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157 records – page 1 of 16.

Abdominal malignancies in patients with Wilson's disease.

https://arctichealth.org/en/permalink/ahliterature18250
Source
QJM. 2003 Sep;96(9):657-62
Publication Type
Article
Date
Sep-2003
Author
J M Walshe
E. Waldenström
V. Sams
H. Nordlinder
K. Westermark
Author Affiliation
Department of Neurology, The Middlesex Hospital, London, UK. penicillamine@waitrose.com
Source
QJM. 2003 Sep;96(9):657-62
Date
Sep-2003
Language
English
Publication Type
Article
Keywords
Abdominal Neoplasms - complications - epidemiology - genetics
Adenocarcinoma - complications - epidemiology - genetics
Adolescent
Adult
Age of Onset
Biliary Tract Neoplasms - complications - epidemiology - genetics
Carcinoma, Hepatocellular - complications - epidemiology - genetics
Child
Cholangiocarcinoma - complications - epidemiology - genetics
Female
Hepatolenticular Degeneration - complications - epidemiology - genetics
Humans
Incidence
Liver Neoplasms - complications - epidemiology - genetics
Long-Term Care
Male
Mutation
Pancreatic Neoplasms - complications - epidemiology - genetics
Retrospective Studies
Sweden - epidemiology
Time Factors
Abstract
BACKGROUND: Wilson's disease is associated with heavy copper overload, primarily in the liver. Copper is a toxic metal, and might be expected to be associated with cancer induction, as iron is in haemochromatosis. However, liver cancer is currently believed to be extremely rare in this disease, and other intra-abdominal malignancies have not been reported. AIM: To assess the frequency of abdominal malignant disease in patients with Wilson's disease on long-term follow-up. DESIGN: Retrospective study in two specialist Wilson's disease clinics: Cambridge/London and Uppsala. METHODS: We reviewed the case records of 363 patients seen at three centres: Addenbrooke's Hospital, Cambridge, 1955-1987; the Middlesex Hospital, London, 1987-2000; and the University Hospital, Uppsala, Sweden, 1966-2002. Patients were grouped by length of follow-up: 10-19 years; 20-29 years; 30-39 years; and 40 years or more. RESULTS: No cancers were seen in patients followed for
PubMed ID
12925721 View in PubMed
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[Acute intermittent porphyria increases the risk of liver cancer. Early diagnosis of the cancer and varying surgery may improve the prognosis]

https://arctichealth.org/en/permalink/ahliterature21547
Source
Lakartidningen. 1998 Jun 24;95(26-27):3043-4
Publication Type
Article
Date
Jun-24-1998
Author
C. Andersson
L. Bjersing
F. Lithner
Author Affiliation
Medicinska kliniken, Norrlands Universitetssjukhus, Umeå.
Source
Lakartidningen. 1998 Jun 24;95(26-27):3043-4
Date
Jun-24-1998
Language
Swedish
Publication Type
Article
Keywords
Female
Humans
Liver Neoplasms - diagnosis - etiology - mortality - surgery
Male
Porphyria, Acute Intermittent - complications - mortality
Prognosis
Risk factors
Sweden - epidemiology
PubMed ID
9679414 View in PubMed
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Acute liver failure in Sweden: etiology and outcome.

https://arctichealth.org/en/permalink/ahliterature161905
Source
J Intern Med. 2007 Sep;262(3):393-401
Publication Type
Article
Date
Sep-2007
Author
G. Wei
A. Bergquist
U. Broomé
S. Lindgren
S. Wallerstedt
S. Almer
P. Sangfelt
A. Danielsson
H. Sandberg-Gertzén
L. Lööf
H. Prytz
E. Björnsson
Author Affiliation
Section of Gastroenterology and Hepatology, Department of Internal Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
Source
J Intern Med. 2007 Sep;262(3):393-401
Date
Sep-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Female
Humans
Liver Failure, Acute - etiology - surgery
Liver Transplantation
Male
Middle Aged
Retrospective Studies
Sweden - epidemiology
Abstract
To determine the causes and outcome of all patients with acute liver failure (ALF) in Sweden 1994-2003 and study the diagnostic accuracy of King's College Hospital (KCH) criteria and the model for end-stage liver disease (MELD) score with transplant-free deaths as a positive outcome.
Adult patients in Sweden with international normalized ratio (INR) of >or=1.5 due to severe liver injury with and without encephalopathy at admission between 1994-2003 were included.
A total of 279 patients were identified. The most common cause of ALF were acetaminophen toxicity in 42% and other drugs in 15%. In 31 cases (11%) no definite etiology could be established. The KCH criteria had a positive-predictive value (PPV) of 67%, negative-predictive value (NPV) of 84% in the acetaminophen group. Positive-predictive value and negative-predictive value of KCH criteria in the nonacetaminophen group were 54% and 63% respectively. MELD score>30 had a positive-predictive value of 21%, negative-predictive value of 94% in the acetaminophen group. The corresponding figures for the nonacetaminophen group were 64% and 76% respectively.
Acetaminophen toxicity was the most common cause in unselected patients with ALF in Sweden. KCH criteria had a high NPV in the acetaminophen group, and in combination with MELD score
PubMed ID
17697161 View in PubMed
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Adverse outcomes of pregnancy in women with non-alcoholic fatty liver disease.

