SEARCH · PubMed Health

Results for “CD4 Lymphocyte Count”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources

PubMed2003

Sarcoidosis following HIV infection: evidence for CD4+ lymphocyte dependence.

BACKGROUND: The chronic granulomatous inflammation of sarcoidosis has been hypothesized to depend on the CD4+ T-helper lymphocyte. HIV infection, which depletes these cells, has been reported to attenuate the manifestations of sarcoidosis. STUDY OBJECTIVES: We asked whether the development of symptomatic sarcoidosis in the context of preexisting HIV infection was dependent on the CD4+ lymphocyte count. DESIGN: We performed a retrospective standardized chart review of all patients who developed granulomatous inflammation following HIV infection at an urban academic referral center. MEASUREMENTS: We identified seven patients with sarcoidosis within this cohort and compared their CD4+ lymphocyte count to that in a cohort of 16 patients in whom similar granulomatous inflammation was found but who did not have sarcoidosis. We then compared our cases to all reported cases using a systematic literature review. RESULTS: The CD4+ lymphocyte count was > 200 cells/ microL in all of our patients with HIV infection when they developed subsequent sarcoidosis. In contrast, specific etiologies for granulomatous inflammation were found in all 10 HIV-infected patients who presented with granulomatous inflammation and a CD4+ lymphocyte count of < 200 cells/ microL, with infectious etiologies found in 8 patients. Similarly, there was relative preservation of the CD4+ lymphocyte count in previously reported cases, with 14 of 19 patients (74%) having an absolute CD4+ lymphocyte count of > 200 cells/ microL. CONCLUSIONS: We conclude that the development of the chronic granulomatous inflammation of sarcoidosis appears to depend on the preservation or restoration of the peripheral CD4+ lymphocyte count and that in most cases the CD4+ lymphocyte count exceeds 200 cells/ microL. Furthermore, alternative specific etiologies of granulomatous inflammation are generally identifiable in HIV-infected patients with peripheral CD4+ lymphocyte counts of < 200 cells/ microL.

AIDS-Related Opportunistic Infections↗

PubMed1995

Risk factors for cotton-wool spots and for cytomegalovirus retinitis in patients with human immunodeficiency virus infection.

PURPOSE: To investigate the risk factors for cotton-wool spots and for cytomegalovirus retinitis in patients with human immunodeficiency virus infection (HIV). METHODS: A cross-sectional study was performed on 453 consecutive male patients with a positive serodiagnosis for HIV. The possible risk factors of age, race, absolute T-lymphocyte CD4+ count, and mode of HIV acquisition were evaluated. RESULTS: Age and race were not significant predictors of either cotton-wool spots or cytomegalovirus retinitis. Low CD4+ T-lymphocyte counts were the strongest predictor of both types of retinopathy. After adjustment for CD4+ T-lymphocyte counts by logistic regression, patients who had acquired HIV through homosexual or bisexual activity were more likely to have cotton-wool spots (odds ratio, 2.09; P = 0.029) and cytomegalovirus retinitis (odds ratio, 4.14; P = 0.0028) than were patients who had acquired the disease intravenously. CONCLUSIONS: The results of this study showed that the ocular manifestations of HIV infection are associated with low CD4+ counts and HIV acquisition through bisexual or homosexual activity. Patients with these risks factors should be targeted for prophylaxis and prevention strategies for cytomegalovirus retinitis.

Adult↗

PubMed2003

Improved outcomes with earlier initiation of highly active antiretroviral therapy among human immunodeficiency virus-infected patients who achieve durable virologic suppression: longer follow-up of an observational cohort study.

