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Biomedical subjects

N M Graham

Publications and source records attributed to N M Graham.

At least 37 records · Page 2Linked to original sources
PubMed1997

Transmission of Mycobacterium tuberculosis by a fiberoptic bronchoscope. Identification by DNA fingerprinting.

CONTEXT: An ongoing restriction fragment length polymorphism (RFLP) study of Mycobacterium tuberculosis isolates from tuberculosis (TB) cases revealed an identical 10-banded IS6110 RFLP pattern unique to 2 patients diagnosed as having TB 6 months apart. Their only identifiable link was care at the same hospital. OBJECTIVE: To determine if nosocomial transmission had occurred. DESIGN: Traditional and molecular epidemiologic investigation. MEASUREMENTS: We reviewed medical charts and bronchoscopic records, examined hospital locations visited by both patients, evaluated hospital ventilation systems, and observed cleaning and disinfection of bronchoscopes. RESULTS: A patient with cough, hoarseness, and fever underwent bronchoscopy and was diagnosed as having TB. A second patient with a mediastinal mass underwent bronchoscopy 2 days later and was diagnosed as having small cell carcinoma. Following 6 months of chemotherapy and radiation therapy, the second patient developed fever and an infiltrate of the right upper lobe of the lung. Bronchoscopic washings revealed acid-fast bacilli and were culture positive for M tuberculosis. Both patients had undergone bronchoscopy with the same instrument in the same operating room with no intervening bronchoscopies. Bronchoscope cleaning and disinfection procedures were inconsistent with national guidelines. CONCLUSIONS: A contaminated bronchoscope was the most likely source of M tuberculosis transmission between these 2 patients. The RFLP analysis of M tuberculosis isolates was responsible for detecting this nosocomial source of transmission and led to the implementation of public health measures to prevent further spread of infection and disease. This study emphasizes the need for continued vigilance in endoscope cleaning techniques.

Adult↗
PubMed1997

Epidemiology of acquired immunodeficiency syndrome: advancing to an endemic era.

Acquired Immunodeficiency syndrome (AIDS) is now endemic in the United States. Human immunodeficiency virus (HIV) is the leading cause of death in U.S. adults aged 25-44 years. While the rate of infection among men who have sex with men has stabilized, that among women, minorities, and young people is increasing. Improved methods for identifying these subpopulations at risk are needed. More than half the people infected with HIV do not know that they are. Recent studies demonstrate rapid viral replication during clinically asymptomatic disease and support the need for early initiation of combination antiretroviral therapy to slow disease progression and to improve patient longevity. However, significant numbers of individuals, particularly those at highest risk, continue to be diagnosed late in their illness. A recently approved oral test for HIV-1 samples mucosal transudate and provides a less invasive, but equally reliable, alternative to blood testing that may increase the acceptability and accessibility of HIV testing. Nonetheless, it remains to be determined whether this oral testing approach will have a significant public health impact among risk groups with low access to screening and care.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Epidemiology and estimated population burden of selected autoimmune diseases in the United States.

