Hydatid cyst is usually located in the liver and lungs, rare cases showing localization in other organs or tissues. In the unusual location, echinococcosis is an excluding diagnosis that is established only after microscopic evaluation. Our first case occurred in a 67-year-old female previously diagnosed with pulmonary tuberculosis and hospitalized with persistent pain in the hip joint. The clinical diagnosis was tuberculosis of the joint, but the presence of the specific acellular membrane indicated a hydatid cyst of the synovial membrane, without bone involvement. Fewer than 25 cases of joint hydatidosis have been reported in literature to date. In the second case, the intramural hydatid cyst was incidentally discovered at autopsy, in the left heart ventricle of a 52-year-old male hospitalized for a fatal brain hemorrhage, as a result of rupture of an anterior communicating artery aneurysm. The conclusion of our paper is that echinococcosis should be taken into account for the differential diagnosis of cystic lesions, independently from their location.
Aged ; Autopsy ; Diagnosis ; Diagnosis, Differential ; Echinococcosis* ; Echinococcus granulosus ; Female ; Heart Ventricles ; Heart* ; Hip Joint* ; Hip* ; Humans ; Intracranial Aneurysm ; Intracranial Hemorrhages ; Joints ; Liver ; Lung ; Male ; Membranes ; Middle Aged ; Myocardium ; Osteoarthritis, Hip ; Rupture ; Synovial Membrane ; Tuberculosis ; Tuberculosis, Pulmonary

BACKGROUND: Pathogenesis of acute respiratory distress syndrome (ARDS) is a controversial issue. Few studies have analyzed the possible role of vascular endothelial growth factor (VEGF) and its receptors in this lesion. METHODS: We compared the immunohistochemical expression of VEGF, its receptors (VEGFR1, VEGFR2) and CD68, in normal lungs and lungs with ARDS. Fifty necropsy cases and 12 lung biopsies with ARDS were analyzed. In total, eight cases were in the early stage and 54 cases were in late stage of ARDS. In addition, the serum level of VEGF165 was also determined. RESULTS: In normal lungs, all antibodies marked the endothelial cells (EC) and pneumocytes (PC), except for CD68, which was expressed in the alveolar macrophages. In early ARDS, the intensity of VEGF165 and VEGFR2 decreased in both EC and PC. VEGF121 was absent in PC but its expression increased in bronchial epithelium. VEGFR1 was expressed in the integral PC. In late ARDS, VEGF165 down-regulation was more significant in PC and EC but its intensity increased in hyaline membranes (HM). In some cases, HM were CD68 positive. The serum level of VEGF165 was up-regulated, while VEGF165 intensity in PC decreased and the HM appeared in alveolar spaces. CONCLUSIONS: Sporadic positivity of HM for CD68 and decreasing of VEGF165 expression in EC proved that VEGF165 is produced by PC, destroyed macrophages, and extravasated serum.
Antibodies ; Biopsy ; Down-Regulation ; Endothelial Cells ; Epithelium ; Humans ; Hyalin ; Lung ; Macrophages ; Macrophages, Alveolar ; Membranes ; Pneumocytes ; Respiratory Distress Syndrome, Adult ; Vascular Endothelial Growth Factor A