When should antiretroviral therapy for HIV be started?
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
Andrew N Phillips
Publications and source records attributed to Andrew N Phillips.
HIV treatment response and prognosis in Europe and North America in the first decade of highly active antiretroviral therapy: a collaborative analysis.
BACKGROUND: Highly active antiretroviral therapy (HAART) for the treatment of HIV infection was introduced a decade ago. We aimed to examine trends in the characteristics of patients starting HAART in Europe and North America, and their treatment response and short-term prognosis. METHODS: We analysed data from 22,217 treatment-naive HIV-1-infected adults who had started HAART and were followed up in one of 12 cohort studies. The probability of reaching 500 or less HIV-1 RNA copies per mL by 6 months, and the change in CD4 cell counts, were analysed for patients starting HAART in 1995-96, 1997, 1998, 1999, 2000, 2001, and 2002-03. The primary endpoints were the hazard ratios for AIDS and for death from all causes in the first year of HAART, which were estimated using Cox regression. RESULTS: The proportion of heterosexually infected patients increased from 20% in 1995-96 to 47% in 2002-03, and the proportion of women from 16% to 32%. The median CD4 cell count when starting HAART increased from 170 cells per muL in 1995-96 to 269 cells per muL in 1998 but then decreased to around 200 cells per muL. In 1995-96, 58% achieved HIV-1 RNA of 500 copies per mL or less by 6 months compared with 83% in 2002-03. Compared with 1998, adjusted hazard ratios for AIDS were 1.07 (95% CI 0.84-1.36) in 1995-96 and 1.35 (1.06-1.71) in 2002-03. Corresponding figures for death were 0.87 (0.56-1.36) and 0.96 (0.61-1.51). INTERPRETATION: Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality.
Adolescent↗
A comparison between abacavir and efavirenz as the third drug used in combination with a background therapy regimen of 2 nucleoside reverse-transcriptase inhibitors in patients with initially suppressed viral loads.
BACKGROUND: Our objective was to compare the rate of viral rebound and therapy failure in patients receiving abacavir or efavirenz as the third drug (in addition to 2 non-abacavir nucleosides) in combination antiretroviral therapy (cART) and to compare the rate of metabolic alteration associated with these regimens. METHODS: We conducted a multicohort prospective observational study of human immunodeficiency virus-infected patients who had attained viral loads < or = 80 copies/mL while receiving cART, without having previously received antiretrovirals. The rates of virological rebound, therapy failure, and lipid-level alteration during follow-up were calculated as the number of events divided by person-years of follow-up (PYFU). A multivariable analysis was performed using a Poisson regression model. RESULTS: We studied a total of 744 patients; the median age was 37 years, 27% of the patients were female, and 41% were heterosexual. There was a total of 854 PYFU spent receiving efavirenz and 285 spent receiving abacavir. The nucleoside reverse-transcriptase inhibitor pairs most frequently used were zidovudine/lamivudine (66% of PYFU), stavudine/lamivudine (17.6%), and stavudine/didanosine (5.4%). The adjusted relative rates of virological failure and therapy failure for abacavir, compared with those for efavirenz, were 2.17 (95% confidence interval [CI], 1.12-4.18; P = .02) and 1.41 (95% CI, 1.01-2.01; P = .05), respectively. CONCLUSIONS: Patients with virological suppression while receiving regimens containing abacavir appear more likely to experience virological and therapy failure than those receiving efavirenz as their third drug. Although this is a selected group of adherent patients, bias cannot be ruled out, because this is a nonrandomized comparison.
Acquired Immunodeficiency Syndrome↗
Relationship between antiretrovirals used as part of a cART regimen and CD4 cell count increases in patients with suppressed viremia.
