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The additive nonparametric and semiparametric Aalen model as the rate function for a counting process.

https://arctichealth.org/en/permalink/ahliterature188979
Source
Lifetime Data Anal. 2002 Sep;8(3):247-62
Publication Type
Article
Date
Sep-2002
Author
Thomas H Scheike
Author Affiliation
Department of Mathematical Sciences, University of Aalborg, Fredrik Bajers Vej 7G, DK-9220 Aalborg, Denmark. ts@math.auc.dk
Source
Lifetime Data Anal. 2002 Sep;8(3):247-62
Date
Sep-2002
Language
English
Publication Type
Article
Keywords
Data Interpretation, Statistical
Denmark
Humans
Liver Diseases - drug therapy - mortality
Models, Statistical
Regression Analysis
Risk assessment
Survival Analysis
Abstract
We use the additive risk model of Aalen (Aalen, 1980) as a model for the rate of a counting process. Rather than specifying the intensity, that is the instantaneous probability of an event conditional on the entire history of the relevant covariates and counting processes, we present a model for the rate function, i.e., the instantaneous probability of an event conditional on only a selected set of covariates. When the rate function for the counting process is of Aalen form we show that the usual Aalen estimator can be used and gives almost unbiased estimates. The usual martingale based variance estimator is incorrect and an alternative estimator should be used. We also consider the semi-parametric version of the Aalen model as a rate model (McKeague and Sasieni, 1994) and show that the standard errors that are computed based on an assumption of intensities are incorrect and give a different estimator. Finally, we introduce and implement a test-statistic for the hypothesis of a time-constant effect in both the non-parametric and semi-parametric model. A small simulation study was performed to evaluate the performance of the new estimator of the standard error.
PubMed ID
12182121 View in PubMed
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Adverse events associated with treatment of latent tuberculosis in the general population.

https://arctichealth.org/en/permalink/ahliterature137998
Source
CMAJ. 2011 Feb 22;183(3):E173-9
Publication Type
Article
Date
Feb-22-2011
Author
Benjamin M Smith
Kevin Schwartzman
Gillian Bartlett
Dick Menzies
Author Affiliation
Respiratory Division, Montreal Chest Institute, McGill University, Que., Canada.
Source
CMAJ. 2011 Feb 22;183(3):E173-9
Date
Feb-22-2011
Language
English
Publication Type
Article
Keywords
Adult
Age Distribution
Aged
Antitubercular Agents - adverse effects
Case-Control Studies
Comorbidity
Drug-Induced Liver Injury - epidemiology - etiology
Female
Humans
Isoniazid - adverse effects
Latent Tuberculosis - drug therapy - epidemiology
Logistic Models
Male
Middle Aged
Patient Admission - statistics & numerical data
Quebec - epidemiology
Retrospective Studies
Rifampin - adverse effects
Risk assessment
Abstract
Guidelines recommend treatment of latent tuberculosis in patients at increased risk for active tuberculosis. Studies investigating the association of therapy with serious adverse events have not included the entire treated population nor accounted for comorbidities or occurrence of similar events in the untreated general population. Our objective was to estimate the risk of adverse events requiring hospital admission that were associated with therapy for latent tuberculosis infection in the general population.
Using administrative health data from the province of Quebec, we created a historical cohort of all residents dispensed therapy for latent tuberculosis between 1998 and 2003. Each patient was matched on age, sex and postal region with two untreated residents. The observation period was 18 months (from 6 months before to 12 months after initiation of therapy). The primary outcome was hospital admission for therapy-associated adverse events.
During the period of observation, therapy for latent tuberculosis was dispensed to 9145 residents, of whom 95% started isoniazid and 5% started rifampin. Pretreatment comorbid illness was significantly more common among patients receiving such therapy compared with the matched untreated cohort. Of all patients dispensed therapy, 45 (0.5%) were admitted to hospital for a hepatic event compared with 15 (0.1%) of the untreated patients. For people over age 65 years, the odds of hospital admission for a hepatic event among patients treated for latent tuberculosis infection was significantly greater than among matched untreated people after adjustment for comorbidities (odds ratio [OR] 6.4, 95% CI 2.2-18.3). Excluding patients with comorbid illness, there were two excess admissions to hospital for hepatic events per 100 patients initiating therapy compared with the rate among untreated people over 65 years (95% CI 0.1-3.87).
The risk of adverse events requiring hospital admission increased significantly among patients over 65 years receiving treatment for latent tuberculosis infection. The decision to treat latent tuberculosis infection in elderly patients should be made after careful consideration of risks and benefits.
