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Abdominal trauma during thirty years: analysis of a large case series.

https://arctichealth.org/en/permalink/ahliterature40679
Source
Injury. 1981 Sep;13(2):93-9
Publication Type
Article
Date
Sep-1981
Author
D. Bergqvist
H. Hedelin
G. Karlsson
B. Lindblad
T. Mätzsch
Source
Injury. 1981 Sep;13(2):93-9
Date
Sep-1981
Language
English
Publication Type
Article
Keywords
Abdominal Injuries - epidemiology - etiology
Accidents, Traffic
Adolescent
Adult
Aged
Child
Child, Preschool
Female
Humans
Infant
Kidney - injuries
Liver - injuries
Male
Middle Aged
Retrospective Studies
Seasons
Spleen - injuries
Sweden
Abstract
Studies have been made in 1407 patients of the causes, the organs involved and the outcome of injury to the abdomen in patients needing admission to hospital in an area of Southern Sweden, between 1950 and the end of 1979. The proportion of female patients and those aged over 60 increased significantly. The seasonal distribution of the injuries showed significant change, with a drop in the initially high frequency sustained during the summer months. Penetrating injuries were rare, but increased in the 1970s. Road traffic accidents as the cause of abdominal injuries rose to a maximum of 56 per cent in the late 1960s. The numbers of injured organs and the frequency of other associated injuries rose gradually until the mid-1970s, after which there was a slight decrease. The spleen, liver and large blood vessels were the organs which were increasingly often injured. The annual incidence of various visceral injuries per 100 000 population was calculated. The number of patients with a delay of at least 24 hours before operation fell significantly and there was a tendency to shorter hospital stay. The mortality curve showed a peak in the late 1960s.
PubMed ID
7327735 View in PubMed
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[Absorptive and excretory functions of the liver in chronic gastritis and peptic ulcer in children]

https://arctichealth.org/en/permalink/ahliterature42369
Source
Pediatr Akus Ginekol. 1976 Mar-Apr;(2):10-2
Publication Type
Article

[A case of congenital hepatic polycystosis in a child 1 year and 6 months old]

https://arctichealth.org/en/permalink/ahliterature28236
Source
Pediatriia. 1973 Feb;52(2):25
Publication Type
Article
Date
Feb-1973
Author
V P Brei
Source
Pediatriia. 1973 Feb;52(2):25
Date
Feb-1973
Language
Ukrainian
Publication Type
Article
Keywords
Child, Preschool
Cysts - congenital
Follow-Up Studies
Humans
Liver Diseases - congenital
Male
PubMed ID
4702248 View in PubMed
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Acquired aplastic anaemia in seven children with severe hepatitis with or without liver failure.

https://arctichealth.org/en/permalink/ahliterature87545
Source
Acta Paediatr. 2007 Nov;96(11):1660-4
Publication Type
Article
Date
Nov-2007
Author
Honkaniemi Emma
Gustafsson Britt
Fischler Björn
Nemeth Antal
Frost Britt-Marie
Papadogiannakis Nikos
Winiarski Jacek
Author Affiliation
Department of Paediatrics, Karolinska University Hospital, Huddinge, Clintec, Karolinska Institutet, S-141 86 Stockholm, Sweden. emma.honkaniemi@karolinska.se
Source
Acta Paediatr. 2007 Nov;96(11):1660-4
Date
Nov-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Anemia, Aplastic - etiology - therapy
Biopsy
Bone Marrow Cells - pathology
Bone Marrow Transplantation
Child
Child, Preschool
Female
Hepatitis - complications - pathology - physiopathology
Humans
Liver - pathology
Liver Failure - etiology
Male
Medical Records
Parvovirus - pathogenicity
Retrospective Studies
Serologic Tests
Sweden
Time Factors
Abstract
AIM: Aplastic anaemia following hepatitis may develop in as many as 1 of 3 patients with non-A, non-B and non-C hepatitis. Several causative factors have been discussed, such as viral infections and autoimmunity. Here we describe the natural history of this condition in 7 children and investigate possible hepatitis-causing agents. METHODS: We reviewed the medical records, bone marrow and liver biopsies of 7 children with severe hepatitis, with or without liver failure, who subsequently had developed aplastic anaemia. RESULTS: The median time from onset of hepatic symptoms until diagnosed onset of aplasia was 54 days. No associated viral infections could be identified. On liver biopsy, a majority had lobular inflammation but lacked signs of autoimmune hepatitis, findings compatible with a viral aetiology. Three of 6 children had low reticulocyte counts already at onset of hepatitis. All, but one patient is alive at median follow-up of 8 years. CONCLUSION: The unknown pathogenetic mechanism appears to target liver and bone marrow simultaneously, because half of the children concomitantly had low reticulocyte counts and severe liver failure.
PubMed ID
17888058 View in PubMed
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Acute liver failure in children: the first 348 patients in the pediatric acute liver failure study group.

