Acquired hemophilia A (AHA) is a rare antibody-mediated condition in which autoantibodies form against a coagulation factor, most commonly factor VIII (FVIII), causing severe coagulopathy. Here the present report presents a case of AHA in a 35-year-old postpartum woman with continuous polyserous bloody effusions who was admitted to the First Affiliated Hospital of Zhejiang Chinese Medical University (Hangzhou, China) in October 2017 without a history of trauma, anticoagulation treatment or coagulopathy. At presentation, the patient's hemoglobin level was low (70 g/l; normal range: 115–150 g/l) g/l, blood pressure was 89/58 mmHg (normal range, 90–140/60–90 mmHg), and activated partial thromboplastin time was 68.4 sec (normal range: 25.0–36.0 sec), with a normal international normalized ratio (0.94; normal range, 0.8–1.2). The reaction time in thrombography was prolonged (35.8 min; normal range: 5–10 min), coagulation FVIII had markedly decreased activity (12.6%; normal range, 60–150%), and FVIII inhibitor had a high titer [7.4 Bethesda units (BU)/ml; normal range, 0–0.6 BU/ml]. Notably, the patient's autoantibody level was markedly higher than normal (1:320; normal range: <1:100). The patient was successfully treated with bleeding control, eradication of FVIII inhibitor, and treatment of the underlying disease. To the best of our knowledge, this is the first case of AHA with polyserous bloody effusions in a patient with an autoimmune disorder during the postpartum period. Reports of such rare cases will aid the characterization of disease pathogenesis, which may in turn lead to the recognition and timely treatment of this rare disorder.
Nonalcoholic fatty liver disease (NAFLD) causes countless burden to people worldwide, especially when the quality of people’s life is improved constantly. It has clinical significance to find novel methods to deal with this common disease. Here, we aimed to assess whether angiogenesis inhibitor ZM306416 could improve NAFLD. Mice were fed with different diets for 15 weeks and treated with ZM306416 followed by analysis of weight and inflammatory infiltration of adipose tissue, fatty degeneration, and fibrosis by immunohistochemistry, fibrosis-related proteins level by qRT-PCR. Compared to control group, ZM306416 treatment significantly declined mice weight and adipose tissue weight. In addition, ZM306416 decreased blood vessel density of adipose tissues, mitigated inflammatory infiltration, fatty degeneration, and fibrosis. Moreover, ZM304616 alleviated adipose fibrosis-related protein expression, and transcription of inflammatory genes and adipogenesis genes. However, the inhibitor enhanced β-oxidation of fatty acid, Nrf2, and SOD2, while decreased serum markers of liver injury. In conclsuion, angiogenesis inhibitor ZM306416 attenuates adipose fibrosis and degradation, promotes adipose functions and lipid metabolism, thereby alleviating obesity-induced nonalcoholic fatty liver.
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