Papers using progression to AIDS as the outcome measure ranked by study quality (best quality study first)
| Ranking from quality assessment | Reference (date of publication)Setting/country | Design, population and sample size | Relevant outcome measures | Findings | Quality assessment: study strengths | Quality assessment: study weaknesses |
|---|---|---|---|---|---|---|
| CI, confidence interval; OR, odds ratio; PCP, Pneumocystis carinii pneumonia; RH, relative hazard; RR, relative risk. | ||||||
| = 1 | Webber et al (1999)20 Hospital affiliated methadone maintenance programme with on-site primary care in New York City, United States | Prospective cohort study of 524 HIV positive people who attended the methadone programme | Time to AIDS defining condition (by CDC 1993 definition21 but excluding CD4+ cell count ⩽200×106/l) and death | Cigarette smoking did not add information to a model controlling for CD4+ cell counts, constitutional symptoms, crack cocaine use, after adjustment for zidovudine use and age (hazard ratios not provided and data insufficient to calculate) | Wide range of confounders taken into account (age, sex, CD4+ cell counts, constitutional symptoms, crack cocaine use, zidovudine use, type and route of drug use, sexual risk factors, and sociodemographic variables) | Investigators not blinded and smoking status not biochemically validated |
| = 1 | Stephenson et al (1999)22 15 genitourinary medicine clinics in Britain and Ireland | Prospective observational cohort study of 385 women aged over 18 years with a positive HIV antibody test who progressed to AIDS | Incidence of AIDS (criteria for AIDS or AIDS defining condition not stated) | In multivariate analysis, rate of progression to AIDS and mortality were not affected by smoking status. Adjusted hazard ratio for smokers versus non-smokers for progression to AIDS was 1.36 (95% CI 0.75 to 2.45) Crude hazard ratio not provide and data insufficient to calculate | Wide range of confounders taken into account (CD4+ lymphocyte count, antiretroviral drug use, Pneumocystis carinii prophylaxis, age, ethnic origin, number of sexual partners, occupational status, marital status, alcohol use, and use of oral contraception) | Date of HIV seroconversion was unknown but CD4+ lymphocyte count was fitted as a fixed variable to adjust for illness on entry to study. Investigators not blinded and no biochemical validation of smoking status |
| = 1 | Conley et al (1996)23 San Francisco, Denver, and Chicago, United States | Prospective and retrospective cohort study of 232 HIV infected homosexual and bisexual men previously enrolled for a hepatitis B study. Participants classified as either smokers (n = 106) or non-smokers (n = 126) | Included diagnosis of AIDS by CDC definition (1987)26 | Neither univariate analysis nor Kaplan-Meier survival analysis found any association between cigarette smoking and the development of AIDS (univariate RR = 1.0, 95% CI = 0.8 to 1.3), PCP (univariate RR = 0.9, 95% CI = 0.5 to 1.6), or Kaposi’s sarcoma (univariate RR = 0.6, 95% CI = 0.3 to 1.1) | Adequate assessment of baseline characteristics including date of seroconversion | Assessors not blinded, smoking status not biochemically assessed |
| = 4 | Coates et al (1990)24 Toronto, Canada | Prospective cohort study of 159 apparently healthy homosexual or bisexual male contacts of other men known to have AIDS with follow up for 4.5 years | Diagnosis of AIDS by CDC definition (1985)31 | Cox regression models showed no relation between smoking status and progression to AIDS (hazard ratio not provided or raw data to calculate) | Interviewer administered questionnaire of exposure (smoking status) and complete follow up of eligible participants. Confounders taken into account were age, alcohol consumption, recreational drug use, sexually transmitted infections, and intestinal parasites | Smoking status not biochemically confirmed. Disease progression for 143 participants who were HIV seropositive on enrolment assessed by estimated length of HIV infection (rather than known dates or proxy measure such as CD4+ cell count). Assessors not blinded |
| = 4 | Burns et al (1996)25 17 community based clinical centres in 13 cities in the United States | Prospective cohort study of 3221 HIV-1 seropositive men and women with median follow up of 36 months for current smokers and never smokers and 37 months for former smokers | Participants classified as never (n = 760), former (n = 618), or current (n = 1843) smokers on the basis of an enrolment questionnaire (not biochemically validated). Outcome measures were HIV related diagnoses similar to CDC list of AIDS defining illnesses (1987)26 | After adjustment for confounders, there was no difference between current and never smokers for overall risk of opportunistic diseases (adjusted RH = 1.05, 95% CI = 0.9 to 1.23) or death (adjusted RH = 1.00, 95% CI = 0.86 to 1.18). However current smokers were at greater risk than non-smokers of developing bacterial pneumonia (adjusted RH = 1.57, 95% CI = 1.14 to 2.15) and AIDS dementia complex (adjusted RH = 1.80, 95% CI = 1.11 to 2.90). Current smokers were less likely than never smokers to develop Kaposi’s sarcoma (adjusted RH = 0.58, 95% CI = 0.39 to 0.88). Crude RH not provided and data insufficient to calculate | Selection criteria clear and appropriate with important confounders taken into account (age, gender, race/ethnicity, HIV-1 risk behaviour, previous disease progression, baseline CD4+ lymphocyte count, Karnofsky score, use of antiretroviral therapy, use of Pneumocystis carinii prophylaxis, alcohol use, and “street” drug use) | Assessors not blinded, smoking status not biochemically verified |
