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Liver fatty acid binding protein (L‐Fabp) modulates lipid trafficking in enterocytes, hepatocytes, and hepatic stellate cells (HSCs). We examined hepatocyte vs. HSC L‐Fabp deletion in hepatic metabolic adaptation and fibrotic injury. Floxed L‐Fabp mice were bred to different transgenic Cre mice or injected with adeno‐associated virus type 8 (AAV8) Cre and fed diets to promote steatosis and fibrosis or were subjected to either bile duct ligation or CCl4 injury. Albumin‐Cre‐mediated L‐Fabp deletion revealed recombination in hepatocytes and HSCs; these findings were confirmed with 2 other floxed alleles. Glial fibrillary acid protein‐Cre and platelet‐derived growth factor receptor β‐Cre‐mediated L‐Fabp deletion demonstrated recombination only in HSCs. Mice with albumin promoter‐driven Cre recombinase (Alb‐Cre)‐mediated or AAV8‐mediated L‐Fabp deletion were protected against food withdrawal‐induced steatosis. Mice with Alb‐Cre‐mediated L‐Fabp deletion were protected against high saturated fat‐induced steatosis and fibrosis, phenocopying germline L‐Fabp−/− mice. Mice with HSC‐specific L‐Fabp deletion exhibited retinyl ester depletion yet demonstrated no alterations in fibrosis. On the other hand, fibrogenic resolution after CCl4 administration was impaired in mice with Alb‐Cre‐mediated L‐Fabp deletion. These findings suggest cell type‐specific roles for L‐Fabp in mitigating hepatic steatosis and in modulating fibrogenic injury and reversal.—Newberry, E. P., Xie, Y., Lodeiro, C., Solis, R., Moritz, W., Kennedy, S., Barron, L., Onufer, E., Alpini, G., Zhou, T., Blaner, W. S., Chen, A., Davidson, N. O. Hepatocyte and stellate cell deletion of liver fatty acid binding protein reveal distinct roles in fibrogenic injury. FASEB J. 33, 4610–4625 (2019). http://www.fasebj.org

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Systemic anticoagulation use remains a crucial therapeutic strategy in the treatment of COVID-19 disease (respiratory tract infection caused by SARS-CoV-2 RNA) affected patient population. By presenting a sporadic case of chest wall hematoma we bring to light factors surrounding this decision. CASE PRESENTATION: A 77-year-old Hispanic female with a history of Hypertension, Diabetes, and Obesity presented with myalgias, cough, and dyspnea at rest. After being diagnosed with COVID-19 Pneumonia, she was started on Hydroxychloroquine. As the patient's oxygen requirement increased despite receiving Tocilizumab and Remdesivir, systemic anticoagulation with Enoxaparin was initiated. Upon receiving therapeutic Enoxaparin subcutaneous for five days, the patient started to complain of left upper chest wall pain, which was noted to have loculated swelling with diffuse ecchymosis. Upon development of sudden hypotension, lightheadedness, acute anemia, she underwent CT Angiography of Chest diagnosing arterial hematoma and attributed to systemic anticoagulation. The patient received several blood products and evacuation of 600 ml chocolate-colored fluid from loculated hematoma with the placement of an in-dwelling drain. She did not require any embolization or surgical intervention, as there was no active arterial diathesis. Before discharge, her symptoms resolved, and she was weaned to a nasal cannula. She continued to improve, and the catheter was subsequently discontinued. The patient was eventually discharged with no further adverse events. DISCUSSION: The incidence of spontaneous muscle hematomas in patients using anticoagulant therapy is infrequent. The proposed risk factors of pathophysiology in these cases include microangiopathy, diabetes, elderly age, vascular lesions, collagen, or hemostatic disorders1. Current literature suggests COVID 19 to be prothrombotic, with varying degrees of abnormalities noted in coagulation test parameters2,3. Reports suggest better outcomes, lower severity of illness with the use of therapeutic anticoagulation4. Pathology reports show COVID 19 infection to cause proinflammatory changes and microthrombi in arterioles5. However, this patient had a bleeding event contrary to published reports so far, including lower extremity and bowel ischemia6,7. This raises the question of appropriate timing, dosage, and use of anticoagulation in these patients. CONCLUSIONS: We aim to throw light into the conundrum surrounding the use of systemic anticoagulation in the COVID19 patient population by highlighting one of the very rare adverse events in the setting of anticoagulation use.

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