Quantitative volumetric magnetization transfer analysis in multiple sclerosis: estimation of macroscopic and microscopic disease burden.

Magnetization transfer imaging (MTI) has been shown to be sensitive to both macroscopic and microscopic disease in multiple sclerosis (MS). In this study three-dimensional MTI was used to estimate the global burden of disease in large volumes of brain tissue. MTI was performed in 15 MS patients and 11 normal controls.

Hereditary cerebral hemorrhage with amyloidosis-Dutch type: better correlation of cognitive deterioration with advancing age than with number of focal lesions or white matter hyperintensities.

The relationship between cognitive deterioration and abnormalities detected by magnetic resonance imaging (MRI) was investigated to determine the radiological correlates of cognitive deterioration in hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D). Twenty HCHWA-D subjects (12 patients who had suffered one or more strokes and eight who had not suffered a stroke) were studied with MRI and underwent extensive neuropsychological examination. On MRI the number of focal lesions was counted, and white matter hyperintensities (WMHs) were scored semiquantitatively.

White matter lesions and cognitive deterioration in presymptomatic carriers of the amyloid precursor protein gene codon 693 mutation.

Objective: To determine early manifestations of hereditary cerebral hemorrhage with amyloidosis (Dutch).

Design: Survey.

Setting: Neurologic outpatient department of the University Hospital Leiden in the Netherlands.

Involvement of the complement system in the pathogenesis of pulmonary leukostasis in experimental myelocytic leukemia.

The role of the complement system in the pathogenesis of pulmonary leukostasis in myelocytic leukemia was studied in a rat model. Acute myelocytic leukemia was induced in six Brown-Norway rats, and complement levels were assayed during the course of the disease. Whole complement activity (CH50) and hemolytic activity of C1q, C3, and C4 decreased from day 16 after induction of the leukemia, when the rats developed pulmonary leukostasis.

Endothelial activation antigens in pulmonary leukostasis in leukemia.

Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control.

Development of pulmonary leukostasis in experimental myelocytic leukemia in the Brown-Norway rat.

The pathogenesis of pulmonary leukostasis in leukemia was studied in a rat model by investigating the course of its development. Leukemia was induced by inoculating rats with leukemic cells. The earliest stage of leukostasis was found from day 14 onward, when leukemic cells appeared in the peripheral blood, and was characterized by accumulation of leukemic cells at the capillary level.

Leucostasis, an underestimated cause of death in leukaemia.

Massive sludging of leukaemic cells in blood vessels is a frequent and often lethal complication of leukaemia. In a retrospective clinicopathological study on the causes of death in 52 patients with acute myeloid leukaemia and myeloproliferative disease, pulmonary leucostasis was found in 40% of the patients. In many of these patients the vessels of the heart, brain and testes were also involved.

Pulmonary leukostasis: radiologic-pathologic study.

The terminal chest radiographs of ten patients with pulmonary leukostasis were correlated with the autopsy findings. In six patients, no abnormalities attributable to leukostasis were seen on chest radiographs. In four patients, diffuse alveolar consolidations were caused by alveolar edema following leukostasis.