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Biomedical subjects

E L Amorosi

Publications and source records attributed to E L Amorosi.

14 recordsLinked to original sources
PubMed1988

The association of progressive, atrophying, chronic, granulomatous dermohypodermitis with Hodgkin's disease.

The case of a patient with an unusual skin disorder--progressive, atrophying, chronic, granulomatous dermohypodermitis (PACGD)--who developed Hodgkin's disease is reported. A review of the literature revealed only two other cases of PACGD, one of which affected a patient who also was found to have Hodgkin's disease. In an additional report, the diagnosis of Hodgkin's disease was made in a patient who may have had the same dermatologic disorder. The case is reported because the association of these two rare diseases is believed to be more than a chance event.

Adult↗
PubMed1983

Simultaneous occurrence of mycosis fungoides and Hodgkin disease: clinical and histologic correlations in three cases with ultrastructural studies in two.

We present three patients who manifested both Hodgkin disease and mycosis fungoides. Ages ranged from 39 to 66 and two were male. Skin lesions were present from 3 to 40 years before the diagnosis of Hodgkin disease. In all cases, mycosis fungoides was confirmed histologically by skin biopsy; the clinical course of the mycosis fungoides was indolent in all cases. Hodgkin disease was confirmed histologically in three, and confirmed by electron microscopy in two. All three patients responded to appropriate treatment for Hodgkin disease and are alive and well at the present time.

Adult↗
PubMed1982

Evolution of Sézary syndrome in the course of hairy cell leukemia.

A patient with a history of "leukemia" for 19 yr and documented hairy cell (HC) leukemia for 10 yr developed mycosis fungoides and the Sézary syndrome. The manifestations of both diseases were diagnostic on clinical and pathologic grounds. Ultrastructural, immunohistochemical, and surface marker techniques proved the HC to have phenotypic characteristics of the T-helper subset of lymphocytes to which the Sézary cells (SC) also belonged. Both types of cells contained tartrate-resistant acid phosphatase. HC did not infiltrate the skin. SC did not contain ribosome lamellar complexes. Because of otherwise overlapping morphology and the apparent replacement of HC by SC, it is likely that the Sézary cells constituted a genetic variant of the original neoplastic clone represented by the hairy cells. Since the biologic and therapeutic implications of such clonal evolution may be important, subtle phenotypic changes should be looked for repeatedly in patients with these diseases.

Aged↗
PubMed1979

Procainamide-induced agranulocytosis and thrombocytopenia.

Procainamide therapy has frequently been reported as a cause of agranulocytosis, but severe thrombocytopenia associated with the use of this drug has been noted only once. We report a case of simultaneously occurring agranulocytosis and profound thrombocytopenia in a patient receiving procainamide hydrochloride. Different mechanisms appeared to be responsible for the two cytopenias.

Aged↗
PubMed1968

In vivo lability of glucose-6-phosphate dehydrogenase in GdA- and GdMediterranean deficiency.

A decreased level of glucose-6-phosphate dehydrogenase might result from decreased rate of synthesis, synthesis of an enzyme of lower catalytic efficiency, increased lability, or a combined mechanism. To test the hypothesis of increased lability, the rate of decline of the enzyme in vivo was measured in three groups of individuals, controls, Gd(-),A-males, and Gd(-), Mediterranean males, by the slope of decline of activity in fractions containing erythrocytes of progressively increasing mean age. These fractions were obtained by ultracentrifugation on a discontinuous density gradient of erythrocyte suspensions free of contaminating platelets and leukocytes. The rate of in vivo decline of pyruvate kinase (another age-dependent enzyme) was also measured and found very similar in the three groups. The in vivo decline of glucose-6-phosphate dehydrogenase was found to follow an exponential rate, with a half-life of 62 days for controls and 13 days for Gd(-),A- erythrocytes. The activity in normal reticulocytes was estimated at 9.7 U and in Gd(-),A- reticulocytes at 8.8 U. These estimates were confirmed by direct measurements in reticulocytes isolated from patients with extreme reticulocytosis. In Gd(-),Mediterranean erythrocytes activity could be demonstrated only in reticulocytes, which were estimated to average 1.4 U. The rate of decline is so extreme that no activity could be detected in mature erythrocytes. These data suggest that the glucose-6-phosphate dehydrogenase deficiency of both the Gd(A-) and the GdMediterranean variant results from different degrees of in vivo instability of the abnormal enzyme.

Black People↗