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Natural History of Opportunistic Disease in an HIV-Infected Urban Clinical Cohort

Richard D. Moore, MD, MHSc; and Richard E. Chaisson, MD
[+] Article and Author Information

From Johns Hopkins University School of Medicine, Baltimore, Maryland. Acknowledgments: The authors thank Jeanne Keruly, Darrell Forney, Joel Gibson, Lisa-Marie Castro, Cathy Riggin, Shelia Kasey, and Kim Veney for technical support. Grant Support: By grant RO1 HS07809 from the Agency for Health Care Policy and Research. Requests for Reprints: Richard D. Moore, MD, Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8059, Baltimore, MD 21205. Current Author Addresses: Dr. Moore: Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8059, Baltimore, MD 21205.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1996;124(7):633-642. doi:10.7326/0003-4819-124-7-199604010-00003
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Objective: To determine the effect of contemporary clinical care on the natural history of opportunistic disease in an urban population infected with the human immunodeficiency virus (HIV).

Setting: Urban university HIV clinic.

Design: Retrospective and prospective observational study.

Patients: 1246 HIV-infected patients with CD4+ counts of 300 cells/mm3 or less.

Measurements: Incidence rates and Kaplan-Meier estimates of the probability of developing opportunistic disease with time, distribution of the CD4+ counts at which opportunistic disease develops, survival after the development of opportunistic disease, and the association between preventive drug therapies and the occurrence of opportunistic infection.

Results: The most common opportunistic disease was Candida esophagitis, which had an incidence of 13.3 events per 100 person-years and a 3-year Kaplan-Meier probability of 0.30. Pneumocystis carinii pneumonia, Mycobacterium avium complex bacteremia, cytomegalovirus, and the acquired immunodeficiency syndrome dementia complex occurred at rates of 5 to 9 events per 100 person-years and 3-year Kaplan-Meier probabilities of 0.15 to 0.22. Toxoplasmosis, cryptococcal meningitis, herpes zoster, the wasting syndrome, and Kaposi sarcoma occurred at rates of about 2 to 4 events per 100 person-years and with 3-year Kaplan-Meier probabilities of 0.05 to 0.10. Non-Hodgkin lymphoma, M. tuberculosis infection, progressive multifocal leukoencephalopathy, and cryptosporidiosis were the least common disorders, with an incidence of about 1 to 2 events per 100 person-years and a 3-year Kaplan-Meier probability less than 0.05. Only the incidences of cryptococcal meningitis, secondary P. carinii pneumonia, and herpes zoster decreased (P < 0.05) between 1989-1992 and 1993-1995. Fluconazole use was associated with a decreased relative rate of 0.49 (P = 0.06) for cryptococcal meningitis and a decreased relative rate of 0.61 (P = 0.005) for esophageal candidiasis. Rifabutin use was associated with a decreased relative rate of 0.37 (P = 0.002) for M. avium complex bacteremia, and trimethoprim-sulfamethoxazole use was associated with decreased relative rates of 0.33 (P = 0.02) for secondary P. carinii pneumonia and 0.55 (P = 0.08) for primary P. carinii pneumonia. Candidiasis, herpes zoster, and M. tuberculosis infection first occurred at a median CD4+ count greater than 100 cells/mm3, but all other opportunistic diseases first occurred at a median CD4+ count less than 50 cells/mm3. Median survival after diagnosis varied from 35 days for non-Hodgkin lymphoma to 680 days for herpes zoster.

Conclusions: In the patients studied, the incidences of secondary P. carinii pneumonia, cryptococcal meningitis, and herpes zoster have declined in the past 5 years. The incidences of primary P. carinii pneumonia and Kaposi sarcoma appear to be declining compared with historical estimates. However, although these and other opportunistic diseases continue to be relatively frequent complications of HIV infection, they are first occurring at more advanced immunosuppression than in the past. Continued efforts are needed to develop effective strategies for preventing opportunistic disease in very advanced HIV infection.

Figures

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Figure 1.
Boxplot of the median (line inside the box), first quartile (bottom of the box), third quartile (top of the box), and mean (asterisk) CD4+ lymphocyte count at the time of the development of opportunistic disease.CandidaMycobacterium aviumPneumocystis cariniiPneumocystis cariniiToxoplasma gondii

Can = esophagitis; CMV = cytomegalovirus infection; Crp = cryptosporidiosis; Cry = cryptococcal meningitis; DEM = acquired immunodeficiency virus dementia complex; HSV = herpes simplex virus infection; HZos = herpes zoster; KS = Kaposi sarcoma; MAC = complex bacteremia; NHL = non-Hodgkin lymphoma; PCP = primary pneumonia; PCP2 = secondary pneumonia; PML = progressive multifocal leukoencephalopathy; Tox = encephalitis; WS = the wasting syndrome.

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Grahic Jump Location
Figure 2.
Kaplan-Meier product-limit estimates of the probability of developing opportunistic disease over 3 years (probability greater than 0.CandidaMycobacterium aviumPneumocystis cariniiPneumocystis carinii

10). CAN equals esophagitis; CMV equals cytomegalovirus infection; DEM equals acquired immunodeficiency virus dementia complex; MAC equals complex bacteremia; PCP equals primary pneumonia; PCP2 equals secondary pneumonia.

Grahic Jump Location
Grahic Jump Location
Figure 3.
Kaplan-Meier product-limit estimates of the probability of developing opportunistic disease over 3 years (probability less than 0.Mycobacterium tuberculosisToxoplasma gondii

10). CRP equals cryptosporidiosis; CRY equals cryptococcal meningitis; HSV equals herpes simplex virus infection; HZ equals herpes zoster; KS equals Kaposi sarcoma; MTB equals disease; NHL equals non-Hodgkin lymphoma; PML equals progressive multifocal leukoencephalopathy; TOX equals encephalitis; WS equals the wasting syndrome.

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