Gene/Protein Disease Symptom Drug Enzyme Compound
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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

The authors report two cases of acute myocarditis due to Staphylococcus aureus in patients with AIDS. There was no history of opportunist infections in either case but the CD4 lymphocyte levels were very low. The myocarditis caused acute cardiac failure and death. Histological examination showed microabscesses filled with Gram positive cocci throughout the myocardium. Bacteriological studies identified the Staphylococcus aureus. Staphylococcus aureus myocarditis without endocardial or pericardial involvement is very rare. It is the result of septic emboli in the cardiac microcirculation. Bacterial myocarditis has rarely been diagnosed in HIV positive patients. Both our cases featured severe cell-mediated immunodeficiency without associated neutropaenia. The decreased bactericidal activity of the neutrophil polynuclears and/or a deficit in the immunity mediated by the B-cell lymphocytes in AIDS could explain the lethal septic complications observed in our two cases.
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PMID:[Acute Staphylococcus aureus myocarditis in AIDS. 2 cases]. 802 79

We studied 124 homosexual men aged 36.7 +/- 7.6 years (range 23-57) using Doppler echocardiography. One hundred and one patients (Group A) had had acquired immunodeficiency syndrome for 1.6 +/- 1.0 years and 23 patients (Group B) had had HIV infection without opportunistic infections for 3.2 +/- 2.3 years. Doppler echocardiography was normal in 31% of Group A patients and in 61% of Group B. Pericardial effusion was found in 44 Group A patients (44%) and two Group B patients (9%). In Group A, left ventricular dilatation and/or dysfunction were found in 20 patients (20%), aortic root dilatation and regurgitation in eight patients (8%) and an intracardiac echogenic mass in seven patients (7%); in Group B one patient (4%) had an intracardiac mass. Forty-four (44%) Group A patients had cardiac presentations, and of these 22 had cardiomegaly with clinical signs of heart failure; 10 patients had tachyarrhythmias compared to only two in Group B. Although the CD4 lymphocyte count (%) was significantly lower in Group A than in Group B (5.4 +/- 6.1 vs 13.3 +/- 7.3, P < 0.001), the presence of pericardial effusion, left ventricular dysfunction, right-sided cardiac enlargement or the duration of HIV infection, did not relate to the CD4 level in either group. Although often not diagnosed clinically, cardiac involvement in patients with AIDS is a clinical reality, with pericardial effusion, cardiomyopathy and left ventricular dysfunction appearing to have a high prevalence in male homosexual patients with AIDS. These clinical and echocardiographic findings are associated with clinically apparent intercurrent opportunistic infections, rather than the HIV virus per se, or the severity of infection as reflected by the CD4 count.
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PMID:Emerging patterns of heart disease in HIV infected homosexual subjects with and without opportunistic infections; a prospective colour flow Doppler echocardiographic study. 817 86

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

As more effective therapies have produced longer survival times for HIV-infected patients, non-infectious complications of late stage HIV infection such as the development of severe global left ventricular dysfunction (dilated heart muscle disease) have emerged. The demographic and clinical characteristics of HIV-infected patients who develop dilated heart muscle disease as well as potential risk factors are, as yet, poorly characterized. Of 174 patients enrolled in a prospective longitudinal study, a total of nine patients, all with CD4 T cell counts < 200 mm-3, developed symptomatic heart disease (congestive heart failure n = 7, sudden cardiac death n = 1 and cardiac tamponade n = 1); three of these patients developed progressive cardiac dysfunction leading to primary cardiac failure and death. An additional 55 HIV-infected patients referred to our Cardiomyopathy Service were found to have global left ventricular dysfunction, with 84% having New York Heart Association Class III or IV congestive heart failure on presentation. Clinical characteristics associated with severe symptomatic cardiac dysfunction included low CD4 T cell counts, myocarditis associated with non-permissive cardiotropic virus infection on endomyocardial biopsy and persistent elevation of anti-heart antibodies. No relationships to any specific HIV risk factor or opportunistic infection were found. These findings suggest that a severe form of HIV-related dilated heart muscle disease is largely a disease of late stage HIV infection. Virus-related myocarditis and cardiac autoimmunity may play a role in the pathogenesis of progressive cardiac injury. Long-term longitudinal studies of larger HIV-infected cohorts are warranted to identify clinical, behavioral and immunologic risk factors.
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PMID:Dilated heart muscle disease associated with HIV infection. 868 2

A 70 year old patient with a past history of a left ventricular cardiomyopathy with concentric hypertrophy presented with an exacerbation of cardiac failure; radiology revealed bilateral lung infiltrations, predominantly on the right and a restrictive ventilatory disorder. The broncho-alveolar lavage revealed a lymphocytosis with CD4 prominence. Microbiological examination was negative. With a worsening radiological picture despite increased anti-failure treatment a video-assisted surgical biopsy was performed. The histological examination revealed diffuse interstitial pulmonary amyloidosis. This observation underlined the value of looking for this rare cause of cardiac failure and pulmonary infiltration in a situation where the pulmonary images did not improve on diuretics.
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PMID:[An unusual case of cardiac insufficiency]. 903 4


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