On the basis of studies with relatively short follow-up, treatment guidelines currently recommend that highly active antiretroviral therapy (HAART) be initiated in asymptomatic human immunodeficiency virus-infected patients when the CD4+ lymphocyte count is < or =200 cells/mm3. We assessed the development of a new opportunistic infection or death among 1173 patients initiating HAART. Durable virologic suppression was defined as having more undetectable (<400 copies/mL) than detectable virus loads after the initiation of therapy. The median durations of therapy and follow-up were 29 and 36 months, respectively. Among patients who achieved durable virologic suppression, those with baseline CD4+ lymphocyte counts of <200 cells/mm3 tended to progress faster than those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 (P=.09) and progressed faster than those with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.01). Among those with durable virologic suppression, there was no difference in disease progression between those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 and those with durable virologic suppression with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.40). Initiating HAART with a CD4+ lymphocyte count of <200 cells/mm3 was associated with a higher risk of disease progression, even with durable virologic suppression. HAART should be initiated at CD4+ lymphocyte counts of >200 cells/mm3.

Adult↗

PubMed2005

Stavudine entry into cerebrospinal fluid after single and multiple doses in patients infected with human immunodeficiency virus.

STUDY OBJECTIVE: To establish the pharmacokinetics of stavudine within the cerebrospinal fluid (CSF) of patients infected with human immunodeficiency virus (HIV). DESIGN: Pharmacokinetic study. SETTING: General clinical research center. PATIENTS: Thirty-six patients infected with HIV; 21 were receiving long-term stavudine therapy, 15 were not (single-dose treatment group). INTERVENTION: After an overnight fast, all patients received a single dose of stavudine 40 mg. Fifteen patients in the long-term treatment group and all 15 patients in the single-dose treatment group were randomized to undergo lumbar puncture 2, 4, or 6 hours after dosing (five patients for each time point from each group). The six other patients in the long-term treatment group underwent lumbar puncture 0 or 8 hours after dosing. MEASUREMENTS AND MAIN RESULTS: Serum stavudine concentrations were obtained just before dosing, 1 hour after dosing (approximate peak), and at the time of lumbar puncture. The CSF was also analyzed for cell counts, protein, and glucose levels. The mean peak serum stavudine concentration in the long-term treatment group was estimated to be 580.7 ng/ml (2.59 micromol/L), occurring approximately 1.3 hours after dosing. The CSF concentrations over 0-8 hours were 0.0-109.9 ng/ml (0.00-0.49 micromol/L) with an overall mean of 51.6 ng/ml (0.23 micromol/L). Mean peak CSF concentration was estimated to be 62.8 ng/ml (0.28 micromol/L), occurring 4.7 hours after dosing. For the 15 patients not taking stavudine, both the serum and the CSF estimated peaks were significantly lower than those of the long-term group: 475.3 ng/ml (2.12 micromol/L) and 40.4 ng/ml (0.18 micromol/L), respectively. However, time to peak was similar at 1.2 hours and 5.0 hours, respectively. In both groups, no correlation was found between CSF and baseline or peak serum stavudine concentrations, CSF white blood cell count, baseline CD4 + lymphocyte count, or plasma viral load. CONCLUSION: Mean CSF stavudine concentrations equaled or exceeded the mean concentration producing 50% of the maximal effect in vivo (EC 50 ) for HIV. The CSF concentrations were higher in the stavudine-experienced patients, indicating that concentrations rise with progressive doses until steady state is reached.

Adult↗

PubMedDate not supplied

CD4 lymphocyte numbers after splenectomy in patients infected with the human immunodeficiency virus.

Splenectomy has been reported to alter inconsistently the CD4 lymphocyte numbers in patients infected with the human immunodeficiency virus (HIV). To further assess the effect of splenectomy we have retrospectively examined the charts of 10 patients who were infected with HIV and who had undergone splenectomy. There was a significant increase in the mean CD4 numbers following splenectomy (mean increase of 326/microliters, or 2.1-fold, P = 0.0009), the total lymphocyte numbers (mean increase of 1.55/ml, or 2.2-fold, P = 0.001) and in the CD8 lymphocyte count (mean increase of 968/microliters, or 2.3-fold, P = 0.014). No significant difference was observed in the percentage CD4 lymphocytes (P = 0.95) or in the CD4:CD8 lymphocyte ratio (P = 0.76). In two patients, symptoms suggestive of impaired immune function developed post-splenectomy, at a time when their CD4 lymphocyte numbers were markedly higher than their pre-splenectomy values. One developed oral candidiasis (CD4 960/microliters, percentage CD4 32%), and in one patient a 7 kg weight loss was associated with recurrent mouth ulcers (CD4 680/microliters, percentage CD4 7%). We conclude that the total CD4 count increases significantly after splenectomy while the percentage CD4 lymphocyte count and CD4:CD8 lymphocyte ratio do not. Our data suggest that the CD4 lymphocyte count overestimates the immune function in these patients, although our findings are not conclusive.