Notes
Cites: Chest. 2005 Jul;128(1):116-2316002924
Cites: JAMA. 1999 Mar 17;281(11):1014-810086436
Cites: Am J Respir Crit Care Med. 2006 Oct 15;174(8):935-5217021358
Cites: JAMA. 1999 Dec 15;282(23):2207-810605965
Cites: J Clin Epidemiol. 2000 Feb;53(2):183-9410729691
Cites: Am J Respir Crit Care Med. 2000 Apr;161(4 Pt 2):S221-4710764341
Cites: JAMA. 2001 Sep 26;286(12):1445-611596606
Cites: CMAJ. 2002 Mar 19;166(6):759-6111944762
Cites: Am J Respir Crit Care Med. 2003 Aug 15;168(4):443-712746255
Cites: Bibl Tuberc. 1970;26:28-1064903501
Cites: Am Rev Respir Dis. 1972 Sep;106(3):357-655080707
Cites: Gastroenterology. 1975 Aug;69(2):289-3021150039
Cites: Bull Int Union Tuberc. 1976;51(1):203-81030282
Cites: Am Rev Respir Dis. 1978 Jun;117(6):991-1001666111
Cites: Ann Intern Med. 1981 Jun;94(6):817-97235427
Cites: Am Rev Respir Dis. 1992 Feb;145(2 Pt 1):494-71736764
Cites: J Clin Epidemiol. 1992 Jun;45(6):613-91607900
Cites: West J Med. 1993 Nov;159(5):560-48279152
Cites: J Clin Epidemiol. 1995 Aug;48(8):999-10097775999
Cites: Chest. 1995 Sep;108(3):706-117656620
Cites: West J Med. 1996 Jun;164(6):486-918764622
Comment In: Evid Based Med. 2011 Dec;16(6):169-7021646317
PubMed ID
21220436 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 late adolescence is associated with an increased risk of severe liver disease later in life.

https://arctichealth.org/en/permalink/ahliterature301635
Source
J Hepatol. 2018 03; 68(3):505-510
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
03-2018
Author
Hannes Hagström
Tomas Hemmingsson
Andrea Discacciati
Anna Andreasson
Author Affiliation
Centre for Digestive Diseases, Division of Hepatology, Karolinska University Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Electronic address: hannes.hagstrom@ki.se.
Source
J Hepatol. 2018 03; 68(3):505-510
Date
03-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Alcohol drinking - epidemiology
Follow-Up Studies
Humans
Liver Diseases - diagnosis - epidemiology
Long Term Adverse Effects - diagnosis - epidemiology
Male
Middle Aged
Risk assessment
Risk factors
Severity of Illness Index
Sweden - epidemiology
Abstract
High alcohol consumption is associated with an increased risk of severe liver disease. Current recommendations suggest it is safe for men to consume 30 grams of alcohol per day. We investigated the association between alcohol consumption early in life and later development of severe liver disease.
We used data on alcohol consumption at conscription to military service from 43,296 men (18-20?years) in Sweden between 1969 and 1970. Outcomes were defined as incident diagnoses of severe liver disease from systematic national registration of clinical events until the end of 2009. A Cox regression model adjusted for body mass index, smoking, use of narcotics, cognitive ability and cardiovascular capacity was applied.
During a mean follow-up of 37.8?years, 383 men developed severe liver disease. Alcohol consumption was associated with an increased risk of development of severe liver disease in a dose-response pattern (adjusted hazard ratio for every one gram/day increase 1.02; 95% CI 1.01-1.02). No evidence of a threshold effect was found. Importantly, a clear trend pointed towards an increased risk of severe liver disease in men who consumed less than 30 grams of alcohol per day.
Alcohol consumption in young men is associated with an increased risk of severe liver disease, up to 39?years later in life. The risk was dose-dependent, with no sign of a threshold effect. Current guidelines for safe alcohol intake in men might have to be revised.
We investigated more than 43,000 Swedish men in their late teens enlisted for conscription in 1969-1970. After almost 40?years of follow-up, we found that alcohol consumption was a significant risk factor for developing severe liver disease, independent of confounders. This risk was dose-dependent, and was most pronounced in men consuming two drinks per day or more.