BACKGROUND: It is unknown if the CD4 cell count response differs according to antiretroviral drugs used in combination antiretroviral therapy (cART) in patients with maximal virological suppression [viral load (VL) < 50 copies/ml]. OBJECTIVES: To compare the change in CD4 cell count over consecutive measurements with VL < 50 copies/ml at both time-points according to nucleoside backbones and other antiretrovirals used. METHODS: Generalized linear models, accounting for multiple measurements within patients, were used to compare CD4 cell count changes after adjustment for antiretrovirals, time from starting cART, age, CD4 at first VL < 50 copies/ml, prior antiretroviral treatment, and change in CD4 cell count since starting cART. RESULTS: We studied 28418 instances of VL < 50 copies/ml in 4041 patients. The mean annual change in CD4 cell count was +45.5/microl [95% confidence interval (CI) +39.4 to +51.6/microl). Comparing two drug nucleoside backbones, there was a lower annual change in CD4 cell count for zidovudine/lamivudine (n = 13038; -15.4/microl; P = 0.012) and for those on tenofovir (n = 1809; -27.3/microl; P = 0.029) compared to lamivudine/stavudine (n = 7339). Compared to the boosted-protease inhibitor regimen (n = 5915), use of an abacavir-based triple-nucleoside regimen was associated with a lower annual change in CD4 cell count (n = 2504 pairs; -26.1/microl; P = 0.011). CONCLUSIONS: A nucleoside backbone of zidovudine/lamivudine or any tenofovir-based backbone was associated with significantly poorer increases in CD4 cell count compared to a nucleoside backbone of stavudine/lamivudine, as was an abacavir-based triple nucleoside regimen compared to a boosted protease inhibitor regimen. Long-term studies are needed to determine whether the differences in immunological response seen here translate into differences in the risk of clinical disease.
Adenine↗
Changes over time in risk of initial virological failure of combination antiretroviral therapy: a multicohort analysis, 1996 to 2002.
BACKGROUND: Triple-combination antiretroviral therapy (CART) for human immunodeficiency virus infection has been in use for almost a decade, but the extent to which treatment success has changed is uncertain. We examined risk of initial virological failure of CART according to the year of starting therapy. METHODS: We included subjects from 5 complete clinic cohorts in Europe and Canada who started CART without previous antiretroviral therapy from 1996 to 2002 with 1 or more pre-CART viral load (VL) measurement and CD4 count. Based on the first VL measurement from 6 to 12 months after CART initiation, virological failure was defined as a VL of more than 500 copies/mL. We used the following 3 inclusion strategies: (1) including all subjects, with missing VL measurement counted as virological failure (n = 3825; strategy A); (2) including all subjects with VL measurement (n = 3120; strategy B); and (3) including all subjects receiving antiretroviral therapy at VL measurement (n = 2890; strategy C). RESULTS: From 1996 to 2002, risk of virological failure fell from 38.9% to 24.8% for strategy A, 28.4% to 12.0% for strategy B, and 22.8% to 8.2% for strategy C. Estimated relative reductions in risk (95% confidence interval) over the 7-year period, adjusted for cohort, demographic factors, pre-CART VL and CD4 count, and previous AIDS, were 48% (39%-56%), 64% (53%-73%), and 79% (69%-85%) for strategies A, B, and C, respectively. Reductions in risk were greatest from 1996 to 1999, with weaker trends subsequently. Trends remained but were attenuated after further adjustment for the starting regimen. CONCLUSIONS: Over a 7-year period of CART use in clinical practice, risk of initial virological failure of treatment has halved at least. These data suggest the trend is due to improvements in CART regimens and greater effectiveness of their use.
Adult↗
Deaths in the era of HAART: contribution of late presentation, treatment exposure, resistance and abnormal laboratory markers.
