Florin Mitu, Alexandra Maștaleru, Clementina Cojocaru, Mihai Roca, Ovidiu Mitu and Maria-Magdalena Leon-Constantin
Catecholamine tumoral syndrome is caused by lesions of the medulosuprarenal cromafin tissue (pheochromocytoma or pheochromocytoblastoma) or of the neural crest (paraganglioma), from the ganglionar cells (ganglioneurinoma or ganglioneuroblastoma) or from the sympathetic nervous cells (sympathogonia – sympathoblastoma and sympathoblasts – neuroblastoma), tumors that excessively secrete cathecolamines (adrenaline and noradrenaline), but also neuropeptides. Indications for testing are associated with the clinical context. Because the pheochromocytoma means a heterogeneous group of secretory tumours, there is no analysis achieving the 100% accuracy. The diagnosis can be established by hormonal dosages for basal determinations and by dynamic tests or through nonspecific tests. Imagistic explorations like computer tomography, abdominal and pelvic MRI can localise the tumour. Plasma and urinary metanephrines dosage are the first intention tests because have a higher accuracy compared to catecholamines or other metabolites. Considering the low prevalence of catecholamine secreting tumours, we considered it necessary to systematise diagnostic possibilities.
Maria-Magdalena Leon-Constantin, Alexandra Maștaleru, Ovidiu Mitu, Madalina Zota, Teodor Vasilcu, Radu Gavril and Florin Mitu
Coumarin anticoagulants era (warfarin, acenocumarol) seems to be coming to an end with the launch of the novel anticoagulants like dabigatran, rivaroxaban, apixaban and edoxaban. Dabigatran (Pradaxa) is a prothrombin (factor II) inhibitor that doesn't necessitate monitoring by coagulation tests, doesn't have food or drug interactions, except for P-gp inhibitors. Rivaroxaban (Xarelto) is a direct inhibitor of factor X and is approved for the prevention of thromboembolic events in patients with non-valvular atrial fibrillation and for the prevention of deep venous thrombosis in patients undergoing orthopaedic surgery (hip and knee prosthesis). Apixaban (Eliquis) is a direct inhibitor of factor X and is indicated for the prevention of venous thromboembolic events in patients undergoing hip or knee arthroplasty, the prevention of thromboembolic events in patients with non-valvular atrial fibrillation and treatment or prevention of recurrences in patients with deep vein thrombosis or pulmonary embolism. Edoxaban (Savaysa), recently approved is USA, is a direct inhibitor of factor X and is indicated for deep venous thrombosis, pulmonary embolism and for the prevention of thromboembolic events in patients with non-valvular atrial fibrillation. The most recent studies focus on antidotes specifically designed to bind and neutralise the anticoagulant activity of both direct thrombin inhibitors and direct factor Xa inhibitors. The drugs currently being studied are idarucizumab, a specific antidote, andexanet alfa, a class-specific antidote and ciraparantag, a universal antidote. Of these, only idarucizumab was approved by the FDA.
Manta Andrei, Maștaleru Alexandra, Oancea Andra, Anghel Razvan Constantin, Roca Mihai, Leon-Constantin Maria Magdalena and Mitu Florin
Obesity, a component of the metabolic syndrome, is a rising public health problem, continuously increasing in the European countries. The therapeutic success of the patient with metabolic syndrome requires a multidisciplinary approach to lifestyle changes, weight loss, continuous and dynamic dietary improvement, sedentary reduction, normalization of blood pressure, glycemia and lipid parameters. We performed a retrospective study that was conducted in the Clinical Rehabilitation Hospital in Iasi, with 4627 patients that were admitted in the Cardiovascular Rehabilitation Clinic from January 2011 to December 2015 with the diagnosis of metabolic syndrome according to WHO definition (Group 1) or with other comorbidities (Group 2). In the first group were included 1064 patients diagnosed with metabolic syndrome. This group has predominantly smoking female patients. Also, in group 1 were diagnosed more patients with left ventricular hypertrophy and coronary heart disease compared to group 2. Most of the patients with inflammatory syndrome were included in the group without metabolic syndrome (group 2). The results of our study confirm that metabolic syndrome is a cluster of abnormalities whose evolution determines the development of coronary heart disease. All this would advocate for treating metabolic syndrome as the primary method of preventing cardiovascular disease.
Oana Irina Gavril, Lidia Iuliana Arhire, Ovidiu Mitu, Radu Sebastian Gavril, Alexandra Mastaleru, Madalina Ioana Zota, Maria-Magdalena Leon-Constantin, Teodor Vasilcu, Laura Mihalache and Florin Mitu
Introduction. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic expression of the metabolic syndrome, both conditions presenting similar clinical features.
Aim. The aim of this study was to evaluate, among diabetic subjects, the relationship between fatty liver load and the presence of metabolic syndrome criteria.
Methods. An observational study was conducted on 92 subjects with type 2 diabetes. We followed anthropometric measurments, lipid profile, blood pressure and the degree of hepatic steatosis using ultrasonography.
Results. The average age of the study group was 60,38 ± 10,37 years, with an approximately equal distribution by gender (48% male and 52% female). More than half of the subjects presented hypercholesterolemia, hypertriglyceridemia, and low HDL cholesterol level. Most of the patients included in the study had varying degrees of liver fat load (only 9,89% of cases of apparently normal liver on ultrasound), and met the criteria for metabolic syndrome (81,31%). It was found that the frequency of the cases with fatty liver impairment was significantly higher in subjects with metabolic syndrome (32,43% compared to 5,88% for those without metabolic syndrome, p = 0,01) and the frequency of the cases with normal liver were significantly higher in subjects without metabolic syndrome (23,53% to 6,76%, p=0,02).
Conclusion. We can say that NAFLD is a risk factor for the presence of metabolic syndrome and it can be considered the hepatic expression of this syndrome.