Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoimmune hemolytic anemia often develops in patients with chronic lymphocytic leukemia, particularly elderly women. It is heralded by a drop in the hematocrit, elevation of reticulocytes, development of jaundice, or a rise in the indirect fraction of serum bilirubin. Evidence of hemolysis supports the diagnosis, and a positive result of the Coombs test confirms it. Survival time is considerably shorter in patients who have both diseases than in those with chronic lymphocytic leukemia alone. Presenting symptoms in patients with the two diseases may include weakness, dizziness, fever, or hemorrhagic phenomena. If the anemia is severe, palpitations, otic pulsations, and cardiac decompensation are common. Physical examination may show enlargement of reticuloendothelial structures. On the other hand, some patients may be essentially asymptomatic. The hemolytic process must be treated as a separate entity, as even vigorous treatment of the leukemia often does not control it. Corticosteroid therapy is preferred, with splenectomy as a second line of defense. If the patient is not a good surgical risk, chemotherapy should be considered. Transfusions are usually incompatible but should be risked if progressive congestive failure, neurologic disturbance, angina, or signs of an impending infarct are present.
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PMID:When autoimmune hemolytic anemia complicates chronic lymphocytic leukemia. 63 66

We describe a patient with acute myelogenous leukaemia who developed angina pectoris during pretransplant conditioning for autologous peripheral blood stem cell transplantation (PBSCT); the conditioning regimen consisted of cytotoxic drugs in combination with granulocyte colony-stimulating factor (G-CSF). Neutrophilia and hypercoagulability were observed at the time of angina pectoris. Recurrence of angina pectoris was not seen after nitrate and aspirin therapy. Exercise stress testing performed after PBSCT suggested the presence of myocardial ischaemia. Therefore cases at risk of vascular events should be carefully managed with prophylactic treatment during G-CSF administration.
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PMID:Angina pectoris occurring during granulocyte colony-stimulating factor-combined preparatory regimen for autologous peripheral blood stem cell transplantation in a patient with acute myelogenous leukaemia. 920 19

Coronary artery disease (CAD) is based on the atherosclerosis of coronary artery and may manifest with myocardial infarction or angina pectoris. Although it is widely accepted that genetic factors are linked to CAD and several disease-related genes have been reported, only a few could be replicated suggesting that there might be some other CAD-related genes. To identify novel susceptibility loci for CAD, we used microsatellite markers in the screening and found six different candidate CAD loci. Subsequent single nucleotide polymorphism (SNP) association studies revealed an association between CAD and megakaryoblastic leukemia factor-1 gene (MKL1). The association with a promoter SNP of MKL1, -184C > T, was found in a Japanese population and the association was replicated in another Japanese population and a Korean population. Functional analysis of the MKL1 promoter SNP suggested that the higher MKL1 expression was associated with CAD. These findings suggest that MKL1 is involved in the pathogenesis of CAD.
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PMID:Megakaryoblastic leukemia factor-1 gene in the susceptibility to coronary artery disease. 1951 52

The term "leukopenic myelosis" is used to describe a type of "myeloblastic leukaemia" in which the leukocyte content of the peripheral blood is subnormal for the whole or the greater part of the course of the disease. Separation from the frankly leukaemic cases is made only on the grounds of clinico-haematological convenience.Twenty-two cases have been seen in the past four years. The age-incidence varied from 3-73 years; 10 were in males and 12 in females. Acute, subacute, and chronic types may be recognized. In all the main characteristic is a progressive anaemia; in acute cases haemorrhagic phenomena and necrotic angina are common.The blood-count is characterized by orthochromic or hyperchromic anaemia, sometimes with reticulocytosis and erythroblastosis. Leukopenia may persist throughout the course, or a terminal leukaemia may occur-especially in the chronic cases. The features of the differential count are the presence of myeloblasts-although the percentage may be below 5%-and the hiatus leukaemicus. Thrombocytopenia usually means a rapid course.This clinico-haematological picture may be mimicked more or less closely by pernicious anaemia, aplastic anaemia, agranulocytosis, and the leuko-erythroblastic anaemias. The sternal puncture findings are, however, diagnostic, and show a great preponderance of primitive myeloid cells, most frequently with a predomincnce of myeloblasts. In two cases evidence was found that the erythropoietic tissues shared in the hyperplasia.
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PMID:Leukopenic Myelosis: (Section of Medicine). 1999 28

