Data from: Quantitative PCR as a marker for preemptive therapy and its role in therapeutic control in Trypanosoma cruzi/HIV coinfection
Background: Trypanosoma cruzi and HIV coinfection can evolve with depression of cellular immunity and increased parasitemia. We applied quantitative PCR (qPCR) as a marker for preemptive antiparasitic treatment to avoid fatal Chagas disease reactivation and analyzed the outcome of treated cases. Met...
Gespeichert in:
Hauptverfasser: | , , , , , , , , , , , , , , , |
---|---|
Format: | Dataset |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext bestellen |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Background: Trypanosoma cruzi and HIV coinfection can evolve with
depression of cellular immunity and increased parasitemia. We applied
quantitative PCR (qPCR) as a marker for preemptive antiparasitic treatment
to avoid fatal Chagas disease reactivation and analyzed the outcome of
treated cases. Methodology: This mixed cross-sectional and longitudinal
study included 171 Chagas disease patients, 60 coinfected with HIV. Of
these 60 patients, ten showed Chagas disease reactivation, confirmed by
parasites identified in the blood, cerebrospinal fluid, or tissues, 12
exhibited high parasitemia but no reactivation, and 38 had low parasitemia
and no reactivation. Results: We showed, for the first time, the success
of the timely introduction of benznidazole in the non-reactivated group
with high levels of parasitemia detected by qPCR and the absence of
parasites in reactivated cases with at least 58 days of benznidazole. HIV+
and HIV+ without reactivation had a 4.0 – 5.1 higher chance of having
parasitemia than HIV seronegative cases. A positive correlation was found
between parasite and viral loads. Remarkably, treated T.
cruzi/HIV-coinfected patients had 77.3% conversion from positive to
negative parasitemia compared to 19.1% of untreated patients.
Additionally, untreated patients showed ~13.6 times higher odds of having
positive parasitemia in the follow-up period compared with treated
patients. Treated and untreated patients showed no differences regarding
the evolution of Chagas disease. The main factors associated with
all-cause mortality were higher parasitemia, lower CD4 counts/µL, higher
viral load, and absence of antiretroviral therapy. Conclusion: We
recommend qPCR prospective monitoring of T. cruzi parasitemia in HIV+
patients and point out the value of pre-emptive therapy for patients with
temporary high parasitemia. In parallel, an early antiretroviral therapy
introduction is advisable, aiming at viral load control, immune response
restoration, and major survival. We also suggest an earlier antiparasitic
treatment for all coinfected patients, followed by effectiveness analysis
alongside antiretroviral therapy. |
---|---|
DOI: | 10.5061/dryad.05qfttf8f |