CD4-CD8 Ratio↗

PubMed2001

Salivary calprotectin levels are raised in patients with oral candidiasis or Sjögren's syndrome but decreased by HIV infection.

Calprotectin levels were determined in whole saliva from patients predisposed to oral candidiasis due to HIV infection or Sjögren's syndrome and from patients with candidiasis associated with various oral disorders (e.g. lichen planus, oral ulceration). Mean calprotectin levels were higher in whole saliva (2 microgram/ml) than in parotid saliva (0.3 microgram/ml). Oral candidiasis was associated with raised whole saliva calprotectin levels in all groups studied. HIV infection was associated with lower levels of salivary calprotectin, in the presence of high or low salivary Candida counts, although CD4+ lymphocyte counts did not significantly correlate with calprotectin concentrations. Calprotectin levels were elevated in saliva from Sjögren's syndrome patients with oral candidiasis, consistent with mucosal transudation of calprotectin from inflamed mucosa and limited dilution due to decreased salivary flow rates. This study indicates that oral candidiasis is associated with raised calprotectin levels secondary to mucosal inflammation, but that diminution of this candidacidal factor due to HIV infection may be a predisposing factor in the aetiology of oral candidiasis.

CD4 Lymphocyte Count↗

PubMed2001

Association of immune complexes and plasma viral load with CD4+ cell depletion, CD8+ DR+ and CD16+ cell counts in HIV+ hemophilia patients. Implications for the immunopathogenesis of HIV-induced CD4+ lymphocyte depletion.

OBJECTIVE: There is evidence that HIV induces CD4+ depletion in part by the formation of immune complexes (IC) that attach to CD4+ blood lymphocytes. In the present study we examined the relationship of IC-coated CD4+ blood cells with retroviral replication in HAART-treated patients. PATIENTS AND METHODS: 52 hemophilia patients were studied from 1997 to 1999. Lymphocyte subsets, IgM, IgG and gp120 on CD4+ blood cells, in vitro responses of lymphocytes to mitogens, plasma neopterin and plasma viral load were measured. RESULTS: Patients with detectable viral replication and without ICs on CD4+ blood lymphocytes had a lower viral load (4100 versus 21000 HIV-1 mRNA copies/ml; P = 0.079) and higher CD4+ cell counts (310/microl versus 161/microl; P = 0.035) than patients with ICs on circulating CD4+ lymphocytes. Among patients with < 80 HIV-1 mRNA copies/ml, IC- individuals had slightly higher CD4+ lymphocyte counts than IC+ patients (384/microl versus 316/microl; n.s.). Further evidence for the clinical relevance of the ICs was obtained when 18 patients who had an undetectable viral load at previous investigations were analyzed. Among patients with a stable undetectable viral load, CD4+ counts increased in 6 of 8 IC- but in none of 2 IC+ individuals. In patients whose viral load increased during the observation period, 5 of 6 IC- but none of 2 IC+ individuals showed higher CD4+ cell counts. Impaired virus killing is suggested by lower CD16+ (35/microl versus 107/microl; P = 0.016), higher CD3+ DR+ (178/microl versus 66/microl; P = 0.006), and higher CD8+ DR+ (142/microl versus 34/microl; P = 0.017) cell counts in IC(-) patients compared to IC- patients without detectable viral load. Strong retroviral replication induced strong T cell dysfunctions. Fewer CD3+ 25+ blood lymphocytes (19/microl versus 47/microl; P = 0.006) and a lower in vitro response of T lymphocytes to the mitogens Con A (RR: 0.3 versus 1.2; P=0.023) and CD3 mab (RR: 0.5 versus 2.4; P = 0.012) was observed in IC+ patients with detectable versus undetectable viral load. CONCLUSION: Our data suggest that ICs on circulating CD4+ blood lymphocytes are primarily associated with CD4+ lymphocyte depletion whereas the plasma viral load is primarily associated with decreased T lymphocyte activation, lower CD16+ counts, and higher CD8+ DR+ lymphocytes which might be the effector cells for virus elimination.