OBJECTIVES: To describe the characteristics of deaths that occur among HIV-positive individuals in the HAART era. DESIGN: Observational database. METHODS: Deaths were reviewed that occurred among HIV-positive individuals seen at the Royal Free Hospital, London between January 1998 and December 2003. RESULTS: Over the study period, there were 121 deaths; death rates declined from approximately 2.0/100 person-years of follow-up in 1998-2000 to approximately 1.0/100 person-years of follow-up in 2001-2003. Approximately one half of deaths (45.5%) were from AIDS-related causes and 74 deaths (61.2%) occurred in individuals who had received HAART: patients had been exposed to a median of seven (range 2-14) antiretroviral drugs and two-fifths had started treatment in the pre-HAART era. Another 15 patients had received only non-HAART treatment regimens prior to death. The median pre-death CD4 cell counts were 68 and 167 cells/microl among those who had and had not received HAART; 23 (31.1%) and 4 (8.5%) had HIV RNA < 400 copies/ml, respectively. Of the patients exposed to HAART for at least 6 months and who experienced viral rebound, information was available on resistance for 26 (21.5% of the total deaths) and 19 of those tested had at least one resistance mutation (median 5, range, 1-16). CONCLUSIONS: While mortality rates among HIV-infected individuals at our centre have fallen since 1988, the deaths that do now occur are more diverse and are the result of a number of factors, including late presentation, delayed uptake of HAART and the previous use of treatment combinations that are now viewed as suboptimal.
Adolescent↗
Limited but increasing use of treatment for hepatitis C across Europe in patients coinfected with HIV and hepatitis C.
Uptake of hepatitis C (HCV) treatment in HIV-coinfected patients is not well described. Of 2356 HCV-seropositive patients, 180 (7.6%) started HCV treatment with interferon-based therapies. In multivariate Poisson-regression models, there was a 38% increase per year in the incidence of starting HCV treatment (95% CI 26 - 51%, p<0.0001); this increased from 3.9 per 1000 person-years follow-up (PYFU) before 1998 (95% CI 1.6 - 6.1) to 32.6 per 1000 PYFU at/after 2004 (95% CI 22.5 - 42.7). Although prescription of HCV therapy is increasing in HIV-coinfected patients, it remains infrequent and variable across regions of Europe.
Antiviral Agents↗
Regional changes over time in initial virologic response rates to combination antiretroviral therapy across Europe.
BACKGROUND: Changes in virologic response to initial combination antiretroviral therapy (cART) over calendar time may indicate improvements in cART or emergence of primary resistance. Regional variations may identify differences in available antiretroviral drugs or patient management. METHODS: Virologic response (viral load < 500 copies/mL) 6 to 12 months after starting cART was analyzed in antiretroviral-naive EuroSIDA patients. Analyses were stratified by region (south, central west, north, east) or time started cART (early, 1996-1997; mid, 1998-1999; late, 2000-1904). RESULTS: Virologic suppression was achieved by 60% of 2102 patients: 57% south (n = 560), 61% central west (n = 466), 63% north (n = 606), 58% east (n = 470) (P = 0.091). An increase was observed over time: 52% early cART, 56% mid cART, 69% late cART (P < 0.001). Overall, there were significant effects of region (P = 0.026) and time (P < 0.001) on virologic response after adjustment for confounders. Stratified by period, regional differences were less evident (early cART, P = 0.967; mid cART, P = 0.291; late cART, P = 0.163). Stratified by region, temporal changes were observed (south, P = 0.061; central west, P < 0.001; north: P = 0.070; east, P = 0.001). CONCLUSIONS: There was some evidence of regional differences in initial virologic response to cART. Improvements over time were observed, suggesting that so far, the effect of primary resistance has not been of sufficient magnitude to prevent increasing suppression rates.
Anti-HIV Agents↗
Is there evidence for an increase in the death rate from liver-related disease in patients with HIV?
