Causes of the people death from drunkenness and alcoholism

We analyzed causes of 1008 people death, who abused by alcohol. Among them 2 groups were separated out: people died due to drunkenness and due to alcoholism. The structure of the death was similar in the both groups, however depended on alcoholism stages. The major cause of the death in group of drunkenness people was acute heart insufficiency, less commonly--lung pathology, and very rarely--brain vessels pathology and liver cirrhosis. In group of people, who died due to alcoholism, lung pathology was the major cause of these deaths, acute heart insufficiency was occurred less commonly, and very rare brain pathology because of delirium tremens or alcohol withdrawal syndrome, as so liver cirrhosis with complications. Hemorrhagic pancreonecrosis after alcoholic excess was found out in both groups, but it was more often in people, who died due to drunkenness. Obtained results show importance of chronic alcoholism identification as a disease with several stages including drunkenness and alcoholism.     

The role of respiratory control disorders in SIDS

Although sudden death in infants resulting from cardiac arrhythmias are well documented these appear to account for no more than 5-10% of SIDS cases. Sudden respiratory failure currently is viewed as the most likely cause of death in the remainder. Accidental asphyxiation appears to have a causal role in less then 50% of deaths diagnosed as SIDS. The rest are most likely do to some form of acute respiratory failure. Although failure of autoresuscitation or failure to arouse from sleep likely contribute to the final sequence of events leading to at least some SIDS deaths, these cannot be regarded as causes of the primary respiratory failure initiating the fatal sequence. Past and current studies provide strong circumstantial evidence that obstructive sleep apnea and/or apnea of prematurity likely account for respiratory failure leading to SIDS in some or many deaths. In drawing conclusions it is well to recognize that mechanisms leading to death in SIDS are heterogeneous and therefore there is room for several plausible theories for respiratory or circulatory abnormalities contributing to SIDS.     

54例心源性猝死患者心传导系统病变的分析

目的 探讨心源性猝死的死亡原因。方法 采用本组建立的心脏传导系统检查法,对１２０例心源性猝死者进行常规组织学检查。结果 发现５４例猝死与ＣＣＳ病变有关。猝死者８５．２％为年青人,２０－３０岁为猝死高峰年龄,男性我于女性。病变以ＣＣＳ炎症最多见,其后顺序是脂肪浸润,肥厚性心肌病伴发ＣＣＳ病变,出血,发育异常,心脏神经组织病变,纤维化及肿瘤等。     

Cardiac disease and risk of sudden death in the young: the burden of the phenomenon

Sudden cardiovascular death is a rare but catastrophic event in young men and women throughout the world. Sudden death is difficult to study. Factors that need elucidation are (1) the definition of sudden death; (2) diagnosis of the cause of sudden death; (3) the true incidence of sudden death, and (4) age and gender of individuals being studied. The “burden” of sudden death is far-reaching and involves medical, emotional, and economic burdens on the family members at risk, the entire family of the victim, and society in general. The pathologist trying to evaluate a case of sudden death also has a burden to make the correct diagnosis, especially since the cause of the sudden death may determine risk to the victim's family members. Sudden death is difficult to prevent since it may be the first and last manifestation of the cardiovascular disease. Also, paradoxically, the greatest number of deaths occurs in “low-risk” groups. The most common causes of cardiovascular deaths in the young are cardiomyopathy, coronary anomaly, obstructive coronary artery disease, myocarditis, valvular disease, channelopathy, and aortic disease leading to dissection or rupture. Many sudden deaths in the young occur during or shortly after exercise. Appropriate pre-participation screening of competitive athletes can reduce the incidence of sudden cardiovascular death in the young. Which measures to try to prevent these rare deaths are indicated and/or cost effective is a matter of discussion and controversy.     