Notes
CommentIn: J Hepatol. 2018 Mar;68(3):389-390 PMID 29395456
CommentIn: J Hepatol. 2018 Jul;69(1):252-253 PMID 29636187
CommentIn: J Hepatol. 2018 Jul;69(1):251-252 PMID 29650335
CommentIn: Ann Hepatol. 2018 Apr 9;17(3):343-344 PMID 29735793
PubMed ID
29395457 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
Cites: J Stud Alcohol. 1977 Jul;38(7):1434-9895152
Cites: Gut. 1980 Oct;21(10):870-77439807
Cites: J Stud Alcohol. 1982 Nov;43(11):1157-707182675
Cites: Hepatology. 1989 Oct;10(4):430-62777204
Cites: Am J Surg Pathol. 1995 Dec;19(12):1409-177503362
Cites: Gastroenterology. 1996 May;110(5):1496-5028613055
Cites: Gut. 1996 Apr;38(4):610-58707097
Cites: Gut. 1997 Dec;41(6):845-509462221
Cites: Alcohol Alcohol. 1998 Jul-Aug;33(4):381-929719397
Cites: Gastroenterology. 2005 Feb;128(2):343-5015685546
Cites: Hepatology. 2005 Jan;41(1):48-5415690481
Cites: Clin Gastroenterol Hepatol. 2005 Nov;3(11):1150-916271348
Cites: Gut. 2006 Mar;55(3):403-816020491
Cites: Hepatology. 2006 May;43(5):1118-2416628644
Cites: Clin Chim Acta. 2006 Oct;372(1-2):184-716790238
Cites: Psychol Addict Behav. 2006 Sep;20(3):333-716938072
Cites: J Clin Gastroenterol. 2011 Jan;45(1):76-8220818236
Cites: Aliment Pharmacol Ther. 2011 Feb;33(3):378-8821118396
Cites: Eur Addict Res. 2011;17(2):90-621178356
Cites: Drug Test Anal. 2011 Apr;3(4):195-20021438164
Cites: Hepatology. 2000 Jan;31(1):7-1110613720
Cites: Best Pract Res Clin Gastroenterol. 2001 Aug;15(4):563-7511492968
Cites: Alcohol Clin Exp Res. 2001 Dec;25(12):1729-3311781505
Cites: Gastroenterology. 2002 Feb;122(2):281-911832443
Cites: J Viral Hepat. 2002 May;9(3):235-4112010513
Cites: Am J Gastroenterol. 2002 Jul;97(7):1807-1212135040
Cites: Hepatology. 2004 Mar;39(3):826-3414999703
Cites: J Hepatol. 2004 Jul;41(1):25-3015246203
Cites: Alcohol Clin Exp Res. 2004 Sep;28(9):1347-5515365305
Cites: J Gastroenterol. 2008;43(9):720-818807134
Cites: Scand J Gastroenterol. 2009;44(3):366-7419016382
Cites: J Stud Alcohol Drugs. 2009 Mar;70(2):296-30319261242
Cites: Alcohol Alcohol. 2009 Sep-Oct;44(5):464-719535495
Cites: J Clin Gastroenterol. 2010 Jan;44(1):58-6519581812
PubMed ID
22791946 View in PubMed
Less detail

Alcoholic Cirrhosis Increases Risk for Autoimmune Diseases: A Nationwide Registry-Based Cohort Study.

https://arctichealth.org/en/permalink/ahliterature274866
Source
Clin Gastroenterol Hepatol. 2015 Nov;13(11):2017-22
Publication Type
Article
Date
Nov-2015
Author
Lisbet Grønbæk
Hendrik Vilstrup
Bent Deleuran
Reiner Wiest
Aleksander Krag
Peter Jepsen
Source
Clin Gastroenterol Hepatol. 2015 Nov;13(11):2017-22
Date
Nov-2015
Language
English
Publication Type
Article
Keywords
Aged
Autoimmune Diseases - epidemiology
Cohort Studies
Denmark - epidemiology
Female
Hospitalization
Humans
Incidence
Liver Cirrhosis, Alcoholic - complications
Male
Middle Aged
Risk assessment
Abstract
Alcoholic cirrhosis is associated with hyperactivation and dysregulation of the immune system. In addition to its ability to increase risk for infections, it also may increase the risk for autoimmune diseases. We studied the incidence of autoimmune diseases among patients with alcoholic cirrhosis vs controls in Denmark.
We collected data from nationwide health care registries to identify and follow up all citizens of Denmark diagnosed with alcoholic cirrhosis from 1977 through 2010. Each patient was matched with 5 random individuals from the population (controls) of the same sex and age. The incidence rates of various autoimmune diseases were compared between patients with cirrhosis and controls and adjusted for the number of hospitalizations in the previous year (a marker for the frequency of clinical examination).
