Extensive Vascular Invasion Research Articles

Fatal Cunninghamella bertholletiae Infection in an Immunocompetent Patient

The first fatal Cunninghamella bertholletiae infection in a clinically immunocompetent host is reported. This case differs from previously reported cases by the lack of extensive vascular invasion and thrombosis.

Mucormycosis in Patients with Renal Failure

Nine fatal cases of systemic mucormycosis observed in association with renal failure are described. Four patients were hospitalized for chronic renal failure as a consequence of chronic glomerulonephritis, myeloma kidney, chronic pyelonephritis, and polycystic kidney disease, respectively; and five patients presented with acute renal failure. The underlying causes in three of these five patients were gentamycin nephrotoxicity, acute gastroenteritis, and allograft rejection, respectively, and in the remaining two, acute renal failure was the result of extensive renal vascular and parenchymal invasion by mucor hyphae. Tissue invasion with mucormycosis was documented during life in two patients and at autopsy in seven patients. The infection was disseminated in five patients, and isolated pulmonary and rhinocerebral involvement occurred in two patients each. Our observations have shown that patients with renal failure are prone to develop mucormycosis, which carries a grave prognosis if therapy is not instituted in time.

Vascular spaces in endolymphatic stromal myosis

Endolymphatic stromal myosis usually has extensive vascular invasion and yet has an excellent prognosis. To resolve this paradox, we studied the involved vascular spaces by electron microscopy, immunoperoxidase identification of factor VIII as a marker for endothelium and serial sections for light microscopy. The spaces were shown to be indeed vascular. However, in many spaces the tumor was not present within the lumina. Sheets of tumor cells had indented and invaginated the endothelium creating the illusion that tumor was present within the lumina. The tumor cells were separated from the lumina by intact endothelial cells and basement membrane. The presence of cell junction modifications between endothelial cells and well-developed basement membrane material demonstrated that at least some of the spaces were blood vessels, probably postcapillary venules, and not lymphatics.

MESENCHYMAL TUMORS OF THE UTERUS. V. INTRAVENOUS LEIOMYOMATOSIS. A CLINICAL AND PATHOLOGIC STUDY OF 14 CASES

Fourteen examples of intravenous leiomyomatosis in the FIP files were studied. Growth beyond the uterus occurred in 10 of the 14 examples, largely in vessels in the broad ligament and in uterine and iliac veins. Metastasis to the heart occurred in 1 example. The study provides evidence that is consistent with both theories of origin of intravenous leiomyomatosis; namely, that it may arise either from the wall of veins within the myometrium or be a result of unusually extensive vascular invasion from a leiomyoma of the myometrium. Intravenous leiomyomatosis should be distinguished from a leiomyoma with vascular invasion by arbitrarily limiting the designation of leiomyoma with vascular invasion to neoplasms in which the vascular growth is a microscopic finding and confined within the leiomyoma. Criteria are given for distinguishing intravenous leiomyomatosis from endometrial stromal sarcoma, leiomyosarcoma, leiomyoma with vascular invasion, and leiomyomatosis peritonealis disseminata.

Mesenchymal tumors of the uterus. V. Intravenous leiomyomatosis: A clinical and pathologic study of 14 cases

AbstractFourteen examples of intravenous leiomyomatosis in the AFIP files were studied. Growth beyond the uterus occurred in 10 of the 14 examples, largely in vessels in the broad ligament and in uterine and iliac veins. Metastasis to the heart occurred in 1 example. The study provides evidence that is consistent with both theories of origin of intravenous leiomyomatosis; namely, that it may arise either from the wall of veins within the myometrium or be a result of unusually extensive vascular invasion from a leiomyoma of the myometrium. Intravenous leiomyomatosis should be distinguished from a leiomyoma with vascular invasion by arbitrarily limiting the designation of leiomyoma with vascular invasion to neoplasms in which the vascular growth is a microscopic finding and confined within the leiomyoma. Criteria are given for distinguishing intravenous leiomyomatosis from endometrial stromal sarcoma, leiomyosarcoma, leiomyoma with vascular invasion, and leiomyomatosis peritonealis disseminata.

Mesenchymal tumors of the uterus. V. Intravenous leiomyomatosis. A clinical and pathologic study of 14 cases.

Fourteen examples of intravenous leiomyomatosis in the FIP files were studied. Growth beyond the uterus occurred in 10 of the 14 examples, largely in vessels in the broad ligament and in uterine and iliac veins. Metastasis to the heart occurred in 1 example. The study provides evidence that is consistent with both theories of origin of intravenous leiomyomatosis; namely, that it may arise either from the wall of veins within the myometrium or be a result of unusually extensive vascular invasion from a leiomyoma of the myometrium. Intravenous leiomyomatosis should be distinguished from a leiomyoma with vascular invasion by arbitrarily limiting the designation of leiomyoma with vascular invasion to neoplasms in which the vascular growth is a microscopic finding and confined within the leiomyoma. Criteria are given for distinguishing intravenous leiomyomatosis from endometrial stromal sarcoma, leiomyosarcoma, leiomyoma with vascular invasion, and leiomyomatosis peritonealis disseminata.