Increased risk for lethal forms of liver disease among HBsAg-positive blood donors in the United States

We have used a death-record search to define the frequency of lethal outcomes of hepatitis B virus infection among a population of more than 15,000 overtly healthy blood donors found positive in routine HBsAg testing. We have compared the study population with a control group of some 18,000 donors selected on the basis of a negative test result. The index and control groups were observed for periods reflecting a total of 55 and 59 thousand person-years, respectively. Twenty percent of the 134 deaths identified among HBsAg positive donors were in some way liver related, including seven deaths due to hepatitis, seven to cirrhosis and six to hepatoma. In contrast, only one of the 95 deaths in the control population was liver related, and was due to fatty degeneration of the liver. The majority (four) of the hepatoma deaths occurred among blacks, three of whom were less than 35 at the time of death. In contrast, deaths from cirrhosis were all among whites. We conclude that there is significant mortality associated with the HBsAg positive state, even though the affected individuals may be asymptomatic and well enough to give blood at some stage. We estimate the standardised mortality ratio for hepatoma among HBsAg-positive persons in the United States is at least 27, confirming the association observed in other populations. The risk for hepatoma among young, HBsAg positive black males appears to approach that reported for HBsAg positive males in Taiwan. Data on the feasibility of AFP testing for early detection of hepatoma are included and discussed.     

Fatty acid oxidation disorders as primary cause of sudden and unexpected death in infants and young children: an investigation performed on cultured fibroblasts from 79 children who died aged between 0-4 years.

BACKGROUND: Disorders of fatty acid metabolism are known to be responsible for cases of sudden and unexpected death in infancy. At least 14 disorders are known at present. 120 cases of sudden infant death syndrome (SIDS) had been examined for a prevalent mutation (G985) causing medium chain acyl CoA dehydrogenase deficiency, which is inherited in an autosomal recessive mode. No over-representation of either homozygous or heterozygous cases was found. AIMS: To investigate a broader spectrum of fatty acid oxidation disorders in a wider range of sudden deaths in infants and young children. METHODS: Seventy nine cases of unexpected death in infants and young children younger than 4 years old were examined for a minimum of nine fatty acid oxidation disorders, using the global [9, 10-3H] myristic acid oxidation assay in cultured fibroblasts from achilles tendon biopsies taken at postmortem examination. RESULTS: Three cases with fatty acid oxidation disorders and two carriers of the G985 mutation were found, all categorized as non-SIDS or borderline SIDS. The global assay used has the advantage of simplicity. CONCLUSIONS: These results indicate that disorders of fatty acid oxidation play a small but significant role in the cause of unexpected death in infants and young children, and that infants and children dying in this way should be regarded as high risk candidates for metabolic diseases.     

Maximizing the effectiveness of the autopsy in cases of sudden death

Autopsies are essential in the investigation of sudden unexpected deaths. To maximize the effectiveness of the autopsy in these cases, the pathologist must assess the circumstances leading to the person's death, should be knowledgeable of the diseases most often responsible for sudden death, and should use dissection techniques most appropriate for their disclosure. In adults, the great majority of sudden deaths are cardiogenic and related to diseases of the coronary arteries, cardiac valves, or myocardium. In infants and young children, however, extracardiac diseases are prevalent in the causation of sudden deaths. Approximately one third of these are inexplicable (sudden infant death syndrome).     

Fatty acid ethyl esters in adipose tissue. A laboratory marker for alcohol-related death

Fatty acid ethyl esters, a family of ethanol metabolites, are formed by esterification of ethanol with fatty acids and have been detected in human organs commonly damaged by ethanol abuse. Because alcohol-related deaths may occur up to six times as often as reported on death certificates, we undertook quantitation of these potentially longer-lived alcohol metabolites in postmortem human adipose tissue to assess their usefulness as a measure of recent ethanol exposure. After isolation and identification using sequential thin-layer and gas chromatography, fatty acid ethyl esters were present in adipose tissue of chronic alcoholics (mean +/- SEM equals 300 +/- 46 nmol/g), even though blood ethanol concentration at the time of death was undetectable. Unintoxicated nonalcoholic subjects who had no history of alcohol abuse had concentrations seven times lower (mean +/- SEM equals 43 +/- 13 nmol/g). In vitro studies demonstrate that fatty acid ethyl esters are synthesized by human adipose tissue in proportion to the ethanol concentration present and their half-life in adipose tissue of laboratory animals is 16 +/- 1.6 hours, ie, fourfold greater than that of alcohol. These results indicate that fatty acid ethyl esters are long-lived ethanol metabolites whose persistence and accumulation in adipose tissue may allow an accurate diagnosis of significant alcohol consumption even when ethanol has been completely eliminated from the body.     

