Biomedical subjects
Publications and source records attributed to R E Slavin.
The microcomputer-based SNOMED encoding system, recently announced by the CAP, has been evaluated in a setting designed to emulate the typical surgical pathology environment. Key features such as minimization of manual entry, ease of use, data integrity, and convenient retrieval capabilities were examined. The system was found to perform satisfactorily in all such features.
Histopathologic changes in the lung in a patient with Behçet's disease are described and the literature dealing with pulmonary pathologic changes in this disease is summarized. The basic lesion is a lymphocytic and necrotizing vasculitis involving all sized pulmonary arteries, veins and septal capillaries. Complications include aneurysms of elastic pulmonary arteries, arterial and venous thromboses, pulmonary infarcts, and bronchial erosion by pulmonary artery aneurysms. Striking periadventitial fibrosis develops and is believed to be related to repetitive vascular inflammatory insults. Peculiar newly formed collateral vessels, lacking elastic lamellae and derived from smooth muscle metaplasia around arterioles, are found in the periadventitial fibrous tissues around thrombosed arteries and aneurysms. Cases of pulmonary artery aneurysms of obscure origin, including those found in the Hughes-Stoven syndrome, are reviewed and both clinical and pathologic findings in these reports are found to be remarkably similar to those observed in Behçet's disease. It is suggested that such cases represent unrecognized or incomplete expressions of Behçet's disease.
Two studies evaluated the effects of a group contingency on electricity conservation. In Study 1, residents of 166 apartment units in three towers held meetings and received biweekly payments of the value of electricity saved compared to predicted use. The group contingencies were initiated in each tower in a multiple-baseline design. The program produced substantial savings in one tower (11.2% of temperature-adjusted baseline), moderate savings in another (4.0%), and minimal savings in a third (1.7%). Overall, the residents saved 6.2%. In Study 2, residents of 255 apartment units, also in three towers, received the same treatment, except only 50% of the value of their savings were paid, and they received a one-time bonus of $5 for using >/= 10% less than baseline. Towers in Study 2 showed savings of 9.5%, 4.7%, and 8.3%, an average of 6.9%.
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1. The clinical and pathologic findings in 100 patients with late generalized tuberculosis (LGT) are described and a comparison made between the findings occurring in the preantibiotic era with those in the early antibiotic period. The clinical presentation of LGT as seen in a general hospital has changed. Whereas, in the preantibiotic era, LGT was often the primary disease, occurring principally in young adults and frequently associated with pulmonary symptoms, in the antibiotic era, LGT commonly occurred together with and was frequently obscured by other diseases, often afflicted the elderly and was much less frequently accompanied by pulmonary symptoms. Symptoms related to extrapulmonary organ tuberculosis in this era were absent in 30% of patients. 2. Diagnostic difficulties in LGT arose because 20% of patients exhibited no constitutional symptoms prior to hospitalization, a history of tuberculosis often was lacking, fever curves and hematologic findings, with the exception of a left shift, commonly were non-specific, monocytosis frequently was absent, chest x-rays were non-diagnostic in about 50% of the cases, and anergy occured particularly in the elderly. 3. Caseous foci responsible for hematogenous spread generally derived from reactivated old caseous lesions located principally in the lungs, lymph nodes, bone, central nervous system, adrenals, and genito-urinary tract. Simultaneous reactivation of anatomically unrelated foci in multiple organs and lymph nodes occurred in 54% of cases. Although chronic pulmonary tuberculosis commonly was associated with LGT in the preantibiotic era, this association was uncommon in recent times. Chronic pulmonary tuberculosis served as the sole source for hematogenous dissemination infrequently and the pulmonary lesions responsible were acute. 5. Large caseous foci located in lymph nodes, bone, prostate gland, and central nervous system frequently occurred in the absence of clinical symptoms and therefore were undiagnosable. 6. The clinical course of LGT was often rapid, although histologic features indicated that the course in some patients was protracted or even episodic. 7. Miliary tubercles very frequently showed caseation and often they enlarged to cause progressive or complicated lesions. Chest x-rays and culture diagnoses were dependent on the formation of these complicated lesions. 8. Liver biopsy is recommended as a diagnostic procedure since 97% of patients exhibited granulomata in this organ. Of diagnostic importance is the fact that 90% of these granulomata exhibited caseous necrosis. Twenty-two percent of patients with liver granulomatas did not show tubercles in the bone marrow. 9. Multiple pathways rather than an exlcusive lymphangitic route were available for tubercle bacilli to gain access to the blood stream and cause hematogenous dissemination.
