Abstract

Objective and aims: Liver disease is currently one of the leading causes of death among people living with HIV. Although platelets alterations are well recognized in the course of liver disease, the impact of thrombocytopenia (TCP: platelet counts <150,000 per microliter), which is highly prevalent among Hazardous Alcohol Users (HAU), is unclear. This lack of information limits the possibility to identify those at risk and to create targeted interventions. Methods: In this study, a total of 400 people living with HIV underwent laboratory assessments to determine if in addition to alcohol, TCP or its related factors (i.e., serotonin) were associated with non-invasive markers of liver fibrosis. The FIB-4 and the APRI scores were calculated using the Sterling’s and the Wai’s formulas, respectively. Results: Liver fibrosis was present in almost half of the study population (47%). As expected, APRI values of Hepatitis C co-infected subjects were higher than in HIV mono-infected patients (0.96 ± 0.18 vs. 0.5 ± 0.45, p=0.01). Notably, the risk was higher among marijuana users (OR= 9 95% CI 1.3-9.5, p=0.02). The risk of moderate fibrosis was also higher in the HAU (OR = 1.3; 95% CI, 1-2.5, p=0.04) when compared to non-HAU. Additional analyses indicated that consumption of liquor even 1-2 drinks per day, and high daily intakes of beer or wine (> 3 drinks per day) increases the risk of liver fibrosis. Thrombocytopenia, which is still prevalent (HAU=15% versus Hep C=22%) significantly increased the odds of moderate fibrosis (OR = 9; 95% CI, 3.6-23; p=0.0001). The odds of having severe fibrosis were 52% higher in the TCP group (95% CI, 13-97; p=0.0000). Serotonin, which is stored in the platelets, was also reduced among subjects with liver fibrosis levels (55.7 ± 6.7 vs. 87.3 ± 7.8 ng/mL, p=0.003). Multivariate analysis identified gender, hepatitis C, liquor use, TCP, marijuana and serotonin alterations as risk factors associated with liver fibrosis. Conclusion: Liver fibrosis is a condition that was associated with modifiable risk factors such as HAU, marijuana, TCP and viral hepatitis C. These results indicated that health care providers must be attentive for signs of these conditions to avert the risk of this terminal liver disease. From the clinical perspectives, analyses suggest that platelet-based interventions and serotonin agonist could be potential therapeutic targets.

Highlights

  • Thrombocytopenia (TCP), a platelet count of less than 150,000 per microliter, is a common hematological complication which affects a sizable proportion of the people living with HIV (PLWH) [1,2,3]

  • These opposite observations let us with a plethora of unanswered questions that we aim to address in this article

  • Since the main focus of this cohort study was to assess the potential effects of alcohol, the DSM-IV-TR questionnaire was applied [25], and those participants who were dependent on drugs or injecting illicit psychoactive substances were excluded

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Summary

Introduction

Thrombocytopenia (TCP), a platelet count of less than 150,000 per microliter, is a common hematological complication which affects a sizable proportion of the people living with HIV (PLWH) [1,2,3]. Platelets exert a variety of other functions These multifunction effects derive from various inflammatory mediators, growth factors, and proteases stored in the platelets, that either enhance or limit tissue injury [8,9]. Initially related to liver fibrosis, other studies have implicated the release of serotonin by platelets as a mediator of liver regeneration and repair after partial hepatectomy [9,11,12]. These opposite observations let us with a plethora of unanswered questions that we aim to address in this article

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