Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia

The Roles of Glucagon-Like Peptide 1 (GLP-1) Receptor Agonists and Sodium-Glucose Cotransporter 2 (SGLT-2) Inhibitors in Decreasing the Occurrence of Adverse Cardiorenal Events in Patients With Type 2 Diabetes

“…SGLT-2i may increase high-density lipoprotein (HDL) cholesterol and decrease triglycerides, which is considered to be beneficial; however, they have also been shown to increase low-density lipoprotein (LDL) cholesterol [ 19 ]. SGLT-2i also significantly reduces serum uric acid levels in the body by interacting with GLUT-9 (SLC2A9), a facilitated glucose transporter that secretes uric acid into the urine and thus decreases serum uric acid in the body [ 20 ]. This ultimately results in a decreased risk of cardiovascular disease, nephrolithiasis, and gout.…”

Efficacy of Lipid Ratios and Platelet Distribution Width for Assessment of Liver Fibrosis in Patients With Non-alcoholic Fatty Liver Disease

“…A decreased platelet count has been observed in patients with severe fibrosis due to reduced production of thrombopoietin by damaged liver cells and increased splenic sequestration and destruction of platelets. Because of the significant failure of platelets and increased interleukin-6 (IL-6) levels induced by inflammation, the platelet life cycle is shorter in patients with NAFLD [6]. The latter stimulates platelet production by bone marrow and promotes the release of larger, reticulated platelets into the bloodstream.…”

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.…”

“…Since 2014, we have been conducting prospective studies to assess the presence of thrombocytopenia (less than 100 Â 10 9 /L platelets) in persons with NAFLD without overt liver cirrhosis. [1][2][3][4] The concept was initially entertained by Dasanu et al in 2010. 5 To define the presence of NAFLD, several methods can be employed: liver biopsy, serologic determinations (Fibromax), and liver transient elastography (TE/Fibroscan).…”