Autoimmune diseases cause significant and chronic morbidity and disability. The actual number of persons in the United States that are affected by autoimmune diseases and the resultant magnitude of their impact on the public's health are limited to a few specific diseases. In order to understand the clinical, public health and economic importance of these diseases it is necessary to have estimates of incidence and prevalence rates in the population. In this analysis, we estimate the number of persons affected by 24 autoimmune diseases in the United States by applying mean weighted prevalence and incidence rates obtained from published articles to U. S. Census data. The study was restricted to 24 autoimmune predefined diseases for which there was direct or indirect evidence for autoimmune pathogenesis. Subsequently, we used computerized search software and ancestry searching (bibliographies) to conduct a comprehensive search of articles published from 1965 to the present. Eligible studies included those which adhered to standard disease definitions and which included population-based estimates of incidence or prevalence rates. Mean weighted incidence and prevalence rates were calculated from eligible published studies with greater weight proportionately given to larger studies. The mean rates were then applied to the U.S. Census population figures to estimate the number of persons currently afflicted with each disease and the number of new cases occurring each year in the United States. Only U.S. and European studies were used to estimate prevalence and incidence rates when there were at least six eligible studies available for a disease. When there were fewer than six studies, all available studies were included, regardless of country of origin. The number of eligible incidence and prevalence studies found in the literature varied considerably between the 24 autoimmune diseases selected. The largest number of eligible prevalence studies were conducted on multiple sclerosis (MS), rheumatoid arthritis, and systemic lupus erythematosus (SLE) (>/=23), followed by insulin-dependent diabetes (IDDM), myasthenia gravis, primary biliary cirrhosis, and scleroderma (>/=7). There were only one to four eligible studies done on 11 other diseases, and no prevalence studies on 6 diseases. Incidence studies were less frequent but the largest number of studies were conducted on IDDM (n = 37) and MS (n = 28), followed by Graves' disease/hyperthyroidism, glomerulonephritis, primary biliary cirrhosis, rheumatic fever, rheumatoid arthritis, scleroderma, and SLE (>/=9). On the other 11 diseases, there were one to six eligible studies, and no studies on 5 diseases. There were no eligible incidence or prevalence studies on Goodpasture's syndrome, idiopathic thrombocytopenia purpura, or relapsing polychondritis. Overall we estimate that 8,511,845 persons in the United States or approximately 1 in 31 Americans are currently afflicted with one of these autoimmune diseases. The diseases with the highest prevalence rates were Graves'/hyperthyroidism, IDDM, pernicious anemia, rheumatoid arthritis, thyroiditis, and vitiligo, comprising an estimated 7,939, 280 people or 93% of the total number estimated. Glomerulonephritis, MS, and SLE added an estimated 323,232 people. The prevalence of the other diseases reviewed were rare, less than 5.14/100,000. Most diseases were more common in women. From the incidence data we estimate that 237,203 Americans will develop an autoimmune disease in 1996 and that approximately 1,186,015 new cases of these autoimmune diseases occur in the United States every 5 years. Women were at 2.7 times greater risk than men to acquire an autoimmune disease. After reviewing the medical literature for incidence and prevalence rates of 24 autoimmune diseases, we conclude that many autoimmune diseases are infrequently studied by epidemiologists. As a result the total burden of disease may be an underestimate. (ABSTRACT TRUNCATED)

Autoimmune Diseases↗
PubMed1997

Impact of tuberculosis control measures and crowding on the incidence of tuberculous infection in Maryland prisons.

Our aim was to determine the incidence of tuberculin skin test (TST) conversion in the Maryland state correctional system. We conducted a historical longitudinal cohort study. A sample of 1,289 inmates, incarcerated in 16 of 23 prisons, who had a negative TST and a second test within 24 months was selected. The incidence of recent conversion was 6.3 per 100 person-years. Risk factors for conversion included high prison-population density (relative risk [RR] = 2.4; 95% confidence interval [CI], 1.5-3.8) and incarceration in a higher-security institution (RR = 2.4; 95% CI, 1.4-4.3). Incarceration in an institution with higher levels of isoniazid prophylaxis (> 65% of TST positives) reduced the risk of infection by 50% (RR = 0.5; 95% CI, 0.3-0.7). Crowding was strongly correlated with risk of conversion (r = 0.83; P < .001), while rates of isoniazid prophylaxis initiation were inversely correlated with risk of infection (r = -0.82; P < .001). In stepwise regression, higher prison-population density was the strongest predictor of increased infection. In a final model, inclusion of the rate of isoniazid prophylaxis initiation reduced the risk associated with crowding (RR = 1.4; P = .4). Annual screening programs for prisons can identify recent conversions that may not otherwise be detected.

Adult↗
PubMed1997

Comparison of a tuberculin interferon-gamma assay with the tuberculin skin test in high-risk adults: effect of human immunodeficiency virus infection.