| = 4 | Eskild et al (1994)27 A health clinic for homosexual and bisexual men in Oslo, Norway | Prospective cohort study of 78 HIV infected homosexual and bisexual clinic clients classified as either non-smokers (n = 31), smoking 1–20 cigarettes a day (n = 26) or more than 20 cigarettes daily (n = 21) | Diagnosis of AIDS by CDC definition (1987)26 | No association found between cigarette smoking and progression to AIDS (adjusted relative risk of developing AIDS in smokers versus non-smokers for 1–20 cigarettes per day was 0.4 (95% CI 0.1 to 1.2) and for >20 cigarettes per day was 1.1 (95% CI 0.4 to 2.7). Crude relative risks were 0.4 (95% CI = 0.2 to 1.2) and 1.1 (95% CI = 0.5 to 2.7), respectively. | Important confounders assessed by interview (age, year of HIV diagnosis, number of male lifetime partners, frequency of receptive anal intercourse, alcohol consumption). Small loss to follow up (2.5%). | Disease progression only accounted for reported year of HIV diagnosis. Smoking status not biochemical verified. Assessors not blinded. No statistically significant association found between known risk factors (number of male lifetime partners, frequency of receptive anal intercourse) and progression to AIDS suggesting study may have been underpowered |
| = 4 | Galai et al (1997)28 Baltimore, Chicago, Los Angeles, and Pittsburgh, United States | Prospective cohort study (part of Multicentre AIDS Cohort Study) of 2420 men with HIV | Included diagnosis of AIDS by CDC definition (1987),26 PCP | No association found in Kaplan-Meier or multivariate Cox regression analyses between smoking and AIDS (adjusted hazard ratio 0.96, p = 0.7, CI not provided or data available to calculate) or PCP | Large cohort with important confounders assessed (date of seroconversion, CD4+ lymphocyte count, antiretroviral and anti-PCP therapy) | Smoking status assessed only by participant completed questionnaire and not biochemically verified. Assessors not blinded |
| = 8 | Burns et al (1991)18 See table 2 | See table 2 | HIV-1 antibody seroconversion, diagnosis of AIDS by CDC definition (1987)26 | Participants who were initially HIV-1 seronegative were more likely to become seropositive if they smoked (p = 0.03). No difference between smokers and non-smokers in progression to AIDS (p = 0.31) or development of PCP. Insufficient data provided to calculate relative risk | See table 2 | See table 2 |
| = 8 | Craib et al (1992)29 Two general practices in Vancouver, Canada | Prospective cohort study of 122 seroincident homosexual men classified as either smokers (n = 74) or non-smokers (n = 48) followed up for 3 years | HIV-1 antibody seroconversion, diagnosis of AIDS by CDC definition (1987)26 | No effect of smoking on progression to AIDS (p = 0.829) or diagnosis of PCP (p = 0.894). Insufficient data provided to calculate relative risk | Representative sample with adequate assessment of disease stage at enrolment (measured by CD4+ and CD8+ lymphocyte counts and date of seroconversion). However use of log rank test meant analysis did not adjust for these confounders | Other potential confounders apart from age and disease progression not assessed. Assessors not blind to smoking status. Unclear why only 122 participants included in analysis |
| = 8 | Nieman et al (1993)30 Genitourinary medicine outpatient department in London, UK | Retrospective cohort study of 84 clients (2 women and 82 men) with AIDS (CDC definition),31 of whom 43 were classified as smokers and 41 as non-smokers (never smoked or stopped more than 12 months ago) | Diagnosis of AIDS by CDC definition (1986)31 | Median time to AIDS (all diagnoses) was 8.17 months for smokers and 14.50 months for non-smokers (p = 0.003). Median time to PCP was 9.0 months for smokers and 16.0 months for non-smokers (p = 0.002). No difference was noted between smokers and non-smokers on the development of non-PCP AIDS | Complete follow up and adequate assessment of disease stage at enrolment (CDC stages were not significantly different between smokers and non-smokers at initial assessment) | Other important confounders (eg, CD4+ cell counts and continued risk behaviours) not measured. Smoking status not biochemically verified. Assessors not blinded to smoking status |