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Eosinophilic gastroenteritis (EGE) is a subgroup of the eosinophilic gastro-intestinal disorders (EGIDs), characterized by eosinophilic infiltration and chronic inflammation of the gastrointestinal tract. These are rare diseases with still incompletely elucidated causes and mechanisms, with frequently delayed diagnosis and variable outcome. Despite increased interest in eosinophilic diseases in recent years, fewer data have been published on EGE and no standardized diagnostic and therapeutic approach exists. This paper reports the case of a young male patient diagnosed with EGE in 2017 based on clinical and histopathological criteria and constantly monitored during five years. Besides gastrointestinal eosinophilic infiltration, biopsies also revealed eosinophilic infiltration of the oesophagus, despite no declared characteristic oesophageal symptoms. We found increased specific IgE to multiple foods and progressive blood hypereosinophilia which preceded EGE diagnosis by three years. The EGE management included selective dietary restrictions and pharmacologic therapy based on daily budesonide non-enteric coated tablets, proton pumps inhibitors, antihistamines, cromoglycate, correction of iron, calcium and vitamin D deficiencies. The clinical outcome was good, while blood eosinophilia and endoscopic appearance remained almost unchanged. After one year the patient complained of respiratory symptoms suggesting asthma, needing continuous combined inhaled therapy. The reported case is illustrative for complex presentation, diagnosis and outcome of a rare case of mucosal chronic EGE associated with oesophageal involvement, peripheral eosinophilia, multiple food allergies and asthma.

Background and Objectives: Arterial hypertension remains an important cause of cardiovascular morbidity and mortality, despite all the progress made in the methods of diagnosis, monitoring of target organs’ damage and treatment. The main cause of the increased prevalence of uncontrolled blood pressure values is the low compliance to antihypertensive treatment. The objective of our study was to assess the compliance to the treatment of patients diagnosed with arterial hypertension and monitored in a primary care office. Materials and Methods: The cross-sectional, retrospective study included 129 patients, 65.89% (85) women, previously diagnosed with arterial hypertension. Data from the medical files were analyzed, as well as the patients’ answers to a survey of 18 questions regarding arterial hypertension, comorbidities, complications, treatment and awareness of the condition. Results: The study included 129 patients, with a mean age of 66 ± 8 years. The majority of patients were overweight, 55.81% (72 patients), and 10.85% (14 patients) had grade I obesity. Most of the patients, 55.81% (72 patients) were diagnosed with grade III hypertension, while 37.98% (49 patients) were diagnosed with grade II hypertension and 6.2% (8 patients) with grade I hypertension. One third of the surveyed patients answered that they follow the recommendations of a low-sodium diet, 21.7% are adherent to treatment, but 56% think that the total cost of the medication is an impediment for their compliance to treatment. The majority, 82.17% (106 patients), of respondents had an affirmative answer to the questions: ‘Do you think it would be easier to take one pill instead of 2, 3 or 4 pills?’ Conclusion: The increased compliance to the antihypertensive treatment and control of blood pressure values are associated with the degree of awareness of arterial hypertension and the consequences if left untreated, emphasizing the role of the general practitioner in counseling for secondary prevention.

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Primary cardiac neoplasms are very rare as compared to metastatic tumors. Myxomas are the most common of the primary cardiac tumors. Myxomas represent almost 50% of cardiac masses with an incidence reported at one in 10000 autopsies. A greater percentage (75%) are located in the left atrium, of these, 90% originate from an area in the atrial septum near the fossa ovalis. Right atrial myxoma are un common beign three to four time less frequent that those located in the left atrium. The incidence of those arising in the left and right ventricles is 2.5-4%. We report on case of right ventricular cardiac myxoma, confirmation with histopathological examination, what is first case in forensic medicine practice.

Background: Systemic lupus erythematosus is a multiorganic, chronic immune disease and lupus nephritis, a severe manifestation, represents the strongest predictor of a poor outcome of this pathology. Cytokines play an important role in lupus nephritis and consequently, their use as biomarkers of active systemic lupus erythematosus disease is of particular interest. The purpose of this work was to study the pro-inflammatory role of interleukin-17 in renal involvement in patients with systemic lupus erythematosus (SLE). Methods: We performed a retrospective study of 87 patients diagnosed with SLE according to the Systemic Lupus International Collaborating Clinics 2012 diagnosis criteria. In this study, we determined the serum levels of interleukin-17 by ELISA. Results: It was observed that 49 patients in the study group presented with positive values of interleukin-17, range (1.12-23.66) pg/ml. There was a positive correlation of interleukin-17 with active SLE as assessed by the Systemic Lupus Erythematous Disease Activity Index. No association was found between serum interleukin-17 level and renal pathology at the inclusion or in the clinical history of the patients. Patients with leukocyturia and hematuria presented higher values of serum interleukin-17 than those without these manifestations. In the linear regression model, after adjusting for age, gender and treatment we found an independent association between serum IL-17 levels and leukocyturia presence with OR=2.06, 95% CI range (1.22-2.89). Conclusions: A positive correlation has been observed between serum IL-17 and the SLE disease activity as assessed by the SLEDAI score computed without anti-DNA antibodies. Also, the IL-17 levels was strongly associated with the presence of leukocyturia and hematuria, even in patients with no clinical evidence of renal disease that might have silent lupus nephritis usually associated with a benign renal outcome.

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This review presents current updates of pancreatic enzyme replacement therapy in children with cystic fibrosis based on literature published in the last decade and some special considerations regarding pancreatic enzyme replacement therapy in the era of new therapies, such as cystic fibrosis transmembrane conductance regulator modulator therapies. Few articles evaluate the efficacy of pancreatic enzyme replacement therapy in the pediatric population, and most studies also included children and adults with cystic fibrosis. Approximately 85% of cystic fibrosis patients have exocrine pancreatic insufficiency and need pancreatic enzyme replacement therapy. Fecal elastase is the most commonly used diagnostic test for exocrine pancreatic insufficiency, although this value can fluctuate over time. While it is used as a diagnostic test, it cannot be used for monitoring the effectiveness of pancreatic enzyme replacement therapy and for adjusting doses. Pancreatic enzyme replacement therapy, the actual treatment for exocrine pancreatic insufficiency, is essential in children with cystic fibrosis to prevent malabsorption and malnutrition and needs to be urgently initiated. This therapy presents many considerations for physicians, patients, and their families, including types and timing of administration, dose monitoring, and therapy failures. Based on clinical trials, pancreatic enzyme replacement therapy is considered effective and well-tolerated in children with cystic fibrosis. An important key point in cystic fibrosis treatment is the recent hypothesis that cystic fibrosis transmembrane conductance regulator modulators could improve pancreatic function, further studies being essential. Pancreatic enzyme replacement therapy is addressed a complication of the disease (exocrine pancreatic insufficiency), while modulators target the defective cystic fibrosis transmembrane conductance regulator protein. Exocrine pancreatic insufficiency in cystic fibrosis remains an active area of research in this era of cystic fibrosis transmembrane conductance regulator modulator therapies. This new therapy could represent an example of personalized medicine in cystic fibrosis patients, with each class of modulators being addressed to patients with specific genetic mutations.