Impact of Highly Active Antiretroviral Therapy on Individual AIDS-Defining Illness Incidence and Survival in Australia

Dore, Gregory J.; Li, Yueming; McDonald, Ann; Rée, Hugo; Kaldo, John M.

doi:10.1097/00042560-200204010-00010

Cited by 36 publications

(46 citation statements)

References 23 publications

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“…The incidence of PCP has markedly declined in the era of antiretroviral therapy [9,10]. In a study by Wolff and O'Donnell [9], in the pre-HAART era, 36% of patients referred to a pulmonary specialist had PCP; however, this decreased to 17.6% in the HAART period.…”

Section: Pneumocystis Pneumoniamentioning

confidence: 99%

Pulmonary infections in the HIV-infected patient in the era of highly active antiretroviral therapy: An update

Lazarous

O’Donnell

2007

Curr Infect Dis Rep

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The highly active antiretroviral therapy (HAART) era began in 1996 when the combination of multiple antiretroviral agents was found to improve outcomes in HIV-infected patients. HAART has made a tremendous impact on the progression of HIV and on the morbidity and mortality associated with its opportunistic infections. HIV-positive patients who respond to HAART have a decreased incidence of opportunistic infections. Studies have documented close to a 50% decline in the incidence of pneumocystis pneumonia and bacterial pneumonia with the use of antiretroviral therapy. Primary and secondary prophylaxis for pneumocystis pneumonia can be discontinued in patients who show a sustained response to antiretroviral therapy. Unique to the HAART era, immune reconstitution syndrome is characterized by a paradoxical deterioration of a preexisting infection that is temporally related to the recovery of the immune system. Recently, more and more patients are being admitted for non-AIDS related illnesses in the HAART era.

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Section: Pneumocystis Pneumoniamentioning

confidence: 99%

Pulmonary infections in the HIV-infected patient in the era of highly active antiretroviral therapy: An update

Lazarous

O’Donnell

2007

Curr Infect Dis Rep

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“…[14][15][16][17][18][19][20][21][22][23][24][25] BL accounts for 25% to 40% of acquired immunodeficiency syndrome (AIDS)-related lymphomas (ARLs), even affecting nonimmunocompromised patients. 14,[26][27][28][29] In a pre-HAART study evaluating an intensive cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)-derived chemotherapy regimen (LNH84), the toxicity was acceptable but the 2-year overall survival (OS) was less than 20% in the 21 patients with BL and BM involvement.…”

Section: Introductionmentioning

confidence: 99%

Intensive chemotherapy regimen (LMB86) for St Jude stage IV AIDS-related Burkitt lymphoma/leukemia: a prospective study

Galicier¹,

Fieschi²,

Borie³

et al. 2007

Blood

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“…These include patients with certain genetic diseases, malignancies requiring chemo-or radiation therapy, and AIDS (10,54,56,58). Despite improved treatments for human immunodeficiency virus infection and improved prophylaxis for P. carinii infection, PcP remains one of the most common AIDS-defining illnesses and is directly responsible for significant morbidity and mortality (12,16,17,58,62). Although significant progress has been made in our understanding of PcP, the exact mechanisms of lung injury are still largely undetermined.…”

mentioning

confidence: 99%

Pneumocystis cariniiActivates the NF-κB Signaling Pathway in Alveolar Epithelial Cells

et al. 2005

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Pneumocystis carinii pneumonia (PcP) is a clinically important infection of immunocompromised patients.Although the interaction of Pneumocystis with the alveolar epithelium has been well documented, very little information regarding the epithelial response to Pneumocystis is currently available. In order to study Pneumocystis-epithelium interactions, a murine cell line derived specifically from an alveolar epithelial cell (AEC) was utilized. The coculture of murine AECs with mouse Pneumocystis induced a dose-and time-dependent release of the CXC chemokine MIP-2. Importantly, the specific removal of Pneumocystis from the preparation, or the pretreatment of AECs with sulfasalazine, a potent and specific inhibitor of NF-B, nearly completely abrogated the chemokine response to Pneumocystis. Since the murine MIP-2 promoter contains consensus B binding sequences, the ability of Pneumocystis to stimulate NF-B signaling in AECs was examined. Pneumocystis stimulation of an AEC line stably transfected with a B-dependent reporter construct triggered the NF-B signaling pathway and reporter production. These data were confirmed in gel shift assays, providing direct evidence that Pneumocystis induced the nuclear translocation of the p50/p65 heterodimeric form of NF-B. Maximal NF-B activation was dependent upon direct contact with viable Pneumocystis organisms. These data demonstrate that Pneumocystis activates NF-B signaling in AECs and establish a reporter cell line for studying NF-B activation in AECs. Given the global regulatory functions of the NF-B family, these findings suggest that Pneumocystis directly alters AEC gene expression in a manner that promotes pulmonary immune and inflammatory responses.Pneumocystis carinii is an opportunistic fungal pathogen that causes life-threatening pneumonia in patients suffering from various congenital or acquired immunodeficiencies. These include patients with certain genetic diseases, malignancies requiring chemo-or radiation therapy, and AIDS (10,54,56,58). Despite improved treatments for human immunodeficiency virus infection and improved prophylaxis for P. carinii infection, PcP remains one of the most common AIDS-defining illnesses and is directly responsible for significant morbidity and mortality (12,16,17,58,62). Although significant progress has been made in our understanding of PcP, the exact mechanisms of lung injury are still largely undetermined. Because recent evidence has demonstrated that lung injury during PcP is not only a consequence of the direct effects of the organism but also a function of the host's response to infection (22,23,47,48,63,67), the identification of signals that promote inflammation and contribute to injury is critical to understanding and treating this disease. Early studies demonstrated that the interaction of P. carinii with the alveolar epithelium is one of the initial events in the infectious process (28,35,38,68). However, very little knowledge exists concerning how the pulmonary epithelium responds to P. carinii infection or what signalin...

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Impact of Highly Active Antiretroviral Therapy on Individual AIDS-Defining Illness Incidence and Survival in Australia

Cited by 36 publications

References 23 publications

Pulmonary infections in the HIV-infected patient in the era of highly active antiretroviral therapy: An update

Pulmonary infections in the HIV-infected patient in the era of highly active antiretroviral therapy: An update

Intensive chemotherapy regimen (LMB86) for St Jude stage IV AIDS-related Burkitt lymphoma/leukemia: a prospective study

Pneumocystis cariniiActivates the NF-κB Signaling Pathway in Alveolar Epithelial Cells

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