Systemic lupus erythematosus combined with primary hyperfibrinolysis and protein C and protein S deficiency:A case report

BACKGROUND Systemic lupus erythematosus(SLE)is an autoimmune disease characterized by systemic involvement and multiple autoantibodies in the serum.Patients with protein C(PC)and protein S(PS)deficiency are prone to thrombosis.In contrast,patients with primary hyperfibrino-lysis tend to bleed.CASE SUMMARY A 52-year-old female patient with bilateral pleural effusion was diagnosed with"tuberculous pleurisy"and treated with anti-tuberculosis drugs and prednisone.The coagulation-related laboratory results showed decreased fibrinogen,PC activity,PS activity,and antithrombinШactivity.The immune-related laboratory results showed positive antinuclear antibody,anti-Smith antibody,anticardiolipin antibody(ACL),anti-β2-glycoprotein I antibody(aβ2GPI)and direct Coomb’s test and decreased complement 3 and complement 4.Thoracoscopy was performed and bloody pleural fluid was drained.Pathology of the pleural biopsy showed lymphocytes,plasma cells,and a few eosinophils in adipose and fibrous connective tissue.Results of whole exome sequencing of blood showed no genetic mutations suggesting the presence of hereditary hematological diseases.The patient was finally diagnosed with SLE and primary hyperfibrinolysis,and was treated with prednisolone,hydroxychloroquine,and compound cyclophosphamide.CONCLUSION PC and PS deficiency in SLE might be related to ACL and aβ2GPI.SLE and primary hyperfibrinolysis can coexist in one patient,with both a risk of thrombosis and a risk of bleeding.

The pathogenesis of chronic subdural hematoma in the perspective of neomembrane formation and related mechanisms

Chronic subdural hematoma(CSDH)is a disease characterized by capsuled blood products that progressively occupy the intracranial space,causing intracranial hypertension and compression in the brain.CSDH frequently occurs in all demographics,especially in the elderly,but the pathogenesis of CSDH remains unclear.In this review,we discuss the origin,development,and current treatment strategies of CSDH.For thefirst time,we analyzed the cellular and molecular compositions of hematoma membranes with a focus on neomembrane formation,a complex early-stage interactive event in hematoma pathogenesis.We hypothesize that in patients with CSDH,dural border cells(DBCs)might be induced to synthesize collagen or serum proteins might accumulate at the dura and arachnoid layers at the site of injury,thereby encapsulating the hemorrhage.Membrane formation may trigger inflammatory responses after subdural hemorrhage,promotingfibroblast-involved extracellular matrix(ECM)deposition and aberrant angiogenesis within the outer membrane.Consequently,ECM deposition and angiogenesis mutually influence each other and are modulated by inflammatory processes.By illustrating the complex and interactive mechanism of neomembrane formation,we aim to provide a novel insight into CSDH pathogenesis and propose directions for future research as well as advancements in treatment strategies for this disease.

Effect of sub-hypothermia therapy on coagulopathy after severe head injury

Sub-hypothermia therapy is one of the treatments for patients with severe head injury. The objective of the therapy is to treat traumatic brain injury （TBI） by alleviating brain edema, protecting blood brain barrier （BBB）, and preventing subsequent damage to neurons. It can protect brain function by depressing metabolism, reducing the release of excitatory amino acids and free radicals, reducing the level of lactic acid, and lowering the damage of cytoskeletal structure However,