Antigen-Antibody Complex↗

PubMed1992

Natural history of advanced HIV disease in patients treated with zidovudine. The Zidovudine Epidemiology Study Group.

OBJECTIVE: To describe the natural history of advanced HIV disease in patients treated with zidovudine. DESIGN: Longitudinal, observational study. SETTING: Twelve academic and community-based sites. PATIENTS, PARTICIPANTS: Eight hundred and sixty-three patients with AIDS or AIDS-related complex (ARC) with a CD4+ lymphocyte count less than 250 x 10(6)/l, who first received zidovudine between 15 April 1987 and 14 April 1988. MAIN OUTCOME MEASURES: Survival, progression to AIDS and first development of specific opportunistic illness. RESULTS: Median survival after initiation of zidovudine therapy ranged from greater than 900 days in patients with a baseline CD4+ lymphocyte count greater than or equal to 150 x 10(6)/l to 560 days in patients with a CD4+ lymphocyte count less than 50 x 10(6)/1. Other factors associated significantly with poorer survival were diagnosis of AIDS (versus ARC), baseline age greater than or equal to 40 years, hematocrit less than 35%, and diminished functional status. In patients with ARC at enrollment, median time of progression to AIDS ranged from 810 days in patients with a CD4+ lymphocyte count greater than or equal to 150 x 10(6)/l to 310 days in patients with a CD4+ lymphocyte count less than 50 x 10(6)/l. Rates of development of specific opportunistic infections or neoplasms and HIV encephalopathy were determined for different baseline CD4+ lymphocyte count ranges. Myelosuppression was significantly more common in patients with CD4+ lymphocyte counts greater than or equal to 100 x 10(6)/l. Sixty-five per cent of patients with a CD4+ lymphocyte count greater than or equal to 100 x 10(6)/l and 51% with a CD4+ lymphocyte count less than 100 x 10(6)/l continued to receive zidovudine 2 years after starting therapy. CONCLUSIONS: We describe the natural history of a cohort of patients treated with zidovudine for advanced HIV disease. These CD4+ lymphocyte count-stratified estimates of disease progression should provide prognostic information useful in the clinical management of advanced disease and the design of future studies.

AIDS-Related Complex↗

PubMed1995

Immunodeficiency and elevated CD4 T lymphocyte counts in two patients coinfected with human immunodeficiency virus and human lymphotropic virus type I.

We describe two patients who were coinfected with human immunodeficiency virus (HIV) and human T-cell lymphotropic virus (HTLV) type I. They had clinical evidence of immunodeficiency (anergy, oral candidiasis, and disseminated herpes zoster) despite having elevated CD4 T lymphocyte counts (range, 2,450-5,292/mm3). We conclude that CD4 lymphocyte counts may not be reliable markers of immunologic competence in patients coinfected with HIV and HTLV-I.

Adult↗

PubMed1992

Risk of developing cytomegalovirus retinitis in persons infected with the human immunodeficiency virus.

