Biomedical subjects
J I Spector
Publications and source records attributed to J I Spector.
Carcinoma of the prostate presenting as acute disseminated intravascular coagulation.
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Skin metastases from transitional cell bladder cancer.
Three cases of transitional cell bladder cancer metastatic to skin are described. This manifestation of transitional cell uroepithelial malignancy was previously believed to be quite uncommon. The authors' experience suggests that this occurrence is not that rare and that it may reflect increased longevity in successfully treated patients, allowing previously unusual manifestations of metastatic disease to become evident. The role of aspiration skin biopsy is discussed.
Plasmacytoma of the breast. An unusual case of recurrent myeloma.
An unusual case of multiple myeloma is presented in which recurrence of the disease after a four-year remission was heralded by an infiltrating plasmacytoma of the breast. The clinical and histologic features of this neoplasm are presented and compared with ten previously reported cases of plasmacytoma of the breast.
Skeletal muscle involvement by lymphoma.
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Cyclophosphamide pneumonitis.
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Sweet's syndrome. Association with acute leukemia.
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Cyclophosphamide and interstitial pneumonitis.
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Early-onset cyclophosphamide-induced interstitial pneumonitis.
This article describes three cases of biopsy-proved interstitial pneumonitis secondary to cyclophosphamide therapy. The pulmonary reactions developed after one to three courses of combination chemotherapy in three patients with diffuse histiocytic lymphoma. Resolution of the pulmonary infiltrates and blood gas value abnormalities followed discontinuation of use of this drug without recurrence when chemotherapy regimens excluding cyclophosphamide were subsequently used. Prednisone was given to all patients after the diagnosis was made, but its role in the resolution of the toxic changes is uncertain. The potential for early onset of cyclophosphamide-induced interstitial pneumonitis has not been previously stressed, but should lead to vigorous investigation of pulmonary reactions occurring at any time after initiation of therapy with this drug.
Acute myelofibrosis with peripheral myeloblastosis: an acute myeloproliferative disorder.
Acute myelofibrosis is an uncommon fulminant disorder characterized by pancytopenia, premature myeloid elements in the peripheral blood, and bone marrow fibrosis. We report the case of a 59-year-old man who had acute myelofibrosis and peripheral myeloblastosis clinically suggesting the diagnosis of acute granulocytic leukemia. The disease was unresponsive to cytotoxic drugs or androgens and the patient died five months later. The association of bone marrow fibrosis with large numbers of myeloblasts in the peripheral blood has rarely been reported and suggests a spectrum of morphological changes in acute myeloproliferative disorders, analogous to the merging of chronic myeloproliferative disorders into one another and into leukemic blast crisis.
Immunoblastic lymphadenopathy. A report of two cases.
Two patients with immunoblastic lymphadenopathy had lymphadenopathy, hepatosplenomegaly, rash, dysproteinemia, constitutional symptoms, and typical morphologic findings or lymph node obliteration by immunoblasts and plasma cells, proliferation of aborizing vessels, and infiltration with amorphous, eosinophilic material. One patient had massive pulmonary infiltrates that responded to steroid therapy early in the course of the disease, but recurred and were found, at autopsy, to represent immunoblastic invasion of the lung. In both cases, a severe peripheral neuropathy developed during the course of the disease. One patient was addicted to dextroamphetamine for 20 years. Response to corticosteroids and cytotoxic therapy was initially rapid and complete, but refractoriness developed as seen in postmortem findings of extensive visceral involvement.
Endoscopic evaluation of small-bowel leukemia.
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Polybrene neutralization as a means of monitoring heparin therapy for extracoporeal cirulation.
