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Anal carcinoma in HIV-infected patients in the period 1995-2009: a Danish nationwide cohort study.

https://arctichealth.org/en/permalink/ahliterature117489
Source
Scand J Infect Dis. 2013 Jun;45(6):453-9
Publication Type
Article
Date
Jun-2013
Author
Rebecca Legarth
Marie Helleberg
Gitte Kronborg
Carsten S Larsen
Gitte Pedersen
Court Pedersen
Janne Jensen
Lars Nørregård Nielsen
Jan Gerstoft
Niels Obel
Author Affiliation
Department of Infectious Diseases, Copenhagen University Hospital , Rigshospitalet, DK-2100 Copenhagen Ø , Denmark. Rebeccalegarth@gmail.com
Source
Scand J Infect Dis. 2013 Jun;45(6):453-9
Date
Jun-2013
Language
English
Publication Type
Article
Keywords
Adult
Antiretroviral Therapy, Highly Active
Anus Neoplasms - epidemiology - virology
Cohort Studies
Denmark - epidemiology
Female
HIV Infections - drug therapy - epidemiology - pathology
Humans
Incidence
Male
Middle Aged
Poisson Distribution
Survival Analysis
Treatment Outcome
Abstract
Several studies have demonstrated an increased risk of non-AIDS cancers in HIV patients and, for some cancers, also in relatives of HIV patients. We aimed to estimate (1) the risk of anal carcinoma among HIV patients and their parents, and (2) the mortality after a diagnosis of anal carcinoma.
We used Poisson regression to estimate the incidence rate ratios (IRR) of anal carcinoma in (1) a population of HIV patients identified from the Danish HIV Cohort Study (n = 4993) compared with a population control cohort matched on age and gender (n = 59,916) for the period 1995-2009, and (2) parents of HIV patients compared with parents of controls for the period 1978-2009. Cancer diagnoses were identified from The Danish Cancer Registry. We further estimated the mortality rate ratios (MRR) of HIV patients compared with controls after the diagnosis of anal carcinoma.
Thirty-six HIV patients versus 8 population controls were diagnosed with anal carcinoma. HIV patients had an increased risk of anal carcinoma (IRR 77.9, 95% CI 36.2-167.7), especially among men who have sex with men (MSM) (IRR 101.4, 95% CI 39.3-261.5). Fathers of HIV patients had an increased risk of anal carcinoma (IRR 7.4, 95% CI 1.4-38.3) compared to fathers of population controls. Mortality after diagnosis of anal carcinoma was increased in male HIV patients compared with the male control cohort (MRR 3.2, 95% CI 1.1-9.2).
Danish HIV patients, especially MSM, have a considerably increased risk of anal carcinoma. We cannot exclude that fathers of HIV patients have an increased risk of anal carcinoma.
PubMed ID
23294033 View in PubMed
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Angiographic features and cardiovascular risk factors in human immunodeficiency virus-infected patients with first-time acute coronary syndrome.

https://arctichealth.org/en/permalink/ahliterature120091
Source
Am J Cardiol. 2013 Jan 1;111(1):63-7
Publication Type
Article
Date
Jan-1-2013
Author
Andreas Knudsen
Anders B Mathiasen
René H Worck
Jens Kastrup
Jan Gerstoft
Terese L Katzenstein
Andreas Kjaer
Anne-Mette Lebech
Author Affiliation
Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Denmark. andreas.knudsen@hvh.regionh.dk
Source
Am J Cardiol. 2013 Jan 1;111(1):63-7
Date
Jan-1-2013
Language
English
Publication Type
Article
Keywords
Acute Coronary Syndrome - complications - epidemiology - radiography
Adult
Aged
Coronary Angiography
Denmark - epidemiology
Female
Follow-Up Studies
HIV
HIV Infections - complications - epidemiology
Humans
Incidence
Male
Middle Aged
Retrospective Studies
Risk factors
Abstract
A matched cohort study was conducted comparing patients with first-time acute coronary syndromes infected with human immunodeficiency virus (HIV) to non-HIV-infected patients with and without diabetes matched for smoking, gender, and type of acute coronary syndrome who underwent first-time coronary angiography. A total of 48 HIV-infected patients were identified from a national database. Coronary angiography showed that the HIV-infected patients had significantly fewer lesions with classification B2/C than the 2 control groups (p
PubMed ID
23040592 View in PubMed
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Association Between Educational Level and Risk of Cancer in HIV-infected Individuals and the Background Population: Population-based Cohort Study 1995-2011.

