2010
DOI: 10.1097/maj.0b013e3181bfc83f
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Hypoalbuminemia and Lymphocytopenia in Patients With Decompensated Biventricular Failure

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Cited by 46 publications
(27 citation statements)
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“…Lymphopenia may be caused by lymphocyte apoptosis in atherosclerotic lesions, which gradually increases with atherosclerotic burden [23]. Moreover, several studies showed a relationship between low lymphocyte count and malnutrition [24, 25]. Thus, the combination of elevated neutrophils (nonspecific inflammation) and decreased levels of lymphocytes (regulatory component) into a single composite marker may provide additional information to interpret the pathogenesis of arterial stiffness [26].…”
Section: Discussionmentioning
confidence: 99%
“…Lymphopenia may be caused by lymphocyte apoptosis in atherosclerotic lesions, which gradually increases with atherosclerotic burden [23]. Moreover, several studies showed a relationship between low lymphocyte count and malnutrition [24, 25]. Thus, the combination of elevated neutrophils (nonspecific inflammation) and decreased levels of lymphocytes (regulatory component) into a single composite marker may provide additional information to interpret the pathogenesis of arterial stiffness [26].…”
Section: Discussionmentioning
confidence: 99%
“…23 In HHF specifically, elevated biventricular filling pressures and subsequent splanchnic congestion may cause direct enteric losses of lymphocytes. 24 Furthermore, this splanchnic congestive process may facilitate bacterial endotoxin translocation from the gut into the systemic circulation. 25,26 Robust immune activation and release of cytokines, such as tumor-necrosis factor-1, may directly relate to reductions in lymphocyte counts (particularly T-helper cell and B-cell subpopulations), 27 perhaps mediated by apoptotic mechanisms.…”
Section: Discussionmentioning
confidence: 99%
“…These mechanisms commonly lead to a protein-losing enteropathy, as was manifested in our patient [14]. The loss of immunoglobulins as well as lymphocyte-rich chyle creates a functionally immunocompromised host [14,15]. This immunocompromised state, as well as bacterial overgrowth and bacterial translocation were likely mediators of SBP in this patient and are the same risk factors previously described in the pathogenesis of SBP among cirrhotics [16][17][18].…”
Section: Discussionmentioning
confidence: 56%