https://arctichealth.org/en/permalink/ahliterature169060
Source
J Pediatr. 2006 May;148(5):652-658
Publication Type
Article
Date
May-2006
Author
Robert H Squires
Benjamin L Shneider
John Bucuvalas
Estella Alonso
Ronald J Sokol
Michael R Narkewicz
Anil Dhawan
Philip Rosenthal
Norberto Rodriguez-Baez
Karen F Murray
Simon Horslen
Martin G Martin
M James Lopez
Humberto Soriano
Brendan M McGuire
Maureen M Jonas
Nada Yazigi
Ross W Shepherd
Kathleen Schwarz
Steven Lobritto
Daniel W Thomas
Joel E Lavine
Saul Karpen
Vicky Ng
Deirdre Kelly
Nancy Simonds
Linda S Hynan
Author Affiliation
University of Pittsburgh, Children's Hospital of Pittsburgh, PA 15213, USA. Robert.squires@chp.edu
Source
J Pediatr. 2006 May;148(5):652-658
Date
May-2006
Language
English
Publication Type
Article
Keywords
Adolescent
Canada - epidemiology
Child, Preschool
Cohort Studies
Databases, Factual
Female
Great Britain
Health status
Humans
Infant
Infant, Newborn
Liver Failure, Acute - diagnosis - epidemiology - therapy
Liver Transplantation
Male
Needs Assessment
Predictive value of tests
Prognosis
United States - epidemiology
Abstract
To determine short-term outcome for children with acute liver failure (ALF) as it relates to cause, clinical status, and patient demographics and to determine prognostic factors.
A prospective, multicenter case study collecting demographic, clinical, laboratory, and short-term outcome data on children from birth to 18 years with ALF. Patients without encephalopathy were included if the prothrombin time and international normalized ratio remained > or = 20 seconds and/or >2, respectively, despite vitamin K. Primary outcome measures 3 weeks after study entry were death, death after transplantation, alive with native liver, and alive with transplanted organ.
The cause of ALF in 348 children included acute acetaminophen toxicity (14%), metabolic disease (10%), autoimmune liver disease (6%), non-acetaminophen drug-related hepatotoxicity (5%), infections (6%), other diagnosed conditions (10%); 49% were indeterminate. Outcome varied between patient sub-groups; 20% with non-acetaminophen ALF died or underwent liver transplantation and never had clinical encephalopathy.
Causes of ALF in children differ from in adults. Clinical encephalopathy may not be present in children. The high percentage of indeterminate cases provides an opportunity for investigation.
Notes
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Cites: Yale J Biol Med. 1984 Mar-Apr;57(2):161-846433587
Cites: Pediatr Clin North Am. 1986 Jun;33(3):691-7013714342
Cites: J Pediatr. 1987 Sep;111(3):313-93625398
Cites: Hepatology. 1992 Nov;16(5):1156-621427654
Cites: J Gastroenterol Hepatol. 1996 Jun;11(6):560-58792311
Cites: Hepatology. 1997 Mar;25(3):541-79049195
Cites: J Pediatr Gastroenterol Nutr. 1997 Feb;24(2):128-349106097
Cites: Pediatr Neurol. 1997 May;16(4):337-439258971
Cites: J Pediatr. 1998 Jan;132(1):22-79469995
Cites: Hepatology. 1998 Apr;27(4):1050-59537445
Cites: Pediatr Neurol. 1998 Mar;18(3):251-29568923
Cites: Dig Dis Sci. 1998 Jun;43(6):1311-69635624
PubMed ID
16737880 View in PubMed
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Acute liver failure meets SOPH syndrome: A case report on an intermediate phenotype.