BACKGROUND: Increases in deaths due to liver-related disease (LRD) among HIV-infected individuals have been reported although the influence of combination antiretroviral therapy (cART) on LRD is controversial. AIMS: To determine changes over time in the death rate from LRD and if longer exposure to cART was associated with an increased death rate from LRD in 10 937 patients from EuroSIDA, an observational longitudinal cohort study. RESULTS: A total of 184 (1.7%) died from LRD during 52 236 person-years of follow-up (PYFU). The death rate from LRD declined from 6.9 per 1000 PYFU before 1995 [95% confidence interval (CI), 3.9-9.9] to 2.6 at/after 2004 (95% CI, 1.6-4.0). When the current CD4 cell count and other factors were taken into account, there was a 13% increase in the death rate from LRD per year (95% CI, 5-20%, P = 0.0008). In patients who had started cART, there was a 12% increase in the death rate from LRD per additional year exposure to cART (95% CI, 4-20%, P = 0.022) after adjustment for current CD4 cell count and other factors. CONCLUSIONS: Death rates from LRD appeared to decrease across Europe. However after adjustment for the current CD4 cell count, and therefore increases in CD4 cell counts in patients taking cART, there was a significant increase over time in death rates from LRD. In patients with similar CD4 cell counts, longer exposure to cART was associated with an increased death rate from LRD. This may be due to direct liver toxicity of antiretrovirals, progression of liver disease due to hepatitis B virus or hepatitis C virus over time as patients survive longer, or some other factor.
Adult↗
Incidence of Tuberculosis among HIV-infected patients receiving highly active antiretroviral therapy in Europe and North America.
BACKGROUND: We obtained estimates of the incidence of tuberculosis (TB) among patients receiving HAART and identified determinants of the incidence. METHODS: We analyzed the incidence of TB during the first 3 years after initiation of HAART among 17,142 treatment-naive, AIDS-free persons starting HAART who were enrolled in 12 cohorts from Europe and North America. We used univariable and multivariable Poisson regression models to identify factors associated with the incidence. RESULTS: During the first 3 years (36,906 person-years), 173 patients developed TB (incidence, 4.69 cases per 1000 person-years). In multivariable analysis, the incidence rate was lower for men who have sex with men, compared with injection drug users (relative rate, 2.46; 95% confidence interval [CI], 1.51-4.01), heterosexuals (relative rate, 2.42; 95% CI, 1.64-3.59), those with other suspected modes of transmission (relative rate, 1.66; 95% CI, 0.91-3.06), and those with a higher CD4+ count at the time of HAART initiation (relative rate per log2 cells/microL, 0.87; 95% CI, 0.84-0.91). During 28,846 person-years of follow-up after the first 6 months of HAART, 88 patients developed TB (incidence, 3.1 cases per 1000 person-years of follow-up). In multivariable analyses, a low baseline CD4+ count (relative rate per log2 cells/microL, 0.89; 95% CI, 0.83-0.96), 6-month CD4+ count (relative rate per log2 cells/microL, 0.90; 95% CI, 0.81-0.99), and a 6-month HIV RNA level >400 copies/mL (relative rate, 2.21; 95% CI, 1.33-3.67) were significantly associated with the risk of acquiring TB after 6 months of HAART. CONCLUSION: The level of immunodeficiency at which HAART is initiated and the response to HAART are important determinants of the risk of TB. However, this risk remains appreciable even among those with a good response to HAART, suggesting that other interventions may be needed to control the TB epidemic in the HIV-infected population.
Adult↗
Twenty five years of HIV infection in haemophilic men in Britain: an observational study.
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Adolescent↗
The rate of viral rebound after attainment of an HIV load <50 copies/mL according to specific antiretroviral drugs in use: results from a multicenter cohort study.