A novel, whole blood interferon-gamma (IFN-gamma) assay was evaluated to determine its suitability for detecting Mycobacterium tuberculosis exposure in intravenous drug users with or without human immunodeficiency virus (HIV) infection. Whole heparinized blood was incubated overnight in separate wells with tuberculin purified protein derivative (PPD), saline, and mitogen controls. Levels of IFN-gamma in plasma supernatants were determined by rapid ELISA. Participants were then administered the tuberculin skin test (TST) and tested for cutaneous anergy. The whole blood IFN-gamma test agreed (89%-100%) with a positive TST in both HIV-seropositive and -seronegative subjects, but reactivity to PPD was more detectable by the whole blood assay among those with negative TSTs or anergy. TST induration diameter and IFN-gamma responses were correlated (Spearman's p = .45, P = .0001), but both responses were blunted by HIV infection. In summary, tuberculin reactivity appears to be more detectable by the whole blood IFN-gamma assay than by TST, and the assay requires no return visit for test reading.

Adult↗
PubMed1997

Predicting clinical progression or death in subjects with early-stage human immunodeficiency virus (HIV) infection: a comparative analysis of quantification of HIV RNA, soluble tumor necrosis factor type II receptors, neopterin, and beta2-microglobulin. Multicenter AIDS Cohort Study.

Quantification of human immunodeficiency virus (HIV) RNA by branched-chain DNA signal amplification, measurement of soluble tumor necrosis factor type II receptors (sTNFR-II), neopterin, beta2-microglobulin, or CD4 cell counts can be used to predict the risk of clinical progression or death in HIV infection but have not been compared in the same study. Ninety subjects were categorized into progression groups by their rate of CD4 cell decline and matched into triplets by initial CD4 cell count, age, race, and calendar time. By matched logistic regression, only the sTNFR-II and HIV RNA values were predictive of outcome across the progression groups. Categorization of baseline HIV RNA and sTNFR-II resulted in differences in progression to several clinical outcomes. sTNFR-II concentrations were the only immune marker examined that increased the prognostic utility of HIV RNA determination in early-stage subjects. Further studies in later stages of disease or after therapy are indicated.

CD4 Lymphocyte Count↗
PubMed1997

Low serum vitamin B-12 concentrations are associated with faster human immunodeficiency virus type 1 (HIV-1) disease progression.

We conducted a nonconcurrent prospective cohort study to examine associations between serum concentrations of vitamin B-6, vitamin B-12 and folate and the risk of progression to first acquired immunodeficiency syndrome (AIDS) diagnosis and CD4+ cell decline to < 2 x 10(8) cells/L. The study population was drawn from a cohort of homosexual and bisexual men in the Baltimore-Washington, DC, area. Eligible subjects were human immunodeficiency virus type 1 (HIV-1)-seropositive at study entry and had serum available in the serum repository from their 1984 baseline study visit. Serum micronutrient levels were assessed in 310 subjects. The follow-up period (April 1984 through December 1993) was approximately 9 y. In Kaplan-Meier analyses, participants with low serum vitamin B-12 concentrations (< 120 pmol/L) had significantly shorter AIDS-free time than those with adequate vitamin B-12 concentrations (median AIDS-free time = 4 vs. 8 y, respectively, P = 0.004). This effect persisted in Cox proportional hazards models after adjusting for HIV-1-related symptoms, CD4+ cell count, age, serum albumin, use of antiretroviral therapy before AIDS, frequency of alcohol consumption and serum folate concentration [relative hazard (RH) = 1.89, 95% confidence interval (CI) = 1.15-3.10). To further explore the temporal relation between low serum vitamin B-12 concentrations and disease progression, additional analyses were performed excluding subjects with more advanced disease at baseline. In these analyses, the increase in risk of progression to AIDS for those with low serum vitamin B-12 concentrations remained significant (RH = 2.21, 95% CI = 1.13-4.34), providing further evidence that low vitamin B-12 concentrations preceded disease progression. In contrast, low serum concentrations of vitamin B-6 and folate were not associated with either progression to AIDS or decline in CD4+ lymphocyte count. Intervention studies are needed to determine whether correction of low serum vitamin B-12 concentrations in early HIV-1 infection will influence the natural history of disease progression.

