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At least 73 records · Page 4Linked to original sources
PubMed1988

Erythremic [corrected] myelosis in chronic lymphocytic leukemia.

Two patients who had both B-cell chronic lymphocytic leukemia (CLL) and dyserythropoiesis are described. One patient (Case 2) had both CLL and dyserythropoiesis. Erythrodysplasia developed in the other patient (Case 1) after treatment for CLL with alkylating agents and 2'-deoxycoformycin. The management of these patients and the possible mechanisms responsible for the development of dyserythropoiesis in CLL are discussed.

Blood Cell Count↗
PubMed1989

[Central pontine myelosis. Morphology and forensic importance].

Central pontine myelinolysis (CPM) evidently occurs more frequently than had been assumed up to now owing to the cases that have been substantiated solely on the basis of pathological anatomy. Its genesis is still unclarified. Computed tomography and magnetic resonance methods allow detection of the foci while the affected person is still alive. They are clearly capable of regression and are not automatically accompanied by a poor prognosis. Since an iatrogenic factor (forced compensation of hyponatremia) is increasingly under discussion as the cause of CPM, the condition also has substantial significance from a forensic point of view. On the basis of a prospective study on CPM confirmed in 100 brains of alcoholics, as well as 4 further cases from the forensic autopsy material, it is shown that hyponatremia is not likely to be the sole triggering factor. The course of the condition in the cases investigated shows that the capacity for action may be preserved up to death (which has occurred for other reasons) in not very pronounced CPM. In questionable violent and other unclear deaths, CPM must also be considered a possible cause of death. The various hypotheses on its etiology in the extensive literature are compared with the findings in our own cases and discussed.

Adult↗
PubMed1987

Magnetic resonance imaging (MRI), cranial computerized tomography (CCT), evoked potentials and cerebrospinal fluid (CSF) analysis in five patients with funicular myelosis.

Five Patients with vitamin B12 deficiency were examined by means of MRI, CCT, VEP, BAEP, EEG, and CSF. In 3 patients medianus-SEP and EMG/ENG were recorded as well. Partly, findings of MRI, CCT, VEP, BAEP, SEP, and CSF were similar to those in multiple sclerosis. This is not very surprising considering that the central nervous system lesions in vitamin B12 deficiency consist of disseminated demyelination. Because of this all these investigative techniques must be considered non-specific. Appraisal of findings is only possible in connection with the case history, clinical findings, and supplementary diagnostic measurements.

Antibodies, Anti-Idiotypic↗
PubMed1986

Acute erythremic myelosis (DiGuglielmo) following atypical aplastic anemia.

A patient presented with acute erythromyelosis (DiGuglielmo) which was developed after 3 yr of aplastic anemia. Aplastic anemia differed from the classical form, since erythroid cells and megakaryocytes were relatively preserved in the bone marrow. Treatment with androgens induced the increase of hematocrit and reticulocyte as well as general improvement. The sudden appearance of hemorrhagic syndrome due to thrombocytopenia was associated with aggravation of anemia and granulocytopenia. In the bone marrow, giant multinuclear proerythroblasts with bizarre nuclear morphology and PAS positivity with coarse granules was found. Serum erythropoietin (Ep) level was high. Bone marrow cells culture in vitro revealed two types of erythroid colonies: typical and giant multinuclear cells, both benzidine-positive. The number of colonies was irrespective to the Ep dose. "Autonomous" Ep independent growth of these colonies was also demonstrated. The number of colonies was more than 3 times higher per number of cells seeded when compared to normals, which indicated malignant proliferation and Ep independent growth. Treatment with 6-mercaptopurine and transfusions was without effect and the patient died after 15 days with signs of cerebral bleeding.

Acute Disease↗