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Biomedical subjects

R W Kellermeyer

Publications and source records attributed to R W Kellermeyer.

At least 19 recordsLinked to original sources
PubMed1987

Escalating doses of sequential methotrexate and 5-fluorouracil, doxorubicin, and vincristine for the treatment of metastatic breast cancer.

Antitumor efficacy of sequential methotrexate, 5-fluorouracil, and mid-cycle doxorubicin regimens has been established in advanced gastric cancer. Based on similar theoretical kinetic considerations, we treated 15 women with metastatic breast cancer with a five-drug nonalkylating agent regimen. Six of 14 evaluable patients had an objective response. Three patients achieved a complete remission (duration 9, 14, 19+ months), and 3 attained a partial remission (duration 2, 3, 6 months). Hematologic toxicity was significant, with 8 patients developing moderate to severe (ECOG grade 3 or 4) toxicity. Although significant antitumor activity with this nonalkylating agent regimen was observed, hematologic toxicity was considerable and limits the usefulness of this regimen in its present schedule.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1984

General principles of the evaluation and therapy of anemias.

The etiologic explanation of an anemia is important for the most effective therapy of that anemia. This may also define an underlying disease process. The etiology of the anemia can be achieved by appropriate use of the history, physical examination, and laboratory data. This information may be used to clarify the anemia, define a diagnosis, and direct appropriate therapy.

Anemia↗
PubMed1983

Iron overload disorders: natural history, pathogenesis, diagnosis, and therapy.

Hemochromatosis is a syndrome which, when fully expressed, is manifested by melanoderma , diabetes mellitus, and liver cirrhosis, with iron overload involving parenchymal and reticuloendothelial cells in many organ systems. This clinical presentation may arise as a consequence of either hereditary or acquired abnormalities of iron overload, although the mechanisms are quite different. In hereditary hemochromatosis (also known as primary, or idiopathic, hemochromatosis), increased intestinal iron absorption leads to excessive accumulations of iron, throughout the body, particularly in parenchymal cells. In secondary forms of iron overload including transfusional hemosiderosis, alcoholic cirrhosis, thalassemia, sideroblastic anemia, and porphyria cutanea tarda, iron accumulates in the reticuloendothelial system initially, but with increasing amounts of total body iron, excessive iron deposits eventually accumulate in parenchymal cells throughout the body producing a picture indistinguishable from hereditary hemochromatosis. In this article, the course, prognosis, and therapy of iron overload will be reviewed in detail. Clinical and experimental data concerning the pathogenesis of the different forms of iron overload will be examined critically. In particular, information relating to possible abnormalities of reticuloendothelial function, intestinal mucosal iron transport, and alterations in serum and tissue isoferritin patterns in hereditary hemochromatosis will be analyzed, and possible directions for future research will be suggested. The mode of inheritance and linkage with the major histocompatibility (HLA) complex will be discussed. Theories on the pathogenesis of tissue damage by excess iron will be evaluated. Methods for measuring the extent of iron overload in clinical practice will be described, including measurements of serum iron, serum ferritin, iron absorption, cobalt excretion, desferrioxamine excretion, liver biopsy and tissue iron determinations, and HLA typing. Finally, unresolved problems in the understanding of the disease process, diagnosis, and therapy will be delineated.

Anemia, Hypochromic↗
PubMed1977

Eosinophilopoietin. A circulating low molecular weight peptide-like substance which stimulates the production of eosinophils in mice.

In earlier studies, methods were developed to raise specific antibodies in rabbits against purified suspensions of mouse or human eosinophils. On administration of antieosinophil serum (AES) to mice, the mature eosinophils in tissues, peripheral blood, and bone marrow were depleted, while the immature eosinophil pool in the bone marrow was observed to proliferate. The current investigations explore the generation of eosinophilopoietic factors during AES-induced eosinophilopenia. Mice received three injections of AES, one every other day. As the peripheral eosinophil counts started to recover after the last AES injection, the serum was collected and transferred to normal animals. Within 2 days the recipients showed an increase in peripheral blood as well as in bone marrow eosinophils. The rise in bone marrow eosinophils was due to newly formed cells as evidenced by increased uptake of [(3)H]thymidine. The generation of eosinophilopoietic activity was specifically related to depletion of eosinophils but not neutrophils. The eosinophilopoietic activity was: (a) dependent on the volume of serum transferred, (b) lost on dialysis, and (c) largely heat labile. The activity eluted as a low molecular weight substance on G-25 Sephadex and was digested by pronase but not by trypsin. Active fractions collected from G-25 columns were not chemotactic for the eosinophils in vitro. Thus, specific depletion of mature eosinophils generates a low molecular weight peptide which stimulates eosinophilopoiesis in vivo. It is suggested that this substance be named eosinophilopoietin.

Animals↗
PubMed1975

Delayed cerebrovascular consequences of therapeutic radiation. A clinicopathologic study of a stroke associated with radiation-related carotid arteriopathy.

A young woman, successfully treated for Hodgkin's disease with radiation and MOPP chemotherapy, incurred a devastating stroke months after radiation therapy to the neck and other areas. There was no premonitory clinical history of cerebrovascular attacks. Autopsy showed unilateral thrombotic occlusion of the internal carotid artery unassociated with neoplastic or fibrotic annular constriction of the vessel. There was medial thickening and fibroblastic proliferation within the carotid artery. Areas of focal elastic membrane degeneration involved the cervical portions of the carotid. Thrombus was organized to the damaged vessel wall and was propagated into the intracranial vessels. Aneurysm formation and arterial hemorrhages were absent. These vascular changes occurred in an area of extensive radiation (7200 rads). Pathoanatomical studies in this patient indicate that radiation-induced vascular changes were associated with a "delayed" stroke.

Adult↗
PubMed1975

Hemochromatosis. Pathophysiologic and genetic considerations.

The clinical, genetic, and pathologic findings, and the pertinent case histories in two families with idiopathic hemochromatosis are presented. These studies support the view that idiopathic hemochromatosis is a disease inherited in at least two ways. In one of these families, inheritance appeared to occur in an autosomal recessive manner, whereas in the other, autosomal dominant expression seemed evident. Evidence that an inability of the reticuloendothelial cells to handle iron may play a major role in the pathogenesis of hemochromatosis is presented. The early age of onset and poorer prognosis associated with the recessive inheritance suggest that the defect in reticuloendothelial cell function present in such cases is different from or more severe than those associated with dominant inheritance.

Adolescent↗