https://arctichealth.org/en/permalink/ahliterature283558
Source
Pediatrics. 2017 Jan;139(1)
Publication Type
Article
Date
Jan-2017
Author
Fanny Kortüm
Iris Marquardt
Malik Alawi
Georg Christoph Korenke
Stephanie Spranger
Peter Meinecke
Kerstin Kutsche
Source
Pediatrics. 2017 Jan;139(1)
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
Alleles
Child, Preschool
DNA Mutational Analysis
Developmental Disabilities - diagnosis - genetics
Dwarfism - diagnosis - genetics
Exome - genetics
Female
Heterozygote Detection
Humans
Liver Failure, Acute - diagnosis - genetics
Mutation, Missense - genetics
Neoplasm Proteins - deficiency - genetics
Optic Atrophy - diagnosis - genetics
Pelger-Huet Anomaly - diagnosis - genetics
Phenotype
Syndrome
Abstract
Acute liver failure (ALF) is a life-threatening condition in the absence of preexisting liver disease in children. The main clinical presentation comprises hepatic dysfunction, elevated liver biochemical values, and coagulopathy. The etiology of ALF remains unclear in most affected children; however, the recent identification of mutations in the neuroblastoma amplified sequence (NBAS) gene in autosomal recessively inherited ALF has shed light on the cause of a subgroup of fever-triggered pediatric ALF episodes. Previously, biallelic mutations in NBAS have been reported to be associated with a syndrome comprising short stature, optic atrophy, and Pelger-Huët anomaly (SOPH) specifically occurring in the Yakut population. No hepatic phenotype has been observed in individuals with this disorder who all carry the homozygous NBAS founder mutation c.5741G>A [p.(Arg1914His)]. We present the case of a 4-year-old girl with the cardinal features of SOPH syndrome: characteristic facial dysmorphism, postnatal growth retardation, delay of bone age, slender long bones, optic atrophy, and Pelger-Huët anomaly. During the first 2 years of her life, a series of infections with episodes of fever were accompanied by elevated liver enzyme levels, but hyperammonemia, hypoglycemia, coagulopathy, or encephalopathy suggestive of acute and severe liver disease were never observed. Whole exome sequencing in the patient revealed compound heterozygosity of the 2 NBAS variants, p.(Arg1914His) and p.(Glu943*). This case highlights the variability of clinical presentation associated with NBAS deficiency. Absence of severe liver problems in this case and SOPH-affected Yakut subjects suggests that individuals carrying the NBAS missense mutation p.(Arg1914His) are less susceptible to developing ALF.
PubMed ID
28031453 View in PubMed
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Adiposity, cardiac size and precursors of coronary atherosclerosis in 5 to 15-year-old children: a retrospective study of 210 violent deaths.

https://arctichealth.org/en/permalink/ahliterature34179
Source
Int J Obes Relat Metab Disord. 1997 Aug;21(8):691-7
Publication Type
Article
Date
Aug-1997
Author
M L Kortelainen
Author Affiliation
Department of Forensic Medicine, University of Oulu, Kajaanintie 52 D, 90220 Oulu 22, Finland.
Source
Int J Obes Relat Metab Disord. 1997 Aug;21(8):691-7
Date
Aug-1997
Language
English
Publication Type
Article
Keywords
Adipose Tissue - anatomy & histology
Adolescent
Arteriosclerosis
Autopsy
Body Height
Body Weight
Cardiomegaly - etiology
Child
Child, Preschool
Comparative Study
Coronary Vessels - anatomy & histology
Female
Heart - anatomy & histology
Humans
Kidney - anatomy & histology
Linear Models
Liver - anatomy & histology
Male
Obesity - complications
Organ Size
Retrospective Studies
Sex Factors
Abstract
OBJECTIVE: To determine the relationship between cardiac size and various measures of adiposity in children and the occurrence of coronary fatty streaks in relation to childhood obesity. DESIGN: A retrospective study based on 210 medico-legal autopsies of 5-15 y old children who had suffered violent death in the Province of Oulu, Finland, in 1970-1995. METHODS: Autopsy reports with attached clinical data and police records were recovered from the archives of the Department of Forensic Medicine, University of Oulu, Finland. All 5-15 y old individuals who had died of external trauma and were not documented as having had any chronic illnesses were chosen for investigation. The following data were extracted from the papers: age, sex, height, body weight, heart weight, liver weight, total weight of the kidneys, thickness of the abdominal subcutaneous fat and description of the coronary arteries. Heart weight was indexed to height2.7, and liver weight and kidney weight were indexed to body weight, body surface area and height. The ponderal index (body weight/height3) was calculated, and relative body weight was determined as the percentage deviation of the weight from the mean weight for height according to a growth chart developed for Finnish children. RESULTS: The average absolute heart weight and heart weight/height2.7 were significantly higher in the boys than in the girls over 12 y of age. Abdominal subcutaneous fat was thicker in the girls, but there were no significant differences in the other indicators of obesity. After adjusting for age, there were significant positive correlations between the ponderal index and heart weight/height2.7 in both the boys (P = 0.000) and the girls (P = 0.038), between relative body weight and heart weight/height2.7 in the boys (P = 0.000) and the girls (P = 0.027), and between abdominal subcutaneous fat thickness and heart weight/height2.7 in the boys (P = 0.045) but not in the girls (P = 0.234). Multiple linear regression analysis showed the ponderal index to be a significant predictor of heart weight/height2.7. Coronary intimal fatty streaks were documented in six individuals (2.9%), five of them having a ponderal index above the average and all of them having a relative weight above the average. Kidney weights were higher in the boys and were positively correlated with the measures of obesity and with heart weight/height2.7. CONCLUSIONS: The results point to an important role of excess body weight and adiposity in the development of early myocardial and coronary changes in childhood: coronary fatty streaks were not found at all in the leanest individuals in this relatively large group and the cardiac size adjusted for body size indicated hypertrophy with increasing adiposity. Prospective autopsy studies are needed in order to determine whether adiposity and the regional distribution of fat, especially intra-abdominal fat accumulation, are associated with the earliest signs of myocardial hypertrophy and the initial phase of lesion development in the arterial intima of children.
PubMed ID
15481770 View in PubMed
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Age at diagnosis and disease progression of cystic fibrosis in an area without newborn screening.