https://arctichealth.org/en/permalink/ahliterature269824
Source
J Infect Dis. 2015 Nov 15;212(10):1552-62
Publication Type
Article
Date
Nov-15-2015
Author
Rebecca Legarth
Lars H Omland
Susanne O Dalton
Gitte Kronborg
Carsten S Larsen
Court Pedersen
Gitte Pedersen
Jan Gerstoft
Niels Obel
Source
J Infect Dis. 2015 Nov 15;212(10):1552-62
Date
Nov-15-2015
Language
English
Publication Type
Article
Keywords
Adult
Cohort Studies
Denmark - epidemiology
Educational Status
Female
HIV Infections - complications
Humans
Incidence
Male
Middle Aged
Neoplasms - epidemiology - mortality
Risk assessment
Survival Analysis
Abstract
Human immunodeficiency virus (HIV)-infected individuals have increased risk of cancer. To our knowledge, no previous study has examined the impact of socioeconomic position on risk and prognosis of cancer in HIV infection.
Population-based cohort-study, including HIV-infected individuals diagnosed (without intravenous drug abuse or hepatitis C infection) (n = 3205), and a background population cohort matched by age, gender, and country of birth (n = 22 435) were analyzed. Educational level (low or high) and cancer events were identified in Danish national registers. Cumulative incidences, incidence rate ratios (IRRs), and survival using Kaplan-Meier methods were estimated.
Low educational level was associated with increased risk of cancer among HIV-infected individuals compared to population controls: all (adjusted-IRRs: 1.4 [95% confidence interval {CI}, 1.1-1.7] vs 1.1 [95% CI, .9-1.2]), tobacco- and alcohol-related (2.1 [95% CI, 1.3-3.4] vs 1.3 [95% CI, 1.1-1.6]), and other (1.7 [95% CI, 1.1-2.8] vs 0.9 [95% CI, .7-1.0]). Educational level was not associated with infection-related or ill-defined cancers. One-year-survival was not associated with educational level, but HIV-infected individuals with low educational level had lower 5-year-survival following infection-related and ill-defined cancers.
Education is associated with risk and prognosis of some cancers in HIV infection, and diverges from what is observed in the background population.
PubMed ID
25904603 View in PubMed
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Cause-specific excess mortality in siblings of patients co-infected with HIV and hepatitis C virus.

https://arctichealth.org/en/permalink/ahliterature161814
Source
PLoS One. 2007;2(8):e738
Publication Type
Article
Date
2007
Author
Ann-Brit Eg Hansen
Nicolai Lohse
Jan Gerstoft
Gitte Kronborg
Alex Laursen
Court Pedersen
Henrik Toft Sørensen
Niels Obel
Author Affiliation
Department of Infectious Diseases, Odense University Hospital, Odense, Denmark. ann-brit.eg.hansen@rh.regionh.dk
Source
PLoS One. 2007;2(8):e738
Date
2007
Language
English
Publication Type
Article
Keywords
Cause of Death
Comorbidity
Denmark - epidemiology
HIV Infections - complications - epidemiology - etiology - mortality
Hepatitis C - complications - epidemiology - etiology - mortality
Humans
Registries
Risk assessment
Risk factors
Siblings
Substance-Related Disorders - complications - epidemiology - mortality
Abstract
Co-infection with hepatitis C in HIV-infected individuals is associated with 3- to 4-fold higher mortality among these patients' siblings, compared with siblings of mono-infected HIV-patients or population controls. This indicates that risk factors shared by family members partially account for the excess mortality of HIV/HCV-co-infected patients. We aimed to explore the causes of death contributing to the excess sibling mortality.
