Abstract
ObjectiveThrombocytopenia (TCP<150 × 103 cells/mm3) has emerged as a relevant factor in the clinical course of HIV. However, the mechanisms mediating such observations have not been well characterized, limiting the possibility of creating targeted interventions. Notably, platelets are the storage and transporter system for serotonin and Brain derived neurotrophic factor (BDNF), which recent laboratory studies associated with viral replication and lymphocyte survival. Thus, we posit that (1) TCP will be associated with reduced levels of BDNF and serotonin (2) That these alterations will lead to poor viro-immune responses to antiretroviral therapy.MethodsTo achieve this goal, a total of 400 people living with HIV were consecutively enrolled to characterize the frequency of thrombocytopenia in hazardous and non-hazardous alcohol user populations in the HAART era. Then, participants underwent immune and laboratory assessments, to determine if TCP was associated with alterations in serotonin (5-HT) and brain derived neurotrophic factor (BDNF).ResultsThe prevalence of thrombocytopenia in this antiretroviral treated cohort was 14%. Rates were significantly higher in the heavy alcohol users, HAU versus the non HAU group (Heavy: 25% versus HAU: 15% versusnon-HAU: 10%). Multivariate model analyses indicated that having TCP, low BDNF levels (<5000 pg/ml), and number of drinks per day were predictors of serotonin levels. PLWH with TCP had about 2-fold lower PPP-BDNFlevels (5037.4 ± 381 vs. 9137.5 ± 7062 pg/ml p=0.0001). Other significant predictors of BDNF levels at the last visit included receiving selective serotonin reuptake inhibitors and PPP serotonin levels. Multivariate analyses also confirmed that altered serotonin levels were associated withhigh viral loadsboth low CD4 cell counts.ConclusionsThrombocytopenia is a relatively frequent complication of HIV, andis particularly prevalent among hazardous alcohol users (HAU). These findings suggest that TCP is associated with altered levels of BDNF and serotonin, suggesting that they may be the bridge linking TCP and poor viro-immune responses observed in this group. These results could have important clinical and therapeutic implications.
Highlights
Thrombocytopenia (TCP: a platelet count of less than 150,000 per microliter), is a common hematological complication which affects a sizable proportion of people living with HIV (PLWH) [1,2,3,4,5,6]
Rates were significantly higher in the heavy alcohol users, hazardous alcohol users (HAU) versus the non HAU group (Heavy: 25% versus HAU: 15% versusnon-HAU: 10%)
Multivariate model analyses indicated that having TCP, low brain derived neurotrophic factor (BDNF) levels (
Summary
Thrombocytopenia (TCP: a platelet count of less than 150,000 per microliter), is a common hematological complication which affects a sizable proportion of people living with HIV (PLWH) [1,2,3,4,5,6]. The mechanism mediating this association is uncertain, highlighting the need for further research. In this regards, it needs to be emphasized that the role of platelets has expanded from hemostasis to inflammation, and host defense [8,9]. Confluent pieces of evidence indicate that platelets share structural and functional similarities with granulocytes, known to participate in antimicrobial host defense. Platelets contain a number of broad spectrum antimicrobial peptides, RANTES and MIP-1 that can enact as HIV-suppressive factors [8,9]
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