https://arctichealth.org/en/permalink/ahliterature277352
Source
Liver Int. 2016 Feb;36(2):268-74
Publication Type
Article
Date
Feb-2016
Author
Hannes Hagström
Jonas Höijer
Jonas F Ludvigsson
Matteo Bottai
Anders Ekbom
Rolf Hultcrantz
Olof Stephansson
Knut Stokkeland
Source
Liver Int. 2016 Feb;36(2):268-74
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Adult
Cesarean Section - statistics & numerical data
Cohort Studies
Diabetes, Gestational - epidemiology - etiology
Female
Humans
Infant, Low Birth Weight
Infant, Newborn
Non-alcoholic Fatty Liver Disease - complications - epidemiology
Pre-Eclampsia - epidemiology - etiology
Pregnancy
Pregnancy Complications - epidemiology
Pregnancy Outcome - epidemiology
Premature Birth - epidemiology - etiology
Sweden - epidemiology
Abstract
Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disease in the world, but little is known about its potential association with pregnancy outcomes. We aimed to investigate pregnancy outcomes in NAFLD.
The Swedish Medical Birth Register (MBR) was used to identify births between 1992 and 2011 (N = 1 960 416). By linkage with the National Patient Register, we identified women with a diagnosis of NAFLD. The MBR was then used to identify outcomes: gestational diabetes, pre-eclampsia, Caesarean section, Apgar score
PubMed ID
26114995 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 abuse and the risk of pancreatic cancer.

https://arctichealth.org/en/permalink/ahliterature9936
Source
Gut. 2002 Aug;51(2):236-9
Publication Type
Article
Date
Aug-2002
Author
W. Ye
J. Lagergren
E. Weiderpass
O. Nyrén
H-O Adami
A. Ekbom
Author Affiliation
Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. weiye@mbox.ki.se
Source
Gut. 2002 Aug;51(2):236-9
Date
Aug-2002
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alcoholism - complications
Chi-Square Distribution
Chronic Disease
Female
Humans
Incidence
Liver Cirrhosis, Alcoholic - complications
Male
Middle Aged
Pancreatic Neoplasms - epidemiology - etiology
Pancreatitis - complications
Prospective Studies
Registries
Research Support, Non-U.S. Gov't
Retrospective Studies
Risk
Smoking - adverse effects
Sweden - epidemiology
Abstract
BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.
PubMed ID
12117886 View in PubMed
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Alcohol consumption in patients with primary sclerosing cholangitis.