Adult↗
PubMed1997

Association between serum vitamin A and E levels and HIV-1 disease progression.

OBJECTIVE: To examine the associations between serum vitamin A and E levels and risk of progression to three key outcomes in HIV-1 infection: first AIDS diagnosis, CD4+ cell decline to < 200 cells x 10(6)/l, and mortality. DESIGN: Non-concurrent prospective study. METHODS: Serum levels of vitamins A and E were measured at the enrollment visit of 311 HIV-seroprevalent homo-/bisexual men participating in the Baltimore/ Washington DC site of the Multicenter AIDS Cohort Study. Cox proportional hazards models were used to estimate the relative hazard of progression to each outcome over the subsequent 9 years, adjusting for several independent covariates. RESULTS: Men in the highest quartile of serum vitamin E levels (> or = 23.5 mumol/l) showed a 34% decrease in risk of progression to AIDS compared with those in the lowest quartile [relative hazard (RH), 0.66; 95% confidence interval (CI), 0.41-1.06)]. This effect was statistically significant when comparing the highest quartile of serum vitamin E to the remainder of the cohort (RH, 0.67; 95% CI, 0.45-0.98). Associations between serum vitamin A levels and risk of progression to AIDS were less clear, but vitamin A levels were uniformly in the normal to high range (median = 2.44 mumol/l). Similar trends were observed for each vitamin with mortality as the outcome, but neither vitamin was associated with CD4+ cell decline to < 200 cells x 10(6)/l. Men who reported current use of multivitamin or single vitamin E supplements had significantly higher serum tocopherol levels than those who were not taking supplements (P = 0.0001). Serum retinol levels were unrelated to intake of multivitamin or single vitamin A supplements. CONCLUSIONS: These data suggest that high serum levels of vitamin E may be associated with slower HIV-1 disease progression, but no relationship was observed between retinol levels and disease progression in this vitamin A-replete population.

Acquired Immunodeficiency Syndrome↗
PubMed1997

The influence of drug use patterns on the rate of CD4+ lymphocyte decline among HIV-1-infected injecting drug users.

OBJECTIVES: To assess the relationship between various injecting drug use patterns and the rate of CD4+ lymphocyte decline in HIV-1-infected injecting drug users in Baltimore, Maryland, USA. METHODS: A cohort of 605 HIV-1-infected injecting drug users was recruited between 1988 and early 1989 in East Baltimore using extensive community outreach techniques. The participants were interviewed semi-annually to collect information on drug use practices. The outcome measure of interest was the rate of CD4+ lymphocyte decline between pairs of CD4+ lymphocyte counts. A mixed model was used to evaluate the relationship between the change in CD4+ lymphocyte count per month and previous CD4+ lymphocyte count and various drug use variables. RESULTS: The 605 HIV-infected injecting drug users had a median initial CD4+ lymphocyte count of 513 cells x 10(6)/l. Using 3209 paired observations, the mean change in CD4+ lymphocyte count was -3.2 cells x 10(6)/l per month. The rate of decline was higher in those with a higher level of CD4+ lymphocytes (P < 0.01) and length of drug use (P < 0.01), but did not vary by injection frequency or injection intensity of specific drug types. Although animal studies have suggested that the pattern of drug administration (continuous versus intermittent) and episodes of withdrawal or overdose might impact the rate of CD4+ lymphocyte decline, this was not observed in the present study. CONCLUSION: Patterns of injecting drug use, based on self-report, were not associated with the rate of decline in CD4+ lymphocytes.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Markers of response to zidovudine monotherapy among treated HIV seroconverters. Italian Seroconversion Study.