https://arctichealth.org/en/permalink/ahliterature101753
Source
Paediatr Perinat Epidemiol. 2011 May;25(3):298-305
Publication Type
Article
Date
May-2011
Author
Isabelle de Monestrol
Asa Klint
Pär Sparén
Lena Hjelte
Author Affiliation
Stockholm CF Centre, Karolinska University Hospital Huddinge, Stockholm, Sweden. isabelle.demonestrol@ki.se
Source
Paediatr Perinat Epidemiol. 2011 May;25(3):298-305
Date
May-2011
Language
English
Publication Type
Article
Keywords
Age Distribution
Age Factors
Child, Preschool
Cystic Fibrosis - diagnosis - epidemiology
Disease Progression
Female
Humans
Infant
Infant, Newborn
Liver Diseases - diagnosis - epidemiology
Lung Diseases - diagnosis - epidemiology
Male
Morbidity
Nutrition Disorders - diagnosis - epidemiology
Risk factors
Sweden - epidemiology
Abstract
We studied age at diagnosis and disease progression of cystic fibrosis (CF) patients with a new study design, using data of 119 patients extracted from Stockholm CF Centre registry. Risk factors for overall morbidity and for lung, liver and nutritional morbidity were investigated separately using time to event methodology (Kaplan-Meier curves, proportional hazards regression). The patients were followed from: (i) healthy at diagnosis to morbidity, (ii) diagnosis with symptoms of morbidity to being free of morbidity, and (iii) free of morbidity to relapse of morbidity. Median age at diagnosis was 5.0 months. Of the patients with overall morbidity at diagnosis 50% became free of morbidity after 4.8 years; however, the patients above the age of 24 months at diagnosis had a reduced chance of becoming free of morbidity (crude hazard ratio 0.14 [95 % confidence interval 0.04, 0.45]) compared with those with diagnosis between the ages of 2 and 12 months (P
PubMed ID
21470269 View in PubMed
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Alcohol-attributable deaths and years of potential life lost among American Indians and Alaska Natives--United States, 2001--2005.

https://arctichealth.org/en/permalink/ahliterature92278
Source
MMWR Morb Mortal Wkly Rep. 2008 Aug 29;57(34):938-41
Publication Type
Article
Date
Aug-29-2008
Source
MMWR Morb Mortal Wkly Rep. 2008 Aug 29;57(34):938-41
Date
Aug-29-2008
Language
English
Publication Type
Article
Keywords
Accidents, Traffic - mortality
Adolescent
Adult
Aged
Alaska - epidemiology
Alcohol Drinking - ethnology - mortality
Cause of Death
Child
Child, Preschool
Death Certificates
Female
Health Status Disparities
Humans
Indians, North American
Infant
Life expectancy
Liver Diseases, Alcoholic - ethnology - mortality
Male
Middle Aged
United States - epidemiology
Abstract
Excessive alcohol consumption is a leading preventable cause of death in the United States and has substantial public health impact on American Indian and Alaska Native (AI/AN) populations. To estimate the average annual number of alcohol-attributable deaths (AADs) and years of potential life lost (YPLLs) among AI/ANs in the United States, CDC analyzed 2001-2005 data (the most recent data available), using death certificate data and CDC Alcohol-Related Disease Impact (ARDI) software. This report summarizes the results of that analysis, which indicated that AADs accounted for 11.7% of all AI/AN deaths, that the age-adjusted AAD rate for AI/ANs was approximately twice that of the U.S. general population, and that AI/ANs lose 6.4 more years of potential life per AAD compared with persons in the U.S. general population (36.3 versus 29.9 years). These findings underscore the importance of implementing effective population-based interventions to prevent excessive alcohol consumption and to reduce alcohol-attributable morbidity and mortality among AI/ANs.
PubMed ID
18756193 View in PubMed
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230 records – page 1 of 23.