Dose-response effects of heparin and protamine in 34 adult patients undergoing cardiac operations were monitored by an in vitro analysis utilizing hexadimetharine bromide (Polybrene) neutralization. Heparin administered prior to cannulation for cardiopulmonary bypass in a dose of 3.0 mg (300 units) per kilogram of body weight, and 1.5 mg (150 units) per kilogram for each subsequent hour of bypass, routinely produced circulating heparin concentrations greater than 1.0 units per milliliter of plasma. A protamine dose equal to 80% of the total number of milligrams of heparin given resulted in no detectable plasma heparin in 23 of the 34 patients one-half hour after administration. No patient required protamine in an amount greater than the total number of milligrams in the heparin dose to achieve heparin neutralization. Modest postoperative chest tube drainage (mean, 784 ml in 48 hours) in these patients provides clinical support for low-dose protamine administration for heparin neutralization at the conclusion of cardiopulmonary bypass.
Physiologic effects of normal-or low-oxygen-affinity red cells in hypoxic baboons.
Baboons were bled one-third their red cell mass and were given homologous transfusions of red blood cells to restore the red cell volume. One group of baboons received red blood cells with a normal 2,3-diphosphoglycerate 2,3-DPG) level and normal affinity for oxygen, and in this group the 2,3-DPG level after transfusion was normal. The other group received red blood cells with a 160% of normal 2,3-DPG level and decreased affinity for oxygen, and in this group the 2,3-DPG level after transfusion was 125% of normal. In both groups of baboons, the inspired oxygen concentration was lowered and arterial PO2 tension was maintained at 55-60 mmHg for 2 h after transfusion. During the hypoxic state, systemic oxygen extraction was similar in the two groups, whereas oxygen saturation was lower in the high 2,3-DPG group than in the control animals. Cardiac output was significantly reduced 30 min after the arterial PO2 was restored to normal. These data indicate that red blood cells with decreased affinity for oxygen maintained satisfactory oxygen delivery to tissue during hypoxia.
Letter: Coagulation studies during experimental hemoglobinemia.
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Coagulation studies during experimental hemoglobinemia in humans.
Infusion of autologous hemolyzed blood in humans has served as a model for various experimental investigations for many years. Numerous studies have shown this model to be unattended by any adverse clinical reactions. In this study evidence of subclinical disseminated intravascular coagulation (DIC) was sought in normal humans infused with autologous hemolyzed blood. Hemoglobinemia was induced in 10 experiments by a single injection of frozen-thawed blood and in 4 experiments by such an injection of hemolysate followed by a 5-h maintenance infusion. Mean peak plasma hemoglobin following single dose injections was 540 mg/100 ml, while levels during continuous infusion averaged 240 mg/100 ml. The induction of hemoglobinemia was asymptomatic. Coagulation studies showed no significant alteration in prothrombin time, partial thromboplastin time, thrombin time, clottable fibrinogen, or WBC. Fibrin degradation products were not found. Platelet counts fell slightly in the 5-min postinfusion sample but returned to preinfusion levels within 30 min, suggesting a temporary sequestration of platelets rather than consumption. The induction of moderate brief experimental hemoglobinemia in normal subjects did not result in the development of demonstrable DIC.
Effect of hemoglobin and hematin on plasma clearance of hemopexin, photo-inactivated hemopexin and albumin (38575).
The plasma half clearance time (T1/2) of isotope-labeled rabbit hemopexin was 35.5 plus or minus 1.9 hr in rabbits. After intra-and extra-vascular equilibration of 125I-hemopexin and 131I-albumin, injection of either hematin, hemoglobin or methemoglobin (12.5 mg of heme/kg body wt) resulted in the rapid removal of 60-80% of circulating hemopexin (T1/2 = 7.2 plus or minus 0.6 hr) but did not affect albumin catabolism. After selective photo-inactivation of hemopexin, the T1/2 of this hemopexin was comparable to that of the native molecule. However, its plasma disappearance curve was not appreciably affected by administration of hematin. These findings demonstrate that hemopexin is cleared and catabolized at an enhanced rate during states of plasma heme load, and that modification of critical histidine residues of hemopexin eliminates its biological function in plasma heme disposal.