Rare cause of spontaneous spleen bleeding: a case report and literature review.

Rupture of the spleen is a serious medical condition manifesting as a sudden abdominal event, potentially life-threatening. Spontaneous spleen rupture is a rare condition. Atraumatic rupture of the spleen is a very unlikely condition. Risk factors include splenomegaly, hemato-oncological diseases, and infections, such as malaria or infectious mononucleosis. Extremely rare is splenic rupture described in autoimmune disease or vasculitis. There has been no reported case of spontaneous splenic rupture as a first manifestation of Churg- Strauss syndrome so far.

Use of Fibrinogen Determination Methods in Differential Diagnosis of Hypofibrinogenemia and Dysfibrinogenemia.

BACKGROUND: Fibrinogen plays an important role in hemostasis. The normal concentration of fibrinogen in blood plasma is between 1.8 - 4.2 g/L. Decreased fibrinogen levels are observed in congenital afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, disseminated intravascular coagulation, fibrinolytic therapy, some more severe hepatic parenchymal disorders, and increased blood loss. Elevated fibrinogen levels occur in inflammatory diseases and neoplastic diseases, in pregnancy, and postoperative conditions. Functional fibrinogen measurement is also one of the basic coagulation screening tests. The fibrinogen antigen assay is used to distinguish between qualitative and quantitative fibrinogen disorders. METHODS: The aim of the study was the use of fibrinogen determination methods in differential diagnosis of hypofibrinogenemia and dysfibrinogenemia, statistical evaluation and determine the relationship of fibrinogen Clauss assay, prothrombin time (PT) derived fibrinogen assay, and fibrinogen antigen in the group of 60 patients with congenital fibrinogen disorders (n = 40 dysfibrinogenemia; n = 20 hypofibrinogenemia). RESULTS: The results measured by the PT-derived fibrinogen assay were approximately four times higher compared to the fibrinogen Clauss assay in the group of patients with dysfibrinogenemia. In patients with hypofibrinogenemia, there is a correlation (r = 0.9016) between the fibrinogen Clauss assay and PT-derived fibrinogen assay with a statistical significance of p < 0.0001. Using a linear or quadratic interpolation function, we were able to determine the fibrinogen Clauss assay and the fibrinogen antigen assay before analysis. CONCLUSIONS: The higher level of the PT-derived fibrinogen assay compared to the fibrinogen Clauss assay in the group of patients with dysfibrinogenemia may pose a greater risk to asymptomatic patients who require diagnosis and treatment in case of bleeding. The fibrinogen value using the PT-derived fibrinogen assay could erroneously give a normal level. The use of the interpolation function is important to estimate the value of fibrinogen activity and antigen before the analysis itself by the Clauss assay or analysis by the fibrinogen antigen assay.

Gastrointestinal tract involvement in mixed connective tissue disease (Sharp syndrome).

Mixed connective tissue diseases (MCTD) is a very rare autoimmune disease connecting clinical signs of systemic lupus, systemic sclerosis, polymyositis and rheumatoid arthritis. Clinical manifestations are very diverse. In some patients, the digestive tract is affected in varying degrees. The esophagus is affected most often, and patients are complaining of dysphagia. Morphologically, this disorder is similar to the injure in systemic scleroderma. In this case, we describe a unique case of a severe damage of digestive tract manifested by esophageal motility disorders, cachectization, ascites, and repeated ileus conditions.

Idiopathic Pan-Colonic and Small-Intestine Varices.

Idiopathic colonic varices represent a rare source of gastrointestinal haemorrhage with a presumed incidence around 0.0007%. Herein, we present a case of idiopathic colonic and small-intestine varices. According to our knowledge, this case report is the first description of both pan-colonic and small-intestine idiopathic varices of this extent. A young male patient without any previous notable medical history was admitted to the hospital because of massive enterorrhagia with haemodynamic instability. Colonoscopy revealed massive pan-colonic varices. After stabilization, numerous diagnostic procedures were performed in order to investigate the aetiology of pan-colonic varices without any explanation of the patient's condition. In addition, capsule endoscopy revealed varices through the whole length of the small intestine. The final diagnosis was idiopathic varices of the colon and small intestine. Because of the rapid clinical stabilization, the single incident of haemorrhage and the extension of the disease, a conservative approach was chosen (venotonics and ß-blockers). During the 12-month follow-up period, the patient reported no gastrointestinal haemorrhage.

Platelet Aggregation in Direct Oral Factor Xa Inhibitors-treated Patients With Atrial Fibrillation: A Pilot Study.

BACKGROUND: Activated factor X (factor Xa) plays an important role in regulation of platelets. The aim of this study was to test the effect of direct oral factor Xa inhibitors-rivaroxaban and apixaban-on platelet aggregation in patients with nonvalvular atrial fibrillation. PATIENTS AND METHODS: This single-center pilot study enrolled 21 factor Xa inhibitors-treated (9 rivaroxaban-treated and 12 apixaban-treated) patients with nonvalvular atrial fibrillation. The trough and peak samples of these patients were tested for adenosine diphosphate (ADP)-induced, epinephrine-induced, and collagen-induced platelet aggregation with light transmission aggregometry, and with factor Xa-calibrated anti-Xa chromogenic analysis. RESULTS: The detected trough anti-Xa activity was 57.5 ± 43.4 µg/L. There was a significant increase in peak anti-Xa activity to 175.9 ± 119.6 µg/L (P < 0.001) observed. The platelet aggregation was reduced with reduced inductor concentration. However, no significant changes in ADP-induced, or in epinephrine-induced, or in collagen-induced platelet aggregation were seen comparing trough and peak sample. There were no significant differences in anti-Xa activity or in platelet aggregation comparing rivaroxaban-treated and apixaban-treated patients. CONCLUSIONS: This study showed that factor Xa inhibition does not affect ADP-induced, epinephrine-induced, and collagen-induced platelet aggregation.