This study examines the risk of developing cytomegalovirus (CMV) retinitis as a function of the duration and degree of CD4+ lymphocyte depletion. A retrospective analysis of 135 persons infected with the human immunodeficiency virus (HIV) was performed. Kaplan-Meier estimates for the percentage of patients developing CMV retinitis during the 27-month study period were calculated. Twenty-six patients were diagnosed as having CMV retinitis. In 14 of these patients, T cell phenotyping was done within the 3 months preceding diagnosis. The mean CD4+ lymphocyte count for these patients was 15.6 cells/mm3 (range, 2-33/mm3). At 27 months, the percentage of patients developing CMV retinitis with baseline CD4+ lymphocyte counts of 0-50, 51-100, and 101-250 cells/mm3 was 41.9%, 26.3%, and 14.7%, respectively (log-rank test, p = 0.003). The odds ratio for developing CMV retinitis for those with baseline CD4+ lymphocyte counts of 0-50 cells/mm3 compared with those with CD4+ lymphocyte counts of 101-250 cells/mm3 was 4.62 (p = 0.002). Twenty-four patients had CD4+ lymphocyte counts of < or = 50 cells/mm3 for an average of 13.1 months prior to diagnosis. Twenty-two patients had an acquired immune deficiency syndrome (AIDS)-defining illness diagnosed for an average of 18.0 months prior to the onset of retinitis. CMV retinitis is most likely to develop in patients with AIDS when the CD4+ lymphocyte count is < or = 50 cells/mm3.

Acquired Immunodeficiency Syndrome↗

PubMed2003

Total lymphocyte count and hemoglobin combined in an algorithm to initiate the use of highly active antiretroviral therapy in resource-limited settings.

OBJECTIVE: To develop clinical algorithms that improve the sensitivity of surrogate markers to initiate the use of highly active antiretroviral therapy (HAART) in resource-limited settings. DESIGN: A retrospective evaluation of total lymphocyte counts (TLC) and hemoglobin to predict the CD4 lymphocyte count. METHODS: A total of 3269 members of the Johns Hopkins HIV observational cohort contributed 22 690 paired observations of CD4 lymphocyte counts and TLC. Two methods were used to evaluate the effect of combining TLC and hemoglobin to predict CD4 cell counts below 200 cells/mm3 before the initiation of HAART in 1451 participants; 55.3% of participants had CD4 cell counts below 200 cells/mm3. RESULTS: TLC below 1200 cells/mm3 and hemoglobin below 12 g/dl significantly predicted CD4 cell counts below 200 cells/mm3. For TLC alone sensitivity was 70.7% and specificity was 81.7%. For both men and women, we chose a TLC lower cutoff point of 1200 cells/mm3, an upper cutoff point of 2000 cells/mm3, and hemoglobin of 12 g/dl. For men, method I generated sensitivity of 78.0% and specificity of 77.5%. Method II improved specificity to 81.8%. For women, method I increased sensitivity to 85.6% and decreased specificity to 64.1%. Method II improved specificity to 81.4%. CONCLUSION: TLC below 1200 cells/mm3 were associated with CD4 cell counts below 200 cells/mm3 as in the WHO guidelines, but sensitivity was low. Adding hemoglobin to TLC increased sensitivity, thereby reducing the risk of false-negative results. Our model may serve as a template for the development of algorithms to initiate the use of HAART in resource-limited settings.

Algorithms↗

PubMed1999

Do gender differences in CD4 cell counts matter?

OBJECTIVE: To examine the effect of gender on disease progression and whether gender differences in CD4 lymphocyte counts persisted for the entire course from HIV seroconversion until (death from) AIDS. METHODS: CD4 lymphocyte counts were modelled in 221 female and 443 male seroconverters following seroconversion, backwards from AIDS and backwards from death using regression analysis for repeated measurements. RESULTS: In the period before use of highly active antiretroviral therapy (HAART), progression to AIDS and to death were marginally slower in women than in men as assessed by proportional hazards analysis. Women seroconverted for HIV, developed AIDS and died at higher CD4 cell counts than men (women: 815, 146 and 44 x 10(6) cells/l, respectively; men: 727, 49 and 22 x 10(6) cells/l, respectively), although differences were only statistically significant at AIDS onset. Declines in CD4 lymphocyte counts were not significantly affected by gender and absolute differences between men and women were stable, with exception for the trajectory close to AIDS when the decline became steeper for men than women. CONCLUSION: These gender differences in CD4 lymphocyte counts suggest a delay of initiation of therapy in women compared with men (our model predicted that women reach the threshold of starting HAART at about 12 months later than men). If this delay unfavourably influences progression, treatment guidelines should be revised so that women can benefit equally from HAART.

