejected by the registering authority. The possibility of homicide was considered. Exhumation and autopsy showed multiple abnormalities, including congenital heart disease and the karyotype of DiGeorge's anomaly. The case highlights the value of the autopsy in such cases, and emphasizes the role of cytogenetics, even after considerable postmortem delay.
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PMID:Infant death due to congenital abnormalities presenting as a homicide. 831 Oct 51

Post-mortem hypoxanthine concentrations in the vitreous humor of human infants were investigated. Hypoxanthine is formed from hypoxic degradation of adenosine monophosphate. The concentrations in the vitreous humor can give information about antemortem hypoxia. The post-mortem levels were corrected for the time elapsing between death and the autopsy. Four groups of infants were compared: 17 babies who died of respiratory distress syndrome (RDS), 72 infants who died of sudden infant death syndrome (SIDS), 23 children dying of congenital heart disease (both cyanotic and acyanotic), and 15 children dying acutely in accidents without any known significant time of hypoxia before death. The corrected, median hypoxanthine levels in victims of SIDS (200 mumol/L) was significantly higher (p < 0.01) than in the accident group (0 mumol/L), but no clear difference was found between the SIDS group and the RDS group (101 mumol/L), or the heart group (54 mumol/L). A number of children with "normal" hypoxanthine levels (0 to 38 mumol/L) were found in all four groups, but the numbers were significantly lower (p < 0.005) in the RDS, SIDS and heart groups than in the accident group. It is concluded that SIDS is probably not a sudden event, but may be preceded by relatively long, or repeated intermittent periods of hypoxia (of unknown etiology).
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PMID:Post-mortem concentrations of hypoxanthine in the vitreous humor--a comparison between babies with severe respiratory failure, congenital abnormalities of the heart, and victims of sudden infant death syndrome. 851 58

A total of 206 cases of sudden infant deaths examined at the Institute of Science and Forensic Medicine, Singapore, over a 5 year period (1989-93) were identified to assess the pattern of sudden death in this age group, which was subdivided into the neonatal and post-neonatal periods. A total of 34% (70) of infant deaths occurred in neonatal life and the remaining 66% (136) in the post-neonatal period; 90% of the neonatal deaths were natural, of which over half were due to congenital heart disease and complications of prematurity. Unnatural deaths in this period were uncommon, there being only seven such deaths. In the post-neonatal period, unnatural deaths constituted 25% of the total with trauma and aspiration heading the list. Natural deaths in the post-neonatal period are predominantly due to infections (34%) and a group of sudden natural deaths with minimal findings (31%). The latter group may arguably represent cases of Sudden Infant Death Syndrome (SIDS). The yearly incidence of this group in our study varied between 0.08 to 0.2 per 1000 live births, which is considerably lower than the incidence quoted for Western populations. The criteria for the classification and the impact of sudden infant deaths in Asian countries are discussed.
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PMID:Sudden infant death in a tropical environment: Singapore's experience. 863 69

Environmental tobacco smoke is a complex mixture of many chemical substances. The term passive smoking is used when a person breathes in air contaminated by tobacco smoke. Active and passive smoking expose an individual to the same substances, but the relative concentrations of the various substances differ. Thus, under conditions where individuals are exposed to an amount of nicotine corresponding to their smoking 1/2 a cigarette, they will be exposed to an amount of nitrosodimethylamine corresponding to their smoking about five cigarettes. Exposure of children to environmental tobacco smoke is associated with increased risk of lower respiratory tract infections, middle ear infections and asthma. Accumulating evidence points to passive smoking as a risk factor for the sudden infant death syndrome. Long term exposure to environmental tobacco smoke increases risk of lung cancer and heart disease. It is estimated that in Norway, 50 non-smokers die of lung cancer and 300-500 of heart disease annually, as a result of long term exposure to environmental tobacco smoke.
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PMID:[Health damages from passive smoking]. 865 89

To examine whether pulmonary neuroendocrine cells (PNEC) is associated with sudden infant death syndrome (SIDS), distribution and function of PNEC were investigated in infants from one to twelve months of age, including 19 cases with SIDS and 18 control cases without congenital heart disease and premature birth. In this study, lung tissue sections were immunostained with antibodies against chromogranin A (CGA) and calcitonin gene-related peptide (CGRP). Although the positivity of CGA in SIDS cases was not significantly different from that in control, the positivity of CGRP in SIDS cases was lower than that in control cases among one to four months old (p < 0.05). Our results suggest that respiratory and/or circulatory regulation of cases with SIDS is disturbed by reduction of CGRP expression, because CGRP is well known to be a vasodilator, a neurotransmitter and a promoter for proliferation of epithelium in airways.
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PMID:[Immunohistochemical study on pulmonary neuroendocrine cells containing calcitonin gene-related peptide in sudden infant death syndrome]. 959

