[Massive liver-cell necroses in cardiac insufficiency. Contribution on the etiology of severe liver-parenchyma lesions].
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Biomedical subjects
Publications and source records attributed to C Stambolis.
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In nephrectomy specimens from a series of 24 Wilms' tumors three different types of neoplastic lesion were found in the uninvolved kidney parenchyma: nodular renal blastema, Wilms' tumorlet and metanephric hamartomas. The histologic features of the first two abnormalities are presented. They show the following characteristics: Being found in patients of younger age they occur mostly bilateral. In older children they are associated to Wilms' tumor. They are related, as this is the case with Wilms' tumors, to certain congenital malformation syndromes. Nodular blastema has been also observed in association with Wilms' tumor in siblings. These findings suggest a genetic relationship between nodular renal blastema-nephroblastomatosis complex and Wilms' tumor. Furthermore, such lesions may represent potential progenitor stages of most nephroblastomas. The clinical implications hereof are discussed.
In the uninvolved kidney parenchyma of three cases with Wilms' tumor neoplastic metanephric aberrations were found which represent regressive forms of the nodular renal blastema-nephroblastomatosis complex. Their histopathologic features are demonstrated. They are designated as simple or diffuse metanephric epithelial hamartomas. Small lesions show involution resulting in scars. In the central parts of larger lesions cysts and adenomas were detected. The latter were multicentric and revealed compact-epithelial, papillary-psammomatous, cystic-multilocular and tubulo-papillary forms. Their origin, possible evolution, relationship to nephroblastoma as well as their significance are discussed.
A review of reported cases of cystic metanephric tumors is given. It is shown that among these neoplasms two distinct pathologic entities exist: the cystic nephroblastoma and the benign multilocular cystic nephroma. The former, a benign variant of Wilms' tumor, is found in children of younger age. Its possible precursor is the infantile form of nephroblastomatosis. The second neoplasm, a clinically and biologically benign tumor, occurs in older children and in half of the cases it is also encountered in adults. It derives from metanephric hamartomas which have their origin in the huvenile form of nephroblastomatosis.
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A case of benign multilocular cystic nephroma in a 12 month old male infant is reported. The patho-anatomical features of this rare renal lesion are demonstrated. Its possible histogenesis and relationship to nephroblastoma are discussed.
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The occurrence of a malignant Wilms'tumor in the right kidney and of a benign epithelial nephroblastoma in the left kidney of a 5-year-old girl is reported. Both kidneys contained foci of persistent well differentiated blastema. In the left kidney a direct transformation of the primitive metanephric epithelium into a benign nephroblastoma is shown. This finding suggests an origin of epithelial nephroblastoma from persistent nephrogenic tissue and indicates that the former represents the benign counterpart of the malignant Wilms'tumor.
Necrotising splenic arteritis with numerous extensive anaemic splenic infarcts was found in four cases of Goodpasture's syndrome with the necrotising variant of rapidly progressive glomerulonephritis. The disease was rapidly fatal. Early scanning of splenic infarcts for diagnostic, prognostic and therapeutic purposes of the fulminating form of Goodpasture's syndrome is recommended.
Generalized lymphangiomyomatosis with diffuse pulmonary involvement was diagnosed at post-mortem of a 26-year-old woman. The disease occurs only in women, during or after their reproductive phase, with chylous effusion, especially chylothorax, dyspnoea and chronic progression. It is a multitopic condition starting with a focal lesion, which has its origin in the smooth musculature of the lymphatics and probably develops in dependence on hormonal factors.
From a series of 28 patients subjected to aortic valve replacement with the Björk-Shiley tilting disc valve prosthesis 3 cases are reported in which massive thrombosis with valve dysfunction and fatal outcome occurred in the very early postoperative period. The autopsy findings and the examination of the blood coagulation state during the first 24 hours postoperatively disclosed in all 3 cases a hypercoagulability being responsible for the massive clot formation. The early recognition and establishment of the diagnosis of a hypercoagulability state and an immediate anticoagulant therapy with heparin are necessary for preventing such early fatal complications in patients with cardiac valve replacement.
Massive thrombosis formation on the valve periphery and on the top surface of the valve occurred in three patients (1,5%) in the immediate postoperative period with the Björk-Shiley valve in the aortic position. Between the third and sixth day these patients died of acute heart failure as a result of coronary artery displacement. Upon autopsy operative technical complications and postoperative infections were ruled out as the cause of death. What appears to be clinically important is an increase in clotting time in the immediate postoperative period which can be proven statistically. This increased clotting inclination was only found in these three patients and in one patient with frequent immediate postoperative peripheral embolic episodes. We therefore feel that early anticoagulation therapy is necessary. Heparin administration is preferred as it not only lowers the clotting ability of the blood but also the adhesive quality of the platelets.
The case of a 33-year-old female patient with rheumatoid arthritis who developed a severe pulmonary fibrosis during chrysotherapy of 3.5 months' duration is reported. The course of the fibrosis was progressive and led to respiratory insufficiency and death. The microscopic picture revealed a honeycomb lung with perialveolar proliferation of connective tissue and mononuclear cell infiltration. The clinical and temporal circumstances gave evidence that this pulmonary fibrosis is possibly to be interpreted as a gold-induced lung disease, though a causal connection could not be established with absolute security. However, gold-induced pulmonary fibrosis is usually completely reversible and has no fatal outcome: this would be the first report of a lethal outcome of a gold-induced pulmonary fibrosis. The clinical data of 39 further cases of gold-induced pulmonary fibrosis published elsewhere are presented.