BACKGROUND: Relatively few data are available on the association between the use of specific antiretroviral drugs and the rate of viral rebound in those attaining a viral load (VL) <50 copies/mL while receiving highly active antiretroviral therapy (HAART). METHODS: Patients achieving a VL <50 copies/mL for the first time while receiving HAART were followed until viral rebound (2 consecutive VLs >500 copies/mL). Pre-HAART antiretroviral-naive patients were analyzed separately from those with nucleoside reverse transcriptase inhibitor (NRTI) experience. RESULTS: Of 3565 suppressed antiretroviral-naive patients, 381 experienced viral rebound (rate, 6.26 events/100 person-years of follow-up [pyrs] [95% confidence interval {CI}, 5.63-6.89 events/100 pyrs]). For those receiving efavirenz, the rate was 4.08 (95% CI, 3.16-5.01) events/pyrs. Compared with this, the rebound rate for those receiving indinavir was 1.52 times higher (rate ratio [RR], 1.52 [95% CI, 0.82-2.84]). RRs (95% CIs) for other drugs were: soft-gel saquinavir, 0.54 (0.07-3.97); nelfinavir, 2.44 (1.68-3.54); indinavir/ritonavir, 1.96 (1.02-3.77); saquinavir/ritonavir, 1.12 (0.48-2.61); lopinavir/ritonavir, 1.23 (0.58-2.59); nevirapine, 1.53 (1.11-2.10); and abacavir, 2.03 (1.26-3.25). Of 810 NRTI-exposed patients, 145 experienced viral rebound (rate, 8.29 [95% CI, 6.94-9.64] events/pyrs). For those receiving efavirenz, the rate was 5.25 (95% CI, 3.11-8.30) events/pyrs. Compared with this, the RRs (95% CIs) were: indinavir, 1.75 (0.82-3.73); hard-gel saquinavir, 3.48 (0.36-33.37); nelfinavir, 2.64 (1.37-5.08); indinavir/ritonavir, 0.32 (0.04-2.49); saquinavir/ritonavir, 0.64 (0.23-1.80); nevirapine, 1.65 (0.90-3.02); and abacavir, 1.82 (0.73-4.52). CONCLUSIONS: We must make comparisons of antiretroviral outcomes in observational data with caution; however, our results suggest that, in those with VLs <50 copies/mL, certain drugs may be associated with higher rebound rates than others.
Adult↗
Impact of therapeutic immunization on HIV-1 viremia after discontinuation of antiretroviral therapy initiated during acute infection.
BACKGROUND: Treatment strategies that would induce durable virological control of human immunodeficiency virus (HIV)-1 in the absence of continued antiretroviral therapy (ART) are highly desirable.METHODS. We assessed, in a randomized, double-blind, placebo-controlled trial, whether the addition of therapeutic vaccines (ALVAC-HIV [vCP1452] or ALVAC-HIV and Remune) to ART initiated during acute infection could increase the probability of having a plasma viral load </=1000 HIV-1 RNA copies/mL 24 weeks after planned discontinuation of ART.RESULTS. All 79 randomized subjects completed the immunization schedule, and 78 discontinued ART with no major safety concerns. After immunization, subjects in the vaccine study arms had significantly increased HIV-1-specific CD4(+) and CD8(+) T cell responses, by interferon- gamma enzyme-linked immunospot assay, compared with those in the placebo study arm. Overall, 17.7% of subjects had </=1000 HIV-1 RNA copies/mL 24 weeks after discontinuation of ART, with no significant difference between the vaccine study arms and the placebo study arm (15.4% vs. 22.2%; difference, -6.8% [95% confidence interval, -26.8% to 10.0%]; P=.54).CONCLUSION. Therapeutic immunization and ART, compared with ART alone, generated HIV-1-specific cellular immunity but did not lead to better virological control of HIV-1 24 weeks after discontinuation of ART. Our trial design appears to be feasible and safe for testing future immune-boosting strategies.
AIDS Vaccines↗
Long term probability of detection of HIV-1 drug resistance after starting antiretroviral therapy in routine clinical practice.