One study after another is finding strong associations between a variety of human illness and exposure to environmental tobacco smoke (ETS). A 1986 report by the U.S. Surgeon General concluded that ETS is a cause of disease, including lung cancer, in healthy nonsmokers. Other reports have documented causal associations between ETS and lower respiratory tract infections, middle ear disease and exacerbation of asthma in children, heart disease, retardation of fetal growth, sudden infant death syndrome, and nasal sinus cancer. However, the findings from many of these studies remain controversial. A number of scientists remain skeptical about the association between ETS and serious illness in nonsmokers, charging that scientific journals either fail to publish pro-tobacco findings and meta-analyses or disregard those that are published. They also claim that many epidemiological studies declare causal associations based on marginal odds ratios.
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PMID:Double exposure. Environmental tobacco smoke. 1044 19

Sudden infant death syndrome (SIDS) occurs silently usually during sleep and, though remaining unexplained after autopsy, leaves footprints creating a pattern analogous to that which follows a flood of nitric acid (NO). These footprints in SIDS are associated with serious pathological changes, viz. elevated hepatic iron, bone marrow hyperplasia, hypomyelinated respiratory control centres, elevated lung immunoglobulins, cerebral hypoperfusion resembling lesions induced by chronic hypoxemia, ischemia, congenital heart disease and congenital myopathy. Hypoxia stimulates the immune response and the over-arousal of the immune response triggers a flood of NO. Adenosine triggers sleep. NO and adenosine are additive as dilators of coronary blood vessels. Blood pressure collapses. Selenium increases the activity of the enzyme ferrochelatase during incorporation of heme into cytochrome oxidase. NO binds to cytochrome oxidase, inhibiting respiration. When NO reaches dangerous levels, the cell turns on production of heme oxygenase. Heme is broken down to iron (Fe) carbon monoxide (CO) and bile pigments. NO has a huge affinity for hemoglobin which catalyses NO degradation to nitrate. Furthermore, NO is a product of smoke and SIDS incidence is higher in smoking mothers.
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PMID:Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload. 1079 Jul 39

Although sudden infant death syndrome (SIDS) is a cause for sudden infant death, other causes should be ruled out before diagnosing SIDS. Cardiac causes for sudden infant death include viral myocarditis, congential heart disease particularly congential aortic stenosis, endocardial fibroelastosis, and anomalous origin of the left coronary artery from the pulmonary artery. Other cardiac conditions that may result in sudden death include rhabdomyomas of the heart in tuberous sclerosis and conduction system disorders. The most frequent conduction system disorders resulting in sudden death include histiocytoid cardiomyopathy, congential heart block that may be associated with maternal lupus erythematosus, arrhythmogenic right ventricular dysplasia, noncompaction of the left ventricle, and long QT syndromes.
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PMID:Cardiovascular causes for sudden infant death. 1194 36

It has been proposed that the presence of siderophages in the lungs of infants who die unexpectedly should be considered a marker of a previous hypoxic event, which may preclude a diagnosis of sudden infant death syndrome. The authors retrospectively reviewed all infant deaths (<1 year old) going to autopsy at the Denver Office of the Medical Examiner from January 1999 to January 2001. Lung sections were stained with Prussian blue, and siderophages were counted in 20 high-power fields per lobe sampled. Cell counts were performed by two independent pathologists who were blinded to history and cause of death, with good reproducibility. Iron stain results were then categorized by average number of siderophages per 20 high-power field (category 1 = <5, category 2 = 5-100, category 3A = 100-500, category 3B = >100 in a single lobe, category 4 = >500). The results were subsequently correlated to case history, autopsy findings, and cause/manner of death. Forty-three cases were reviewed. The causes of death included sudden infant death syndrome (16), asphyxia (5), undetermined (6), and other (16). Those deaths were categorized by the above criteria as follows: category 1. (32), category 2. (6), category 3. (4), and category 4. (1). All sudden infant death syndrome deaths were in category 1. Categories 1 and 2 also included deaths in which hypoxia might have been present before death because of such factors as pneumonia and congenital heart disease. Categories 3 and 4 included a known homicidal asphyxia in which repeated episodes of intentional smothering were documented, 2 probable asphyxias, 1 nonaccidental trauma, and 1 undetermined. All 5 cases had questionable circumstances surrounding the death of the infant. Pulmonary siderophages were described in only 1 of the 43 autopsy reports. It was concluded that pulmonary siderophages can be markedly increased in cases of repeated asphyxia. Siderophages may also be increased in cases where hypoxia may have been present for another reason, but not to the same degree. Siderophages are not increased in sudden infant death syndrome. Because iron-laden macrophages often are not recognized on routine examination with hematoxylin and eosin staining, iron stains may be helpful in the evaluation of infant deaths. If siderophages are present in increased amounts without an obvious explanation, further investigation is warranted.
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PMID:Pulmonary siderophages and unexpected infant death. 1246 13


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