We retrieved causes of death from the Danish National Registry of Deaths and estimated cause-specific excess mortality rates (EMR) for siblings of HIV/HCV-co-infected individuals (n = 436) and siblings of HIV mono-infected individuals (n = 1837) compared with siblings of population controls (n = 281,221). Siblings of HIV/HCV-co-infected individuals had an all-cause EMR of 3.03 (95% CI, 1.56-4.50) per 1,000 person-years, compared with siblings of matched population controls. Substance abuse-related deaths contributed most to the elevated mortality among siblings [EMR = 2.25 (1.09-3.40)] followed by unnatural deaths [EMR = 0.67 (-0.05-1.39)]. No siblings of HIV/HCV co-infected patients had a liver-related diagnosis as underlying cause of death. Siblings of HIV-mono-infected individuals had an all-cause EMR of 0.60 (0.16-1.05) compared with siblings of controls. This modest excess mortality was due to deaths from an unknown cause [EMR = 0.28 (0.07-0.48)], deaths from substance abuse [EMR = 0.19 (-0.04-0.43)], and unnatural deaths [EMR = 0.18 (-0.06-0.42)].
HCV co-infection among HIV-infected patients was a strong marker for family-related mortality due to substance abuse and other unnatural causes. To reduce morbidity and mortality in HIV/HCV-co-infected patients, the advances in antiviral treatment of HCV should be accompanied by continued focus on interventions targeted at substance abuse-related risk factors.
Notes
Cites: Lancet. 2000 Nov 25;356(9244):1800-511117912
Cites: J Infect Dis. 2007 Jan 15;195(2):230-517191168
Cites: Am J Psychiatry. 2003 Apr;160(4):687-9512668357
Cites: Lancet. 2003 Nov 22;362(9397):1708-1314643119
Cites: Ugeskr Laeger. 1980 Jan 21;142(4):257-617355510
Cites: Forensic Sci Int. 1993 Nov;62(1-2):157-98300030
Cites: Arch Gen Psychiatry. 1995 Jan;52(1):42-527811161
Cites: Subst Use Misuse. 1997 Dec;32(14):2163-839440160
Cites: Dan Med Bull. 1999 Sep;46(4):354-710514943
Cites: Clin Infect Dis. 2005 Jun 15;40(12):e101-915909251
Cites: Scand J Infect Dis. 2005;37(5):338-4316051569
Cites: Clin Infect Dis. 2005 Sep 1;41(5):713-2016080095
Cites: AIDS. 2005 Oct;19 Suppl 3:S13-916251809
Cites: AIDS. 2005 Oct;19 Suppl 3:S8-1216251833
Cites: Clin Infect Dis. 2006 May 15;42(10):1481-716619163
Cites: AIDS. 2006 May 12;20(8):1171-916691069
Cites: Lancet. 2006 Sep 9;368(9539):938-4516962883
Cites: Ugeskr Laeger. 2001 Aug 6;163(32):4190-511510236
PubMed ID
17710138 View in PubMed
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CD4 decline is associated with increased risk of cardiovascular disease, cancer, and death in virally suppressed patients with HIV.

https://arctichealth.org/en/permalink/ahliterature114835
Source
Clin Infect Dis. 2013 Jul;57(2):314-21
Publication Type
Article
Date
Jul-2013
Author
Marie Helleberg
Gitte Kronborg
Carsten S Larsen
Gitte Pedersen
Court Pedersen
Niels Obel
Jan Gerstoft
Author Affiliation
Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark. mhelleberg@sund.ku.dk
Source
Clin Infect Dis. 2013 Jul;57(2):314-21
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Adult
Anti-Retroviral Agents - therapeutic use
CD4 Lymphocyte Count
Cardiovascular Diseases - epidemiology - mortality
Cohort Studies
Denmark - epidemiology
Female
Follow-Up Studies
HIV Infections - complications - drug therapy - immunology - mortality
Humans
Male
Middle Aged
Neoplasms - epidemiology - mortality
Risk assessment
Survival Analysis
Viral Load
Abstract
The clinical implications of a considerable CD4 decline despite antiretroviral treatment and viral suppression are unknown. We aimed to test the hypothesis that a major CD4 decline could be a marker of cardiovascular disease or undiagnosed cancer.
Patients with human immunodeficiency virus (HIV) were followed in the Danish nationwide, population-based cohort study in the period 1995-2010 with quarterly CD4 measurements. Associations between a CD4 decline of =30% and cardiovascular disease, cancer, and death were analyzed using Poisson regression with date of CD4 decline as a time-updated variable.
