A Rare Cause of Recurrent Pericarditis.

Recurrent pericarditis poses a significant challenge to clinicians, particularly when patients are unresponsive or intolerant to conventional treatments. Accurate diagnosis of recurrent pericarditis, potentially facilitated by collaboration with other medical specialties, is crucial for ensuring timely and appropriate treatment of symptoms and prevention of further episodes. We present a case of a 52-year-old male patient with a history of multiple episodes of pericarditis, who was admitted to the Cardiology Department due to another recurrence. The first episode of pericarditis was diagnosed nearly a year before his current hospitalization. Initially, the patient received high doses of Ibuprofen and colchicine, but there was no favorable response to this treatment regimen. At that point, intravenous prednisolone was initiated, which led to clinical and laboratory improvement. Since then, the patient had experienced two more recurrences while tapering off prednisolone. Immunological tests, Mantoux tuberculin skin test, and chest and abdominal computed tomography (CT) had revealed no evidence of an underlying cause. On admission the patient was febrile and the electrocardiogram showed diffuse ST elevation and PR depression in leads I, II, aVF, V2-V6. Bedside echocardiogram revealed a small pericardial effusion and since the chest X-ray was normal and no other potential infection sites were identified, the diagnosis of recurrent pericarditis was established. During his current hospitalization, intravenous prednisolone was initiated, colchicine was continued and a more detailed history was taken, raising the suspicion upon the presence of an auto-inflammatory disease. Genetic investigation identified an uncommon heterozygous mutation in the familial Mediterranean fever gene (MEFV) and after consideration of patient's history, familial Mediterranean fever was diagnosed. Anakinra was initiated on top of colchicine and gradual tapering of corticosteroids and the patient showed significant improvement, with no other recurrence during the two-year follow-up.

Cardiorenal Syndrome: Challenges in Everyday Clinical Practice and Key Points towards a Better Management.

Under the term cardiorenal syndrome (CRS) falls an increasing number of patients who present with combined heart and kidney dysfunction. Despite the increasing knowledge concerning CRS pathophysiology, diagnosis, and treatment, many of the aforementioned aspects remain obscure in everyday clinical practice. Some of the challenges that clinicians face when they treat CRS nowadays is the need for a patient-centered management with early diagnosis, early intervention, the distinction of true kidney injury from permissive renal function deterioration during decongestion therapy, and the development of therapeutic algorithms to guide therapy.

miR-185 and miR-29a are similarly expressed in the bronchoalveolar lavage cells in IPF and lung cancer but common targets DNMT1 and COL1A1 show disease specific patterns.

Idiopathic pulmonary fibrosis (IPF) and lung cancer (LC) constitute two progressively devastating lung diseases with common risk factors including aging and smoking. There is an increasing interest in the investigation of common pathogenic mechanisms between IPF and LC with therapeutic implications. Several oncomirs, microRNAs associated with malignancy, are also linked with IPF. miR­29a and miR­185 downregulation is probably involved both in carcinogenesis and fibrogenesis. We have previously observed miR­29a and miR­185 downregulation in IPF cells from bronchoalveolar lavage (BAL) and in this study we investigated their expression in LC BAL cells. Common targets of miR­29a and miR­185 such as DNA methyltransferase (DNMT)1, DNMT3b, COL1A1, AKT1 and AKT2 were measured. Potential correlations with pulmonary function tests, smoking status and endobronchial findings were investigated. Similar levels of miR­29a and miR­185 were detected in IPF and LC while their common targets AKT1 and DNMT3b were not found to differ, suggesting potential pathogenetic similarities at the level of key epigenetic regulators. By conrast, COL1A1 mRNA levels were increased in IPF suggesting a disease­specific mRNA signature. Notably, DNMT1 was downregulated in the LC group and its expression was further reduced in the presence of increasing malignant burden as it was implied by the endobronchial findings.