BACKGROUND: Little is known about the long term risk of development of HIV-1 drug resistance for patients starting antiretroviral therapy (ART) with three or four drug regimens in routine clinical practice. METHODS: We analysed a large cohort study of patients seen in one of six large HIV clinics in and around London, UK. The focus of this analysis was on patients who started ART with two nucleosides plus either a single protease inhibitor (PI), a PI with ritonavir, abacavir or a non-nucleoside reverse transcriptase inhibitor (NNRTI). RESULTS: 4306 patients were followed; 1436 (33%) started with a single PI, 279 (6%) with a PI plus ritonavir, 156 (4%) with triple nucleosides and 2435 (57%) with an NNRTI. The overall cumulative risk of viral load failure was 38% by 6 years. Risk of > or =1 major IAS-USA mutation was 27% by 6 years; risk of mutations from at least two of the three main drug classes was 20% over the same period. These are lower limit estimates as test results were not available for many with viral load failure. Risk of PI mutations being detected in people who started ART with regimens containing a PI with ritonavir was significantly lower than the risk of NNRTI mutations being detected in those starting with NNRTI-containing regimens (relative hazard 0.3195% CI 0.15-0.61; p = 0.0008). CONCLUSION: In routine practice, rates of viral load failure and of resistance detection in patients who started ART with three or four drugs are appreciable.
Adult↗
Treatment exhaustion of highly active antiretroviral therapy (HAART) among individuals infected with HIV in the United Kingdom: multicentre cohort study.
OBJECTIVES: To investigate whether there is evidence that an increasing proportion of HIV infected patients is starting to experience increases in viral load and decreases in CD4 cell count that are consistent with exhaustion of available treatment options. DESIGN: Multicentre cohort study. SETTING: Six large HIV treatment centres in southeast England. PARTICIPANTS: All individuals seen for care between 1 January 1996 and 31 December 2002. MAIN OUTCOME MEASURES: Exposure to individual antiretroviral drugs and drug classes, CD4 count, plasma HIV RNA burden. RESULTS: Information is available on 16,593 individuals (13,378 (80.6%) male patients, 10,340 (62.3%) infected via homosexual or bisexual sex, 4426 (26.7%) infected via heterosexual sex, median age 34 years). Overall, 10,207 of the 16,593 patients (61.5%) have been exposed to any antiretroviral therapy. This proportion increased from 41.2% of patients under follow up at the end of 1996 to 71.3% of those under follow up in 2002. The median CD4 count and HIV RNA burden of patients under follow up in each year changed from 270 cells/mm3 and 4.34 log10 copies/ml in 1996 to 408 cells/mm3 and 1.89 log10 copies/ml, respectively, in 2002. By 2002, 3060 (38%) of patients who had ever been treated with antiretroviral therapy had experienced all three main classes. Of these, around one quarter had evidence of "viral load failure" with all these three classes. Patients with three class failure were more likely to have an HIV RNA burden > 2.7 log10 copies/ml and a CD4 count < 200 cells/mm3. CONCLUSIONS: The proportion of individuals with HIV infection in the United Kingdom who have been treated has increased gradually over time. A substantial proportion of these patients seem to be in danger of exhausting their options for antiretroviral treatment. New drugs with low toxicity, which are not associated with cross resistance to existing drugs, are urgently needed for such patients.
Adolescent↗
Risk of AIDS and death at given HIV-RNA and CD4 cell count, in relation to specific antiretroviral drugs in the regimen.
BACKGROUND: It is unknown whether the relationship between the HIV-RNA/CD4 cell count and risk of clinical disease continues to hold true for newer antiretroviral drugs approved without data from clinical endpoint trials. OBJECTIVE: : To determine and compare whether rate ratios of AIDS and death at given, latest HIV-RNA and CD4 cell counts levels were similar, regardless of which nucleoside pair and specific third drugs patients received as antiretroviral therapy. DESIGN: EuroSIDA observational cohort. A total of 9802 prospectively followed patients. METHODS: Analysis included patients taking combination antiretroviral therapy (CART) regimens containing two non-abacavir nucleosides plus a 'third drug' of a non-nucleoside reverse transcriptase inhibitor, a (possibly ritonavir boosted) protease inhibitor or abacavir. RESULTS: A total of 6814 patients contributed a total of 22 766.6 person-years of follow up. Median latest CD4 cell count was 353 x 10 cells/l, HIV-RNA 199 copies/ml. A total of 900 events of new AIDS or death were observed. AIDS/death rates for any given CD4 or HIV-RNA category were similar regardless of specific drugs being used. Adjusted rate ratios (RR) for individual drugs compared with indinavir (for which clinical endpoint trials are available) were all close to 1 and with relatively narrow 95% confidence intervals (CI); for example, nelfinavir RR, 0.99 (95% CI, 0.76-1.28); efavirenz RR, 0.83 (95% CI, 0.57-1.20); abacavir RR, 1.01 (95% CI, 0.64-1.60). Results were similar for different nucleoside pairs. CONCLUSIONS: The results indicate that AIDS/death rates for given CD4 cell count and HIV-RNA categories are similar, regardless of CART regimen being taken and provide reassurance that HIV-RNA and CD4 cell counts in individual patients receiving newer drugs have the same meaning, in terms of AIDS/death risk, regardless of specific antiretroviral regimen.