We followed 2584 virally suppressed HIV patients for 13 369 person-years (PY; median observation time, 4.7 years). Fifty-six patients developed CD4 decline (incidence rate, 4.2/1000 PY [95% confidence interval {CI}, 3.2-5.4]). CD4 counts dropped from a median of 492 cells/µL to 240 cells/µL. CD8, CD3, and total lymphocyte counts dropped concomitantly. No HIV-related factors, apart from treatment with didanosine, were associated with CD4 decline. The risk of cardiovascular disease, cancer, and death increased markedly =6 months after CD4 decline (incidence rate ratio, 11.7 [95% CI, 3.6-37.4] and 13.7 [95% CI, 4.3-43.6], respectively, and mortality rate ratio 4.3 [95% CI, 1.1-17.6]).
A major decline in CD4 count is associated with a marked increased risk of cardiovascular disease, cancer, and death among virally suppressed HIV patients.
PubMed ID
23575194 View in PubMed
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Cell-associated HIV DNA measured early during infection has prognostic value independent of serum HIV RNA measured concomitantly.

https://arctichealth.org/en/permalink/ahliterature7373
Source
Scand J Infect Dis. 2002;34(7):529-33
Publication Type
Article
Date
2002
Author
Terese L Katzenstein
Roberto S Oliveri
Thomas Benfield
Jesper Eugen-Olsen
Claus Nielsen
Jan Gerstoft
Author Affiliation
AIDS-Laboratory, Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark. Katzenstein@dadlnet.dk
Source
Scand J Infect Dis. 2002;34(7):529-33
Date
2002
Language
English
Publication Type
Article
Keywords
Cohort Studies
DNA, Viral - blood
Denmark
Genotype
HIV Infections - blood
Homosexuality, Male
Humans
Male
Prognosis
RNA, Viral - blood
Receptors, CCR5 - genetics
Viral Load
Abstract
Using data from the Danish AIDS Cohort of HIV-infected homosexual men established in the 1980s, the prognostic value of early HIV DNA loads was evaluated. In addition to DNA measurements, concomitant serum HIV RNA levels, CD4 cell counts and CCR5 genotypes were determined. The patients were divided into 3 groups, according to whether their cell-associated HIV DNA load was or = 2,500 DNA copies/10(6) peripheral blood mononuclear cells. Clinical progression rates differed significantly between the groups (p
PubMed ID
12195879 View in PubMed
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Changes in lung function of HIV-infected patients: a 4.5-year follow-up study.

https://arctichealth.org/en/permalink/ahliterature123634
Source
Clin Physiol Funct Imaging. 2012 Jul;32(4):288-95
Publication Type
Article
Date
Jul-2012
Author
Ulrik Sloth Kristoffersen
Anne-Mette Lebech
Jann Mortensen
Jan Gerstoft
Henrik Gutte
Andreas Kjaer
Author Affiliation
Department of Clinical Physiology, Nuclear Medicine & PET, Copenhagen University Hospital, Copenhagen, Denmark. ulriksk@sund.ku.dk
Source
Clin Physiol Funct Imaging. 2012 Jul;32(4):288-95
Date
Jul-2012
Language
English
Publication Type
Article
Keywords
Adult
Anti-Retroviral Agents - therapeutic use
Denmark
Drug Therapy, Combination
Female
Follow-Up Studies
Forced expiratory volume
HIV Infections - complications - drug therapy - physiopathology - virology
Humans
Lung - physiopathology - virology
Lung Volume Measurements
Male
Middle Aged
Outpatient Clinics, Hospital
Prognosis
Prospective Studies
Pulmonary Diffusing Capacity
Pulmonary Disease, Chronic Obstructive - diagnosis - etiology - physiopathology - virology
Smoking - adverse effects
Time Factors
Vital Capacity
Abstract
To investigate the development of lung function in HIV-infected patients.
In a prospective cohort study, 88 HIV-infected patients had a lung function test performed and 63 patients (72%) had their LFT repeated with a median follow-up period of 4.4 years. Forty-eight per cent were smokers, and at the re-examination, 97% were on combination antiretroviral therapy.