Acquired Immunodeficiency Syndrome↗

PubMed2004

The search for a predictor of CD4 cell count continues: total lymphocyte count is not a substitute for CD4 cell count in the management of HIV-infected individuals in a resource-limited setting.

Total lymphocyte count (TLC) has been recommended as a substitute for CD4 cell count for the management of HIV-infected individuals living in resource-limited settings. To confirm this, 151 TLCs and CD4 cell counts were obtained from 109 patients who had not yet started treatment and analyzed. CD4 cell counts of <200 cells/mm3 were found in 42 cases (37.8%) with TLCs of > or =1200 cells/mm3. Thus, 1 in 3 individuals would have been deprived of needed treatment. Therefore, in this setting, TLC is not a reliable predictor of CD4 cell count in HIV-infected individuals.

Adult↗

PubMed2002

The association of serum lactate dehydrogenase level with selected opportunistic infections and HIV progression.

BACKGROUND: The purpose of this study was to determine the association of serum lactate dehydrogenase (LDH) levels with certain opportunistic infection and to determine an association between LDH levels and CD4+ lymphocyte counts. METHOD: We studied 352 patients retrospectively with HIV infection and one of the following infections: histoplasmosis; toxoplasmosis; tuberculosis (pulmonary and disseminated); bacterial pneumonia; Pneumocystis carinii pneumonia. Demographic and clinical data were obtained from the Adult Spectrum of Diseases (ASD) database in New Orleans. Bivariate and multivariate analysis were used to determine the association between LDH levels and opportunistic infections and CD4+ lymphocyte counts. RESULTS: Patients with a serum LDH level <225 IU/L had a mean CD4+ lymphocyte count of 159/dl (SE 19.3) as compared to patients with a serum LDH level > or =225 IU/L, who had a mean CD4+ lymphocyte count of 58/dl (SE 6.9) (P<0.01). Non-Caucasian race, a diagnosis of histoplasmosis, disseminated tuberculosis or Pneumocystis carinii pneumonia, and CD4+ lymphocyte count were significantly associated with a serum LDH level > or =225 IU/L in the bivariate analysis. In a multivariate analysis, after controlling for race and CD4+ lymphocyte count, the only diagnoses that were significantly associated with the serum LDH level were definitive Pneumocystis carinii pneumonia and toxoplasmosis. Having a higher LDH level was not associated with early mortality. CONCLUSIONS: Although not diagnostic, serum LDH levels could be used as an adjunctive marker in certain opportunistic infections. There is an inverse relationship between serum LDH levels and CD4+ lymphocyte counts in this group.

AIDS-Related Opportunistic Infections↗

PubMed1993

Risk for perinatal HIV-1 transmission according to maternal immunologic, virologic, and placental factors.