The aim of the study was to evaluate indicators of response to zidovudine monotherapy in terms of progression to AIDS and death in a cohort of human immunodeficiency virus (HIV) seroconverters. From a larger observational epidemiological cohort of 1,024 HIV seroconverters we identified 315 persons on zidovudine monotherapy. In this treated cohort, age, sex, risk group, constitutional symptoms, CD4 cell count, and p24 antigen levels at initiation of treatment and 6 months later were examined separately for two outcomes, AIDS and death, using standard survival methods. The variables measured at the visit at which zidovudine monotherapy was initiated that predicted more rapid progression to AIDS were CD4 cell count (RH = 2.61); constitutional symptoms (RH = 2.56); p24 antigenaemia level (RH = 2. 17); and subsequent change in CD4 cell count (> 30% decline) contributed additional predictive information (RH = 2.70). Results were similar for mortality, and did not vary significantly by risk group. In a tested subset of patients, p24 antigenaemia was associated with high levels of plasma RNA viral load. The median number of HIV RNA copies was about 28,000 copies/ml among p24 antigen-positive individuals and about 7,700 copies/ml among participants who were persistently negative for p24 antigenaemia. CD4 cell count, symptoms and p24 antigenaemia at the start of therapy and CD4 cell decline after initiation of treatment are early indicators of disease progression in zidovudine-treated patients. The combined use of these indicators may help to better predict who will respond to zidovudine or to other antiretroviral therapies.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Effect of Mycobacterium tuberculosis on HIV replication. Role of immune activation.

The prevalence of Mycobacterium tuberculosis (MTB) has increased worldwide, in part due to the HIV epidemic. Epidemiology data have demonstrated that HIV-infected individuals are more susceptible to MTB disease, which may lead to an acceleration in the progression of HIV disease. The purpose of this study was to determine whether MTB modulates HIV infection in vivo and to delineate the mechanisms involved by using in vitro model systems. Plasma viral load was measured in HIV-infected individuals before, during, and after the development of MTB disease; a 5- to 160-fold increase in viral replication was observed during the acute phase of MTB disease. In order to evaluate the mechanisms involved in this MTB-induced HIV replication, we used an in vitro system of primary PBMC and lymph node mononuclear cells isolated from HIV-infected individuals. The data demonstrated that MTB induced HIV replication in CD8+ T cell-depleted lymphocytes from HIV-infected individuals with a history of purified protein derivative (PPD) positivity but not in those who were PPD negative; this induction of HIV replication correlated with the level of cellular activation. In an in vitro acute HIV infection model, MTB increased HIV replication in PBMC from healthy donors with a history of PPD positivity, but not in PBMC from PPD-negative donors and this induction of viral replication also correlated with cellular activation. In conclusion, MTB increased HIV replication in vivo and in an in vitro model. This MTB-mediated viral production likely occurs through Ag-specific activation and infection of responding T cells.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Effects of micronutrient intake on survival in human immunodeficiency virus type 1 infection.

The authors examined the relation between dietary and supplemental micronutrient intake and subsequent mortality among 281 human immunodeficiency type 1 (HIV-1)-infected participants at the Baltimore, Maryland/Washington, DC, site of the Multicenter Acquired Immunodeficiency Syndrome Cohort Study. Subjects completed a semiquantitative food frequency questionnaire at their baseline visit in 1984. Levels of daily micronutrient intake were examined in relation to subsequent mortality over the 8-year follow-up period by using multivariate Cox models, adjusting for age, symptoms, CD4+ count, energy intake, and treatment. The highest quartile of intake for each B-group vitamin was independently associated with improved survival: B1 (relative hazard (RH) = 0.60, 95% confidence interval (CI) 0.38-0.95), B2 (RH = 0.59, 95% CI 0.38-0.93), B6 (RH = 0.45, 95% CI 0.28-0.73), and niacin (RH = 0.57, 95% CI 0.36-0.91). In a final model, the third quartile of beta-carotene intake (RH = 0.60, 95% CI 0.37-0.98) was associated with improved survival, while increasing intakes of zinc were associated with poorer survival. Intakes of B6 supplements at more than twice the recommended dietary allowance were associated with improved survival (RH = 0.60, 95% CI 0.39-0.93), while intakes of B1 and B2 supplements at levels greater than five times the recommended dietary allowance were associated with improved survival (B1: RH = 0.61, 95% CI 0.38-0.98; B2:RH = 0.60, 95% CI 0.37-0.97). Any intake of zinc supplements, however, was associated with poorer survival (RH = 1.49, 95% CI 1.02-2.18). These data support the performance of clinical trials to assess the effects of B-group vitamin supplements on HIV-1-related survival. Further studies are needed to determine the optimal level of zinc intake in HIV-1-infected individuals.