https://arctichealth.org/en/permalink/ahliterature122648
Source
World J Gastroenterol. 2012 Jun 28;18(24):3105-11
Publication Type
Article
Date
Jun-28-2012
Author
Hannes Hagström
Per Stål
Knut Stokkeland
Annika Bergquist
Author Affiliation
Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, 14186 Stockholm, Sweden. hannes.hagstrom@ki.se
Source
World J Gastroenterol. 2012 Jun 28;18(24):3105-11
Date
Jun-28-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alcohol drinking - epidemiology
Analysis of Variance
Binge Drinking - epidemiology
Chi-Square Distribution
Cholangitis, Sclerosing - diagnosis - epidemiology
Disease Progression
Elasticity Imaging Techniques
Female
Humans
Liver Cirrhosis, Alcoholic - diagnosis - epidemiology
Male
Middle Aged
Predictive value of tests
Questionnaires
Registries
Retrospective Studies
Risk assessment
Risk factors
Sweden - epidemiology
Time Factors
Young Adult
Abstract
To assess the alcohol drinking patterns in a cohort of primary sclerosing cholangitis (PSC) patients and the possible influence on the development of fibrosis.
Ninety-six patients with PSC were evaluated with a validated questionnaire about a patient's lifetime drinking habits: the lifetime drinking history (LDH) questionnaire. In addition, clinical status, transient elastography and biochemistry values were analysed and registered. Patients were defined as having either significant or non-significant fibrosis. Significant fibrosis was defined as either an elastography value of = 17.3 kPa or the presence of clinical signs of cirrhosis. Patients were divided into two groups depending on their alcohol consumption patterns; no/low alcohol consumption (one drink or unit/d) and moderate/high alcohol consumption (= 1 drink or unit/d). LDH data were calculated to estimate lifetime alcohol intake (LAI), current alcohol intake, drinks per year before and after diagnosis of PSC. We also calculated the number of episodes of binge-drinking (defined as consuming = 5 drinks per occasion) in total, before and after the diagnosis of PSC.
The mean LAI was 3882 units of alcohol, giving a mean intake after onset of alcohol consumption of 2.6 units per week. Only 9% of patients consumed alcohol equal to or more than one unit per day. Current alcohol intake in patients with significant fibrosis (n = 26) was less than in patients without significant fibrosis (n = 70), as shown by lower values of phosphatidylethanol (B-PEth) (0.1 ?mol/L vs 0.33 ?mol/L, respectively, P = 0.002) and carbohydrate-deficient transferrin (CDT) (0.88% vs 1.06%, respectively, P = 0.02). Self-reported LAI was similar between the two groups. Patients with significant fibrosis reduced their alcohol intake after diagnosis from 103 to 88 units per year whereas patients without fibrosis increased their alcohol intake after PSC diagnosis from 111 to 151 units/year. There were no correlations between elastography values and intake of alcohol (units/year) (r = -0.036).
PSC patients have low alcohol consumption. The lack of correlation between fibrosis and alcohol intake indicates that a low alcohol intake is safe in these patients.
Notes
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PubMed ID
22791946 View in PubMed
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Alcoholism and cancer risk: a population-based cohort study.

https://arctichealth.org/en/permalink/ahliterature24357
Source
Cancer Causes Control. 1992 Sep;3(5):419-25
Publication Type
Article
Date
Sep-1992
Author
H O Adami
J K McLaughlin
A W Hsing
A. Wolk
A. Ekbom
L. Holmberg
I. Persson
Author Affiliation
Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden.
Source
Cancer Causes Control. 1992 Sep;3(5):419-25
Date
Sep-1992
Language
English
Publication Type
Article
Keywords
Aged
Alcoholism - complications - epidemiology
Cohort Studies
Esophageal Neoplasms - epidemiology - etiology
Female
Humans
Incidence
Laryngeal Neoplasms - epidemiology - etiology
Liver Neoplasms - epidemiology - etiology
Lung Neoplasms - epidemiology - etiology
Male
Middle Aged
Mouth Neoplasms - epidemiology - etiology
Neoplasms - epidemiology - etiology
Research Support, Non-U.S. Gov't
Risk factors
Sweden - epidemiology
Abstract
The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965-83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.3-1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3-1.6) and among women (SIR = 1.5, CI = 1.1-2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9-5.7), esophagus (SIR = 6.8, CI = 4.5-9.9), larynx (SIR = 3.3, CI = 1.7-6.0), and lung (SIR = 2.1, CI = 1.7-2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9-2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6-1.4), large bowel (SIR = 1.1, CI = 0.8-1.5), prostate (SIR = 1.0, CI = 0.8-1.3), urinary bladder (SIR = 1.0, CI = 0.6-1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3-1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6-2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5-9.1).(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed ID
1525322 View in PubMed
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Alcoholism and liver cirrhosis in the etiology of primary liver cancer.