OBJECTIVE: To evaluate how maternal and obstetric factors interact to influence mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission. DESIGN: Prospective, observational cohort study of children born to HIV-infected women to determine child's HIV infection status. The analysis then compared peripartum maternal, placental, and obstetric variables between HIV-1 transmitter and nontransmitter women. SETTING: Two large maternity wards in Kinshasa, Zaire. PARTICIPANTS: Consecutive sample of 324 HIV-1-infected women at delivery, with 254 HIV-seronegative women followed up as control subjects. PRINCIPAL OUTCOME MEASURES: HIV infection status of children, to classify each woman as an HIV-1 transmitter or nontransmitter. RESULTS: The highest transmission risk (TR) was associated with maternal p24 antigenemia (TR, 71%; relative risk [RR], 3.0; 95% confidence interval [CI], 1.7 to 5.2) and maternal CD8+ lymphocyte counts of at least 1.80 x 10(9)/L (1800/microL) (TR, 50%; RR, 2.2; 95% CI, 1.2 to 4.2). Among women with CD8+ lymphocyte counts of less than 1.80 x 10(9)/L, CD4+ lymphocyte counts of less than 0.60 x 10(9)/L were a risk factor (TR, 29%; RR, 2.2; 95% CI, 1.2 to 4.2). In women with neither high CD8+ nor low CD4+ lymphocyte counts, placental membrane inflammation was associated with perinatal transmission (TR, 40%; RR, 4.2; 95% CI, 1.3 to 13.7). In women with neither p24 antigenemia, high CD8+ or low CD4+ lymphocyte counts, nor placental membrane inflammation, the transmission risk was only 7%. Additional correlates of transmission included maternal anemia and fever, but not maternal sexually transmitted diseases. CONCLUSIONS: Identifiable subgroups of HIV-1-infected women based on maternal and placental characteristics had between a 7% and 71% risk of perinatal HIV-1 transmission. Not only the overall rate of transmission but the impact of different risk factors for transmission appear to vary over the course of HIV infection.

AIDS Serodiagnosis↗

PubMed1994

Coinfection with human T-cell lymphotropic virus type I and HIV in Brazil. Impact on markers of HIV disease progression.

OBJECTIVES: To study the effect of human T-cell lymph-tropic virus type I (HTLV-I) on markers of human immunodeficiency virus (HIV) disease progression. DESIGN: A retrospective, nested case-control study. SETTING: A university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. PARTICIPANTS: Human immunodeficiency virus-seropositive adults participating in a prospective HIV cohort study. MAIN OUTCOME MEASURES: The HIV clinical stage, CD4+ lymphocyte counts, and other laboratory parameters in 27 individuals infected with HIV and HTLV-I (coinfection) and 99 age-matched, HIV-seropositive, HTLV-seronegative controls (single infection). RESULTS: Variables independently associated with coinfection included higher CD4+ lymphocyte count (odds ratio [OR], 2.3; 95% confidence limits [CL], 1.3, 4.1), higher CD4+ percentage (OR, 2.0; 95% CL, 1.3, 3.2), beta 2-microglobulin level of 254 nmol/L or more (OR, 6.8; 95% CL, 1.3, 35.4), World Health Organization stages 3 and 4 (OR, 4.4; 95% CL, 1.1, 18.0), and reporting a parenteral risk factor (OR, 7.4; 95% CL, 1.4, 38.9). When stratified by p24 antigenemia, coinfection was associated with an estimated 82% higher CD4+ lymphocyte count (P < .05). CONCLUSION: Coinfection was associated with higher CD4+ lymphocyte counts, more advanced clinical disease, and higher beta 2-microglobulin levels than HIV infection alone. The higher mean CD4+ lymphocyte count does not appear to offer immunologic benefit. Caution should be exercised when using CD4+ lymphocytes as a surrogate marker in studies of HIV infection in populations where HTLV-I is prevalent. Further studies are needed to address whether current CD4+ lymphocyte values for the initiation of antiretroviral therapy and chemoprophylaxis against opportunistic infections in HIV infection are appropriate in coinfection.

Adult↗

PubMed2000

Impact of pulmonary tuberculosis on survival of HIV-infected adults: a prospective epidemiologic study in Uganda.