Gingival enlargement is common among patients and can be caused by a variety of etiological factors. The most common reason is poor oral hygiene and high bacterial load that leads to gingival inflammation and enlargement. Other implicated factors include systemic drugs, such as phenytoin (Dilantin) taken by epileptic patients, calcium channel blockers such as nifedipine (Procardia) and verapamil (Calan) for the treatment of hypertension, arrhythmia and angina. Another class of medication associated with gingival enlargement is immunosuppressive agents given to organ-transplant patients to prevent rejection of the new element such as cyclosporine. Some enlargements could be associated with other conditions such as puberty, pregnancy or diabetes or be a symptom of a systemic disease (leukemia, Wegener's granulomatosis or sarcoidosis). In rare cases the cause for the enlargement is genetic and termed hereditary gingival fibromatosis (HGF). HGF is a genetic disorder characterized by a progressive enlargement of the gingiva. Histologically, the gingiva is characterized by an accumulation of dense fibrous connective tissue. This is believed to be due to an imbalance between synthesis and degradation of extracellular matrix composed mainly of collagen molecules or due to an alteration in fibroblast proliferation. Different pathogenic mechanisms have been proposed and examined over the years but no precise process has been identified. The main objective of this paper is to discuss this genetic anomaly and support it with clinical cases of a mother and her two children. It will focus on the clinical and histologic characteristics of HGF as well as known biologic and genetic features and treatment modalities.
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PMID:Gummy smile: could it be genetic? Hereditary gingival fibromatosis. 2287 May 49

Gingival enlargement is common among patients and can be caused by a variety of etiological factors. The most common reason is poor oral hygiene and high bacterial load that leads to gingival inflammation and enlargement. Other implicated factors include systemic drugs, such as Phenytoin (Dilantin) taken by epileptic patients, Calcium Channel Blockers such as Nifedipine (Procardia) and Verapamil (Calan) for the treatment of hypertension, arrhythmia and angina. Another class of medication associated with gingival enlargement is immunosuppressive agents given to organ-transplant patients to prevent rejection of the new element, such as Cyclosporine. Some enlargements could be associated with other conditions such as puberty, pregnancy or diabetes or be a symptom of a systemic disease (leukemia, Wegener's granulomatosis or sarcoidosis). In rare cases the cause for the enlargement is genetic and termed Hereditary Gingival Fibromatosis (HGF). HGF is a genetic disorder characterized by a progressive enlargement of the gingiva. Histologically, the gingiva is characterized by an accumulation of dense fibrous connective tissue. This is believed to be due to an imbalance between synthesis and degradation of extracellular matrix composed mainly of collagen molecules or due to an alteration in fibroblast proliferation. Different pathogenic mechanisms have been proposed and examined over the years but no precise process has been identified. The main objective of this paper is to discuss this genetic anomaly and support it with clinical cases of a mother and her two children. It will focus on the clinical and histologic characteristics of HGF as well as known biologic and genetic features and treatment modalities.
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PMID:Gummy smile: could it be genetic? Hereditary gingival fibromatosis. 2334 94

Amlodipine (AD) is a calcium channel blocker that is mainly used in the treatment of hypertension and angina. However, latest findings have revealed that its efficacy is not only limited to the treatment of cardiovascular diseases as it has shown to possess antioxidant activity and plays an important role in apoptosis. Therefore, it is also employed in the treatment of cerebrovascular stroke, neurodegenerative diseases, leukemia, breast cancer, and so forth either alone or in combination with other drugs. AD is a photosensitive drug and requires protection from light. A number of workers have tried to formulate various conventional and nonconventional dosage forms of AD. This review highlights all the formulations that have been developed to achieve maximum stability with the desired therapeutic action for the delivery of AD such as fast dissolving tablets, floating tablets, layered tablets, single-pill combinations, capsules, oral and transdermal films, suspensions, emulsions, mucoadhesive microspheres, gels, transdermal patches, and liposomal formulations.
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PMID:Formulations of Amlodipine: A Review. 2782 2