This very interesting report communicates a case of acquired HDL-C deficiency that is remarkable for its infectious origin. Very low or undetectable HDL-C more often originates from assay interference from paraproteins and autoantibodies or secondary to the use of drugs, including anabolic steroids and fibrates. Infectious diseases often induce several responses that may hypothetically reduce HDL-C concentrations; impairment of macrophage activity; a humoral immune response that cross-reacts with reagents in enzymatic HDL assays: inflammation mediated by cytokines that may specifically reduce HDL-C concentrations; and direct or indirect impairment of liver synthetic function. However, it is generally true that undetectable HDL-C is an unusual finding relative to the numbers of septic patients seen in most hospital settings and the patient in this case did not have laboratory findings consistent with acute or chronic liver failure.
This raises the possibility that Babesia directly reduces HDL-C in the course of its pathogenesis. Common parasites such as Toxoplasma gondii, Plasmodium falciparum and other Plasmodium spp., Cryptosporidium parvum, and nonhuman pathogens such as Theileria and Eimeria spp. actively acquire host cholesterol for synthesis of cell membranes and other structures and/or are strict auxotrophs for specific forms of cholesterol such as HDL-C and LDL-C. This underappreciated aspect of parasite pathogenesis has potential significance in humans as well as other animals such as dogs (which are commonly infected with Babesia and, in contrast to humans, have an abundance of HDL-C and very little LDL-C), cattle, and other animals in which lipid synthesis and scavenging pathways are potential therapeutic targets for pathogens that have relatively few treatments. This case invites further study through a larger case series and adds undetectable HDL-C to a list of laboratory findings that may telegraph the presence of otherwise difficult-to-diagnose infections.
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Authors' Disclosures or Potential Conflicts of Interest: No authors declared any potential conflicts of interest.
- Received for publication November 14, 2016.
- Accepted for publication November 22, 2016.
- © 2016 American Association for Clinical Chemistry