Of the 24,679 patients diagnosed with alcoholic cirrhosis, 532 developed an autoimmune disease, yielding an overall increased adjusted incidence rate ratio (aIRR) of 1.36 (95% confidence interval [CI], 1.24-1.50). The strongest associations were with Addison's disease (aIRR, 2.47; 95% CI, 1.04-5.85), inflammatory bowel disease (aIRR, 1.56; 95% CI, 1.26-1.92), celiac disease (aIRR, 5.12; 95% CI, 2.58-10.16), pernicious anemia (aIRR, 2.35; 95% CI, 1.50-3.68), and psoriasis (aIRR, 4.06; 95% CI, 3.32-4.97). There was no increase in the incidence rate for rheumatoid arthritis (aIRR, 0.89; 95% CI, 0.69-1.15); the incidence rate for polymyalgia rheumatica decreased in patients with alcoholic cirrhosis compared with controls (aIRR, 0.47; 95% CI, 0.33-0.67).
Based on a nationwide cohort study of patients in Denmark, alcoholic cirrhosis is a risk factor for several autoimmune diseases.
PubMed ID
26044312 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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Alpha-particle carcinogenesis in Thorotrast patients: epidemiology, dosimetry, pathology, and molecular analysis.

https://arctichealth.org/en/permalink/ahliterature19345
Source
J Environ Pathol Toxicol Oncol. 2001;20(4):311-5
Publication Type
Article
Date
2001
Author
Y. Ishikawa
I. Wada
M. Fukumoto
Author Affiliation
Department of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo.
Source
J Environ Pathol Toxicol Oncol. 2001;20(4):311-5
Date
2001
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alpha Particles - adverse effects
Carcinogens - adverse effects - pharmacokinetics
Carcinoma, Hepatocellular - epidemiology - etiology
Cause of Death
Cholangiocarcinoma - epidemiology - etiology
DNA Damage
DNA Mutational Analysis
Epidemiologic Studies
Europe - epidemiology
Female
Genes, p53
Half-Life
Hemangiosarcoma - epidemiology - etiology
Humans
Japan - epidemiology
Leukemia - epidemiology - etiology
Liver Cirrhosis - epidemiology - etiology
Liver Neoplasms - epidemiology - etiology
Loss of Heterozygosity
Male
Middle Aged
Radiation Injuries
Research Support, Non-U.S. Gov't
Risk assessment
Thorium Dioxide - adverse effects - pharmacokinetics
United States
Abstract
We studied the alpha-radiation risks in patients who received injections of Thorotrast, an X-ray contrast medium used in Europe, Japan, and the United States from 1930 to 1955. Thorotrast was composed of thorium dioxide (ThO2) and Th-232, a naturally occurring radionuclide. Because the physical half-life of ThO2 is 14 billion years and Thorotrast is hardly eliminated from the body, tissues in which it was deposited are irradiated by alpha-radiation for the entire lifetime of the subject. The dosimetry of Thorotrast patients is very complicated, but currently its reliability is quite high compared with other irradiated populations. The major causes of the death of Thorotrast patients are liver cancer, liver cirrhosis, leukemia, and other cancers. Three histologies of liver cancer are found: cholangiocarcinoma, hepatocellular carcinoma, and angiosarcoma. Although cholangiocarcinoma is the most frequent, angiosarcoma is characteristic of alpha-radiation. Among blood neoplasms with a higher incidence of increase than the general population, erythroleukemia and myelodysplastic syndrome were remarkable. Thorotrast patients exhaled a high concentration of radon (Rn-220), a progeny of Th-232, but no excesses of lung cancer in the patients of Japan, Germany, and Denmark were reported. Mutation analyses of p53 genes and loss of heterozygosity (LOH) studies at 17p locus were performed to characterize the genetic changes in Thorotrast-induced liver tumors. Interestingly, LOH, supposedly corresponding to large deletions was not frequent; most mutations were transitions, also seen in tumors of the general population, suggesting that genetic changes of Thorotrast-induced cancers are mainly delayed mutations, and not the result of the direct effects of radiation.
PubMed ID
11797840 View in PubMed
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Analysis of survival predictors in a prospective cohort of patients undergoing transarterial chemoembolization for hepatocellular carcinoma in a single Canadian centre.

https://arctichealth.org/en/permalink/ahliterature127146
Source
HPB (Oxford). 2012 Mar;14(3):162-70
Publication Type
Article
Date
Mar-2012
Author
Karim M Eltawil
Robert Berry
Mohamed Abdolell
Michele Molinari
Author Affiliation
Department of Surgery, Queen Elizabeth II Health Sciences Center, Dalhousie University, Halifax, NS, Canada.