Sickle-cell trait as a risk factor for sudden death in physical training

Case reports of sudden death during exertion have not established an association between the sickle-cell trait (hemoglobin AS) and exercise-related death. To test this association, all deaths occurring among 2 million enlisted recruits during basic training in the U.S. Armed Forces in 1977 to 1981 were classified from autopsy and clinical records as non-sudden deaths or as sudden deaths explained or unexplained by preexisting disease. On the basis of known numbers of entering recruits (according to race, age, and sex) and published prevalence rates for hemoglobin AS (8 percent for black and 0.08 percent for nonblack recruits), death rates (per 100,000) were 32.2 for sudden unexplained deaths, 2.7 for sudden explained deaths, and 0 for non-sudden deaths among black recruits with hemoglobin AS, as compared with 1.2, 1.2, and 0.7 among black recruits without hemoglobin S and 0.7, 0.5, and 1.1 among nonblack recruits without hemoglobin S. Among black recruits the relative risk of sudden unexplained death (hemoglobin AS vs. non-hemoglobin S) was 27.6 (95 percent confidence interval, 9 to 100; P less than 0.001), whereas among all recruits this risk was 39.8 (95 percent confidence interval, 17 to 90; P less than 0.001). The relative risk of sudden unexplained death among all recruits increased with age (P less than 0.04), from 13 (ages 17 to 18) to 95 (ages 26 to 30). We conclude that recruits in basic training with the sickle-cell trait have a substantially increased, age-dependent risk of exercise-related sudden death unexplained by any known preexisting cause.     

Lymphocyte cytotoxicity for autologous human hepatocytes in alcoholic liver disease.

Alcoholic liver disease has been shown to progress even after cessation of ethanol intake and the involvement of an immunological mechanism has been suggested. To study whether lymphocyte cytotoxicity for autologous human hepatocytes is involved in the pathogenic process of alcoholic liver disease, hepatocytes (target cells) obtained by a needle liver biopsy from 36 patients with alcoholic liver disease were isolated by enzymatic digestion and incubated with autologous peripheral lymphocytes (effector cells). Using a microcytotoxicity assay, a cytotoxic effect was observed in patients with active cirrhosis or alcoholic hepatitis, but not in those with inactive cirrhosis, hepatic fibrosis or fatty liver. When lymphocytes were separated into T cell enriched and non-T cell enriched fractions, this cytotoxic effect was significantly greater with the non-T cell enriched lymphocyte fraction than with the T cell enriched fraction. The addition of aggregated IgG reduced the cytotoxic effect of the lymphocytes. These results suggested that antibody-dependent cell-mediated cytotoxicity may be of pathogenic importance in alcoholic liver disease.     

Investigation into sudden infant deaths and unascertained infant deaths in England and Wales, 1995-2003

This article investigates whether the decline in the sudden infant death rates and the rise in unascertained death rates during the period 1995-2003 were linked. It concludes that changes in certification practices surrounding sudden infant deaths and unascertained deaths suggest that it is becoming more difficult to distinguish between these two causes of death. In addition, there is a huge overlap in the characteristics of babies whose deaths are certified as sudden infant death and those whose death is unascertained. These terms are to some extent used interchangeably. Based on this evidence it seems appropriate to include both groups in any analysis of unexplained infant deaths.     