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Sequential chemotherapeutic regimens, primarily used in the treatment of hematopoietic malignancies, and employing ara-C as a basic antineoplastic agent induce mucosal alterations in the entire gastrointestinal tract. These are characterized by surface and glandular epithelial atypia, immaturity, and necrosis. Glandular regeneration is characteristically delayed leading to a state of intestinal aproliferative cytopenia. Other toxic intestinal changes include telangiectasia of blood vessels and the formation of intramural hematomas. Intestinal infections develop frequently and are complicated by peritonitis, liver abscesses, pneumatosis cystoides in testinalis and sepsis. These intestinal lesions are accompanied by a predictable clinical syndrome which begins concomitantly with ara-C infusions and is characterized by diarrhea, ileus, abdominal pain, hematemesis and melena, severe hypokalemia, hypocalcemia and a protein-losing enteropathy. Additional toxic manifestations induced by ara-C include transient weight gains, fever elevations and severe bone marrow depression. The genesis of the intestinal lesions is linked to the three day dose schedule of ara-C infusions which insures both arrest of the cycling intestinal cells in the S-phase and a high cytotoxic index. The severity of these lesions is markedly augmented by prior treatment with ara-C and cyclophosphamide which causes synchronization and probable recruitment of intestinal stem cells, respectively.
A case of radiation enteritis in a patient with non-Hodgkin's lymphoma is described. The patient's complaints suggested recurrence of her lymphoma and radiographic studies were nondiagnostic of radiation-induced enteritis, delaying diagnosis and appropriate therapy. An inadvertent error in radiotherapy technic and fibrous adhesions resulting from the staging laparotomy contributed to the radiation injury. Radiation enteritis is a rare complication of irradiation of abdominal lymphoma, but it must be considered by physicians who encounter a similar situation.
An autopsy case of radiation-induced intracranial malignant fibrous histiocytoma (fibroxanthosarcoma) is reported. The tumor developed in the region of the sella turcica 11 years after high dose radiotherapy of a chromophobe adenoma of the pituitary. The tumor had infiltrated the base of the brain as well as the base of the skull. Metastases were not found. The tumor was composed of an admixture of bizarre fibroblasts, histiocytes and giant cells, xanthoma cells and siderophages, with a storiform fibrous stroma. This appears to be the first documented instance of a malignant fibrous histiocytoma occurring intracranially after local x-irradiation.
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A distinct arterial lesion was observed in the large abdominal muscular arteries in three autopsied patients. The salient histopathologic feature of this arterial lesion was either partial or total mediolysis. This was accompanied by a linear fibrin deposit between the media and adventitia and a variable nonpleomorphic inflammatory infiltrate. Total mediolysis led to the formation of arterial gaps. Disecting aneurysms frequently occurred and began either adjacent to arterial gaps or as a result of capillary hemorrhages in areas of partial mediolysis. Ruptured aneurysms led to massive intraabdominal hemorrhages. Arterial luminal occlusion, either by thrombi or dissection, resulted in ischemic bowel changes and renal infarcts. In addition, the arteries affected by mediolysis also showed medial degenerative changes, akin to cystic medial necrosis. Concomitant changes in the kidney showed mesangial hyperplasia; the heart exhibited histiocytic infiltrates and rare Aschoff-like bodies and capsular inflammation were seen in the spleen. The pathogenesis of the arterial lesions is unknown. A possible explanation is that this arteritis may have been induced by immune complexes and that local arterial medial degenerative changes predispose the involved arteries to immunologic injury.
Pathologic changes induced by high dose intermittent cyclophosphamide therapy are described in 39 patients with solid tumors, lymphohematopoietic malignant disease, and bone marrow transplants. Patients receiving 50 to 120 mg. per kg. daily for one to four days showed transmural bladder injury affecting all component tissue; toxic vasculitis involving small arteries, capillaries, and venules; and interstitial, myocardial, and vascular changes in the heart. Myocardial necrosis with heart failure was the dose limiting factor of very high dose therapy. Patients receiving 15 to 30 mg. per kg. for four days showed variable degrees of bladder injury limited to the mucosa and lamina propria and vascular changes consisting only of telangiectasia. Both groups showed atypia of transitional urinary and esophageal epithelia as well as of mesenchymal cells in the lamina propria of the bladder, persistent and total ablation of spermatogenesis, and long lasting absence of ovarian follicular maturation. Bone marrow hypoplasia and lymphoid depletion developing after cyclophosphamide therapy completely disappeared an average of 3.5 weeks after the last dose.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.