The emergence of the rare syndrome called vaccine-induced immune thrombocytopenia and thrombosis (VITT) after adenoviral vector vaccines, including ChAdOx1 nCov-19, raises concern about one's predisposing risk factors. Here we report the case of a 56-year-old white man who developed VITT leading to death within 9 days of symptom onset. He presented with superior sagittal sinus thrombosis, right frontal intraparenchymal hematoma, frontoparietal subarachnoid and massive ventricular hemorrhage, and right lower extremity arterial and venous thrombosis. His laboratory results showed elevated D-dimer, C-reactive protein, tissue factor, P-selectin (CD62p), and positive anti-platelet factor 4. The patient's plasma promoted higher CD62p expression in healthy donors' platelets than the controls. Genetic investigation on coagulation, thrombophilia, inflammation, and type I interferon-related genes was performed. From rare variants in European or African genomic databases, 68 single-nucleotide polymorphisms (SNPs) in one allele and 11 in two alleles from common SNPs were found in the patient genome. This report highlights the possible relationship between VITT and genetic variants. Additional investigations regarding the genetic predisposition of VITT are needed.
Background: Kounis syndrome is a hypersensitive coronary artery disease caused by the body's exposure to allergens, which is induced by various drugs and environmental factors. This entity has been described primarily in isolated case reports and case series. We report a case of type III Kounis syndrome caused by cefoperazone-sulbactam.
Case presentation: A 79-year-old man who received an infusion of cefoperazone-sulbactam in Respiratory Department of our hospital for recurrent infections. 28 minutes later, he developed skin flushing of the trunk and extremities, soon followed by loss of consciousness and shock. With antianaphylaxis, pressor therapy, and fluid rehydration, the patient was admitted to the ICU for treatment. During which, he experienced recurrent ventricular fibrillation and a progressive increase in troponin I levels. The ECG of the patient showed that the ST segment elevation of lead II, III, avF, and V3R–V5R was 0.10–0.20 MV. An urgent coronary angiography showed an in-stent thrombosis in the middle part of the right coronary artery, occlusion of the distal flow with TIMI grade 0. The diagnosis was type III Kounis syndrome with cardiogenic shock. Despite aggressive treatment, the patient died on day 7 after ICU admission.
Conclusion: Kunis syndrome is a life-threatening disease, and therefore allergic reactions in patients with a history of cephalosporin allergy and coronary stent implantation should be considered and treated promptly.
Background: Ulcerative colitis often leads to gastrointestinal bleeding and venous thromboembolism (VTE). At present, there is no clear conclusion about anticoagulant therapy for these patients. Treatment for ulcerative colitis usually includes 5-aminosalicylic acid, corticosteroid, and biologics. Acute ulcerative colitis, usually caused by infection, is usually severe and can be life-threatening.
Case presentation: We report the development of VTE in a patient with severe acute ulcerative colitis who experienced gastrointestinal bleeding following hormonal therapy. The patient's indicators suggested that his blood was hypercoagulable and that his prognosis was poor.
Conclusion: Patients with ulcerative colitis are prone to form VTE. The use of corticosteroids during treatment increases the risk of thrombus. Anticoagulation strategy for patients with ulcerative colitis after gastrointestinal bleeding is a problem that needs to be discussed.
Genetic and acquired risk factors are extremely important mechanisms in the development of venous thromboembolism (VTE). Inherited antithrombin (AT) deficiency due to mutations in the SERPINC1 gene is a well-known risk factor for genetic thrombophilia. In this case, we reported a 28-year young abroad student who presented with refractory and recurrent VTE in-hospital. This patient presented with a 2-month history of right lower limb pain and 1 week of fever. The ultrasound showed deep venous thrombosis in the right common and superficial femoral veins. The CTPA confirmed acute pulmonary embolism with multiple filling defects in both pulmonary arteries. He was diagnosed with “pulmonary embolism, pneumonia, lower extremity venous thrombosis”. The level of serum antithrombin was normal, yet gene sequencing revealed a heterozygous missense mutation of SERPINC1, c.1277C>T (p.Ser426Leu). The patient underwent anticoagulant therapy of heparin and inferior vena cava filter implantation. The patient had undergone recurrent VTE despite adequate anticoagulation with heparin during the first 2 weeks. The swelling, pain, and thrombosis of lower extremity veins got resolved from warfarin and rivaroxaban. Inherited antithrombin deficiency due to mutations in the SERPINC1 gene is the genetic basis of this patient, and warfarin/rivaroxaban, other than heparin, is beneficial.
An isolated right atrial thrombus is a life-threatening entity that is extremely rare in patients with dilated cardiomyopathy (DCM), which is characterized by a reduced left ventricular function and consequent left ventricular thrombosis. Here, we present the case of a mysterious isolated giant right atrial thrombus in a male patient with DCM. The presence of deep vein thrombosis prompted us to investigate for other underlying diseases for his right atrial thrombus. Interestingly, the elevation of two tumor markers indicated the likelihood of cancer-associated thrombosis. Further, the computed tomography demonstrated a spiculated mass in the lower right lung that was confirmed by an endobronchial biopsy as lung squamous cell carcinoma. Consequently, the giant thrombus in the right atrium should be attributed principally to lung squamous cell carcinoma on the background of DCM. After 3 weeks of enoxaparin, the echocardiogram indicated partial resolution of the thrombus. However, the patient suffered sudden death due to pulmonary embolism.