Undetectable HDL Cholesterol in a Patient with Flu-Like Illness

Bock, Jay L.; Senzel, Lisa; Spitzer, Eric D.; Bifulco, William

doi:10.1373/clinchem.2016.258616

Cited by 4 publications

(4 citation statements)

References 11 publications

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“…Oxidation of HDL-c is more pronounced in older patients due to the small footprint of antioxidants [165]. Similar alterations in the lipid profile are apparent in viral and protozoan-driven sepsis as well [164,[166][167][168]. Some studies quantified quite precisely that a serum level of HDL-c below 25 mg/dL is the threshold of dramatically increased risk for Furthermore, if these conditions persist over a long period, even small deviations may lead to significant impacts [129].…”

Section: Lipid Metabolism During Acute Sepsismentioning

confidence: 97%

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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(1) Background: Sepsis is one of the most common critical care illnesses with increasing survivorship. The quality of life in sepsis survivors is adversely affected by several co-morbidities, including increased incidence of dementia, stroke, cardiac disease and at least temporary deterioration in cognitive dysfunction. One of the potential explanations for their progression is the persistence of lipid profile abnormalities induced during acute sepsis into recovery, resulting in acceleration of atherosclerosis. (2) Methods: This is a targeted review of the abnormalities in the long-term lipid profile abnormalities after sepsis; (3) Results: There is a well-established body of evidence demonstrating acute alteration in lipid profile (HDL-c ↓↓, LDL-C -c ↓↓). In contrast, a limited number of studies demonstrated depression of HDL-c levels with a concomitant increase in LDL-C -c in the wake of sepsis. VLDL-C -c and Lp(a) remained unaltered in few studies as well. Apolipoprotein A1 was altered in survivors suggesting abnormalities in lipoprotein metabolism concomitant to overall lipoprotein abnormalities. However, most of the studies were limited to a four-month follow-up and patient groups were relatively small. Only one study looked at the atherosclerosis progression in sepsis survivors using clinical correlates, demonstrating an acceleration of plaque formation in the aorta, and a large metanalysis suggested an increase in the risk of stroke or acute coronary event between 3% to 9% in sepsis survivors. (4) Conclusions: The limited evidence suggests an emergence and persistence of the proatherogenic lipid profile in sepsis survivors that potentially contributes, along with other factors, to the clinical sequel of atherosclerosis.

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Section: Lipid Metabolism During Acute Sepsismentioning

confidence: 97%

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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“…Compared to Plasmodium , there is less known about Babesia pathogenesis. However, patients infected with Babesia display lipid abnormalities and markedly low HDL levels, suggesting these parasites depend on host lipid metabolism as well ( Cunha et al, 2000 ; Bock et al, 2017 ; Table 1 ). Similar abnormalities have been observed in Babesia -infected cattle and canines ( Goodger et al, 1990 ; Milanović et al, 2019 ).…”

Section: Intracellular Growthmentioning

confidence: 99%

Lipid hijacking: A unifying theme in vector-borne diseases

O’Neal

Butler

Rolandelli

et al. 2020

eLife

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Vector-borne illnesses comprise a significant portion of human maladies, representing 17% of global infections. Transmission of vector-borne pathogens to mammals primarily occurs by hematophagous arthropods. It is speculated that blood may provide a unique environment that aids in the replication and pathogenesis of these microbes. Lipids and their derivatives are one component enriched in blood and are essential for microbial survival. For instance, the malarial parasite Plasmodium falciparum and the Lyme disease spirochete Borrelia burgdorferi, among others, have been shown to scavenge and manipulate host lipids for structural support, metabolism, replication, immune evasion, and disease severity. In this Review, we will explore the importance of lipid hijacking for the growth and persistence of these microbes in both mammalian hosts and arthropod vectors.

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“…Typical laboratory findings include anemia, thrombocytopenia, elevated ferritin levels, low haptoglobin levels, and other indicators of hemolysis (4,21). Markedly reduced levels of high-density lipoprotein cholesterol (HDL-C) in patients with babesiosis have been observed, with extremely low HDL-C levels and very high ferritin levels being strongly associated with disease (38,39). Both HDL-C and ferritin levels appear to normalize posttreatment, potentially permitting their use as biomarkers for diagnosis and treatment efficacy.…”

Section: Clinical Findingsmentioning

confidence: 99%

Babesia microti: from Mice to Ticks to an Increasing Number of Highly Susceptible Humans

et al. 2017

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, a zoonotic intraerythrocytic parasite, is the primary etiological agent of human babesiosis in the United States. Human infections range from subclinical illness to severe disease resulting in death, with symptoms being related to host immune status. Despite advances in our understanding and management of , the incidence of infection in the United States has increased. Therefore, research focused on eradicating disease and optimizing clinical management is essential. Here we review this remarkable organism, with emphasis on the clinical, diagnostic, and therapeutic aspects of human disease.

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Undetectable HDL Cholesterol in a Patient with Flu-Like Illness

Cited by 4 publications

References 11 publications

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Lipid hijacking: A unifying theme in vector-borne diseases

Babesia microti: from Mice to Ticks to an Increasing Number of Highly Susceptible Humans

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