Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old man, who came from Kagoshima prefecture, was hospitalized because of lumbago and lymphadenopathy. On admission, mild anemia and leukocytosis with atypical lymphoid cells were seen in the peripheral blood. Flow cytometry of the abnormal lymphocytes showed that they expressed CD4, and CD25, but not CD8. Anti HTLV I antibody was expressed in the serum. Atypical lymphoid cells had proviral DNA with restriction enzyme EcoRI. Lymphnode biopsy was performed and the specimens of lymphnode showed diffuse infiltration of abnormal lymphocytes. So we diagnosed Adult T-cell leukemia lymphoma. The patient's serum calcium level was increased, so he lost consciousness and became oliguric and developed acute renal failure. Hemodialysis was required to control azotemia. During the time of hemodialysis, cardiac arrest was occurred and he died. Autopsy confirmed the presence of a metastatic calcification in various organs, such as myocardium, alveolar septa of the lungs, and gastric mucosa. A metastatic calcinosis was found in the myocardium, which was thought to be the cause of his heart failure. But at the ATLL cells didn't infiltrate in the myocardium. Calcinosis was a significant complication of neoplastic disease in these patients and contributed to morbidity and mortality.
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PMID:[Adult T-cell leukemia lymphoma with metastatic calcification]. 192 Aug 88

A 65-year-old man with idiopathic myocarditis is described. He was admitted with symptoms of acute heart failure. Examination revealed left ventricular hypokinesis. Results of an endomyocardial biopsy showed "resolving myocarditis". Immunological studies of the peripheral blood showed a low helper-suppressor (CD4/CD8) ratio on admission and depressed natural killer (NK) cell activity coincident with the onset of myocarditis. We considered that this immunological imbalance may have occurred during the progression of myocarditis to dilated cardiomyopathy.
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PMID:Idiopathic myocarditis associated with T-cell subset changes and depressed natural killer activity. 212 66

Establishing the diagnosis of drug-induced pneumonitis is always difficult and requires that the following criteria be met: administration of the drug on a long-term basis; knowledge that the drug is able to induce pulmonary disorders; occurrence during therapy of interstitial pneumonitis with clinical, radiological and functional characteristics of this type of lung disease; exclusion of all other causes of interstitial pneumonitis (cardiac failure, infections, collagen vascular diseases, malignancies); bronchoalveolar lavage specimen, revealing lymphocytosis with an inverted CD4/CD8 lymphocyte ratio, isolated or associated with neutrophil and/or eosinophil alveolitis; finally, full recovery within several weeks or months after drug withdrawal unless irreversible pulmonary fibrosis has occurred. Certain specific characteristics correspond to the therapeutic class of the drug, i.e. antimicrobial, cardiovascular, antiinflammatory, neurological, metabolic, antiallergy or some other drugs.
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PMID:[Drug-induced pneumopathies (excluding cytostatic drugs)]. 261 Apr 52

In a total of 22 failing hearts from human transplant recipients, the expression of major histocompatibility complex (MHC) molecules, the CD phenotype of infiltrating mononuclear cells, and the number of fibroblasts were analyzed by immunohistochemistry. Compared with 10 non-failing control hearts, significantly higher morphometric area fractions of HLA-ABC and HLA-DR with a concomitant increase of CD3-, CD4- and CD8-positive cells were found to be comparable in 12 patients with idiopathic dilated cardiomyopathy and in 10 patients with secondary heart failure. Furthermore, the similarity of T-cell activation in idiopathic and secondary variants of the disease were substantiated by the following observations: (1) the site-specific distribution of MHC molecules and mononuclear cells in the myocardium was comparable in idiopathic and secondary dilated cardiomyopathy; (2) 6 individuals with lymphocytic aggregates in their myocardium in association with the highest levels of HLA-ABC expression were equally distributed among idiopathic and secondary patient subsets; and (3) expression of HLA-ABC and HLA-DR correlated with that of an endothelial cell marker, von Willebrand factor, in failing myocardia of both study groups. In conclusion, no difference was found in increased MHC molecule expression in failing myocardium of idiopathic and secondary variants of dilated cardiomyopathy, and these entities were not differentially associated with infiltration by increased numbers of T lymphocytes. Hence, we postulate that these immunopathological features are consequences rather than causative factors of myocardial degeneration and dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endomyocardial HLA expression is increased to the same extent in idiopathic and secondary dilated cardiomyopathy. 795 4