Dietary ethanol and cholesterol in Macaca nemestrina serum lipid and hepatic changes

This study was designed to evaluate the effects of alcohol ingestion on liver integrity in nonhuman primates consuming a fat-rich diet typical of North American humans. Nineteen young adult male Macaca nemestrina were studied for 18 months. A 2 × 2 factorial design was used such that two groups received a liquid diet with ethanol as 36% of calories and two groups received an elevated dietary cholesterol level of 1.0 mg/kcal. Intereactions between the effects of ethanol and cholesterol were determined. Significant effects of ethanol were found, with the most pronounced of these including increased serum and liver triglyceride concentrations. Dietary cholesterol induced significant increases in serum cholesterol and liver cholesterol concentrations. Significant interactions between ethanol and cholesterol were found in the elevation of liver triglyceride, and serum cholesterol and triglyceride concentrations. Ethanol-fed animals developed fatty livers with giant mitochondria but not alcoholic hepatitis or cirrhosis. Hepatic lipidosis and megamitochondria were apparent after 6 months, and progression in their severity from 6 to 18 months was minimal. Massive hepatic fat accumulation during 18 months of alcohol ingestion with fat-rich diets was not sufficient to cause further hepatic degeneration in these primates.     

Cosleeping and sudden unexpected death in infancy

CONTEXT: The practice of infants cosleeping with adults has long been the subject of controversy. Autopsy findings in cases of sudden infant death syndrome (SIDS) are usually indistinguishable from those found with unintentional or intentional suffocation, and the determination of the cause of death in cases of sudden unexpected death in infancy is often based on investigative findings and the exclusion of natural or traumatic causes. OBJECTIVE: To further elucidate the risk of cosleeping. METHODS: We reviewed 58 cases of sudden unexpected infant deaths. Cases were excluded if there was any significant medical history or evidence of trauma or abuse. RESULTS: Twenty-seven of the infants were cosleeping. Eleven of these cases had been previously diagnosed as SIDS, and in 7 cases parental intoxication was documented. CONCLUSION: Our findings support recent studies that suggest that cosleeping or placing an infant in an adult bed is a potentially dangerous practice. The frequency of cosleeping among cases diagnosed as SIDS in our study suggests that some of these deaths may actually be caused by mechanical asphyxia due to unintentional suffocation by the cosleeping adult and/or compressible bedding materials.     

Right ventricular dysplasia associated with sudden death in young adults.

The frequency of right ventricular dysplasia (RVD) in an autopsy series of young persons with sudden cardiac death in the United States has not been previously reported. We reviewed the autopsies from cases of sudden cardiac deaths in young adults in the state of Maryland and noted three cases of RVD among 547 cardiac deaths (0.55%). These three cases of RVD in young adults and three additional cases from our file are presented. Their ages ranged from 19 to 28 yr, and there were five males and one female. Five deaths occurred during strenuous exercise while the sixth was unwitnessed. Three of these cases had a documented history of arrhythmias and 1 had palpitations. In each case, autopsy revealed right ventricular dilatation with partial absence of the myocardium and extensive fatty infiltrates with and without fibrosis. In four cases, collections of chronic lymphocytic infiltrates were seen, of which two had associated myocyte necrosis. In one patient, the disease was familial, while in the remaining five it was sporadic, suggesting a nongenetic cause.     

Morphological investigation of two sibling autopsy cases of mitochondrial trifunctional protein deficiency

Two sibling autopsy cases of type 2 mitochondrial trifunctional protein (MTP) deficiency are described. MTP is an enzyme complex involved in the mitochondrial beta-oxidation of fatty acids, which is the major pathway for energy production in heart and skeletal muscle. Both cases showed similar pathological findings. Numerous small foci of degeneration of muscle cells and cardiac myocytes were detected. Some of these cells had condensed or fragmented nuclei and most of them were positively stained using the deoxyuridine triphosphate nick-end labeling method. The lipid staining of both cases showed a small- to medium-sized fatty, vesicular morphology for liver cells, muscle cells, cardiac myocytes and proximal tubular cells of the kidney. Bone marrow was severely hypoplastic, and cortical thymocytes were markedly reduced in number. Neither case had hepatic fibrosis nor cirrhosis. The definitive diagnosis of type 2 MTP deficiency was made by verifying completely defective MTP-alpha and MTP-beta subunits in cultured skin fibroblasts of one of 2 patients. Our patients' signs indicate that there is a wider pathological spectrum of type 2 MTP deficiency, while very few autopsy cases of type 2 MTP deficiency have been confirmed. Pathologists should consider the possibility of type 2 MTP deficiency or other beta-oxidation defects in cases of sudden infant death, fatty infiltration of viscera or cardiomyopathy.     