BACKGROUND: Retrospective cohort studies of tuberculosis suggest that active tuberculosis accelerates the progression of HIV infection. The validity of these findings has been questioned because of their retrospective design, diverse study populations, variable compliance with anti-tuberculous therapy and use of anti-retroviral medication. To assess the impact of tuberculosis on survival in HIV infection we performed a prospective study among HIV-infected Ugandan adults with and without tuberculosis. METHODS: In a prospective cohort study, 230 patients with HIV-associated tuberculosis and 442 HIV-infected subjects without tuberculosis were followed for a mean duration of 19 months for survival. To assess changes in viral load over 1 year, 20 pairs of tuberculosis cases and controls were selected and matched according to baseline CD4 lymphocyte count, age, sex and tuberculin skin test status. RESULTS: During the follow-up period, 63 out of of 230 tuberculosis cases (28%) died compared with 85 out of 442 controls (19%), with a crude risk ratio of 1.4 [95% confidence interval (CI), 1.07-1.87]. Most deaths occurred in patients with CD4 lymphocyte counts < 200 x 10(6) cells/l at baseline (n = 99) and occurred with similar frequency in the tuberculosis cases (46%) and the controls (44%). When the CD4 lymphocyte count was > 200 x 10(6)/l, however, the relative risk of death in HIV-associated tuberculosis was 2.1 (95% CI, 1.27-3.62) compared with subjects without tuberculosis. For subjects with a CD4 lymphocyte count > 200 x 10(6)/l, the 1-year survival proportion was slightly lower in the cases than in the controls (0.91 versus 0.96), but by 2 years the survival proportion was significantly lower in the cases than in the controls (0.84 versus 0.91; P < 0.02; log-rank test). For subjects with a CD4 lymphocyte count of 200 x 10(6) cells/l or fewer, the survival proportion at 1 year for the controls was lower than cases (0.59 versus 0.64), but this difference was not statistically significant (P = 0.53; logrank test). After adjusting for age, sex, tuberculin skin test status, CD4 lymphocyte count, and history of HIV-related infections, the overall relative hazard for death associated with tuberculosis was 1.81 (95% CI, 1.24-2.65). In a nested Cox regression model, the relative hazard for death was 3.0 (95% CI, 1.62-5.63) for subjects with CD4 lymphocyte counts > 200 x 10(6)/l and 1.5 (95% CI, 0.99-2.40) for subjects with a CD4 lymphocyte count of 200 x 10(6)/l or fewer. CONCLUSION: The findings from this prospective study indicate that active tuberculosis exerts its greatest effect on survival in the early stages of HIV infection, when there is a reserve capacity of the host immune response. These observations provide a theoretical basis for the treatment of latent tuberculous infection in HIV-infected persons.

AIDS-Related Opportunistic Infections↗

PubMed2002

Evaluation and management of HIV-infected women.

The rate of newly diagnosed AIDS in the United States is increasing fastest in women, who are infected with HIV primarily through heterosexual transmission. Approximately 60% of these women are African American, and 18% are Latina. A gynecologic infection is the most common symptom that leads to initial medical evaluation. Specific studies at baseline should include CD4 lymphocyte count, HIV-1 RNA level, and gynecologic examination with Papanicolaou smear. Decisions about initiation of antiretroviral therapy depend on the patient's clinical diagnoses, her willingness to adhere to treatment, and CD4 lymphocyte and HIV-1 RNA levels. Levels of HIV-1 RNA may be somewhat lower in women than in men at the same CD4 count, whereas women have higher CD4 lymphocyte counts at the time of AIDS diagnosis. However, prospective trials have not yet indicated the need to change the threshold CD4 lymphocyte counts or HIV-RNA levels for initiation of therapy in women. The efficacy of antiretroviral therapy appears to be similar in men and women, although women are more likely to experience toxicities. Abnormal Papanicolaou smears occur in approximately 40% of women at baseline, and 58% are infected with human papillomavirus. The prevalence of both conditions increases with lower CD4 lymphocyte counts and higher HIV-1 RNA levels. Precursor lesions to cervical cancer may be effectively treated, but almost 50% recur within 1 year, mandating careful follow-up. Referral should be sought for specialized gynecologic care and for issues related to HIV itself, since survival is prolonged in patients treated by physicians who are experienced in treating HIV. When they are provided the same access to care, HIV-infected women have similar prognoses as HIV-infected men.

Adult↗