Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis

Thrombospondin 1 and Nuclear Factor Kappa B Signaling Pathways in Non-alcoholic Fatty Liver Disease

“…However, serum liver enzyme levels do not correlate with histological findings in the clinical setting and are not helpful in the diagnosis of NAFLD and in determining the severity of the disease. Despite all this, TSP-1 may be an enchanting target for NASH-induced hepatic fibrosis [30]. The hepatocyte-mediated fibrogenic response is regulated by TSP-1 [31].…”

Pearls and pitfalls in non-alcoholic fatty liver disease: tricky results are common

“…There is accumulating evidence that thrombocytopenia itself can be seen before the development of advanced fibrosis and thus may be an independent manifestation of the NAFLD disease process (see Table 3). In two recent small cohorts, the prevalence of thrombocytopenia in non-cirrhotic NAFLD was found to be 24%-28% and was associated with increased body weight [50,51] . These studies though defined NAFLD based on non-invasive measures; a larger retrospective Brazilian study of 441 patient with biopsyproven NAFLD reported a lower prevalence of thrombocytopenia in non-cirrhotic patients at 3.2% [52] .…”

“…In two recent small cohorts, the prevalence of thrombocytopenia in non-cirrhotic NAFLD was found to be 24%−28% and was associated with increased body weight [ 50 , 51 ] . These studies though defined NAFLD based on non-invasive measures; a larger retrospective Brazilian study of 441 patient with biopsy-proven NAFLD reported a lower prevalence of thrombocytopenia in non-cirrhotic patients at 3.2% [ 52 ] . Nonetheless, whether this mild thrombocytopenia is clinically important remains unclear as rates of bleeding events or need for treatment do not differ from patients with normal platelet levels [ 50 ] .…”

Démonstration de Faisabilité: Nonalcoholic Fatty Liver Disease May Cause Thrombocytopenia

“…Strictly speaking, the cause of the thrombocytopenia we observe in NAFLD is unknown, but several explanations have been offered, such as a certain degree of hypersplenism, bone marrow hypoplasia, reduced peripheral blood cell survival, thrombopoietin deficiency, among others. [1][2][3][4][5][6] Since hypersplenism may lead into granulocytopenia, we also explored the association of NAFLD, granulocytopenia, and thrombocytopenia and found that there is a significant association between these variables, thus suggesting that hypersplenism may somehow be involved in the origin of the cytopenias observed in people with NAFLD. 4 As a result of the studies that have been conducted in this condition, we have learned that the salient features of the NAFLD-associated thrombocytopenia are: (1) it presents in around one-fifth of patients, depending on the method employed to define the liver damage; (2) it is associated with excess weight; (3) it is usually mild, with platelet count above 40 Â 10 9 /L; (4) it is not associated to mucocutaneous bleeding; and (5) it does not need specific treatment to improve the platelet count.…”

“…2 Interestingly, according to a group of researchers in Brazil, employing liver biopsy to define NAFLD, the prevalence of thrombocytopenia was 3%. 6 Since NAFLD is the hepatic component of insulin resistance, we assessed the association of thrombocytopenia and insulin resistance and found that, in the absence of NAFLD, insulin resistance by itself is not associated with thrombocytopenia. 3 It seems that changes in the intrahepatic circulation and/or structure are needed to induce the drop in platelet count.…”