Source
HPB (Oxford). 2012 Mar;14(3):162-70
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Carcinoma, Hepatocellular - blood - mortality - pathology - therapy
Chemoembolization, Therapeutic - adverse effects - mortality
Female
Humans
Kaplan-Meier Estimate
Liver Neoplasms - blood - mortality - pathology - therapy
Male
Middle Aged
Multivariate Analysis
Neoplasm Staging
Nova Scotia
Palliative Care
Proportional Hazards Models
Prospective Studies
Risk assessment
Risk factors
Time Factors
Treatment Outcome
Tumor Burden
alpha-Fetoproteins - metabolism
Abstract
Despite advances in the treatment of hepatocellular carcinoma (HCC), a great proportion of patients are eligible only for palliative therapy for reasons of advanced-stage disease or poor hepatic reserve. The use of transarterial chemoembolization (TACE) in the palliation of non-resectable HCC has shown a survival benefit in European and Asian populations. The aim of this study was to assess the efficacy of TACE by analysing overall 5-year survival, interval changes of tumour size and serum alpha-fetoprotein (AFP) levels in a prospective North American cohort.
From September 2005 to December 2010, 46 candidates for TACE were enrolled in the study. Collectively, they underwent 102 TACE treatments. Data on tumour response, serum AFP and survival were prospectively collected.
In compensated cirrhotic patients, serial treatment with TACE had a stabilizing effect on tumour size and reduced serum AFP levels during the first 12 months. Overall survival rates at 1, 2 and 3 years were 69%, 58% and 20%, respectively. Younger individuals and patients with a lower body mass index, affected by early-stage HCC with involvement of a single lobe, had better survival in univariate analysis. After adjustment for risk factors, early tumour stage (T1 and T2 vs. T3 and T4) at diagnosis was the only statistically significant predictor for survival.
In compensated cirrhotic patients, TACE is an effective palliative intervention and HCC stage at diagnosis seems to be the most important predictor of longterm outcomes.
Notes
Cites: Ann Surg Oncol. 2000 Sep;7(8):593-60011005558
Cites: Hepatobiliary Pancreat Dis Int. 2011 Apr;10(2):143-5021459720
Cites: Hepatology. 2002 May;35(5):1164-7111981766
Cites: Arch Surg. 2002 Jun;137(6):653-7; discussion 657-812049535
Cites: Lancet. 2002 May 18;359(9319):1734-912049862
Cites: BMC Gastroenterol. 2002;2:211835693
Cites: Hepatology. 2003 Feb;37(2):429-4212540794
Cites: Major Probl Clin Surg. 1964;1:189-2244949992
Cites: JAMA. 1981 Mar 20;245(11):1123-76162038
Cites: Am J Clin Oncol. 1982 Dec;5(6):649-557165009
Cites: Hepatology. 1984 Jan-Feb;4(1 Suppl):3S-6S6319264
Cites: J Surg Oncol. 1995 Oct;60(2):116-217564377
Cites: N Engl J Med. 1996 Mar 14;334(11):693-98594428
Cites: Am J Med. 1996 Oct;101(4):422-348873514
Cites: Dig Dis Sci. 1996 Dec;41(12):2332-99011438
Cites: J Clin Gastroenterol. 1999 Jun;28(4):334-4010372931
Cites: Semin Liver Dis. 1999;19(3):271-8510518307
Cites: Hepatology. 2005 Nov;42(5):1208-3616250051
Cites: J Clin Oncol. 2006 May 10;24(14):2137-5016682732
Cites: Gastroenterology. 2006 Aug;131(2):461-916890600
Cites: Clin Oncol (R Coll Radiol). 2006 Nov;18(9):684-9217100154
Cites: Hepatobiliary Pancreat Dis Int. 2008 Jun;7(3):237-5718522878
Cites: Korean J Radiol. 2008 Nov-Dec;9(6):534-4019039270
Cites: Eur J Cancer. 2009 Jan;45(2):228-4719097774
Cites: Ann Oncol. 2009 Jun;20 Suppl 7:vii1-vii619497945
Cites: Clin Transplant. 2009 Dec;23 Suppl 21:61-719930318
Cites: Cardiovasc Intervent Radiol. 2010 Feb;33(1):41-5219908093
Cites: J Gastroenterol Hepatol. 2010 May;25(5):951-620546449
Cites: HPB (Oxford). 2010 Apr;12(3):174-8020590884
Cites: J Gastroenterol Hepatol. 2010 Aug;25(8):1426-3420659234
Cites: Hepatology. 2011 Mar;53(3):1020-221374666
Cites: Int J Cancer. 2001 Oct 15;94(2):153-611668491
PubMed ID
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