Some conditions of metabolic origin are, at least in part, considered to be associated or driven by HIV infection or its treatment. These include hyperlipidaemia, lipodystrophy, type 2 diabetes, non-alcoholic fatty liver disease (non-ALFLD), fragility fractures, and some elements of cardiovascular disease.
There are several behavioural factors, particularly diet exercise, alcohol, smoking, and there are some antiretroviral drugs, that contribute to the high incidence of metabolic disease in people living with HIV (PLWH). Some fundamental biological and cellular mechanisms may be important in driving metabolic abnormalities in PLWH. Irisin, a cleaved part of a protein encoded by the FNDC5 (Fibronectin type III domain-containing protein 5) gene, has been correlated in PLWH with adiposity, and inversely correlated with fat free mass and some strength parameters. HIV may disrupt fundamental metabolic host cell processes and further enable a preferential environment for virion assembly. The metabolic syndrome and obesity appear to be key for many cases of liver fibrosis in PLWH with concomitant hepatitis virus infection. The METAFIB study found that adipokines and SCD163 (a soluble form of Cluster of Differentiation receptor163), were significantly associated with fibrosis of the liver.
To improve metabolic health outcomes in PLWH, we need further studies to increase our evidence base and develop better therapies. Therapeutic strategies include the identification of risk factors for metabolic disease in PLWH, such as fatty liver, and screening for diabetes, affording the opportunity to encourage behavioural change such as diet and exercise, and the selection of appropriate antiretroviral medication.