A 41-year-old patient with chronic myelogenous leukemia in the accelerated phase was treated with mitoxantrone. She developed pyrexia 7 days after receiving the third administration of mitoxantrone. After 3 more days, she experienced dry cough and dyspnea. Bilateral fine crackles were audible, but no signs of heart failure were found. A chest X-ray film revealed diffuse reticulogranular infiltrates bilaterally. An increase in the prednisolone dosage led to an improvement. Specimens of the bronchoalveolar lavage revealed an increase in CD4-/CD8- lymphocytes. The peripheral lymphocytes also expressed neither CD4 nor CD8. Specimens of a transbronchial lung biopsy disclosed thickening of the alveolar wall with infiltration of lymphoid cells.
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PMID:Interstitial pneumonitis possibly due to mitoxantrone. 829 77

A 26 year old Japanese male who had a history of leukocytosis in 1985 and received chemotherapy because of myeloblastic crisis of chronic myelogenous leukemia (CML) from May 1986, was admitted in November 1987. He had lymphadenopathy, lymphoid tumor of paranasal sinus and pleural effusion with marked lymphoid cells infiltration. On admission, laboratory data of peripheral blood and bone marrow revealed remission; lymphoid cells of pleural effusion were positive for CD3, CD4 and CD8. Second induction chemotherapy was performed successfully. After a few months, however, myeloblastic crisis recurred. Intensive chemotherapy ended in failure and he died of renal and heart failure. Chromosome analysis showed Ph1 and additional abnormalities at myeloblastic crisis and normal at T lymphoid crisis, but the same rearrangement of breakpoint cluster region existed in both crisis cells. Therefore we supposed that more than two-step pathogenesis is involved in the development of Ph1 positive or Ph1 negative CML clone of this patient.
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PMID:[Ph1 positive myeloblastic crisis followed by Ph1 negative, bcr rearrangement positive T lymphoid crisis in a CML case]. 847 87

Peripartum cardiomyopathy is a classic but uncommon entity in African women about which there is little etiologic understanding. From January 1990 to March 1996 a series of 30 cases of peripartum cardiomyopathy was collected at the Principal Hospital in Dakar, Senegal. Peripartum cardiomyopathy was defined as the occurrence of cardiac insufficiency in a woman with no previous history of heart disease, during the period between the second and twentieth weeks after delivery confirmed by ultrasound evidence of dilated cardiomyopathy. The overall incidence of peripartum cardiomyopathy during the study period was 30 out of 1200 deliveries. The mean age of the women in the study was 34 years and mean parity was 5.2. In 13.3% of cases births involved twins. There were no predisposing socio-economic or climatic factors. The clinical picture was severe cardiac failure in 80.3% of cases and left ventricular insufficiency in 16.6%. In all cases ultrasound findings were typical of dilated cardiomyopathy. Serum selenium and vitamin B1 levels were normal. Measurements of T CD4 and CD8 in eight patients were normal. Conversion enzyme inhibitors were administered to twenty patients. Complete remission was achieved in 14 patients, three patients died, and thirteen patients presented ultrasonic evidence of persistent dilated cardiomyopathy. One patient relapsed after a subsequent delivery. These findings are in agreement with previous reports concerning the clinical and prognostic features of peripartum cardiomyopathy in Africa.
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PMID:[Etiopathogenic, ultrasonographic and prognostic features of postpartum cardiomyopathy]. 913 97

Sphingolipids and their metabolic products are now known to have second-messenger functions in a variety of cellular signaling pathways. Lactosylceramide (LacCer), a glycosphingolipid (GSL) present in vascular cells such as endothelial cells, smooth muscle cells, macrophages, neutrophils, platelets, and monocytes, contributes to atherosclerosis. Large amounts of LacCer accumulate in fatty streaks, intimal plaque, and calcified intimal plaque, along with oxidized low density lipoproteins (Ox-LDLs), growth factors, and proinflammatory cytokines. A possible role for LacCer in vascular cell biology was suggested when this GSL was found to stimulate the proliferation in vitro of aortic smooth muscle cells (ASMCs). A further link of LacCer in atherosclerosis was uncovered by the finding that Ox-LDLs stimulated specifically the biosynthesis of LacCer. Ox-LDL-stimulated endogenous synthesis of LacCer by activation of UDP-Gal:GlcCer,beta1-4galtransferase (GalT-2) is an early step in this signaling pathway. In turn, LacCer serves as a lipid second messenger that orchestrates a signal transduction pathway, ultimately leading to cell proliferation. This signaling pathway includes LacCer-mediated activation of NADPH oxidase that produces superoxide. Such superoxide molecules stimulate the GTP loading of p21(ras). Subsequently, the kinase cascade (Raf-1, Mek2, and p44MAPK [mitogen-activated protein kinase]) is activated. The phosphorylated form of p44MAPK translocates from the cytoplasm to the nucleus and engages in c-fos expression, proliferating cell nuclear antigen (PCNA) such as cyclin activation, and cell proliferation takes place. Interestingly, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, can abrogate the Ox-LDL-mediated activation of GalT-2, the signal kinase cascade noted above, as well as cell proliferation. Additional studies have revealed that LacCer mediates the tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor-kappaB expression and intercellular adhesion molecule (ICAM-1) expression in vascular endothelial cells via the redox-dependent transcriptional pathway. LacCer also stimulates the expression of CD11/CD8, or Mac-1, on the surface of human neutrophils. Collectively, this phenomenon may contribute to the adhesion of neutrophils or monocytes to the endothelial cell surface and thus initiate the process of atherosclerosis. In addition, the LacCer-mediated proliferation of ASMCs may contribute to the progression of atherosclerosis. On the other hand, programmed cell death (apoptosis) by proinflammatory cytokines such as TNF-alpha, interleukin-1, and high concentrations of Ox-LDL occur via activation of a cell membrane-associated neutral sphingomyelinase (N-SMase). N-SMase hydrolyzes sphingomyelin into ceramide and phosphocholine. In turn, ceramide or a homologue serves as an important stress-signaling molecule. Interestingly, an antibody against N-SMase can abrogate Ox-LDL- and TNF-alpha-induced apoptosis and therefore may be useful for in vivo studies of apoptosis in experimental animals. Because plaque stability is an integral aspect of atherosclerosis management, activation of N-SMase and subsequent apoptosis may be vital events in the onset of plaque rupture, stroke, or heart failure. Interestingly, in human liver cells, N-SMase action mediates the TNF-alpha-induced maturation of the sterol regulatory-element binding protein. Moreover, a cell-permeable ceramide can reconstitute the phenomenon above in a sterol-independent fashion. Such findings may provide new avenues for therapy for patients with atherosclerosis. The findings described here indicate an important role for sphingolipids in vascular biology and provide an exciting opportunity for further research in vascular disease and atherosclerosis.
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PMID:Sphingolipids in atherosclerosis and vascular biology. 976 22