Carbon monoxide diffusion capacity was reduced and decreased over time in both smokers and non-smokers. Alveolar volume decreased and forced vital capacity increased similarly in both smokers and non-smokers. No changes were observed in forced expiratory volume or peak flow, but smokers had reduced values compared with those of the non-smokers at both examinations. FEV1/FVC was reduced especially in smokers and declined in both smokers and non-smokers.
Carbon monoxide diffusion capacity is reduced in HIV-infected patients and seems to decline over time. Additionally, signs of obstructive lung disease are present in HIV-infected patients and seem to increase over time, although only modestly.
PubMed ID
22681606 View in PubMed
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Characterization of HIV-1 from patients with virological failure to a boosted protease inhibitor regimen.

https://arctichealth.org/en/permalink/ahliterature137635
Source
J Med Virol. 2011 Mar;83(3):377-83
Publication Type
Article
Date
Mar-2011
Author
Marie Rathcke Lillemark
Jan Gerstoft
Niels Obel
Gitte Kronborg
Court Pedersen
Louise Bruun Jørgensen
Tina Vasehus Madsen
Terese Lea Katzenstein
Author Affiliation
Department of Virology, State Serum Institute, Copenhagen, Denmark. mml@ssi.dk
Source
J Med Virol. 2011 Mar;83(3):377-83
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
Anti-HIV Agents - blood - therapeutic use
Antiretroviral Therapy, Highly Active
Cohort Studies
Denmark
Drug Resistance, Viral
Female
Genes, gag
Genes, pol
HIV Infections - drug therapy - epidemiology - virology
HIV-1 - drug effects - genetics
Humans
Male
Mutation
Protease Inhibitors - blood - therapeutic use
Ritonavir - blood - therapeutic use
Treatment Outcome
Viral Load
Abstract
The use of highly active antiretroviral treatment (HAART) regimens with unboosted protease inhibitors (PIs) has resulted in a high level of virological failure primarily due to the development of resistant virus. Current boosted PI regimens combine successfully low-dose ritonavir (r) with a second PI. The aim of the study was to estimate the proportion of patients, in a population based setting, who develop virological failure on a PI/r regimen. Through The Danish HIV Cohort Study 1,007 patients who received PI/r based treatment between 1995 and 2008 were identified. Twenty-three (2.3%) experienced virological failure, of whom 19 (83%) started PI/r treatment before 2001. Patients from Copenhagen (n=19) were selected to study the development of protease (PR) and gag cleavage site (CS) mutations during PI/r treatment and PI plasma levels at the time of virological failure. Three patients (16%) developed major PI resistance mutations. Mutations in the p7/p1 and p1/p6 gag CS only developed in patients with major or minor mutations in PR. Drug concentrations were low or undetectable in 10 out of the 19 patients. In total PR resistance mutations and low drug levels could account for 12 (63%) of the failure cases. In conclusion, virological failure to PI/r is a low and decreasing problem primarily caused by low plasma drug levels and to a lesser extent major PR mutations. Gag CS mutations did not contribute significantly to resistance development and virological failure.
PubMed ID
21264856 View in PubMed
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Comorbidity acquired before HIV diagnosis and mortality in persons infected and uninfected with HIV: a Danish population-based cohort study.

https://arctichealth.org/en/permalink/ahliterature134959
Source
J Acquir Immune Defic Syndr. 2011 Aug 1;57(4):334-9
Publication Type
Article
Date
Aug-1-2011
Author
Nicolai Lohse
Jan Gerstoft
Gitte Kronborg
Carsten Schade Larsen
Court Pedersen
Gitte Pedersen
Lars Nielsen
Henrik Toft Sørensen
Niels Obel
Author Affiliation
Department of Clinical Epidemiology, Århus University Hospital, Århus, Denmark. niclohse@gmail.com
Source
J Acquir Immune Defic Syndr. 2011 Aug 1;57(4):334-9
Date
Aug-1-2011
Language
English
Publication Type
Article
Keywords
Adult
Cause of Death
Cohort Studies
Comorbidity
Denmark - epidemiology
Female
HIV Infections - complications - epidemiology - mortality
Hepatitis C - epidemiology - mortality
Humans
Life expectancy
Male
Middle Aged
Vital statistics
Abstract
We aimed to estimate the impact of comorbidity acquired before HIV diagnosis on mortality in individuals infected with HIV.