Acquired Immunodeficiency Syndrome↗
Changes over time in post-seroconversion CD4 cell counts in the Italian HIV-Seroconversion Study: 1985-2002.
OBJECTIVE: To determine whether there has been a tendency for early post-seroconversion CD4 cell counts to change over calendar time. DESIGN: A prospective cohort study of individuals with well-estimated dates of seroconversion. METHODS: We studied 1251 individuals who seroconverted to HIV in Italy between 1985 and 2002, and for whom the first CD4 count was measured within 2 years of seroconversion and before any use of antiretrovirals. Linear regression models were used to assess evidence for a trend in post-seroconversion CD4 cell count over time. RESULTS: The median post-seroconversion CD4 cell count was 674 x 10 cells/l in those seroconverting between 1985 and 1990, 588 x 10 cells/l for 1991 to 1994, 559 x 10 cells/l for 1995 to 1998 and 494 x 10 cells/l for 1999 to 2002. The post-seroconversion CD4 cell count decreased by an average of 8.4 x 10 cells/l per year (95% confidence interval, 4.0-12.9; P < 0.001), after adjustment for potential confounders, including interval between HIV-negative and HIV-positive tests, lag time for first CD4 cell count measurement, age at seroconversion, gender, HIV-transmission group, and clinical centre. The finding was consistent in sensitivity analyses restricted to those with information on acute infection. CONCLUSION: These data suggest a possible decreasing trend in CD4 cell count immediately following seroconversion in Italy which requires further investigation.
AIDS-Related Opportunistic Infections↗
Decline in esophageal candidiasis and use of antimycotics in European patients with HIV.
BACKGROUND: Esophageal candidiasis (EC) remains one of the most common AIDS defining illnesses in patients with human immunodeficiency virus (HIV) in the era of highly active antiretroviral therapy (HAART), but little is known about factors associated with EC after starting HAART. OBJECTIVES: To describe changes in the use of antimycotic medication, the incidence of EC and factors associated with EC before and after starting HAART. METHODS: Patients from EuroSIDA, a pan-European longitudinal, prospective observational study. Generalized linear models and poisson regression models were used to investigate the relationships. RESULTS: A total of 9,873 patients did not have EC at recruitment, subsequently 537 (15.8%) developed EC. The proportion of patients taking any antimycotic dropped from 18% at January 1995 to 2% at January 2004 (p < 0.0001); the duration of treatment declined from 10 to 3 months over the same period (p < 0.0001). There was a 32% annual decline in the incidence of EC (95% CI 30-35%, p < 0.0001). There was a significant annual decline in the incidence of EC pre-HAART in time-updated, adjusted models, (incidence rate ratio (IRR) 0.80, 95% CI 0.76-0.85, p < 0.0001) but not post-HAART (IRR 0.97; 95% CI 0.90-1.06, p= 0.54). Older patients and those with low CD4 counts had the greatest incidence of EC in the post-HAART era. CONCLUSIONS: There has been a marked decline in the incidence of EC between 1994 and 2004. This was accompanied by a decline in markers associated with fungal disease, including use of antimycotics and a decline in duration of treatment.
AIDS-Related Opportunistic Infections↗