Viral myocarditis is an important cause of heart failure and dilated cardiomyopathy. T lymphocytes are implicated in myocardial damage in murine models of coxsackievirus B3 (CVB3) myocarditis. We used knockout mice lacking CD4 (CD4(-/-)), CD8 (CD8(-/-)), both coreceptors (CD4(-/-)CD8(-/-)), or the T-cell receptor beta chain (TCRbeta(-/-)) to address the contribution of T-cell subpopulations to host susceptibility to CVB3 myocarditis. Severity of disease was magnified in CD8(-/-) mice but attenuated in CD4(-/-) mice, consistent with a pathogenic role for CD4(+) lymphocytes. Elimination of both CD4 and CD8 molecules from T lymphocytes by genetic knockout better protected mice from myocarditis, demonstrating that both CD4(+) and CD8(+) T cells contribute to host susceptibility. The same benefit occurred in TCRbeta(-/-) mice, with prolonged survival and minimal myocardial disease observed after CVB3 infection. Elevated interferon-gamma and decreased tumor necrosis factor-alpha expression are associated with attenuated myocardial damage in CD4(-/-)CD8(-/-) mice. These results show that the presence of TCRalphabeta(+) T cells enhances host susceptibility to myocarditis. The severity of myocardial damage and associated mortality are dependent on the predominant T-cell type available to respond to CVB3 infection. One mechanism by which CD4(+) and CD8(+) T-cell subsets influence the pathogenesis of myocarditis may involve specific cytokine expression patterns.
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PMID:Susceptibility to myocarditis is dependent on the response of alphabeta T lymphocytes to coxsackieviral infection. 1048 59

Periodontitis, a prime cause of tooth loss in humans, is implicated in the increased risk of systemic diseases such as heart failure, stroke, and bacterial pneumonia. The mechanisms by which periodontitis and antibacterial immunity lead to alveolar bone and tooth loss are poorly understood. To study the human immune response to specific periodontal infections, we transplanted human peripheral blood lymphocytes (HuPBLs) from periodontitis patients into NOD/SCID mice. Oral challenge of HuPBL-NOD/SCID mice with Actinobacillus actinomycetemcomitans, a well-known Gram-negative anaerobic microorganism that causes human periodontitis, activates human CD4(+) T cells in the periodontium and triggers local alveolar bone destruction. Human CD4(+) T cells, but not CD8(+) T cells or B cells, are identified as essential mediators of alveolar bone destruction. Stimulation of CD4(+) T cells by A. actinomycetemcomitans induces production of osteoprotegerin ligand (OPG-L), a key modulator of osteoclastogenesis and osteoclast activation. In vivo inhibition of OPG-L function with the decoy receptor OPG diminishes alveolar bone destruction and reduces the number of periodontal osteoclasts after microbial challenge. These data imply that the molecular explanation for alveolar bone destruction observed in periodontal infections is mediated by microorganism-triggered induction of OPG-L expression on CD4(+) T cells and the consequent activation of osteoclasts. Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis.
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PMID:Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection. 1099 85


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