Presentation of pericardial hydatid cyst as acute cardiac tamponade.

We report a case of a 47-year-old man with isolated pericardial hydatid cyst (without myocardial involvement) that presented as acute pericardial tamponade. After initial investigation and transthoracic echocardiography, emergent pericardial drainage was performed for downgrading the urgency of a definitive treatment for a hydatid cyst. A computed tomography examination after the pericardial drainage showed a pericardial cyst without heart muscle involvement, making the treatment possible through anterior thoracotomy and without performing cardiopulmonary bypass. Complete surgical removal of the cyst was performed. The postoperative course was uneventful. The patient received postoperative albendazole treatment. He remained asymptomatic and no recurrence was observed during a 1-year follow-up period.

Peroxisome proliferator-activated receptor gamma as modulator of inflammation in pulmonary sarcoidosis.

Peroxisome proliferator-activated receptor (PPAR) includes the family of ligand-activated transcription factors which belong to the group of nuclear hormone receptors and are connected to retinoid, glucocorticoid and thyroid hormone receptors. There are three subtypes of PPARs: PPARalpha (also known as NR1C3), PPARgamma (known as NR1C1) and PPARdelta (known as PPARbeta or NR1C2). All of them take part in the metabolism, cell proliferation and immune response. PPARgamma and PPARalpha are identified as important immunomodulators and potentially represent an anti-inflammatory target for respiratory diseases. PPARgamma deficiency in the lungs has been observed in the inflammatory diseases such as asthma, pulmonary alveolar proteinosis, fibrosis and sarcoidosis, as well as in the animal models of the lung inflammation. A small number of papers concerned with PPARgamma in sarcoidosis pointto the lowered activity of this factor in the alveolar macrophages and a lowered gene expression for the PPARgamma, while the activity is preserved in healthy individuals. At the same time, an increased activity of the nuclear factor kappa B (NF-kappaB) in the bronchoalveolar lavage has been recorded in patients with sarcoidosis. The reason for the decrease in the production of PPARgamma in sarcoidosis remains unknown. Several possible mechanisms are mentioned: genetic defect with lowered production, down-regulation due to the increased values of IFN-gamma or an increased decomposition of PPARgamma. Further investigation will explain the mechanisms regarding the decreased production of PPARgamma in sarcoidosis.

Giant primary retroperitoneal myxoid leiomyoma: a case report.

INTRODUCTION: Leiomyomas are benign smooth muscle tumors that usually arise from the uterus. CASE REPORT: We present a patient with a 6-month history of vague abdominal discomfort, occasional nausea, vomiting and urinary incontinence. On examination, there was an extremely large firm unpainfull palpable abdominal mass. Laboratory investigation revealed mild leukocytosis and blood creatinine elevation. Abdominopelvic ultrasonography and computed tomography revealed a massive well bordered, encapsulated intraabdominal tumor, extending from the pelvis to epigastrium and almost completely fulfilling the pelvic and abdominal cavity. At laparotomy, tumor arising from the retroperitoneum was excised in toto. Histopathological examination disclosed that the tumor was composed mainly of smooth muscle cells and very rare fibrous connective tissue elements with myxomatous alteration and with no mitotic activity. The negative results of numerous additional parameters analyzed (pancytokeratin, epithelial membrane antigen, S100 protein, CD68, CD34, desmin, aktin) ruled out different origin of a tumor. One year after resection the patient had no complaints and no radiological evidence of tumor recurrence. CONCLUSION: Considering current limitations in radiological diagnosis, in toto resection of these tumors is necessary to rule out malignancy.

Tumor necrosis factor alpha gene polymorphism in serbian patients with sarcoidosis.

INTRODUCTION: Sarcoidosis is a multisystemic disease of unknown etiology. Genetic factors play a considerable role in the onset of the disease. Tumor necrosis factor alpha (TNF-a) is a proinflammatory cytokine which plays an important role in the pathogenesis of the disease and the formation of granuloma by regulating cellular proliferation and apoptosis. OBJECTIVE: The aim of this study was to investigate the role of TNF-alpha-308 G/A polymorphism in the development of sarcoidosis and to evaluate the association between the aforementioned type of polymorphism and the clinical course of the disease. METHODS: Seventy patients with sarcoidosis and 50 healthy volunteers were genotyped for the TNF-alpha-308G/A polymorphism. Polymorphism variants were examined by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism) on the DNA isolated from blood leukocytes. RESULTS: There were no significant differences in TNF-alpha-308A allele frequency distribution between sarcoidosis patients and the control group, but the TNF-alpha-308A allele was observed significantly more frequently in the sarcoidosis patients with Löfgren's syndrome when compared with non-Löfgren's patients. CONCLUSION: We have found that the TNF-alpha-308A variant is associated with Löfgren's syndrome in Serbian patients with sarcoidosis.