Adult↗
PubMed1996

Survival in HIV-infected patients who have received zidovudine: comparison of combination therapy with sequential monotherapy and continued zidovudine monotherapy. Multicenter AIDS Cohort Study Group.

BACKGROUND: Among patients who begin receiving zidovudine during intermediate-stage human immunodeficiency virus (HIV) infection, it is unclear whether changing to combination therapy (adding didanosine or zalcitabine) or sequential monotherapy (changing to didanosine or zalcitabine) significantly improves survival. OBJECTIVE: To determine, among patients who began receiving zidovudine during intermediate-stage HIV infection, the differential effects of changing to combination therapy (zidovudine with didanosine or zalcitabine) or sequential monotherapy (with didanosine or zalcitabine) or continuing zidovudine monotherapy. PATIENTS: 1077 HIV-seropositive men in the Multicenter AIDS (acquired immunodeficiency syndrome) Cohort Study who began receiving zidovudine before an AIDS-defining illness developed. SETTING: University-affiliated clinics in Baltimore, Chicago, Los Angeles, and Pittsburgh. DESIGN: Longitudinal cohort study, Treatment groups and important prognostic variables were modeled as time-dependent covariates in Cox proportional hazards models. MEASUREMENTS: Progression to AIDS and death. RESULTS: Compared with patients receiving continued zidovudine monotherapy, patients receiving combination therapy had a 45% improvement in survival (relative risk, 0.55 [95% Cl, 0.41 to 0.74; P < 0.001]) and patients who changed to sequential monotherapy had a 32% improvement in survival (relative risk, 0.68 [Cl, 0.52 to 0.89; P = 0.005]). In the landmark analyses, the median prolongation of survival associated with changing therapy was, at best, 3 to 6 months. Survival curves converged at 3.5 years for the 50 cells/mm3 disease-stage landmark, at 4.4 years for the 100 cells/mm3 landmark and at 4.9 years for the 150 cells/mm3 landmark. Mortality within these periods was 100%, regardless of treatment group or landmark. CONCLUSIONS: For patients who began receiving zidovudine during intermediate-stage disease, changing to either combination therapy or sequential monotherapy was associated with a statistically significant survival benefit compared with continuation of zidovudine monotherapy. The absolute increase in survival was modest, however, and long-term survival remained poor. Simultaneous time-dependent adjustment for changes in therapy and in important prognostic variables is necessary to derive relatively unbiased estimates of treatment effects in observational studies of HIV infection.

Antiviral Agents↗
PubMed1996

Effect of isoniazid chemoprophylaxis on HIV-related mycobacterial disease.