https://arctichealth.org/en/permalink/ahliterature11847
Source
Int J Cancer. 1992 Jul 30;51(6):898-902
Publication Type
Article
Date
Jul-30-1992
Author
H O Adami
A W Hsing
J K McLaughlin
D. Trichopoulos
D. Hacker
A. Ekbom
I. Persson
Author Affiliation
Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden.
Source
Int J Cancer. 1992 Jul 30;51(6):898-902
Date
Jul-30-1992
Language
English
Publication Type
Article
Keywords
Aged
Alcoholism - complications - epidemiology
Cohort Studies
Female
Follow-Up Studies
Humans
Incidence
Liver Cirrhosis - complications - epidemiology
Liver Cirrhosis, Alcoholic - complications - epidemiology
Liver Neoplasms - epidemiology - etiology
Male
Middle Aged
Registries
Research Support, Non-U.S. Gov't
Sweden - epidemiology
Abstract
The aim of this study was to determine the risk of developing primary liver cancer in patients with a diagnosis of alcoholism, liver cirrhosis, or both. Three population-based, mutually exclusive cohorts were defined on the basis of hospital discharge diagnosis between 1965 and 1983. Complete follow-up through 1984--excluding the first year of follow-up--showed that among 8,517 patients with a diagnosis of alcoholism, 13 cancers occurred, vs. 4.2 expected (standardized incidence ratio (SIR) = 3.1; 95% confidence interval (CI) = 1.6 to 5.3); among 3,589 patients with liver cirrhosis, 59 cancers occurred, vs. 1.7 expected (SIR = 35.1; 95% CI = 26.7 to 45.3), and among 836 patients with both diagnoses, 11 cancers occurred, vs. 0.3 expected (SIR = 34.3; 95% CI = 17.1 to 61.3). Thus, alcoholism alone entailed a moderately increased risk and alcoholism with liver cirrhosis did not increase the high relative risk for liver cancer more than cirrhosis alone. We conclude that alcohol intake may be a liver carcinogen only by being causally involved in the development of cirrhosis; and further, that the risk of developing liver cancer following cirrhosis in this population is similar to or higher than that after chronic hepatitis-B-virus infection in other Western countries.
PubMed ID
1639537 View in PubMed
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Alcoholism in social classes and occupations in Sweden.

https://arctichealth.org/en/permalink/ahliterature11036
Source
Int J Epidemiol. 1997 Jun;26(3):584-91
Publication Type
Article
Date
Jun-1997
Author
T. Hemmingsson
I. Lundberg
A. Romelsjö
L. Alfredsson
Author Affiliation
Department of Occupational Health, NVSO, Karolinska Hospital, Stockholm, Sweden.
Source
Int J Epidemiol. 1997 Jun;26(3):584-91
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Alcohol drinking - epidemiology
Alcoholism - epidemiology
Cohort Studies
Confidence Intervals
Cross-Sectional Studies
Databases, Factual
Employment - statistics & numerical data
Female
Humans
Liver Cirrhosis, Alcoholic - epidemiology
Male
Military Personnel - statistics & numerical data
Occupations - classification - statistics & numerical data
Odds Ratio
Registries
Research Support, Non-U.S. Gov't
Retrospective Studies
Social Class
Sweden - epidemiology
Twins - statistics & numerical data
Abstract
BACKGROUND: A number of studies have shown variations in the occurrence of alcoholism between different socioeconomic groups and occupations, but it has not been clear to what extent this is related to the average alcohol consumption in the same socioeconomic groups or occupations. METHODS: The relationship between socioeconomic group and occupation and hospital discharge 1981-1983 due to 'diagnoses related to alcoholism' (AD) (alcohol psychosis, alcoholism, and alcohol intoxication) and liver cirrhosis was studied in a cohort of 375,035 men and 140,139 women in 13 counties in Sweden who had reported the same occupation in the censuses of 1960 and 1970. Data on alcohol consumption in different socioeconomic groups and occupations were collected from a conscription investigation and from the Swedish twin registry with data from 1969/70 and 1973 respectively. RESULTS: Intermediate or higher non-manual employees had lower risk of AD as well as of liver cirrhosis compared to manual workers for both sexes. Among males several, mostly blue-collar, occupations had increased relative risks of AD. A high level of association was found between the relative risks of AD and liver cirrhosis in socioeconomic groups, and the relative risk of AD in occupations, and the average alcohol consumption in the same socioeconomic groups/occupations among males. Such an association was not evident among women. CONCLUSION: The study shows, contrary to previous Swedish evidence, that there is a strong relationship between the incidence of alcoholism in socioeconomic groups and occupations and the average alcohol consumption in these groups among men.
PubMed ID
9222784 View in PubMed
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157 records – page 1 of 16.