This cohort study compared 2 different cohorts. The prospective population-based nationwide observational Danish HIV Cohort Study was used to compare all adults diagnosed with HIV in Denmark from 1997 with a matched general population cohort. Comorbidity history was ascertained from the Danish National Patient Registry and vital statistics obtained from the Danish Civil Registration System. Cox regression was used to estimate the impact of Charlson comorbidity index (CCI) and hepatitis C virus coinfection on mortality, and population attributable risk was used to assess the proportional impact of comorbidity on mortality.
CCI comorbidity was present before HIV diagnosis in 11.3% of 1638 persons with HIV, and in 8.0% of 156,506 persons in the general population. The risk for death in patients with HIV with at least 1 CCI point was 1.84 times higher than in those with no CCI points (adjusted mortality rate ratio, 95% confidence interval: 1.32 to 2.57). The annual risk of dying for patients with HIV vs general population with 0, 1, 2, and 3+ CCI points was 1.70% (1.44 to 2.00) vs 0.27% (0.26 to 0.28), 4.37% (3.01 to 6.32) vs 1.36% (1.26 to 1.47), 8.06% (4.94 to 13.16) vs 2.44% (2.22 to 2.68), and 10.15% (5.08 to 20.30) vs 5.84% (5.19 to 6.58), respectively. Comorbidity acquired before HIV, hepatitis C virus coinfection, and background mortality accounted for 45% of total mortality in the population infected with HIV.
Almost half of deaths in persons diagnosed with HIV in a health care setting with free access to highly active antiretroviral therapy stemmed from factors unrelated to HIV disease.
PubMed ID
21522017 View in PubMed
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Copenhagen comorbidity in HIV infection (COCOMO) study: a study protocol for a longitudinal, non-interventional assessment of non-AIDS comorbidity in HIV infection in Denmark.

https://arctichealth.org/en/permalink/ahliterature283204
Source
BMC Infect Dis. 2016 Nov 26;16(1):713
Publication Type
Article
Date
Nov-26-2016
Author
Andreas Ronit
Judith Haissman
Ditte Marie Kirkegaard-Klitbo
Thomas Skårup Kristensen
Anne-Mette Lebech
Thomas Benfield
Jan Gerstoft
Henrik Ullum
Lars Køber
Andreas Kjær
Klaus Kofoed
Jørgen Vestbo
Børge Nordestgaard
Jens Lundgren
Susanne Dam Nielsen
Source
BMC Infect Dis. 2016 Nov 26;16(1):713
Date
Nov-26-2016
Language
English
Publication Type
Article
Keywords
Acquired Immunodeficiency Syndrome - epidemiology
Adult
Blood pressure
Cardiovascular Diseases - diagnostic imaging - epidemiology
Cohort Studies
Comorbidity
Computed Tomography Angiography
Denmark - epidemiology
HIV Infections - drug therapy - epidemiology
Humans
Leukocytes, Mononuclear
Life expectancy
Liver Diseases - epidemiology
Longitudinal Studies
Observational Studies as Topic
Risk factors
Abstract
Modern combination antiretroviral therapy (cART) has improved survival for people living with HIV (PLWHIV). Non-AIDS comorbidities have replaced opportunistic infections as leading causes of mortality and morbidity, and are becoming a key health concern as this population continues to age. The aim of this study is to estimate the prevalence and incidence of non-AIDS comorbidity among PLWHIV in Denmark in the cART era and to determine risk factors contributing to the pathogenesis. The study primarily targets cardiovascular, respiratory, and hepatic non-AIDS comorbidity.
The Copenhagen comorbidity in HIV-infection (COCOMO) study is an observational, longitudinal cohort study. The study was initiated in 2015 and recruitment is ongoing with the aim of including 1500 PLWHIV from the Copenhagen area. Follow-up examinations after 2 and 10 years are planned. Uninfected controls are derived from the Copenhagen General Population Study (CGPS), a cohort study including 100,000 uninfected participants from the same geographical region. Physiological and biological measures including blood pressure, ankle-brachial index, electrocardiogram, spirometry, exhaled nitric oxide, transient elastography of the liver, computed tomography (CT) angiography of the heart, unenhanced CT of the chest and upper abdomen, and a number of routine biochemical analysis are uniformly collected in participants from the COCOMO study and the CGPS. Plasma, serum, buffy coat, peripheral blood mononuclear cells (PBMC), urine, and stool samples are collected in a biobank for future studies. Data will be updated through periodical linking to national databases.