OBJECTIVES: The aims of this study were to (1) identify trends and risk factors for mycobacterial disease and (2) determine the effect of expanded access to isoniazid chemoprophylaxis on tuberculosis incidence. METHODS: A prospective observational cohort study was conducted among community-based injecting drug users (IDUs); 2960 IDUs (942 human immunodeficiency virus [HIV] seropositive) were followed up from January 1988 to June 1994. Directly observed chemoprophylaxis with twice-weekly isoniazid (10 to 15 mg/kg) was offered to purified protein derivative (PPD) tuberculin-positive (> or = 5-mm induration diameter in HIV-seropositive subjects and > or = 10-mm diameter in HIV-seronegative subjects) individuals but not to those with cutaneous anergy. Overall and annual incidence rates of disease due Mycobacterium tuberculosis, Mycobacterium avium complex, and other atypical mycobacteria were estimated using Poisson regression. RESULTS: HIV seropositivity was the strongest risk factor for tuberculosis, M avium complex, and other mycobacterial disease (relative risk [RR], 3.8, 17.2, and 6.9, respectively). Median CD4 lymphocyte cell counts for the three groups of mycobacterial disease were 0.17, 0.03, and 0.02 x 10(9)/L (167/microL, 30/microL, 18/microL) within 6 months of diagnosis (before or after). Overall incidence rates of tuberculosis, M avium complex disease, and other mycobacterial disease were 1.9, 8.8, and 2.7 per 1000 person-years, respectively. Tuberculosis incidence peaked in 1991 at six per 1000 person-years. However, after access to directly observed preventive therapy was expanded for tuberculin-positive subjects, incidence fell to only one case in 1992 and zero cases for 24 months from mid-1992 to mid-1994. During this period the number of PPD-positive patients who completed at least 26 weeks of therapy (or were still receiving isoniazid) more than tripled (from 21 to 70). None of the 12 patients with tuberculosis diagnosed during follow-up had received any preventive therapy. In addition, no tuberculosis developed among participants with cutaneous anergy. Calendar trends in risk for M avium complex and tuberculosis diverged after expanded access to isoniazid prophylaxis. Compared with 1988-1989, risk of M avium complex increased sevenfold. Tuberculosis risk fell 83% from the peak risk in 1990-1991. CONCLUSIONS: Expanded access to directly observed isonazid therapy for tuberculin-positive IDUs with and without HIV infection was associated with an 83% drop in tuberculosis incidence, while in the same period M avium complex incidence significantly increased. These population-based data are consistent with those obtained from clinical trials of isoniazid prophylaxis and were obtained without offering chemoprophylaxis to HIV-infected patients with cutaneous energy.

AIDS-Related Opportunistic Infections↗
PubMed1996

Use of antiherpes drugs and the risk of Kaposi's sarcoma: data from the Multicenter AIDS Cohort Study.

To determine if use of antiherpes drugs protects against the development of AIDS-associated Kaposi's sarcoma (KS), data from 935 homosexual men with AIDS from the Multicenter AIDS Cohort Study were analyzed. In nested case-control analysis, neither acyclovir use for human immunodeficiency virus infection (odds ratio [OR], 0.84; 95% confidence interval [CI], 0.56-1.26; P = .39) nor acyclovir use for any indication (OR, 1.02; 95% CI, 0.76-1.38; P = .89) was associated with a reduced risk of KS as initial AIDS diagnosis. In longitudinal analysis, acyclovir was also not protective against developing KS as a late manifestation of AIDS (after initial non-KS AIDS diagnosis). Among men with cytomegalovirus disease, ganciclovir use (relative risk [RR], 0.56; 95% CI, 0.22-1.44; P = .23) and foscarnet use (RR, 0.40; 95% CI, 0.051-3.10; P = .38) were associated (although not significantly) with a reduced risk of KS. Thus, acyclovir use does not appear to reduce the risk of KS, but further study of other antiherpes drugs such as ganciclovir and foscarnet is warranted.

AIDS-Related Opportunistic Infections↗
PubMed1996

The effect of latent Mycobacterium tuberculosis infection on human immunodeficiency virus (HIV) disease progression and HIV RNA load among injecting drug users.

To examine the relationship between latent Mycobacterium tuberculosis infection and human immunodeficiency virus (HIV) disease progression, two studies were done among a cohort of HIV-infected injecting drug users. First, the decline in CD4 cell count after baseline tuberculin skin testing was prospectively compared for 37 tuberculin-positive (induration > or = 5 mm) and 284 tuberculin-negative (induration < or = 2 mm) persons. After adjustment for baseline immune function, the mean 6-month CD4 cell decline was not significantly different (34.5 vs. 45.6 cells, respectively, P = .14). Second, the plasma HIV burden at baseline skin testing was compared for 33 tuberculin-positive cases and 33 matched tuberculin-negative controls. HIV RNA was detected in 8 cases and 10 controls (odds ratio = 0.67, 95% confidence interval = 0.19-2.36). Among the 14 pairs with HIV detected in > or = 1 member, the HIV concentration was higher for the case in 4 and for the control in 10 (P = .18). These findings suggest that unlike active tuberculosis, latent M. tuberculosis infection does not hasten HIV progression.

Adult↗