Mysterious Case of Reduction in HDL Cholesterol in a Patient with B-cell Monocytosis

Abstract

<h3>Lead Author's Financial Disclosures</h3> Nothing to disclose. <h3>Study Funding</h3> None. <h3>Background/Synopsis</h3> We review a clinical scenario involving a 66-year-old male seen in clinic for acute change in clinical status. This is intended to highlight reduction in HDL levels associated with progressive anemia, thrombocytopenia, and splenomegaly suspicious for B-cell predominant lymphoma. <h3>Objective/Purpose</h3> To review the relationship of HDL cholesterol levels and inflammatory states suspected for lymphoma and its impact on clinical management. <h3>Methods</h3> In addition to close follow-up at primary care clinic, he was referred to hematology for further evaluation for workup such as bone marrow biopsy. <h3>Results</h3> A 66-year-old male with history of hypothyroidism, chronic kidney disease, and dyslipidemia on statin was now found to have progressive worsening fatigue over weeks along with hematologic changes such as anemia, thrombocytopenia and splenomegaly. Initial referral to hematology for clinical change did not raise any concern due to grossly borderline hematologic laboratory values. However, importantly, patient was noted to have significant acute drop of ∼40% in HDL levels during this period. This finding along with a clinical change prompted further workup from hematology revealing atypical lymphocytes observed on peripheral smear with 43.6% CD19 positive B cells with CD5 and CD10 negative on flow cytometry as well as a bone marrow and lymph node biopsy. <h3>Conclusions</h3> Cholesterol plays an integral role in structural maintenance of cell membranes, intracellular and intercellular signaling, and metabolism. Several cohort studies have shown an inverse correlation between serum HDL cholesterol levels and malignancy such as breast cancer, lymphoma and leukemia, particularly non-hodgkin's lymphoma (NHL). Based on many epidemiologic and prospective studies, it has been hypothesized that chronic inflammation may result in reduction of HDL cholesterol and perhaps may act as a potential marker of severity of systemic inflammation and inflammation-induced NHL risk. Interestingly, HDL cholesterol seems to modulate inflammatory responses independent of non-HDL cholesterol levels by inhibiting cytokine-induced expression of endothelial cell adhesion molecules and by suppressing chemotactic activity of monocytes and lymphocytes. In our clinical case, our patient may not be adequately evaluated based on borderline hematological laboratory abnormalities. However, a drastic drop (∼40%) in HDL cholesterol levels along with a change in clinical status promptly acted as a marker for further evaluation of a concerning and potentially fatal inflammatory state.