As life expectancy for PLWHIV improves, it is essential to study long-term impact of HIV and cART. We anticipate that findings from this cohort study will increase knowledge on non-AIDS comorbidity in PLWHIV and identify targets for future interventional trials. Recognizing the demographic, clinical and pathophysiological characteristics of comorbidity in PLWHIV may help inform development of new guidelines and enable us to move forward to a more personalized HIV care.
ClinicalTrials.gov: NCT02382822 .
Notes
Cites: Am J Cardiol. 2016 Jan 15;117(2):214-2026639041
Cites: Lancet. 2013 Nov 2;382(9903):1525-3324152939
Cites: Clin Infect Dis. 2011 Dec;53(11):1130-921998280
Cites: JAMA Intern Med. 2013 Apr 22;173(8):614-2223459863
Cites: AIDS. 2010 Jun 19;24(10):1537-4820453631
Cites: Clin Exp Immunol. 2011 Jan;163(1):33-4920939860
Cites: Clin Physiol Funct Imaging. 2012 Jul;32(4):288-9522681606
Cites: N Engl J Med. 2015 Aug 27;373(9):795-80726192873
Cites: Lancet. 2014 Jul 19;384(9939):241-825042234
Cites: Lancet. 2014 Jul 19;384(9939):258-7124907868
Cites: Open Forum Infect Dis. 2016 Jan 21;3(1):ofw00926925429
Cites: Clin Gastroenterol Hepatol. 2010 Feb;8(2):183-9119800985
Cites: Am J Respir Crit Care Med. 2000 Feb;161(2 Pt 1):381-9010673175
Cites: AIDS. 2015 Sep 24;29(15):1927-3526352879
Cites: AIDS. 2016 Jul 17;30(11):1731-4326752282
Cites: J Acquir Immune Defic Syndr. 2016 Aug 1;72(4):437-4326990826
Cites: Lancet Infect Dis. 2015 Jul;15(7):810-826070969
Cites: AIDS. 2013 May 15;27(8):1303-1123299176
Cites: J Acquir Immune Defic Syndr. 2015 Feb 1;68(2):209-1625588033
Cites: Am J Respir Crit Care Med. 2011 Feb 1;183(3):388-9520851926
Cites: Lancet Respir Med. 2014 Jul;2(7):583-9224831854
Cites: Am J Respir Crit Care Med. 2011 Sep 1;184(5):602-1521885636
Cites: Eur Respir J. 2005 Aug;26(2):319-3816055882
Cites: Clin Infect Dis. 2010 Feb 15;50(4):502-1120085465
Cites: Thorax. 2006 Jun;61(6):472-716517577
Cites: Ann Intern Med. 2015 Mar 3;162(5):335-4425732274
Cites: Am J Respir Crit Care Med. 2000 Aug;162(2 Pt 1):612-610934095
Cites: Behav Res Methods. 2009 Nov;41(4):1149-6019897823
Cites: PLoS Med. 2012;9(5):e100121222563304
Cites: N Engl J Med. 2008 Oct 30;359(18):1897-90818971492
Cites: J Immunol Methods. 2007 Apr 30;322(1-2):57-6917382342
Cites: Clin Infect Dis. 2014 Dec 15;59(12):1787-9725182245
Cites: Dan Med Bull. 2006 Nov;53(4):441-917150149
Cites: Curr Opin Infect Dis. 2016 Feb;29(1):31-826555039
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):30-321775347
Cites: Clin Infect Dis. 2011 Dec;53(11):1120-621998278
Cites: AIDS. 2015 Nov;29(17 ):2297-30226544701
Cites: AIDS. 2014 May 15;28(8):1181-9124901259
Cites: AIDS. 2016 Mar 27;30(6):889-9826959353
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):38-4121775349
Cites: J Hepatol. 2015 Jul;63(1):237-6425911335
PubMed ID
27887644 View in PubMed
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67 records – page 1 of 7.