Metabolic perturbations associated with HIV and antiretroviral therapies are widespread. Unfortunately, research has predominantly focused in cardiometabolic problems, neglecting other important areas. In fact, the immune-calcium–skeletal interface has been understudied despite its potential relevance in people living with HIV (PLWH).
Using a case-control methodology, 200 PLWH receiving medical care were enrolled and stratified according to hazardous vs. non-hazardous alcohol intake (HAU vs. non-HAU) and calcium (Ca) levels by analyzing baseline data. The group was chosen to represent relatively "pure" HAU with minimal drug use and no psychiatric diagnoses.
With these narrow parameters in place, we found evidence that HAU significantly increases TNF-α levels compared to Non-HAU (2.8 ± 0.6 vs. 1.9 ± 0.3 pg/ml, p = 0.05) and decreases blood Ca levels (9 ± 0.6 vs. 9.4 ± 0.5, p = 0.03).
Our analyses also suggest that chronic inflammation, as indicated by increased TNF-α levels, is associated with hypocalcemia (hypoCa <8.6). Despite the limited prevalence of hypoCa, these findings are clinically significant given that hypoCA PLWH exhibited decreased CD4 (253 ± 224 vs. 417.7 ± 281, p = 0.02), B cells (147 ± 58 vs. 248 ± 151, p = 0.03) and NK cells (146.8 ± 90 vs. 229 ± 148, p = 0.008) and elevated CD8 (902.5 ± 438 vs. 699 ± 510, p = 0.09) compared to those with normal calcium.
Furthermore, calcium effects on viral load were also evident with hypoCA exhibiting the highest loads (140,187 ± 111 vs. 35,622 ± 7770 HIV copies, p = 0.01).
Multivariate analyses confirmed the significance of hypoCa in predicting viroimmune parameters.
This paper provides the first evidence that hypoCa accounts for some of the variation in viroimmune measures in HAART recipients and suggests that hypoCa may be mediating alcohol's deleterious effects.
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