Hepatic triglyceride accumulation and the ethanol physical withdrawal syndrome in mice.

Physical dependence on ethanol was induced in TO strain mice by chronic administration of ethanol by inhalation. The severity of the behavioral syndrome of withdrawal from ethanol was quantified by a subjective scoring method. During the chronic administration of ethanol, triglycerides accumulated in livers of male or female mice with a time course similar to that of the induction of physical dependence. When ethanol was withdrawn from adult or weaning dependent mice, a relationship was observed between the decline of triglyceride concentrations in liver and the duration of the ethanol withdrawal syndrome. The addition of DL-carnitine (7% w/w) to diet during the administration of ethanol markedly inhibited the accumulation of triglycerides, and significantly reduced the intensity of the ethanol withdrawal syndrome. Administration of carbon tetrachloride ((1.3 ml/kg i.p.), however, although augmenting hepatic triglyceride accumulation, had no significant effect on the withdrawal syndrome. The results are interpreted as suggesting either that ethanol-induced liver dysfunction plays a part in dependence, or, more likely, that triglyceride accumulation reflects an ethanol-induced metabolic disorder which is itself related to the induction of dependence.     

Alcohol induced liver disease.

Alcohol induces a variety of changes in the liver: fatty change, hepatitis, fibrosis, and cirrhosis. The histopathological appearances of these conditions are discussed, with special attention to differential diagnosis. Many forms of alcoholic liver disease are associated with Mallory body formation and fibrosis. Mallory bodies are formed, at least in part, from intermediate filaments. Associated changes in intermediate filament organisation in alcoholic liver disease also occur. Their significance in the pathogenesis of hepatocyte death may be related to abnormalities in messenger RNA function. The mechanisms underlying hepatic fibrogenesis are also discussed.     

心脏传导系统部位肿瘤的形态观察

目的观察心脏传导系统部位的肿瘤发病率及其与猝死关系。方法采用本组建立的心脏传导系统检查法,对无心外原因猝死者１４９例及死于非心脏疾病者７３７例作组织学检查。结果发现１２例心脏传导系统有肿瘤,占１．３５％,加上会诊１例共１３例。其中原发性良性心脏肿瘤累及心脏传导系统１０例,转移性恶性肿瘤３例。１０例良性肿瘤主要为纤维瘤、血管瘤、心房间隔脂肪瘤样肥厚、房室结间皮瘤和横纹肌瘤,其中８例位于窦房结和房室结,转移瘤全部累及窦房结。１３例中３例引起猝死。结论心脏传导系统肿瘤是可致猝死的人体最小肿瘤。     

Retrospective review of Japanese sudden unexpected death in infancy: the importance of metabolic autopsy and expanded newborn screening

Sudden unexpected death in infancy is defined as sudden unexpected death occurring before 12 months of age. The common causes of sudden unexpected death in infancy are infection, cardiovascular anomaly, child abuse, and metabolic disorders. However, the many potential inherited metabolic disorders are difficult to diagnose at autopsy and may therefore be underdiagnosed as a cause of sudden unexpected death in infancy. In the present study we retrospectively reviewed 30 Japanese sudden unexpected death in infancy cases encountered between 2006 and 2009 at our institute. With postmortem blood acylcarnitine analysis and histological examination of the liver, we found two cases of long-chain fatty acid oxidation defects. Molecular analysis revealed that the one patient had a compound heterozygote for a novel mutation (p.L644S) and a disease-causing mutation (p.F383Y) in the carnitine palmitoyltransferase 2 gene. Furthermore, retrospective acylcarnitine analysis of the newborn screening card of this patient was consistent with carnitine palmitoyltransferase II deficiency. Metabolic autopsy and expanded newborn screening would be helpful for forensic scientists and pediatricians to diagnose fatty acid oxidation disorders and prevent sudden unexpected death in infancy.